1
40
328
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.09.021</a>
Pages
10–19
Volume
101
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
4-Hydroxynonenal dependent alteration of TRPV1-mediated coronary microvascular signaling.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*4-Hydroxynonenal; *Coronary regulation; *Lipid peroxidation; *Post-translational modification; *Protein Processing; *Reactive oxygen species; *Signal Transduction; *TRPV1; Action Potentials/drug effects; Aldehydes/antagonists & inhibitors/metabolism/*pharmacology; Animal; Animals; Blood Flow Velocity; Calcium Signaling/drug effects; Capsaicin/*pharmacology; Cardiovascular Agents/*pharmacology; Coronary Circulation/drug effects; Coronary Vessels/metabolism/physiopathology; Cysteine/genetics/metabolism; Diabetes Mellitus/drug therapy/*metabolism/physiopathology; Disease Models; Femoral Artery/metabolism/physiopathology; HEK293 Cells; Humans; Inbred C57BL; Lipid Peroxidation; Male; Mice; Patch-Clamp Techniques; Post-Translational; TRPV Cation Channels/genetics/*metabolism; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Sinharoy Pritam; Connell Patrick J; Fahmy Joseph N; Cappelli Holly C; Thodeti Charles K; Geldenhuys Werner J; Damron Derek S; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent regulation of coronary blood flow (CBF) is disrupted in diabetes. Further, we have shown that endothelial TRPV1 is differentially regulated, ultimately leading to the inactivation of TRPV1, when exposed to a prolonged pathophysiological oxidative environment. This environment has been shown to increase lipid peroxidation byproducts including
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.09.021</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*4-Hydroxynonenal
*Coronary regulation
*Lipid peroxidation
*Post-translational modification
*Protein Processing
*Reactive oxygen species
*Signal Transduction
*TRPV1
2016
Action Potentials/drug effects
Aldehydes/antagonists & inhibitors/metabolism/*pharmacology
Animal
Animals
Blood Flow Velocity
Bratz Ian N
Calcium Signaling/drug effects
Cappelli Holly C
Capsaicin/*pharmacology
Cardiovascular Agents/*pharmacology
Connell Patrick J
Coronary Circulation/drug effects
Coronary Vessels/metabolism/physiopathology
Cysteine/genetics/metabolism
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetes Mellitus/drug therapy/*metabolism/physiopathology
Disease Models
Fahmy Joseph N
Femoral Artery/metabolism/physiopathology
Free radical biology & medicine
Geldenhuys Werner J
HEK293 Cells
Humans
Inbred C57BL
Lipid Peroxidation
Male
Mice
NEOMED College of Medicine
Patch-Clamp Techniques
Post-Translational
Sinharoy Pritam
Thodeti Charles K
TRPV Cation Channels/genetics/*metabolism
Vasodilation/drug effects
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.115.306590" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.115.306590</a>
Pages
1729–1731
Issue
11
Volume
116
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A bouquet for a broken heart: can flowers repair a damaged heart?
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-05
Subject
The topic of the resource
angiogenesis; Animals; coronary vessels; Coronary Vessels/*physiopathology; Editorials; endocardium; Endocardium/*physiopathology; endothelial cells; Endothelium; myocardial infarction; Myocardial Infarction/*physiopathology; Vascular/*physiopathology
Creator
An entity primarily responsible for making the resource
Thodeti Charles K
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.115.306590" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.115.306590</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
angiogenesis
Animals
Circulation research
Coronary Vessels
Coronary Vessels/*physiopathology
Department of Integrative Medical Sciences
Editorials
endocardium
Endocardium/*physiopathology
endothelial cells
Endothelium
myocardial infarction
Myocardial Infarction/*physiopathology
NEOMED College of Medicine
Thodeti Charles K
Vascular/*physiopathology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/ATVBAHA.114.303929" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.114.303929</a>
Pages
1854–1859
Issue
9
Volume
34
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A brief etymology of the collateral circulation.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-09
Subject
The topic of the resource
*Cardiology; *Collateral Circulation/physiology; *Terminology as Topic; Blood Vessels/embryology/growth & development; collateral circulation; Humans; myocardial ischemia; Neovascularization; peripheral arterial disease; Physiologic/physiology; stroke
Creator
An entity primarily responsible for making the resource
Faber James E; Chilian William M; Deindl Elisabeth; van Royen Niels; Simons Michael
Description
An account of the resource
It is well known that the protective capacity of the collateral circulation falls short in many individuals with ischemic disease of the heart, brain, and lower extremities. In the past 15 years, opportunities created by molecular and genetic tools, together with disappointing outcomes in many angiogenic trials, have led to a significant increase in the number of studies that focus on: understanding the basic biology of the collateral circulation; identifying the mechanisms that limit the collateral circulation's capacity in many individuals; devising methods to measure collateral extent, which has been found to vary widely among individuals; and developing treatments to increase collateral blood flow in obstructive disease. Unfortunately, accompanying this increase in reports has been a proliferation of vague terms used to describe the disposition and behavior of this unique circulation, as well as the increasing misuse of well-ensconced ones by new (and old) students of collateral circulation. With this in mind, we provide a brief glossary of readily understandable terms to denote the formation, adaptive growth, and maladaptive rarefaction of collateral circulation. We also propose terminology for several newly discovered processes that occur in the collateral circulation. Finally, we include terms used to describe vessels that are sometimes confused with collaterals, as well as terms describing processes active in the general arterial-venous circulation when ischemic conditions engage the collateral circulation. We hope this brief review will help unify the terminology used in collateral research.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.114.303929" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.114.303929</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cardiology
*Collateral Circulation/physiology
*Terminology as Topic
2014
Arteriosclerosis, thrombosis, and vascular biology
Blood Vessels/embryology/growth & development
Chilian William M
Collateral Circulation
Deindl Elisabeth
Department of Integrative Medical Sciences
Faber James E
Humans
myocardial ischemia
NEOMED College of Medicine
Neovascularization
peripheral arterial disease
Physiologic/physiology
Simons Michael
stroke
van Royen Niels
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.00154.2018" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00154.2018</a>
Pages
H1262–H1263
Issue
6
Volume
314
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A chicken and egg conundrum: coronary microvascular dysfunction and heart failure with preserved ejection fraction.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-06
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn; Sisakian Hamayak; Peketi Punita; Parikh Ankur; Chilian William
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00154.2018" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00154.2018</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
American journal of physiology. Heart and circulatory physiology
Chilian William
Department of Integrative Medical Sciences
NEOMED College of Medicine
Ohanyan Vahagn
Parikh Ankur
Peketi Punita
Sisakian Hamayak
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/ncomms8466" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/ncomms8466</a>
Pages
7466–7466
Volume
6
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A metabolic stress-inducible miR-34a-HNF4alpha pathway regulates lipid and lipoprotein metabolism.
Publisher
An entity responsible for making the resource available
Nature communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-06
Subject
The topic of the resource
Animals; Apolipoproteins E/genetics; Atherosclerosis/genetics/metabolism; Diabetes Mellitus; Experimental/genetics/metabolism; Hep G2 Cells; Hepatocyte Nuclear Factor 4/*genetics/metabolism; Humans; Knockout; LDL/genetics; Lipid Metabolism/*genetics; Lipoproteins/metabolism; Liver/metabolism; Mice; MicroRNAs/*genetics/metabolism; Middle Aged; Non-alcoholic Fatty Liver Disease/*genetics/metabolism; Physiological/*genetics; Receptors; Stress; Triglycerides/*metabolism
Creator
An entity primarily responsible for making the resource
Xu Yang; Zalzala Munaf; Xu Jiesi; Li Yuanyuan; Yin Liya; Zhang Yanqiao
Description
An account of the resource
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases, but its underlying mechanism is poorly understood. Here we show that hepatocyte nuclear factor 4alpha (HNF4alpha), a liver-enriched nuclear hormone receptor, is markedly inhibited, whereas miR-34a is highly induced in patients with non-alcoholic steatohepatitis, diabetic mice and mice fed a high-fat diet. miR-34a is essential for HNF4alpha expression and regulates triglyceride accumulation in human and murine hepatocytes. miR-34a inhibits very low-density lipoprotein secretion and promotes liver steatosis and hypolipidemia in an HNF4alpha-dependent manner. As a result, increased miR-34a or reduced HNF4alpha expression in the liver attenuates the development of atherosclerosis in Apoe(-/-) or Ldlr(-/-) mice. These data indicate that the miR-34a-HNF4alpha pathway is activated under common conditions of metabolic stress and may have a role in the pathogenesis of NAFLD and in regulating plasma lipoprotein metabolism. Targeting this pathway may represent a novel approach for the treatment of NAFLD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/ncomms8466" target="_blank" rel="noreferrer noopener">10.1038/ncomms8466</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Animals
Apolipoproteins E/genetics
Atherosclerosis/genetics/metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus
Experimental/genetics/metabolism
Hep G2 Cells
Hepatocyte Nuclear Factor 4/*genetics/metabolism
Humans
Knockout
LDL/genetics
Li Yuanyuan
Lipid Metabolism/*genetics
Lipoproteins/metabolism
Liver/metabolism
Mice
MicroRNAs/*genetics/metabolism
Middle Aged
Nature communications
NEOMED College of Medicine
Non-alcoholic Fatty Liver Disease/*genetics/metabolism
Physiological/*genetics
Receptors
Stress
Triglycerides/*metabolism
Xu Jiesi
Xu Yang
Yin Liya
Zalzala Munaf
Zhang Yanqiao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1124/jpet.106.111369" target="_blank" rel="noreferrer noopener">http://doi.org/10.1124/jpet.106.111369</a>
Pages
877–884
Issue
2
Volume
320
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A noninflammatory interleukin-1beta fragment stimulates fetal lung fluid absorption in guinea pigs.
Publisher
An entity responsible for making the resource available
The Journal of pharmacology and experimental therapeutics
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-02
Subject
The topic of the resource
Absorption; Adrenergic; Adrenocorticotropic Hormone/blood; Animals; beta/analysis; Body Fluids/drug effects/metabolism; Epithelial Sodium Channels/genetics; Female; Fetus/drug effects; Guinea Pigs; Hydrocortisone/biosynthesis; Interleukin-1beta/*pharmacology; Lung/*drug effects/metabolism; Messenger/analysis; Oxytocin/pharmacology; Peptide Fragments/*pharmacology; Pregnancy; Receptors; RNA
Creator
An entity primarily responsible for making the resource
Li Tianbo; Varadarajulu Shilpa; Beard LaMonta L; Yun June; Folkesson Hans G
Description
An account of the resource
We have previously demonstrated that full-length interleukin (IL)-1beta can induce and stimulate lung fluid absorption in near-term guinea pig fetuses via stimulation of fetal cortisol synthesis and release. To develop a potentially clinically useful drug, we tested the hypothesis that maternal administration of a noninflammatory IL-1beta-fragment (IL-1beta(Fr)) induced cortisol synthesis and stimulated lung fluid absorption in preterm fetuses. IL-1beta(Fr) was administered s.c. daily to timed-pregnant guinea pigs for 3 days with and without simultaneous cortisol synthesis inhibition by metyrapone. Fetuses were obtained by abdominal hysterotomy at 61 and 68 days gestation and instilled with isosmolar 5% albumin into the lungs, and lung fluid absorption was measured over 1 h by mass balance. Lung fluid absorption was induced at 61 days and stimulated at 68 days gestation by IL-1beta(Fr), which both were attenuated by cortisol synthesis inhibition. Moreover, induction of labor by oxytocin stimulated lung fluid absorption at 61 days but had no stimulatory effect at 68 days gestation when given with the IL-1beta(Fr). Plasma adrenocorticotropin and cortisol concentrations were increased by IL-1beta(Fr) at 61 days gestation and remained high but unstimulated by IL-1beta(Fr) at 68 days gestation, and metyrapone always reduced cortisol concentrations. Prenatal lung fluid absorption, when present as well as IL-1beta(Fr)-induced, was always propranolol- and amiloride-sensitive, suggesting that beta-adrenoceptor stimulation and the epithelial Na(+) channel (ENaC) were critical for the induced/stimulated lung fluid absorption. ENaC expression was increased by IL-1beta(Fr) and attenuated by cortisol synthesis inhibition. Thus, our results suggest a potential clinical use of IL-1beta(Fr) therapeutically to induce lung fluid absorption in fetuses at risk of preterm delivery.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1124/jpet.106.111369" target="_blank" rel="noreferrer noopener">10.1124/jpet.106.111369</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2007
Absorption
Adrenergic
Adrenocorticotropic Hormone/blood
Animals
Beard LaMonta L
beta/analysis
Body Fluids/drug effects/metabolism
Department of Integrative Medical Sciences
Epithelial Sodium Channels/genetics
Female
Fetus/drug effects
Folkesson Hans G
Guinea Pigs
Hydrocortisone/biosynthesis
Interleukin-1beta/*pharmacology
Li Tianbo
Lung/*drug effects/metabolism
Messenger/analysis
NEOMED College of Medicine
Oxytocin/pharmacology
Peptide Fragments/*pharmacology
Pregnancy
Receptors
RNA
The Journal of pharmacology and experimental therapeutics
Varadarajulu Shilpa
Yun June
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1210/me.2009-0482" target="_blank" rel="noreferrer noopener">http://doi.org/10.1210/me.2009-0482</a>
Pages
1151–1164
Issue
6
Volume
24
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A novel bile acid-activated vitamin D receptor signaling in human hepatocytes.
Publisher
An entity responsible for making the resource available
Molecular endocrinology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-06
Subject
The topic of the resource
Calcitriol/*metabolism; Calcitriol/pharmacology; Cell Membrane/drug effects/metabolism; Cell Nucleus/drug effects/metabolism; Cholesterol 7-alpha-Hydroxylase/antagonists & inhibitors/genetics; Enzyme Activation/drug effects; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors; Genetic/genetics; Hep G2 Cells; Hepatocyte Nuclear Factor 4/metabolism; Hepatocytes/*drug effects/enzymology/*metabolism; Humans; Intracellular Space/drug effects/metabolism; Ligands; Lithocholic Acid/*pharmacology; Mitogen-Activated Protein Kinase Kinases/metabolism; Phosphorylation/drug effects; Phosphotyrosine/metabolism; Promoter Regions; Protein Kinase Inhibitors/pharmacology; Protein Transport/drug effects; Proto-Oncogene Proteins c-raf/metabolism; Receptors; Retinoid X Receptor alpha/metabolism; Signal Transduction/*drug effects; src-Family Kinases/metabolism; Steroid Hydroxylases/genetics/metabolism; Vitamin D3 24-Hydroxylase
Creator
An entity primarily responsible for making the resource
Han Shuxin; Li Tiangang; Ellis Ewa; Strom Stephen; Chiang John Y L
Description
An account of the resource
Vitamin D receptor (VDR) is activated by natural ligands, 1alpha,
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1210/me.2009-0482" target="_blank" rel="noreferrer noopener">10.1210/me.2009-0482</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Calcitriol/*metabolism
Calcitriol/pharmacology
Cell Membrane/drug effects/metabolism
Cell Nucleus/drug effects/metabolism
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/antagonists & inhibitors/genetics
Department of Integrative Medical Sciences
Ellis Ewa
Enzyme Activation/drug effects
Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors
Genetic/genetics
Han Shuxin
Hep G2 Cells
Hepatocyte Nuclear Factor 4/metabolism
Hepatocytes/*drug effects/enzymology/*metabolism
Humans
Intracellular Space/drug effects/metabolism
Li Tiangang
Ligands
Lithocholic Acid/*pharmacology
Mitogen-Activated Protein Kinase Kinases/metabolism
Molecular endocrinology (Baltimore, Md.)
NEOMED College of Medicine
Phosphorylation/drug effects
Phosphotyrosine/metabolism
Promoter Regions
Protein Kinase Inhibitors/pharmacology
Protein Transport/drug effects
Proto-Oncogene Proteins c-raf/metabolism
Receptors
Retinoid X Receptor alpha/metabolism
Signal Transduction/*drug effects
src-Family Kinases/metabolism
Steroid Hydroxylases/genetics/metabolism
Strom Stephen
Vitamin D3 24-Hydroxylase
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/mus.27191" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/mus.27191</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
ISSN
1097-4598 0148-639X
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1002/mus.27191" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1002/mus.27191</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
February 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Pediatrics
Department of Integrative Medical Science
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A Novel Exercise Testing Algorithm to Diagnose Mitochondrial Myopathy.
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-02-03
Subject
The topic of the resource
Cardiopulmonary exercise testing; Mitochondrial myopathy; Oxygen uptake (V&c.dotab;O2); Oxygen Uptake Efficiency Slope (OUES); V&c.dotab;O2 /Work slope
Creator
An entity primarily responsible for making the resource
Bhatia Rajeev;Cohen BH;McNinch N
Description
An account of the resource
INTRODUCTION: Oxygen uptake efficiency slope (OUES) is a non-invasive cardiopulmonary exercise testing (CPET) measurement based on oxygen uptake (V&c.dotab;O(2) ) and minute ventilation (V&c.dotab;(E) ) and is a marker of the efficiency of oxygen utilization by the body. However, it has not been studied in mitochondrial disorders. We explored noninvasive CPET parameters including OUES as a way to reliably diagnose mitochondrial myopathy. METHODS: We performed cycle ergometer maximal exercise testing on definite and suspected mitochondrial myopathy subjects (MM-D & MM-S) and their age and sex matched controls. OUES was corrected for body surface area (OUES/BSA) to eliminate the effect of body size. RESULTS: 40 participants [20 mitochondrial myopathy subjects {13 MM-D (6 males; aged 14-64 years) / 7 MM-S (5 males, aged 11-30 years} and 20 controls] completed the study. MM-D subjects showed lower aerobic fitness than controls. OUES/BSA was lower in MM-D subjects suggesting inefficient oxygen utilization. Area under the curve (AUC) and 95% Confidence Interval (CI) for OUES/BSA [0.91 (0.80, 1.00)], Peak V&c.dotab;O(2) % predicted [0.95 (0.86, 1.00)] and V&c.dotab;O(2) /Work slope [0.94 (0.85, 1.00)] showed excellent ability to diagnose mitochondrial myopathy in MM-D subjects. We applied a diagnostic approach based on the above parameters to MM-S subjects and their controls and were able to support or disprove the diagnosis of mitochondrial myopathy. DISCUSSION: We proposed and applied an approach based on the above three CPET parameters to reliably diagnose mitochondrial myopathy and found it to be clinically useful. This article is protected by copyright. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/mus.27191" target="_blank" rel="noreferrer noopener">10.1002/mus.27191</a>
Format
The file format, physical medium, or dimensions of the resource
journalArticle
Publisher
An entity responsible for making the resource available
Muscle & Nerve
2021
Bhatia Rajeev
Cardiopulmonary exercise testing
Cohen BH
Department of Integrative Medical Sciences
Department of Pediatrics
February 2021 List
journalArticle
McNinch N
Mitochondrial myopathy
Muscle & nerve
NEOMED College of Medicine
O2 /Work slope
O2)
Oxygen uptake (V&c.dotab
Oxygen Uptake Efficiency Slope (OUES)
V&c.dotab
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/RES.0000000000000311" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/RES.0000000000000311</a>
Pages
E106-E106
Issue
12
Volume
125
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1161/RES.0000000000000311" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1161/RES.0000000000000311</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
March 2020 Update
NEOMED College
NEOMED College of Medicine; NEOMED College of Graduate Studies
NEOMED Department
NEOMED Student Publications; NEOMED Student Publications; Department of Anatomy & Neurobiology; Department of Integrative Medical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A Novel Murine Model to Study Postnatal Coronary Collateral Growth by Lineage Tracing
Publisher
An entity responsible for making the resource available
Circulation Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-12
Creator
An entity primarily responsible for making the resource
Jamaiyar Anurag; Juguilon Cody; Richardson Devan; Gadd James; Wang Tao; Enrick Molly; Chilian William M; Yin Liya
Identifier
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<a href="http://doi.org/10.1161/RES.0000000000000311" target="_blank" rel="noreferrer noopener">10.1161/RES.0000000000000311</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Chilian William M
Circulation research
Department of Anatomy & Neurobiology
Department of Integrative Medical Sciences
Enrick Molly
Gadd James
Jamaiyar Anurag
Juguilon Cody
NEOMED College of Graduate Studies Student
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
NEOMED Student Publications
Richardson Devan
Wang Tao
Yin Liya
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/sctm.17-0046" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/sctm.17-0046</a>
Pages
1759–1766
Issue
9
Volume
6
Dublin Core
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Title
A name given to the resource
A Novel Role for CAMKK1 in the Regulation of the Mesenchymal Stem Cell Secretome.
Publisher
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Stem cells translational medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-09
Subject
The topic of the resource
Calcium/calmodulin-dependent protein kinase kinase-1; Cardiac disease; Cardiac regeneration; Mesenchymal stem cells; Secretome
Creator
An entity primarily responsible for making the resource
Dong Feng; Patnaik Shyam; Duan Zhong-Hui; Kiedrowski Matthew; Penn Marc S; Mayorga Maritza E
Description
An account of the resource
Transplantation of adult stem cells into myocardial tissue after acute myocardial infarction (AMI), has been shown to improve tissue recovery and prevent progression to ischemic cardiomyopathy. Studies suggest that the effects of mesenchymal stem cells (MSC) are due to paracrine factors released by MSC, as the benefits of MSC can be achieved through delivery of conditioned media (CM) alone. We previously demonstrated that downregulation of Dab2 enhances MSC cardiac protein expression and improves cardiac function after AMI following MSC engraftment. In order to define the molecular mechanisms that regulate MSC secretome, we analyzed gene arrays in MSC following downregulation of Dab2 via TGFbeta1 pretreatment or transfection with Dab2:siRNA or miR-145. We identified 23 genes whose expressions were significantly changed in all three conditions. Among these genes, we have initially focused our validation and functional work on calcium/calmodulin-dependent protein kinase kinase-1 (CAMKK1). We quantified the effects of CAMKK1 overexpression in MSC following injection of CM after AMI. Injections of CM from MSC with CAMKK1 over-expression correlated with an increase in vascular density (CAMKK1 CM: 2,794.95 +/- 44.2 versus Control: 1,290.69 +/- 2.8 vessels/mm(2) ) and decreased scar formation (CAMKK1 CM 50% +/- 3.2% versus Control: 28% +/- 1.4%), as well as improved cardiac function. Direct overexpression of CAMKK1 in infarcted tissue using a CAMKK1-encoding plasmid significantly improved ejection fraction (CAMKK1: 83.2% +/- 5.4% versus saline: 51.7% +/- 5.8%. Baseline: 91.3% +/- 4.3%) and decreased infarct size after AMI. Our data identify a novel role for CAMKK1 as regulator of the MSC secretome and demonstrate that direct overexpression of CAMKK1 in infarcted cardiac tissue, results in therapeutic beneficial effects. Stem Cells Translational Medicine 2017;6:1759-1766.
Identifier
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<a href="http://doi.org/10.1002/sctm.17-0046" target="_blank" rel="noreferrer noopener">10.1002/sctm.17-0046</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Calcium/calmodulin-dependent protein kinase kinase-1
Cardiac disease
Cardiac regeneration
Department of Integrative Medical Sciences
Dong Feng
Duan Zhong-Hui
Kiedrowski Matthew
Mayorga Maritza E
Mesenchymal stem cells
NEOMED College of Medicine
Patnaik Shyam
Penn Marc S
Secretome
Stem cells translational medicine
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1053/j.gastro.2007.08.042" target="_blank" rel="noreferrer noopener">http://doi.org/10.1053/j.gastro.2007.08.042</a>
Pages
1660–1669
Issue
5
Volume
133
Dublin Core
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Title
A name given to the resource
A novel role of transforming growth factor beta1 in transcriptional repression of human cholesterol 7alpha-hydroxylase gene.
Publisher
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Gastroenterology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-11
Subject
The topic of the resource
Bile Acids and Salts/metabolism; Carcinoma; Cell Line; Cells; Cholesterol 7-alpha-Hydroxylase/*genetics/*metabolism; Cultured; Enzyme Inhibitors/pharmacology; Genetic/drug effects/*physiology; Hepatocellular/*metabolism/pathology; Hepatocyte Nuclear Factor 4/metabolism; Hepatocytes/drug effects/*metabolism/pathology; Humans; Hydroxamic Acids/pharmacology; Liver Neoplasms/*metabolism/pathology; Messenger/metabolism; RNA; Signal Transduction/physiology; Smad3 Protein/metabolism; Transcription; Transforming Growth Factor beta1/*metabolism; Tumor
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chiang John Y L
Description
An account of the resource
BACKGROUND & AIMS: Inhibition of cholesterol 7alpha-hydroxylase (CYP7A1) by bile acids and inflammatory cytokines provides an important mechanism to protect hepatocytes from bile acid toxicity during cholestasis. Transforming growth factor beta1 (TGFbeta1) released by hepatic stellate cells during chronic liver injury plays a critical role in liver inflammation and fibrogenesis. The objective of this study is to investigate the role of TGFbeta1 in hepatic bile acid synthesis. METHODS: mRNA expressions in primary human hepatocytes and HepG2 cells were measured by quantitative real-time polymerase chain reaction. Reporter assay, glutathione-S-transferase pull-down assay, adenovirus-mediated gene transduction, and chromatin immunoprecipitation assay were used to study the mechanism of TGFbeta1 regulation of CYP7A1 gene transcription. RESULTS: TGFbeta1 inhibited the mRNA expression of CYP7A1 and bile acid synthesis in HepG2 cells and primary human hepatocytes. Mothers against decapentaplegic homolog (Smad3) inhibited both CYP7A1 promoter activity and mRNA expression by inhibiting
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1053/j.gastro.2007.08.042" target="_blank" rel="noreferrer noopener">10.1053/j.gastro.2007.08.042</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2007
Bile Acids and Salts/metabolism
Carcinoma
Cell Line
Cells
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics/*metabolism
Cultured
Department of Integrative Medical Sciences
Enzyme Inhibitors/pharmacology
Gastroenterology
Genetic/drug effects/*physiology
Hepatocellular/*metabolism/pathology
Hepatocyte Nuclear Factor 4/metabolism
Hepatocytes/drug effects/*metabolism/pathology
Humans
Hydroxamic Acids/pharmacology
Li Tiangang
Liver Neoplasms/*metabolism/pathology
Messenger/metabolism
NEOMED College of Medicine
RNA
Signal Transduction/physiology
Smad3 Protein/metabolism
Transcription
Transforming Growth Factor beta1/*metabolism
Tumor
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/nature10111" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/nature10111</a>
Pages
506–510
Issue
7352
Volume
474
Dublin Core
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Title
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A nuclear-receptor-dependent phosphatidylcholine pathway with antidiabetic effects.
Publisher
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Nature
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-06-23
Subject
The topic of the resource
BILE acids; HOMEOSTASIS; HYPOGLYCEMIC agents; INSULIN resistance; LABORATORY mice; LECITHIN; TRIGLYCERIDES
Creator
An entity primarily responsible for making the resource
Lee Jae Man; Lee Yoon-Kwang; Mamrosh Jennifer L; Busby Scott A; Griffin Patrick R; Pathak Manish C; Ortlund Eric A; Moore David D
Description
An account of the resource
Nuclear hormone receptors regulate diverse metabolic pathways and the orphan nuclear receptor LRH-1 (also known as NR5A2) regulates bile acid biosynthesis. Structural studies have identified phospholipids as potential LRH-1 ligands, but their functional relevance is unclear. Here we show that an unusual phosphatidylcholine species with two saturated 12 carbon fatty acid acyl side chains (dilauroyl phosphatidylcholine (DLPC)) is an LRH-1 agonist ligand in vitro. DLPC treatment induces bile acid biosynthetic enzymes in mouse liver, increases bile acid levels, and lowers hepatic triglycerides and serum glucose. DLPC treatment also decreases hepatic steatosis and improves glucose homeostasis in two mouse models of insulin resistance. Both the antidiabetic and lipotropic effects are lost in liver-specific Lrh-1 knockouts. These findings identify an LRH-1 dependent phosphatidylcholine signalling pathway that regulates bile acid metabolism and glucose homeostasis. [ABSTRACT FROM AUTHOR]
Identifier
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<a href="http://doi.org/10.1038/nature10111" target="_blank" rel="noreferrer noopener">10.1038/nature10111</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2011
BILE acids
Busby Scott A
Department of Integrative Medical Sciences
Griffin Patrick R
Homeostasis
HYPOGLYCEMIC agents
Insulin Resistance
LABORATORY mice
LECITHIN
Lee Jae Man
Lee Yoon-Kwang
Mamrosh Jennifer L
Moore David D
Nature
NEOMED College of Medicine
Ortlund Eric A
Pathak Manish C
triglycerides
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/mc.20305" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/mc.20305</a>
Pages
564–575
Issue
7
Volume
46
Dublin Core
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Title
A name given to the resource
A plant lignan, 3'-O-methyl-nordihydroguaiaretic acid, suppresses papillomavirus E6 protein function, stabilizes p53 protein, and induces apoptosis in cervical tumor cells.
Publisher
An entity responsible for making the resource available
Molecular carcinogenesis
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-07
Subject
The topic of the resource
Apoptosis Regulatory Proteins/metabolism; Apoptosis/*drug effects; bcl-2-Associated X Protein/metabolism; Caspase 3/metabolism; Caspase 9/metabolism; Cultured/drug effects; Enzyme Activation/drug effects; Female; Genetic; Humans; Luciferases; Masoprocol/*analogs & derivatives/therapeutic use; Oncogene Proteins; Plants/chemistry; Proto-Oncogene Proteins/metabolism; Repressor Proteins/*metabolism; Transcription; Tumor Cells; Tumor Suppressor Protein p53/genetics/*metabolism; Uterine Cervical Neoplasms/*drug therapy/metabolism/pathology; Viral/*metabolism
Creator
An entity primarily responsible for making the resource
Allen Kristi L; Tschantz Deidra R; Awad Keytam S; Lynch William P; DeLucia Angelo L
Description
An account of the resource
Persistent infection with oncogenic human papillomaviruses (HPVs) is the most important factor in the induction of uterine cervical cancer, a leading cause of cancer mortality in women worldwide. Upon cell transformation, continual expression of the viral oncogenes is required to maintain the transformed phenotype. The viral E6 protein forms a ternary complex with the cellular E6-AP protein and p53 protein which promotes the rapid degradation of p53. Recent studies have revealed that lignans from the creosote bush (3'-O-methyl-nordihydroguaiaretic acid) can repress the viral promoter responsible for E6 gene expression. Work reported here shows that the lignan can subvert viral oncogene function resulting in stabilized p53 protein within treated HPV-containing tumor cells. The stabilized p53 is transcriptionally active as demonstrated by a luciferase reporter vector and induction of genes for Bax and PUMA proteins. Apoptosis is detected by annexin V binding to treated cells as analyzed by flow cytometry. Programmed cell death is confirmed by the induction of active caspases and TUNEL assay. Initiator caspase-9 is activated first, followed later by the effector caspase-3 enzyme. The stabilization and induced apoptosis are not observed within treated HPV-negative cervical tumor cells. Quantitative real time RT-PCR analysis of endogenous E6 gene transcription from the integrated HPV 16 promoter shows at least a fivefold repression of expression as compared to untreated cells. These results indicate that the loss of E6 protein in treated cells could be, in part, responsible for the stabilization of p53 within the lignan treated cells.
Identifier
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<a href="http://doi.org/10.1002/mc.20305" target="_blank" rel="noreferrer noopener">10.1002/mc.20305</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2007
Allen Kristi L
Apoptosis Regulatory Proteins/metabolism
Apoptosis/*drug effects
Awad Keytam S
bcl-2-Associated X Protein/metabolism
Caspase 3/metabolism
Caspase 9/metabolism
Cultured/drug effects
DeLucia Angelo L
Department of Integrative Medical Sciences
Enzyme Activation/drug effects
Female
Genetic
Humans
Luciferases
Lynch William P
Masoprocol/*analogs & derivatives/therapeutic use
Molecular carcinogenesis
NEOMED College of Medicine
Oncogene Proteins
Plants/chemistry
Proto-Oncogene Proteins/metabolism
Repressor Proteins/*metabolism
Transcription
Tschantz Deidra R
Tumor Cells
Tumor Suppressor Protein p53/genetics/*metabolism
Uterine Cervical Neoplasms/*drug therapy/metabolism/pathology
Viral/*metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M513420200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M513420200</a>
Pages
10081–10088
Issue
15
Volume
281
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A Prospero-related homeodomain protein is a novel co-regulator of hepatocyte nuclear factor 4alpha that regulates the cholesterol 7alpha-hydroxylase gene.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006-04
Subject
The topic of the resource
*Gene Expression Regulation; Aged; Amino Acid Motifs; Bile Acids and Salts/metabolism; Cell Line; Cell Nucleus/metabolism; Cells; Cholesterol 7-alpha-Hydroxylase/*chemistry/*genetics; Cultured/metabolism; Enzymologic; Female; Genes; Genetic; Gluconeogenesis; Glutathione Transferase/metabolism; Hepatocyte Nuclear Factor 4/metabolism/*physiology; Hepatocytes/metabolism; Homeodomain Proteins/metabolism/*physiology; Humans; Immunoprecipitation; Liver/metabolism; Luciferases/metabolism; Male; Messenger/metabolism; Middle Aged; Phosphoenolpyruvate Carboxykinase (ATP)/metabolism; Plasmids/metabolism; Protein Structure; Reporter; Response Elements; Reverse Transcriptase Polymerase Chain Reaction; RNA; Small Interfering/metabolism; Tertiary; Time Factors; Transcription; Transcriptional Activation; Transfection; Tumor Suppressor Proteins; Two-Hybrid System Techniques
Creator
An entity primarily responsible for making the resource
Song Kwang-Hoon; Li Tiangang; Chiang John Y L
Description
An account of the resource
Prox1, an early specific marker for developing liver and pancreas in foregut endoderm has recently been shown to interact with alpha-fetoprotein transcription factor and repress cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription. Using a yeast two-hybrid assay, we found that Prox1 strongly and specifically interacted with hepatocyte nuclear factor (HNF)4alpha, an important transactivator of the human CYP7A1 gene in bile acid synthesis and phosphoenolpyruvate carboxykinase (PEPCK) gene in gluconeogenesis. A real time PCR assay detected Prox1 mRNA expression in human primary hepatocytes and HepG2 cells. Reporter assay, GST pull-down, co-immunoprecipitation, and yeast two-hybrid assays identified a specific interaction between the N-terminal LXXLL motif of Prox1 and the activation function 2 domain of HNF4alpha. Prox1 strongly inhibited HNF4alpha and peroxisome proliferators-activated receptor gamma coactivator-1alpha co-activation of the CYP7A1 and PEPCK genes. Knock down of the endogenous Prox1 by small interfering RNA resulted in significant increase of CYP7A1 and PEPCK mRNA expression and the rate of bile acid synthesis in HepG2 cells. These results suggest that Prox1 is a novel co-regulator of HNF4alpha that may play a key role in the regulation of bile acid synthesis and gluconeogenesis in the liver.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M513420200" target="_blank" rel="noreferrer noopener">10.1074/jbc.M513420200</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
2006
Aged
Amino Acid Motifs
Bile Acids and Salts/metabolism
Cell Line
Cell Nucleus/metabolism
Cells
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*chemistry/*genetics
Cultured/metabolism
Department of Integrative Medical Sciences
Enzymologic
Female
Genes
Genetic
Gluconeogenesis
Glutathione Transferase/metabolism
Hepatocyte Nuclear Factor 4/metabolism/*physiology
Hepatocytes/metabolism
Homeodomain Proteins/metabolism/*physiology
Humans
Immunoprecipitation
Li Tiangang
Liver/metabolism
Luciferases/metabolism
Male
Messenger/metabolism
Middle Aged
NEOMED College of Medicine
Phosphoenolpyruvate Carboxykinase (ATP)/metabolism
Plasmids/metabolism
Protein Structure
Reporter
Response Elements
Reverse Transcriptase Polymerase Chain Reaction
RNA
Small Interfering/metabolism
Song Kwang-Hoon
Tertiary
The Journal of biological chemistry
Time Factors
Transcription
Transcriptional Activation
Transfection
Tumor Suppressor Proteins
Two-Hybrid System Techniques
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M004531" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M004531</a>
Pages
2223–2233
Issue
8
Volume
51
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A putative role of micro RNA in regulation of cholesterol 7alpha-hydroxylase expression in human hepatocytes.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-08
Subject
The topic of the resource
3' Untranslated Regions/genetics; Base Sequence; Chenodeoxycholic Acid/pharmacology; Cholesterol 7-alpha-Hydroxylase/*genetics; Enzymologic/drug effects/*genetics; Fibroblast Growth Factors/pharmacology; Gene Expression Regulation; Genetic/drug effects/genetics; Hep G2 Cells; Hepatocytes/drug effects/enzymology/*metabolism; Humans; Isoxazoles/pharmacology; MicroRNAs/*genetics/*metabolism; Oligonucleotide Array Sequence Analysis; Post-Transcriptional/drug effects/genetics; RNA Processing; Transcription
Creator
An entity primarily responsible for making the resource
Song Kwang-Hoon; Li Tiangang; Owsley Erika; Chiang John Y L
Description
An account of the resource
Cholesterol 7alpha-hydroxylase (CYP7A1) plays a critical role in regulation of bile acid synthesis in the liver. CYP7A1 mRNAs have very short half-lives, and bile acids destabilize CYP7A1 mRNA via the 3'-untranslated region (3'-UTR). However, the underlying mechanism of translational regulation of CYP7A1 mRNA remains unknown. Screening of a human micro RNA (miRNA) microarray has identified five differentially expressed miRNAs in human primary hepatocytes treated with chenodeoxycholic acid, GW4064, or fibroblast growth factor (FGF)19. These compounds also significantly induced the expression of miR-122a, a liver-specific and the predominant miRNA in human hepatocytes. The putative recognition sequences for miR-122a and miR-422a were localized in the 3'-UTR of human CYP7A1 mRNA. The miR-122a and miR-422a mimics inhibited, whereas their inhibitors stimulated CYP7A1 mRNA expression. These miRNAs specifically inhibited the activity of the CYP7A1-3'-UTR reporter plasmids, and mutations of miRNA binding sites in 3'-UTR abrogated miRNA inhibition of reporter activity. These results suggest that miR-122a and miR-422a may destabilize CYP7A1 mRNA to inhibit CYP7A1 expression. However, these miRNAs did not play a role in mediating FGF19 inhibition of CYP7A1 transcription. Under certain conditions, miRNA may reduce CYP7A1 mRNA stability to inhibit bile acid synthesis, and the miR-122a antagomirs may stimulate bile acid synthesis to reduce serum cholesterol and triglycerides.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M004531" target="_blank" rel="noreferrer noopener">10.1194/jlr.M004531</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
3' Untranslated Regions/genetics
Base Sequence
Chenodeoxycholic Acid/pharmacology
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics
Department of Integrative Medical Sciences
Enzymologic/drug effects/*genetics
Fibroblast Growth Factors/pharmacology
Gene Expression Regulation
Genetic/drug effects/genetics
Hep G2 Cells
Hepatocytes/drug effects/enzymology/*metabolism
Humans
Isoxazoles/pharmacology
Journal of lipid research
Li Tiangang
MicroRNAs/*genetics/*metabolism
NEOMED College of Medicine
Oligonucleotide Array Sequence Analysis
Owsley Erika
Post-Transcriptional/drug effects/genetics
RNA Processing
Song Kwang-Hoon
Transcription
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.4161/chan.24328" target="_blank" rel="noreferrer noopener">http://doi.org/10.4161/chan.24328</a>
Pages
211–214
Issue
3
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A TRP to cardiac fibroblast differentiation.
Publisher
An entity responsible for making the resource available
Channels (Austin, Tex.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-06
Subject
The topic of the resource
Female; Humans; Male; Animals; TRPV4; *Wound Healing; TRPV Cation Channels/*metabolism; integrin; *Cell Differentiation; cardiac fibroblast; myofibroblast; *Calcium Signaling; *Cell Transdifferentiation; Atrial Fibrillation/*metabolism; differentiation; ECM stiffness; Fibroblasts/*metabolism/*physiology; mechanical signaling; Myofibroblasts/*cytology/*metabolism; Rho/ROCK; TRPC Cation Channels/*metabolism; TRPM Cation Channels/*metabolism; Cellular; *Mechanotransduction
Creator
An entity primarily responsible for making the resource
Thodeti Charles K; Paruchuri Sailaja; Meszaros J Gary
Description
An account of the resource
The differentiation of cardiac fibroblasts to myofibroblasts is one of the key events during cardiac remodeling, however, the molecular mechanism underlying this process is not well known. Calcium signaling plays an important role in the regulation of cardiac fibroblast function, but its role in the differentiation of fibroblasts is undefined. Recently four Transient Receptor Potential (TRP) channels TRPM7, TRPC3, TRPC6 and TRPV4 were shown to be crucial for the differentiation of cardiac fibroblasts to myofibroblasts. This addendum sums up the roles described for these four TRP channels in cardiac fibroblast differentiation, and discusses the possible molecular mechanisms underlying this process and its relevance for cardiac remodeling in disease.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.4161/chan.24328" target="_blank" rel="noreferrer noopener">10.4161/chan.24328</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Calcium Signaling
*Cell Differentiation
*Cell Transdifferentiation
*Mechanotransduction
*Wound Healing
2013
Animals
Atrial Fibrillation/*metabolism
cardiac fibroblast
Cellular
Channels (Austin, Tex.)
Department of Integrative Medical Sciences
differentiation
ECM stiffness
Female
Fibroblasts/*metabolism/*physiology
Humans
integrin
Male
mechanical signaling
Meszaros J Gary
myofibroblast
Myofibroblasts/*cytology/*metabolism
NEOMED College of Medicine
Paruchuri Sailaja
Rho/ROCK
Thodeti Charles K
TRPC Cation Channels/*metabolism
TRPM Cation Channels/*metabolism
TRPV Cation Channels/*metabolism
TRPV4
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.111.252734" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.111.252734</a>
Pages
851–856
Issue
6
Volume
110
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Absence of type VI collagen paradoxically improves cardiac function, structure, and remodeling after myocardial infarction.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-03
Subject
The topic of the resource
Animal; Animals; Apoptosis/physiology; Cardiac/pathology/physiology; Collagen Type VI/*genetics/*metabolism; Disease Models; Echocardiography; Extracellular Matrix/metabolism/pathology; Fibrosis/genetics/pathology/physiopathology; Knockout; Male; Mice; Myocardial Infarction/diagnostic imaging/*genetics/*physiopathology; Myocytes; Ventricular Remodeling/*physiology
Creator
An entity primarily responsible for making the resource
Luther Daniel J; Thodeti Charles K; Shamhart Patricia E; Adapala Ravi K; Hodnichak Cheryl; Weihrauch Dorothee; Bonaldo Paolo; Chilian William M; Meszaros J Gary
Description
An account of the resource
RATIONALE: We previously reported that type VI collagen deposition increases in the infarcted myocardium in vivo. To date, a specific role for this nonfibrillar collagen has not been explored in the setting of myocardial infarction (MI). OBJECTIVE: To determine whether deletion of type VI collagen in an in vivo model of post-MI wound healing would alter cardiac function and remodeling in the days to weeks after injury. METHODS AND RESULTS: Wild-type and Col6a1(-/-) mice were subjected to MI, followed by serial echocardiographic and histological assessments. At 8 weeks after MI, infarct size was significantly reduced, ejection fraction was significantly preserved (43.9% +/- 3.3% versus 29.1% +/- 4.3% for wild-type), and left ventricular chamber dilation was attenuated in the Col6a1(-/-) MI group (25.8% +/- 7.9% increase versus 62.6% +/- 16.5% for wild-type). The improvement in cardiac remodeling was evident as early as 10 days after MI in the Col6a1(-/-) mice. Myocyte apoptosis within the infarcted zones was initially greater in the Col6a1(-/-) group 3 days after MI, but by day 14 this was significantly reduced. Collagen deposition also was reduced in the infarcted and remote areas of the Col6a1(-/-) hearts. The reductions in chronic myocyte apoptosis and fibrosis are critical events leading to improved long-term remodeling and functional outcomes. CONCLUSIONS: These unexpected results demonstrate for the first time that deletion of type VI collagen in this knockout model plays a critical protective role after MI by limiting infarct size, chronic apoptosis, aberrant remodeling, and fibrosis, leading to preservation of cardiac function.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.111.252734" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.111.252734</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Adapala Ravi K
Animal
Animals
Apoptosis/physiology
Bonaldo Paolo
Cardiac/pathology/physiology
Chilian William M
Circulation research
Collagen Type VI/*genetics/*metabolism
Department of Integrative Medical Sciences
Disease Models
Echocardiography
Extracellular Matrix/metabolism/pathology
Fibrosis/genetics/pathology/physiopathology
Hodnichak Cheryl
Knockout
Luther Daniel J
Male
Meszaros J Gary
Mice
Myocardial Infarction/diagnostic imaging/*genetics/*physiopathology
Myocytes
NEOMED College of Medicine
Shamhart Patricia E
Thodeti Charles K
Ventricular Remodeling/*physiology
Weihrauch Dorothee
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/circ.142.suppl_3.17248" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/circ.142.suppl_3.17248</a>
Pages
A17248-A17248
Issue
Suppl 3
Volume
142
ISSN
0009-7322
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Update Year & Number
December 2020 List
NEOMED College
NEOMED College of Medicine Student
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
NEOMED Student Publications
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Title
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Abstract 17248: The role of microRNA-21 in regulating the coronary microcirculation in diabetes
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An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-11-17
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An entity primarily responsible for making the resource
Juguilon C; Wang Z; Gadd J;Ohanyan VA; Anurag J; Molly E; Wang T; Kolz C; William MC; Yin L
Description
An account of the resource
Introduction: Coronary microvascular dysfunction is prevalent among diabetics and intersects with deficits in endothelial-dependent vasodilation. These deficits occur early in the progression of the disease, but the mechanisms remain incompletely understood. Nitric oxide (NO) is the major endothelial-dependent mediator of vasodilation in the healthy coronary circulation, but the mediator switches to hydrogen peroxide (H2O2) in coronary artery disease (CAD) patients. Diabetes is a risk factor for CAD, so we hypothesized that a similar switch would occur.Methods: Coronary arteries were isolated and endothelial-dependent vasodilation was assessed using myography. Quantitative polymerase chain reaction (qPCR) was performed for gene expression analysis and myocardial blood flow (MBF) was measured by contrast echocardiography.Results: Nitric oxide synthase inhibitor (L-NAME) inhibited vasodilation in wild type (WT) mice, but the H2O2 scavenger (PEG-catalase) had no effect. In contrast, vasodilation in diabetic mice was blunted by PEG-catalase, but not L-NAME. This suggests that the mediator of coronary vasodilation switched from NO to H2O2 in diabetes. Importantly, we found that microRNA-21 (miR-21) is upregulated in diabetes and the deficiency modulates the mediator switch from NO to H2O2 in diabetic mice.Conclusions: The switch in the mediator of coronary vasodilation from NO to H2O2 contributes to microvascular dysfunction in diabetes and miR-21 regulates this switch. Further genetic profiling will elucidate the pathways and mechanisms converging with miR-21 to regulate microvascular function in diabetes. This is the first mouse model that recapitulates the switch in mediator of coronary vasodilation from NO to H2O2 seen in CAD patients.
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<a href="http://doi.org/10.1161/circ.142.suppl_3.17248" target="_blank" rel="noreferrer noopener">10.1161/circ.142.suppl_3.17248</a>
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journalArticle
2020
Anurag J
Circulation
December 2020 List
Department of Integrative Medical Sciences
Gadd J
journalArticle
Juguilon C
Kolz C
Molly E
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED Student Publications
Ohanyan VA
Wang T
Wang Z
William MC
Yin L
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/onc.2015.83" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/onc.2015.83</a>
Pages
314–322
Issue
3
Volume
35
Dublin Core
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Title
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Activation of mechanosensitive ion channel TRPV4 normalizes tumor vasculature and improves cancer therapy.
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Oncogene
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
Animals; Calcium Signaling/genetics; Carcinoma; Cell Line; Cell Proliferation/drug effects; Cisplatin/administration & dosage; Endothelium; Gene Expression Regulation; Humans; Leucine/administration & dosage/analogs & derivatives; Lewis Lung/drug therapy/*genetics/pathology; Mice; Neoplastic/drug effects; Neovascularization; Pathologic/drug therapy/*genetics/pathology; Sulfonamides/administration & dosage; TRPV Cation Channels/agonists/biosynthesis/*genetics; Tumor; Vascular Endothelial Growth Factor A/genetics; Vascular/drug effects/*pathology
Creator
An entity primarily responsible for making the resource
Adapala R K; Thoppil R J; Ghosh K; Cappelli H C; Dudley A C; Paruchuri S; Keshamouni V; Klagsbrun M; Meszaros J G; Chilian W M; Ingber D E; Thodeti C K
Description
An account of the resource
Tumor vessels are characterized by abnormal morphology and hyperpermeability that together cause inefficient delivery of chemotherapeutic agents. Although vascular endothelial growth factor has been established as a critical regulator of tumor angiogenesis, the role of mechanical signaling in the regulation of tumor vasculature or tumor endothelial cell (TEC) function is not known. Here we show that the mechanosensitive ion channel transient receptor potential vanilloid 4 (TRPV4) regulates tumor angiogenesis and tumor vessel maturation via modulation of TEC mechanosensitivity. We found that TECs exhibit reduced TRPV4 expression and function, which is correlated with aberrant mechanosensitivity towards extracellular matrix stiffness, increased migration and abnormal angiogenesis by TEC. Further, syngeneic tumor experiments revealed that the absence of TRPV4 induced increased vascular density, vessel diameter and reduced pericyte coverage resulting in enhanced tumor growth in TRPV4 knockout mice. Importantly, overexpression or pharmacological activation of TRPV4 restored aberrant TEC mechanosensitivity, migration and normalized abnormal angiogenesis in vitro by modulating Rho activity. Finally, a small molecule activator of TRPV4, GSK1016790A, in combination with anticancer drug cisplatin, significantly reduced tumor growth in wild-type mice by inducing vessel maturation. Our findings demonstrate TRPV4 channels to be critical regulators of tumor angiogenesis and represent a novel target for anti-angiogenic and vascular normalization therapies.
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<a href="http://doi.org/10.1038/onc.2015.83" target="_blank" rel="noreferrer noopener">10.1038/onc.2015.83</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Adapala R K
Animals
Calcium Signaling/genetics
Cappelli H C
Carcinoma
Cell Line
Cell Proliferation/drug effects
Chilian W M
Cisplatin/administration & dosage
Department of Integrative Medical Sciences
Dudley A C
Endothelium
Gene Expression Regulation
Ghosh K
Humans
Ingber D E
Keshamouni V
Klagsbrun M
Leucine/administration & dosage/analogs & derivatives
Lewis Lung/drug therapy/*genetics/pathology
Meszaros J G
Mice
NEOMED College of Medicine
Neoplastic/drug effects
Neovascularization
Oncogene
Paruchuri S
Pathologic/drug therapy/*genetics/pathology
Sulfonamides/administration & dosage
Thodeti C K
Thoppil R J
TRPV Cation Channels/agonists/biosynthesis/*genetics
Tumor
Vascular Endothelial Growth Factor A/genetics
Vascular/drug effects/*pathology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1124/jpet.104.073155" target="_blank" rel="noreferrer noopener">http://doi.org/10.1124/jpet.104.073155</a>
Pages
502–508
Issue
2
Volume
312
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Activation of metabotropic glutamate receptor 1 dimers requires glutamate binding in both subunits.
Publisher
An entity responsible for making the resource available
The Journal of pharmacology and experimental therapeutics
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-02
Subject
The topic of the resource
Blotting; Calcium Channels/drug effects/metabolism; DNA/biosynthesis/genetics; Dose-Response Relationship; Drug; Fluorescent Antibody Technique; Genes; Glutamic Acid/*metabolism; Humans; Membrane Potentials/drug effects; Metabotropic Glutamate/genetics/*metabolism; myc/genetics; Patch-Clamp Techniques; Plasmids/genetics; Receptors; Signal Transduction/drug effects; Superior Cervical Ganglion/cytology/drug effects/metabolism; Sympathetic Nervous System/cytology/drug effects/metabolism; Western
Creator
An entity primarily responsible for making the resource
Kammermeier Paul J; Yun June
Description
An account of the resource
Group I metabotropic glutamate receptors (mGluRs) form stable, disulfide-linked homodimers. Lack of a verifiably monomeric mGluR1 mutant has led to difficulty in assessing the role of dimerization in the molecular mechanism of mGluR1 activation. The related GABA(B) receptor exhibits striking intradimer cross talk (ligand binding at one subunit effectively produces G protein activation at the other), but it is unclear whether group I mGluRs exhibit analogous cross talk. Signaling of heterologously expressed mGluR1 was examined in isolated rat sympathetic neurons by measuring glutamate-mediated inhibition of native calcium currents. To examine mGluR1 activity when only one dimer subunit has access to glutamate ligand, wildtype mGluR1 was coexpressed with mGluR1 Y74A, a mutant with impaired glutamate binding, and the activity of the heterodimer (mutant/wild type) was examined. The mGluR1 Y74A mutant alone had a dose-response curve that was shifted by about 2 orders of magnitude. The half-maximal dose of glutamate shifted from 1.3 (wild-type mGluR1) to about 450 (mGluR1 Y74A) microM. However, the maximal effect was similar. Wild-type mGluR1 was expressed with excess Y74A mGluR1 to generate a receptor population consisting largely of mutant homodimers and mutant/wild-type heterodimers but without detectable wild-type homodimers. Under these conditions, no glutamate-mediated calcium current inhibition was observed below approximately 300 microM glutamate, although wild-type mGluR1 protein was detectable with immunofluorescence. These data suggest that mutant/wild-type heterodimeric receptors are inactive at ligand concentrations favoring glutamate association with receptor dimers at only one subunit.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1124/jpet.104.073155" target="_blank" rel="noreferrer noopener">10.1124/jpet.104.073155</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2005
Blotting
Calcium Channels/drug effects/metabolism
Department of Integrative Medical Sciences
DNA/biosynthesis/genetics
Dose-Response Relationship
Drug
Fluorescent Antibody Technique
Genes
Glutamic Acid/*metabolism
Humans
Kammermeier Paul J
Membrane Potentials/drug effects
Metabotropic Glutamate/genetics/*metabolism
myc/genetics
NEOMED College of Medicine
Patch-Clamp Techniques
Plasmids/genetics
Receptors
Signal Transduction/drug effects
Superior Cervical Ganglion/cytology/drug effects/metabolism
Sympathetic Nervous System/cytology/drug effects/metabolism
The Journal of pharmacology and experimental therapeutics
Western
Yun June
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1111/acer.14429" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/acer.14429</a>
ISSN
1530-0277 0145-6008
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1111/acer.14429" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1111/acer.14429</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
August 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Acute alcohol intoxication impairs SHH-GLI1 signaling and activation of primitive hematopoietic precursor cells in the early stage of host response to bacteremia.
Publisher
An entity responsible for making the resource available
Alcoholism, Clinical and Experimental Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-08-09
Subject
The topic of the resource
bacteremia; alcohol; hematopoietic stem cells; host response; sonic hedgehog
Creator
An entity primarily responsible for making the resource
Shi X; Simms KJ; Zhang P
Description
An account of the resource
BACKGROUND: Activation of hematopoietic stem cells [HSCs, lineage(lin)(-) stem cell growth factor receptor(c-kit)(+) stem cell antigen-1(Sca-1)(+) or LKS cells in mice], is critical for initiating the granulopoietic response. This study determined the effect of alcohol exposure on sonic hedgehog (SHH) signaling in the regulation of HSC activation during bacteremia. METHODS: Acute alcohol intoxication was induced in mice by intraperitoneal (i.p.) injection of 20% alcohol (5 g alcohol/kg body weight). Control mice received i.p. saline. Thirty minutes later, mice were intravenously (i.v.) injected with Escherichia coli (E. coli, 1 - 5 x 10(7) CFUs/mouse) or saline. RESULTS: SHH expression by lineage negative bone marrow cells (BMCs) was significantly increased 24 h after E. coli infection. Extracellular signal-regulated kinase 1/2 (ERK1/2)-specificity protein 1 (Sp1) signaling promotes SHH expression. ERK1/2 was markedly activated in BMCs 8 h following E. coli infection. Alcohol suppressed both the activation of ERK1/2 and up-regulation of SHH expression following E. coli infection. E. coli infection up-regulated GLI family zinc finger 1 (Gli1) gene expression by BMCs and increased Gli1 protein content in LKS cells. The extent of Gli1 expression was correlated with the activity of proliferation in LKS cells. Alcohol inhibited up-regulation of Gli1 expression and activation of LKS cells in response to E. coli infection. Alcohol also interrupted the granulopoietic response to bacteremia. CONCLUSION: These data show that alcohol disrupts SHH-Gli1 signaling and HSC activation in the early stage of the granulopoietic response, which may serve as an important mechanism underlying the impairment of immune defense against bacterial infection in host excessively consuming alcohol.
Identifier
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<a href="http://doi.org/10.1111/acer.14429" target="_blank" rel="noreferrer noopener">10.1111/acer.14429</a>
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journalArticle
2020
Alcohol
alcoholism
Alcoholism, Clinical and Experimental Research
August 2020 List
bacteremia
Clinical and Experimental Research
Department of Integrative Medical Sciences
hematopoietic stem cells
host response
journalArticle
NEOMED College of Medicine
Shi X
Simms KJ
sonic hedgehog
Zhang P
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1111/acer.14429" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/acer.14429</a>
ISSN
1530-0277
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1111/acer.14429" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1111/acer.14429</a>
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Update Year & Number
September 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Acute alcohol intoxication impairs sonic hedgehog-GLI1 signaling and activation of primitive hematopoietic precursor cells in the early stage of host response to bacteremia.
Publisher
An entity responsible for making the resource available
Alcoholism, Clinical And Experimental Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-08-09
Subject
The topic of the resource
Alcohol; Bacteremia; Hematopoietic Stem Cells; Host Response; Sonic Hedgehog
Creator
An entity primarily responsible for making the resource
Shi X;Simms KJ;Zhang P
Description
An account of the resource
Background: Activation of hematopoietic stem cells [HSCs, lineage(lin) - stem cell growth factor receptor (c-kit) + stem cell antigen-1(Sca-1) + , or LKS cells in mice] is critical for initiating the granulopoietic response. This study determined the effect of alcohol exposure on sonic hedgehog (SHH) signaling in the regulation of HSC activation during bacteremia.; Methods: Acute alcohol intoxication was induced in mice by intraperitoneal (i.p.) injection of 20% alcohol (5 g alcohol/kg body weight). Control mice received i.p. saline. Thirty minutes later, mice were intravenously (i.v.) injected with Escherichia coli (E. coli, 1 to 5 × 10 7 CFUs/mouse) or saline.; Results: SHH expression by lineage-negative bone marrow cells (BMCs) was significantly increased 24 hours after E. coli infection. Extracellular signal-regulated kinase 1/2 (ERK1/2)-specificity protein 1 (Sp1) signaling promotes SHH expression. ERK1/2 was markedly activated in BMCs 8 hours following E. coli infection. Alcohol suppressed both the activation of ERK1/2 and up-regulation of SHH expression following E. coli infection. E. coli infection up-regulated GLI family zinc finger 1 (Gli1) gene expression by BMCs and increased Gli1 protein content in LKS cells. The extent of Gli1 expression was correlated with the activity of proliferation in LKS cells. Alcohol inhibited up-regulation of Gli1 expression and activation of LKS cells in response to E. coli infection. Alcohol also interrupted the granulopoietic response to bacteremia.; Conclusion: These data show that alcohol disrupts SHH-Gli1 signaling and HSC activation in the early stage of the granulopoietic response, which may serve as an important mechanism underlying the impairment of immune defense against bacterial infection in host excessively consuming alcohol. (© 2020 by the Research Society on Alcoholism.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/acer.14429" target="_blank" rel="noreferrer noopener">10.1111/acer.14429</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
Alcohol
alcoholism
Alcoholism, Clinical and Experimental Research
bacteremia
Clinical and Experimental Research
Department of Integrative Medical Sciences
hematopoietic stem cells
host response
journalArticle
NEOMED College of Medicine
September 2020 List
Shi X
Simms KJ
sonic hedgehog
Zhang P
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/jappl.1990.69.2.694" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jappl.1990.69.2.694</a>
Pages
694–699
Issue
2
Volume
69
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Administration of a synthetic antiprotease reduces smoke-induced lung injury.
Publisher
An entity responsible for making the resource available
Journal of applied physiology (Bethesda, Md. : 1985)
Date
A point or period of time associated with an event in the lifecycle of the resource
1990
1990-08
Subject
The topic of the resource
*Lung Injury; alpha-Macroglobulins/physiology; Animals; Endopeptidases/physiology; Female; Gabexate; Guanidines/*pharmacology; Neutrophils/physiology; Pulmonary Edema/etiology/prevention & control; Pulmonary Gas Exchange/drug effects; Serine Proteinase Inhibitors/*pharmacology; Sheep; Smoke Inhalation Injury/*drug therapy/etiology/physiopathology
Creator
An entity primarily responsible for making the resource
Niehaus G D; Kimura R; Traber L D; Herndon D N; Flynn J T; Traber D L
Description
An account of the resource
Our previous studies suggest that a neutrophil-mediated inflammatory injury causes a major fraction of the pulmonary edema that occurs after smoke inhalation. Because activated neutrophils extrude cytotoxic proteases, the current study was conducted to evaluate the role of proteases in the pulmonary microvascular injury. Twelve sheep, instrumented for collection of lung lymph, were insufflated with cotton smoke. The sheep were treated 30 min after smoke inhalation with either gabexate mesilate (an inhibitor of serine proteases) or vehicle. Smoke inhalation resulted in an increased protease activity in the lung interstitium, as evidenced by decreases in both antiprotease activity and immunoreactive alpha 2-macroglobulin. Intravenous infusion of gabexate mesilate prevented the decrease in antiprotease activity. The protease inhibitor significantly attenuated the smoke-induced increase in transvascular fluid and protein flux, with untreated animals exhibiting 460% increases in flux compared with 180% in the inhibitor treated sheep. The protease inhibitor also eliminated the functional degradation in gas exchange that was observed in the untreated sheep. These studies strongly suggest that an increase in pulmonary proteolytic enzyme activity is responsible for a significant fraction of the degradation in microvascular integrity and gas exchange that is associated with smoke inhalation injury.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jappl.1990.69.2.694" target="_blank" rel="noreferrer noopener">10.1152/jappl.1990.69.2.694</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Lung Injury
1990
alpha-Macroglobulins/physiology
Animals
Department of Integrative Medical Sciences
Endopeptidases/physiology
Female
Flynn J T
Gabexate
Guanidines/*pharmacology
Herndon D N
Journal of applied physiology (Bethesda, Md. : 1985)
Kimura R
NEOMED College of Medicine
Neutrophils/physiology
Niehaus G D
Pulmonary Edema/etiology/prevention & control
Pulmonary Gas Exchange/drug effects
Serine Proteinase Inhibitors/*pharmacology
Sheep
Smoke Inhalation Injury/*drug therapy/etiology/physiopathology
Traber D L
Traber L D
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/jbt.2570050303" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jbt.2570050303</a>
Pages
147–153
Issue
3
Volume
5
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Aflatoxin B1 metabolism by 3-methylcholanthrene-induced hamster hepatic cytochrome P-450s.
Publisher
An entity responsible for making the resource available
Journal of biochemical toxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
1990
1905-06
Subject
The topic of the resource
Animals; Rats; Gene Expression Regulation; Liver/enzymology; Antibodies/immunology; Cricetinae; Enzyme Induction/drug effects; Mesocricetus; Aflatoxin B1; Liver/drug effects/*enzymology; Methylcholanthrene/*pharmacology; Aflatoxins/immunology/*metabolism; Cytochrome P-450 Enzyme System/biosynthesis/isolation & purification/*metabolism; Mutagenicity Tests; Salmonella typhimurium/enzymology/genetics; Subcellular Fractions/drug effects/enzymology; Inbred Strains; Enzymologic; Microsomes
Creator
An entity primarily responsible for making the resource
Lai T S; Chiang J Y
Description
An account of the resource
We have studied the activation of aflatoxin B1 by hamster liver microsomes and purified hamster cytochrome P-450 isozymes using a umu mutagen test. The hamster liver microsomes or S-9 fractions were much more active than rat liver microsomes or S-9 fractions in the activation of umu gene expression by aflatoxin B1 metabolites. 3-Methyl-cholanthrene treatment increased aflatoxin B1 activation by hamster liver microsomes. Two major 3-methylcholanthrene-inducible cytochrome
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/jbt.2570050303" target="_blank" rel="noreferrer noopener">10.1002/jbt.2570050303</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1990
Aflatoxin B1
Aflatoxins/immunology/*metabolism
Animals
Antibodies/immunology
Chiang J Y
Cricetinae
Cytochrome P-450 Enzyme System/biosynthesis/isolation & purification/*metabolism
Department of Integrative Medical Sciences
Enzyme Induction/drug effects
Enzymologic
Gene Expression Regulation
Inbred Strains
Journal of biochemical toxicology
Lai T S
Liver/drug effects/*enzymology
Liver/enzymology
Mesocricetus
Methylcholanthrene/*pharmacology
Microsomes
Mutagenicity Tests
NEOMED College of Medicine
Rats
Salmonella typhimurium/enzymology/genetics
Subcellular Fractions/drug effects/enzymology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.pharmthera.2019.03.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.pharmthera.2019.03.001</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Alcohol abuse and disorder of granulopoiesis.
Publisher
An entity responsible for making the resource available
Pharmacology & therapeutics
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-03
Subject
The topic of the resource
*stem cells; Alcohol abuse; Bacterial infection; Bone marrow; Cell signaling; Granulopoiesis; Immune defense; Leukopenia; Progenitor cells; The granulopoietic response
Creator
An entity primarily responsible for making the resource
Shi Xin; DeLucia Angelo L; Bao Jianxin; Zhang Ping
Description
An account of the resource
Granulocytes are the major type of phagocytes constituting the front line of innate immune defense against bacterial infection. In adults, granulocytes are derived from hematopoietic stem cells in the bone marrow. Alcohol is the most frequently abused substance in human society. Excessive alcohol consumption injures hematopoietic tissue, impairing bone marrow production of granulocytes through disrupting homeostasis of granulopoiesis and the granulopoietic response. Because of the compromised immune defense function, alcohol abusers are susceptible to infectious diseases, particularly septic infection. Alcoholic patients with septic infection and granulocytopenia have an exceedingly high mortality rate. Treatment of serious infection in alcoholic patients with bone marrow inhibition continues to be a major challenge. Excessive alcohol consumption also causes diseases in other organ systems, particularly severe alcoholic hepatitis which is life threatening. Corticosteroids are the only therapeutic option for improving short-term survival in patients with severe alcoholic hepatitis. The existence of advanced alcoholic liver diseases and administration of corticosteroids make it more difficult to treat serious infection in alcoholic patients with the disorder of granulopoieis. This article reviews the recent development in understanding alcohol-induced disruption of marrow granulopoiesis and the granulopoietic response with the focus on progress in delineating cell signaling mechanisms underlying the alcohol-induced injury to hematopoietic tissue. Efforts in exploring effective therapy to improve patient care in this field will also be discussed.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.pharmthera.2019.03.001" target="_blank" rel="noreferrer noopener">10.1016/j.pharmthera.2019.03.001</a>
*Stem cells
2019
Alcohol abuse
bacterial infection
Bao Jianxin
bone marrow
cell signaling
DeLucia Angelo L
Department of Integrative Medical Sciences
Granulopoiesis
Immune defense
Leukopenia
NEOMED College of Medicine
Pharmacology & therapeutics
progenitor cells
Shi Xin
the granulopoietic response
Zhang Ping
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1111/acer.14059">http://doi.org/10.1111/acer.14059</a>
Pages
101A–101A
Volume
43
ISSN
0145-6008
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Title
A name given to the resource
ALCOHOL INHIBITS UPREGULATION OF GBP7 EXPRESSION BY HEMATOPOIETIC STEM/PROGENITOR CELLS DURING THE GRANULOPOIETIC RESPONSE TO SEPTIC INFECTION
Publisher
An entity responsible for making the resource available
Alcoholism-Clinical and Experimental Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
Substance Abuse
Creator
An entity primarily responsible for making the resource
Shi X; Simms K J; Ewing T J; Zhang P
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/acer.14059">http://doi.org/10.1111/acer.14059</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Description
An account of the resource
Alcohol impairs activation of hematopoietic stem/progenitor cells (HSPCs) during the granulopoietic response to serious bacterial infection. This study investigated the involvement of guanylate‐binding protein 7 (GBP7) in the regulation of HSPC function during the granulopoietic response and the effect of alcohol on this signaling system. Male Balb/c mice were fed on Lieber‐DeCarli low fat liquid alcohol diet for 5 weeks. Binge alcohol administration was given to mice at the end of the 5‐week feeding by intraperitoneally (i.p.) injecting a single dose of alcohol (20% alcohol in saline, 5 g alcohol/kg). Pair‐fed mice on the control diet received an i.p. injection of saline. Septicemia was induced in mice via intravenous (i.v.) injection of E. coli (E11775, ATCC, Rockville, MD, ˜5 × 107 CFUs/mouse) 30 min after the binge alcohol intoxication. E. coli septicemia caused a markedly upregulation of GBP7 expression at both mRNA and protein levels in HSPCs. This upregulation of GBP7 expression was accompanied with activation of HSPCs. Chronic plus binge alcohol administration suppressed the upregulation of GBP7 expression along with inhibition of HSPC activation in response to E. coli septicemia. Searching murine GBP7 gene promoter region identified multiple Fos/Jun binding sites. Alcohol suppressed activation of c‐Jun N‐terminal kinases (JNK1/2) in marrow cells during E. coli septicemia. Inhibition of JNK1/2 activation with specific inhibitor (SP600125) suppressed lipopolysaccharide‐induced up‐regulation of GBP7 expression by HSPCs. The predominant localization of GBP7 was in the nuclei of HSPCs, which might imply its close association with nuclear signaling pathways driving cell cycling. Septicemia caused marked increases in cyclin D1 expression and enhancement of proliferation in HSPCs, both of which were suppressed by alcohol. Knockout of GBP7 gene in murine HSC line EML cells profoundly inhibited their proliferation as reflected by the marked decrease in cell BrdU incorporation. GBP7 gene knockout also significantly reduced granulocyte/monocyte colony‐formatting activity In EML cells. These results indicate that GBP7 plays an important role in the activation of HSPCs during the granulopoietic response. Alcohol disrupts GBP7 signaling, which may serve as a mechanism underlying the impairment of primitive hematopoietic precursor cell activation during the granulopoietic response to septic infection in hosts intoxicated with alcohol (Supported by NIH grant AA022816).
2019
Alcoholism-Clinical and Experimental Research
Department of Integrative Medical Sciences
Ewing T J
June 2019 Update
NEOMED College of Medicine
Shi X
Simms K J
Substance Abuse
Zhang P
-
Text
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URL Address
<a href="http://doi.org/" target="_blank" rel="noreferrer noopener">http://doi.org/</a>
Pages
78-79
Issue
1
Volume
53
ISSN
1073-2322
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Update Year & Number
January 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Science
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Title
A name given to the resource
Alcohol intoxication disrupts SHH-GLI1 signaling in mediating activation of primitive hematopoietic precursor cells during the granulopoietic response to bacteremia
Publisher
An entity responsible for making the resource available
Shock
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-06
Creator
An entity primarily responsible for making the resource
Shi X; Simms KJ; Zhang P
Identifier
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<a href="http://doi.org/" target="_blank" rel="noreferrer noopener"></a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
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journalArticle
2020
Department of Integrative Medical Sciences
January 2021 List
journalArticle
NEOMED College of Medicine
Shi X
Shock
Simms KJ
Zhang P
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M015859" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M015859</a>
Pages
1561–1568
Issue
8
Volume
52
Dublin Core
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Title
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Aldo-keto reductase 1B7 is a target gene of FXR and regulates lipid and glucose homeostasis.
Publisher
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Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
*Aldehyde Reductase/genetics/metabolism; Adenoviridae; Animal; Animals; Blood Glucose/*metabolism; Cholesterol/analysis; Cytoplasmic and Nuclear/genetics/*metabolism; Diabetes Mellitus/genetics/*metabolism/physiopathology; Disease Models; Fatty Liver/genetics/*metabolism/physiopathology; Gene Expression; Genetic Vectors; Gluconeogenesis/genetics; Homeostasis; Humans; Liver/*metabolism/physiopathology; Malondialdehyde/blood; Mice; Polymerase Chain Reaction; Receptors; Transfection; Transgenic; Triglycerides/analysis
Creator
An entity primarily responsible for making the resource
Ge Xuemei; Yin Liya; Ma Huiyan; Li Tiangang; Chiang John Y L; Zhang Yanqiao
Description
An account of the resource
Aldo-keto reductase 1B7 (AKR1B7) is proposed to play a role in detoxification of by-products of lipid peroxidation. In this article, we show that activation of the nuclear receptor farnesoid X receptor (FXR) induces AKR1B7 expression in the liver and intestine, and reduces the levels of malondialdehyde (MDA), the end product of lipid peroxidation, in the intestine but not in the liver. To determine whether AKR1B7 regulates MDA levels in vivo, we overexpressed AKR1B7 in the liver. Overexpression of AKR1B7 in the liver had no effect on hepatic or plasma MDA levels. Interestingly, hepatic expression of AKR1B7 significantly lowered plasma glucose levels in both wild-type and diabetic db/db mice, which was associated with reduced hepatic gluconeogenesis. Hepatic expression of AKR1B7 also significantly lowered hepatic triglyceride and cholesterol levels in db/db mice. These data reveal a novel function for AKR1B7 in lipid and glucose metabolism and suggest that AKR1B7 may not play a role in detoxification of lipid peroxides in the liver. AKR1B7 may be a therapeutic target for treatment of fatty liver disease associated with diabetes mellitus.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M015859" target="_blank" rel="noreferrer noopener">10.1194/jlr.M015859</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Aldehyde Reductase/genetics/metabolism
2011
Adenoviridae
Animal
Animals
Blood Glucose/*metabolism
Chiang John Y L
Cholesterol/analysis
Cytoplasmic and Nuclear/genetics/*metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus/genetics/*metabolism/physiopathology
Disease Models
Fatty Liver/genetics/*metabolism/physiopathology
Ge Xuemei
Gene Expression
Genetic Vectors
Gluconeogenesis/genetics
Homeostasis
Humans
Journal of lipid research
Li Tiangang
Liver/*metabolism/physiopathology
Ma Huiyan
Malondialdehyde/blood
Mice
NEOMED College of Medicine
Polymerase Chain Reaction
Receptors
Transfection
Transgenic
Triglycerides/analysis
Yin Liya
Zhang Yanqiao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s00395-017-0631-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-017-0631-4</a>
Pages
41–41
Issue
4
Volume
112
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Alignment of inducible vascular progenitor cells on a micro-bundle scaffold improves cardiac repair following myocardial infarction.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-07
Subject
The topic of the resource
*Cardiovascular regeneration; *Ischemic heart diseases; *Micro-bundle scaffold; *Myocardial infarction; *Neovascularization; *Stem cells; *Tissue Scaffolds; *Vascular progenitor cells; Animal; Animals; Cell Differentiation; Cell Proliferation; Cell Survival; Cells; Coculture Techniques; Cultured; Disease Models; Endothelial Progenitor Cells/metabolism/*transplantation; Fibroblast Growth Factor 2/metabolism; Lactic Acid/*chemistry; Muscle; Myocardial Infarction/metabolism/pathology/physiopathology/*surgery; Myocardium/metabolism/*pathology; Myocytes; Paracrine Communication; Phenotype; Physiologic; Polyglycolic Acid/*chemistry; Polylactic Acid-Polyglycolic Acid Copolymer; Rats; Signal Transduction; Smooth; Smooth Muscle/metabolism/*transplantation; Sprague-Dawley; Time Factors; Tissue Engineering/*methods; Vascular Endothelial Growth Factor A/metabolism; Vascular/metabolism/*transplantation; Ventricular Remodeling
Creator
An entity primarily responsible for making the resource
Jamaiyar Anurag; Wan Weiguo; Ohanyan Vahagn; Enrick Molly; Janota Danielle; Cumpston Devan; Song Hokyung; Stevanov Kelly; Kolz Christopher L; Hakobyan Tatev; Dong Feng; Newby Bi-Min Zhang; Chilian William M; Yin Liya
Description
An account of the resource
Ischemic heart disease is still the leading cause of death even with the advancement of pharmaceutical therapies and surgical procedures. Early vascularization in the ischemic heart is critical for a better outcome. Although stem cell therapy has great potential for cardiovascular regeneration, the ideal cell type and delivery method of cells have not been resolved. We tested a new approach of stem cell therapy by delivery of induced vascular progenitor cells (iVPCs) grown on polymer micro-bundle scaffolds in a rat model of myocardial infarction. iVPCs partially reprogrammed from vascular endothelial cells (ECs) had potent angiogenic potential and were able to simultaneously differentiate into vascular smooth muscle cells (SMCs) and ECs in 2D culture. Under hypoxic conditions, iVPCs also secreted angiogenic cytokines such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) as measured by enzyme-linked immunosorbent assay (ELISA). A longitudinal micro-scaffold made from poly(lactic-co-glycolic acid) was sufficient for the growth and delivery of iVPCs. Co-cultured ECs and SMCs aligned well on the micro-bundle scaffold similarly as in the vessels. 3D cell/polymer micro-bundles formed by iVPCs and micro-scaffolds were transplanted into the ischemic myocardium in a rat model of myocardial infarction (MI) with ligation of the left anterior descending artery. Our in vivo data showed that iVPCs on the micro-bundle scaffold had higher survival, and better retention and engraftment in the myocardium than free iVPCs. iVPCs on the micro-bundles promoted better cardiomyocyte survival than free iVPCs. Moreover, iVPCs and iVPC/polymer micro-bundles treatment improved cardiac function (ejection fraction and fractional shortening, endocardial systolic volume) measured by echocardiography, increased vessel density, and decreased infarction size [endocardial and epicardial infarct (scar) length] better than untreated controls at 8 weeks after MI. We conclude that iVPCs grown on a polymer micro-bundle scaffold are new promising approach for cell-based therapy designed for cardiovascular regeneration in ischemic heart disease.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-017-0631-4" target="_blank" rel="noreferrer noopener">10.1007/s00395-017-0631-4</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cardiovascular regeneration
*Ischemic heart diseases
*Micro-bundle scaffold
*Myocardial infarction
*Neovascularization
*Stem cells
*Tissue Scaffolds
*Vascular progenitor cells
2017
Animal
Animals
Basic research in cardiology
Cell Differentiation
Cell Proliferation
Cell Survival
Cells
Chilian William M
Coculture Techniques
Cultured
Cumpston Devan
Department of Integrative Medical Sciences
Disease Models
Dong Feng
Endothelial Progenitor Cells/metabolism/*transplantation
Enrick Molly
Fibroblast Growth Factor 2/metabolism
Hakobyan Tatev
Jamaiyar Anurag
Janota Danielle
Kolz Christopher L
Lactic Acid/*chemistry
Muscle
Myocardial Infarction/metabolism/pathology/physiopathology/*surgery
Myocardium/metabolism/*pathology
Myocytes
NEOMED College of Medicine
Newby Bi-Min Zhang
Ohanyan Vahagn
Paracrine Communication
Phenotype
Physiologic
Polyglycolic Acid/*chemistry
Polylactic Acid-Polyglycolic Acid Copolymer
Rats
Signal Transduction
Smooth
Smooth Muscle/metabolism/*transplantation
Song Hokyung
Sprague-Dawley
Stevanov Kelly
Time Factors
Tissue Engineering/*methods
Vascular Endothelial Growth Factor A/metabolism
Vascular/metabolism/*transplantation
Ventricular Remodeling
Wan Weiguo
Yin Liya
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/hep.26699" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.26699</a>
Pages
1750–1760
Issue
5
Volume
59
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
All-trans-retinoic acid ameliorates hepatic steatosis in mice by a novel transcriptional cascade.
Publisher
An entity responsible for making the resource available
Hepatology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-05
Subject
The topic of the resource
Animals; Basic Helix-Loop-Helix Transcription Factors/genetics; Blood Glucose/analysis; Cytoplasmic and Nuclear/*physiology; Fatty Liver/*drug therapy/metabolism; Gene Expression Regulation; Genetic; Inbred C57BL; Lipid Metabolism; Liver/metabolism; Male; Mice; Non-alcoholic Fatty Liver Disease; PPAR gamma/*genetics; Receptors; Repressor Proteins/genetics; Retinoic Acid Receptor alpha; Retinoic Acid/physiology; Transcription; Tretinoin/pharmacology/*therapeutic use
Creator
An entity primarily responsible for making the resource
Kim Seong-Chul; Kim Chun-Ki; Axe David; Cook Aaron; Lee Mikang; Li Tiangang; Smallwood Nicole; Chiang John Y L; Hardwick James P; Moore David D; Lee Yoon-Kwang
Description
An account of the resource
UNLABELLED: Mice deficient in small heterodimer partner (SHP) are protected from diet-induced hepatic steatosis resulting from increased fatty acid oxidation and decreased lipogenesis. The decreased lipogenesis appears to be a direct consequence of very low expression of peroxisome proliferator-activated receptor gamma 2 (PPAR-gamma2), a potent lipogenic transcription factor, in the SHP(-/-) liver. The current study focused on the identification of a SHP-dependent regulatory cascade that controls PPAR-gamma2 gene expression, thereby regulating hepatic fat accumulation. Illumina BeadChip array (Illumina, Inc., San Diego, CA) and real-time polymerase chain reaction were used to identify genes responsible for the linkage between SHP and PPAR-gamma2 using hepatic RNAs isolated from SHP(-/-) and SHP-overexpressing mice. The initial efforts identify that hairy and enhancer of split 6 (Hes6), a novel transcriptional repressor, is an important mediator of the regulation of PPAR-gamma2 transcription by SHP. The Hes6 promoter is specifically activated by the retinoic acid receptor (RAR) in response to its natural agonist ligand, all-trans retinoic acid (atRA), and is repressed by SHP. Hes6 subsequently represses hepatocyte nuclear factor 4 alpha (HNF-4alpha)-activated PPAR-gamma2 gene expression by direct inhibition of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.26699" target="_blank" rel="noreferrer noopener">10.1002/hep.26699</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Animals
Axe David
Basic Helix-Loop-Helix Transcription Factors/genetics
Blood Glucose/analysis
Chiang John Y L
Cook Aaron
Cytoplasmic and Nuclear/*physiology
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Fatty Liver/*drug therapy/metabolism
Gene Expression Regulation
Genetic
Hardwick James P
Hepatology (Baltimore, Md.)
Inbred C57BL
Kim Chun-Ki
Kim Seong-Chul
Lee Mikang
Lee Yoon-Kwang
Li Tiangang
Lipid Metabolism
Liver/metabolism
Male
Mice
Moore David D
NEOMED College of Medicine
NEOMED College of Pharmacy
Non-alcoholic Fatty Liver Disease
PPAR gamma/*genetics
Receptors
Repressor Proteins/genetics
Retinoic Acid Receptor alpha
Retinoic Acid/physiology
Smallwood Nicole
Transcription
Tretinoin/pharmacology/*therapeutic use
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1096/fasebj.2020.34.s1.03648" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fasebj.2020.34.s1.03648</a>
Issue
1
Volume
34
ISSN
0892-6638
Search for Full-text
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1096/fasebj.2020.34.s1.03648" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1096/fasebj.2020.34.s1.03648</a>
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Update Year & Number
September 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
NEOMED Student Publications
Department of Integrative Medical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Alzheimers disease-related pathology and impaired cognitive function associate with reduced O-GLCNAC transferase in aged metabolic syndrome KKAY(+/-) mice
Publisher
An entity responsible for making the resource available
Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
Creator
An entity primarily responsible for making the resource
Jinka S;Lallo Jason;Gupta S;Mathias A;Khanal S;Al-Rhayyel Y;Herman D;Fleming S;Raman P
Description
An account of the resource
Metabolic syndrome (MetS) refers to a cluster of anomalies including type 2 diabetes, obesity, insulin resistance and dyslipidemia. Patients with MetS are 1.5 times more likely to develop late‐onset Alzheimer’s Disease (AD), with impaired glucose metabolism, defective insulin signaling, increased oxidative stress and inflammation being shared between the comorbid diseases. Notably, risk of AD is profoundly enhanced in the aging MetS population. Recent studies in AD patients and AD mouse models suggest a putative link between hyperphosphorylated tau neurofibrillary tangles, a commonly accepted AD pathology, and cerebral glucose hypometabolism. Impaired glucose metabolism is characterized by reduced glucose flux through the hexosamine metabolic pathway triggering attenuated signaling via O‐linked N‐acetylglucosamine (O‐GlcNAc) transferase (OGT), a major regulator of intracellular protein O‐GlcNAcylation. However, the role of OGT in the etiology of MetS‐induced AD remains incompletely understood. The goal of the present study was to examine the link between cognitive function, AD pathology and OGT signaling in a mouse model of MetS (KKAy+/−) that develops increased body weight, hyperglycemia, elevated total cholesterol and total triglyceride levels. Briefly, male and female obese agouti KKAy+/−, lean non‐agouti KKAy−/− and normal C57BL/6 control mice weaned at 4 wks of age on regular chow diet were subjected to periodic body weight and random blood glucose monitoring followed by a battery of behavioral tests at 12+ months of age. Plasma and brain (frontal cortex and hippocampus) tissues were then harvested from each genotype for biochemical and molecular studies. In an object recognition test of attention and memory, obese KKAy+/− mice showed a more severe impairment in discrimination between a novel and familiar object compared to lean KKAy−/− and normal C57BL/6 mice. Additionally, in a test of spontaneous activity obese KKAy+/− mice made significantly fewer rears vs lean KKAy−/− mice and wild‐type C57BL/6 controls; these results suggest diminished cognitive function in the obese KKAy+/− mice. Furthermore, immunoblotting of brain tissue lysates derived from the agouti KKAy+/− mice revealed increased ptau expression coupled with reduced pERK (signaling mediator of neuronal function) and pGSK (inactive form of tau kinase GSK3β) expression compared to non‐agouti KKAy−/−. Importantly, augmented tau phosphorylation was concomitant to attenuated OGT expression in brain lysates of obese KKAy+/− mice. Together, these data demonstrate a direct association between cognitive dysfunction, AD‐related pathology and reduced OGT expression in aged MetS KKAy+/− mice. Overall, our study implicates a role of OGT in MetS‐induced cognitive decline and AD pathogenesis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1096/fasebj.2020.34.s1.03648" target="_blank" rel="noreferrer noopener">10.1096/fasebj.2020.34.s1.03648</a>
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journalArticle
2020
Al-Rhayyel Y
Department of Integrative Medical Sciences
Faseb Journal
Fleming S
Gupta S
Herman D
Jinka S
journalArticle
Khanal S
Lallo Jason
Mathias A
NEOMED College of Medicine
NEOMED College of Medicine Student
NEOMED Student Publications
Raman P
September 2020 List
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.ijcard.2018.02.053" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ijcard.2018.02.053</a>
Pages
168–169
Volume
259
Dublin Core
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Title
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AMP-activated kinase "Keaps" ischemia/reperfusion-induced necroptosis under control.
Publisher
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International journal of cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-05
Subject
The topic of the resource
*AMP-Activated Protein Kinases; *AMPK; *Apoptosis; *Ischemia/reperfusion; *Myocardium; *Necroptosis; *Necrosis; Apoptosis; Humans; Myocardial Reperfusion Injury; Myocardium
Creator
An entity primarily responsible for making the resource
Kanugula Anantha K; Thodeti Charles K
Identifier
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<a href="http://doi.org/10.1016/j.ijcard.2018.02.053" target="_blank" rel="noreferrer noopener">10.1016/j.ijcard.2018.02.053</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*AMP-Activated Protein Kinases
*AMPK
*Apoptosis
*Ischemia/reperfusion
*Myocardium
*Necroptosis
*Necrosis
2018
Apoptosis
Department of Integrative Medical Sciences
Humans
International journal of cardiology
Kanugula Anantha K
Myocardial Reperfusion Injury
Myocardium
NEOMED College of Medicine
Thodeti Charles K
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/HYPERTENSIONAHA.107.098459" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/HYPERTENSIONAHA.107.098459</a>
Pages
704–711
Issue
3
Volume
51
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Angiotensin II-induced extracellular signal-regulated kinase 1/2 activation is mediated by protein kinase Cdelta and intracellular calcium in adult rat cardiac fibroblasts.
Publisher
An entity responsible for making the resource available
Hypertension (Dallas, Tex. : 1979)
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-03
Subject
The topic of the resource
Acetophenones/pharmacology; Angiotensin II/*physiology; Animals; Benzopyrans/pharmacology; Calcium/*metabolism; Cell Proliferation; Cells; Cultured; Enzyme Activation; ErbB Receptors/metabolism; Fibroblasts/*metabolism; Male; Mitogen-Activated Protein Kinase 1/*metabolism; Mitogen-Activated Protein Kinase 3/*metabolism; Myocardium/*cytology/metabolism; Phorbol Esters/pharmacology; Phosphorylation; Protein Kinase C-delta/genetics/*metabolism; Rats; Signal Transduction/physiology; Sprague-Dawley
Creator
An entity primarily responsible for making the resource
Olson Erik R; Shamhart Patricia E; Naugle Jennifer E; Meszaros J Gary
Description
An account of the resource
Angiotensin II (Ang II)-induced proliferation of cardiac fibroblasts is a major contributing factor to the pathogenesis of cardiac fibrosis. Ang II activates extracellular signal-regulated kinase (ERK) 1/2 to induce cardiac fibroblast proliferation, but the signaling pathways leading to ERK 1/2 activation have not been elucidated in these cells. The goal of the current study was to identify the intracellular mediators of Ang II-induced ERK 1/2 activation in adult rat cardiac fibroblasts. We determined that 100 nmol/L of Ang II-induced ERK 1/2 phosphorylation is inhibited by simultaneous chelation of cytosolic calcium and downregulation of protein kinase C (PKC) by phorbol ester or by the specific PKCdelta inhibitor rottlerin, as well as PKCdelta small interfering RNA, but not by inhibition of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate, phorbol ester, rottlerin, or PKCdelta small interfering RNA alone. We also found that Ang II does not transactivate the epidermal growth factor receptor in adult cardiac fibroblasts, because pretreatment with 1 mumol/L of AG 1478 did not significantly inhibit [(3)H]-thymidine incorporation or ERK 1/2 activation. In addition, immunoprecipitation of the epidermal growth factor receptor demonstrated no significant Ang II-induced phosphorylation of tyrosine residues. Inhibition of phosphatidylinositide 3-kinase, PKCzeta, and src tyrosine kinase had no effect on Ang II-induced ERK 1/2 activation. Collectively, these data demonstrate that Ang II does not transactivate the epidermal growth factor receptor in adult rat cardiac fibroblasts to activate ERK 1/2, a common pathway described in vascular smooth muscle and other cell types, but rather occurs via activation of distinct parallel signaling pathways mechanistically controlled by intracellular Ca(2+) and PKCdelta.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/HYPERTENSIONAHA.107.098459" target="_blank" rel="noreferrer noopener">10.1161/HYPERTENSIONAHA.107.098459</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2008
Acetophenones/pharmacology
Angiotensin II/*physiology
Animals
Benzopyrans/pharmacology
Calcium/*metabolism
Cell Proliferation
Cells
Cultured
Department of Integrative Medical Sciences
Enzyme Activation
ErbB Receptors/metabolism
Fibroblasts/*metabolism
Hypertension (Dallas, Tex. : 1979)
Male
Meszaros J Gary
Mitogen-Activated Protein Kinase 1/*metabolism
Mitogen-Activated Protein Kinase 3/*metabolism
Myocardium/*cytology/metabolism
Naugle Jennifer E
NEOMED College of Medicine
Olson Erik R
Phorbol Esters/pharmacology
Phosphorylation
Protein Kinase C-delta/genetics/*metabolism
Rats
Shamhart Patricia E
Signal Transduction/physiology
Sprague-Dawley
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1039/c6nr00398b" target="_blank" rel="noreferrer noopener">http://doi.org/10.1039/c6nr00398b</a>
Pages
6542–6554
Issue
12
Volume
8
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Anti-atherogenic effect of trivalent chromium-loaded CPMV nanoparticles in human aortic smooth muscle cells under hyperglycemic conditions in vitro.
Publisher
An entity responsible for making the resource available
Nanoscale
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-03
Subject
The topic of the resource
*Comovirus; Aorta/*metabolism; Atherosclerosis/*drug therapy/therapy; Azo Compounds/chemistry; Cell Proliferation; Cells; Chlorides/*chemistry; Chromium Compounds/*chemistry; Cultured; Cytokines/metabolism; Drug Delivery Systems; Electron; Fluorescence; Glucose/chemistry; Humans; Hyperglycemia/*metabolism; Lipids/chemistry; Microscopy; Myocytes; Nanoparticles/chemistry; NF-kappa B/metabolism; Proliferating Cell Nuclear Antigen/chemistry; Smooth Muscle/*metabolism; Spectrophotometry; Transforming Growth Factor beta/metabolism; Transmission; Ultraviolet
Creator
An entity primarily responsible for making the resource
Ganguly Rituparna; Wen Amy M; Myer Ashley B; Czech Tori; Sahu Soumyadip; Steinmetz Nicole F; Raman Priya
Description
An account of the resource
Atherosclerosis, a major macrovascular complication associated with diabetes, poses a tremendous burden on national health care expenditure. Despite extensive efforts, cost-effective remedies are unknown. Therapies for atherosclerosis are challenged by a lack of targeted drug delivery approaches. Toward this goal, we turn to a biology-derived drug delivery system utilizing nanoparticles formed by the plant virus, Cowpea mosaic virus (CPMV). The aim herein is to investigate the anti-atherogenic potential of the beneficial mineral nutrient, trivalent chromium, loaded CPMV nanoparticles in human aortic smooth muscle cells (HASMC) under hyperglycemic conditions. A non-covalent loading protocol is established yielding CrCl3-loaded CPMV (CPMV-Cr) carrying 2000 drug molecules per particle. Using immunofluorescence microscopy, we show that CPMV-Cr is readily taken up by HASMC in vitro. In glucose (25 mM)-stimulated cells, 100 nM CPMV-Cr inhibits HASMC proliferation concomitant to attenuated proliferating cell nuclear antigen (PCNA, proliferation marker) expression. This is accompanied by attenuation in high glucose-induced phospho-p38 and pAkt expression. Moreover, CPMV-Cr inhibits the expression of pro-inflammatory cytokines, transforming growth factor-beta (TGF-beta) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB), in glucose-stimulated HASMCs. Finally glucose-stimulated lipid uptake is remarkably abrogated by CPMV-Cr, revealed by Oil Red O staining. Together, these data provide key cellular evidence for an atheroprotective effect of CPMV-Cr in vascular smooth muscle cells (VSMC) under hyperglycemic conditions that may promote novel therapeutic ventures for diabetic atherosclerosis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1039/c6nr00398b" target="_blank" rel="noreferrer noopener">10.1039/c6nr00398b</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Comovirus
2016
Aorta/*metabolism
Atherosclerosis/*drug therapy/therapy
Azo Compounds/chemistry
Cell Proliferation
Cells
Chlorides/*chemistry
Chromium Compounds/*chemistry
Cultured
Cytokines/metabolism
Czech Tori
Department of Integrative Medical Sciences
Drug Delivery Systems
Electron
Fluorescence
Ganguly Rituparna
Glucose/chemistry
Humans
Hyperglycemia/*metabolism
Lipids/chemistry
Microscopy
Myer Ashley B
Myocytes
Nanoparticles/chemistry
Nanoscale
NEOMED College of Medicine
NF-kappa B/metabolism
Proliferating Cell Nuclear Antigen/chemistry
Raman Priya
Sahu Soumyadip
Smooth Muscle/*metabolism
Spectrophotometry
Steinmetz Nicole F
Transforming Growth Factor beta/metabolism
Transmission
Ultraviolet
Wen Amy M
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3389/fnins.2019.01166" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fnins.2019.01166</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1166
Volume
13
ISSN
1662-4548
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.3389/fnins.2019.01166" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.3389/fnins.2019.01166</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
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Title
A name given to the resource
Astrocyte Infection Is Required for Retrovirus-Induced Spongiform Neurodegeneration Despite Suppressed Viral Protein Expression
Publisher
An entity responsible for making the resource available
Frontiers In Neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
1905-07
Subject
The topic of the resource
astrocytes; retrovirus; neural stem cells; glia; spongiform neurodegeneration; neural progenitor cells; neurotropism; virus suppression
Creator
An entity primarily responsible for making the resource
Cardona Sandra M; Dunphy Jaclyn M; Das Alvin S; Lynch Connor R; Lynch William P
Description
An account of the resource
The ability of retroviruses (RVs) to cause neurodegeneration is critically dependent upon two activities of the envelope protein (Env). First, Env facilitates viral genome delivery to CNS target cells through receptor binding and membrane fusion. Second, Env expression within one or more targets indirectly alters the physiology of certain neurons. Although the major Env expressing CNS cell types have been identified for many neurovirulent RVs, it remains unresolved, which targets play a causal role in neuropathogenesis. Moreover, this issue is complicated by the potential for post-infection virus suppression. To address these questions we explored herein, whether and how cryptic neurotropism differences between ecotropic and amphotropic murine leukemia viruses (MLVs) impacted neurovirulence. Neurotropism was first explored ex vivo using (1) acute primary glial cell cultures and (2) neural progenitor cell (NPC)- neural stem cell (NSC) neural sphere (NPH) chimeras. These experiments indicated that primary astrocytes and NPCs acutely restrict amphotropic but not ecotropic virus entry. CNS tropism was investigated using NSC transplant-based Cre-vector pseudotyping wherein mTmG transgenic fluorescent protein reporter mice revealed both productive and suppressed infection. Cre-pseudotyping with FrCasE, a prototypic neurovirulent ecotropic virus, identified glia and endothelia, but not neurons, as targets. Almost two-thirds (62%) of mGFP+ cells failed to show Env expression, suggesting widespread virus suppression. To circumvent RV superinfection interference confounds, targets were also identified using ecotropic packaging NSCs. These experiments identified known ecotropic targets: microglia, oligodendrocyte progenitor cells (OPCs) and endothelia. Additionally, one third of mGFP+ cells were identified as protoplasmic astrocytes, cells that rarely express virus in vivo. A CNS targeting comparison between isogenic ecotropic (FrCasE) and amphotropic (FrAmE) viruses showed a fourfold higher astrocyte targeting by FrCasE. Since ecotropic Env pseudotyping of amphotropic virus in the CNS dramatically exacerbates neurodegeneration, these results strongly suggest that astrocyte infection is a major disease requirement. Moreover, since viral Env protein expression is largely subdetectable in astrocytes, minimal viral protein expression appears sufficient for affecting neuronal physiology. More broadly, these findings raise the specter that subdetectable astrocyte expression of exogenous or endogenous RVs could play a major role in human and animal neurodegenerative diseases.
Identifier
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<a href="http://doi.org/10.3389/fnins.2019.01166" target="_blank" rel="noreferrer noopener">10.3389/fnins.2019.01166</a>
PMID: 31736699 PMCID: PMC6828646
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Astrocytes
Cardona Sandra M
Das Alvin S
Department of Integrative Medical Sciences
Dunphy Jaclyn M
Frontiers in neuroscience
glia
Journal Article
Lynch Connor R
Lynch William P
NEOMED College of Medicine
neural progenitor cells
Neural stem cells
neurotropism
November 2019 Update
retrovirus
spongiform neurodegeneration
virus suppression
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCULATIONAHA.116.024826" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCULATIONAHA.116.024826</a>
Pages
1240–1252
Issue
13
Volume
135
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Augmentation of Muscle Blood Flow by Ultrasound Cavitation Is Mediated by ATP and Purinergic Signaling.
Publisher
An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-03
Subject
The topic of the resource
Adenosine Triphosphate – Metabolism; Adenosine Triphosphate/*metabolism; Animal Studies; Animals; contrast echocardiography; Equipment and Supplies; Hemodynamics; Humans; Inbred C57BL; Male; Mice; microbubbles; Microbubbles; microcirculation; Muscle; Neurotransmitter Agents – Metabolism; perfusion; Purinergic Agents/*metabolism; Signal Transduction; Skeletal – Blood Supply; Skeletal/*blood supply; Ultrasonography – Methods; Ultrasonography/*methods
Creator
An entity primarily responsible for making the resource
Belcik J Todd; Davidson Brian P; Xie Aris; Wu Melinda D; Yadava Mrinal; Qi Yue; Liang Sherry; Chon Chae Ryung; Ammi Azzdine Y; Field Joshua; Harmann Leanne; Chilian William M; Linden Joel; Lindner Jonathan R
Description
An account of the resource
BACKGROUND: Augmentation of tissue blood flow by therapeutic ultrasound is thought to rely on convective shear. Microbubble contrast agents that undergo ultrasound-mediated cavitation markedly amplify these effects. We hypothesized that purinergic signaling is responsible for shear-dependent increases in muscle perfusion during therapeutic cavitation. METHODS: Unilateral exposure of the proximal hindlimb of mice (with or without ischemia produced by iliac ligation) to therapeutic ultrasound (1.3 MHz, mechanical index 1.3) was performed for 10 minutes after intravenous injection of 2x10(8) lipid microbubbles. Microvascular perfusion was evaluated by low-power contrast ultrasound perfusion imaging. In vivo muscle ATP release and in vitro ATP release from endothelial cells or erythrocytes were assessed by a luciferin-luciferase assay. Purinergic signaling pathways were assessed by studying interventions that (1) accelerated ATP degradation; (2) inhibited P2Y receptors, adenosine receptors, or KATP channels; or (3) inhibited downstream signaling pathways involving endothelial nitric oxide synthase or prostanoid production (indomethacin). Augmentation in muscle perfusion by ultrasound cavitation was assessed in a proof-of-concept clinical trial in 12 subjects with stable sickle cell disease. RESULTS: Therapeutic ultrasound cavitation increased muscle perfusion by 7-fold in normal mice, reversed tissue ischemia for up to 24 hours in the murine model of peripheral artery disease, and doubled muscle perfusion in patients with sickle cell disease. Augmentation in flow extended well beyond the region of ultrasound exposure. Ultrasound cavitation produced an approximately 40-fold focal and sustained increase in ATP, the source of which included both endothelial cells and erythrocytes. Inhibitory studies indicated that ATP was a critical mediator of flow augmentation that acts primarily through either P2Y receptors or adenosine produced by ectonucleotidase activity. Combined indomethacin and inhibition of endothelial nitric oxide synthase abolished the effects of therapeutic ultrasound, indicating downstream signaling through both nitric oxide and prostaglandins. CONCLUSIONS: Therapeutic ultrasound using microbubble cavitation to increase muscle perfusion relies on shear-dependent increases in ATP, which can act through a diverse portfolio of purinergic signaling pathways. These events can reverse hindlimb ischemia in mice for \textgreater24 hours and increase muscle blood flow in patients with sickle cell disease. CLINICAL TRIAL REGISTRATION: URL: http://clinicaltrials.gov. Unique identifier: NCT01566890.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCULATIONAHA.116.024826" target="_blank" rel="noreferrer noopener">10.1161/CIRCULATIONAHA.116.024826</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Adenosine Triphosphate – Metabolism
Adenosine Triphosphate/*metabolism
Ammi Azzdine Y
Animal Studies
Animals
Belcik J Todd
Chilian William M
Chon Chae Ryung
Circulation
contrast echocardiography
Davidson Brian P
Department of Integrative Medical Sciences
Equipment and Supplies
Field Joshua
Harmann Leanne
Hemodynamics
Humans
Inbred C57BL
Liang Sherry
Linden Joel
Lindner Jonathan R
Male
Mice
Microbubbles
Microcirculation
Muscle
NEOMED College of Medicine
Neurotransmitter Agents – Metabolism
Perfusion
Purinergic Agents/*metabolism
Qi Yue
Signal Transduction
Skeletal – Blood Supply
Skeletal/*blood supply
Ultrasonography – Methods
Ultrasonography/*methods
Wu Melinda D
Xie Aris
Yadava Mrinal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1006/bbrc.1998.9759" target="_blank" rel="noreferrer noopener">http://doi.org/10.1006/bbrc.1998.9759</a>
Pages
109–113
Issue
1
Volume
253
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Basic transcription element binding protein (BTEB) transactivates the cholesterol 7 alpha-hydroxylase gene (CYP7A).
Publisher
An entity responsible for making the resource available
Biochemical and biophysical research communications
Date
A point or period of time associated with an event in the lifecycle of the resource
1998
1998-12
Subject
The topic of the resource
*Gene Expression Regulation; Animals; Bile Acids and Salts/genetics; Binding Sites/genetics; Carcinoma; Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism; Complementary/analysis; Cultured; DNA; DNA-Binding Proteins/metabolism/*physiology; Electrophoresis; Enzyme Activation/genetics; Genetic; Hepatocellular; Humans; Kruppel-Like Transcription Factors; Liver/enzymology; Podophyllin/analogs & derivatives/metabolism; Podophyllotoxin/analogs & derivatives; Polyacrylamide Gel; Promoter Regions; Protein Binding/genetics; Rats; Transcription Factors/metabolism/*physiology; Tumor Cells
Creator
An entity primarily responsible for making the resource
Foti D; Stroup D; Chiang J Y
Description
An account of the resource
Cholesterol 7 alpha-hydroxylase catalyzes the first and rate-limiting step in the conversion of cholesterol to bile acids in the liver. Previously, we have identified two bile acid response elements located in nt -74 to -54 (BARE-I) and -148 to -118 (BARE-II) regions. The nucleotide sequences in these BAREs are highly conserved and shared a novel sequence, AGTTCAAG. To identify and isolate nuclear protein factors that bind to these BAREs, we have screened a human liver cDNA expression library with oligonucleotide probes containing the sequence from nt -149 to -127. Twenty positive clones were selected and purified. Partial nucleotide sequences of these clones were determined. Nucleotide homology search of DNA databases of the sequences of these clones revealed that sequence of one clone, G13, is identical to basic transcription element binding protein (BTEB), a GC box-binding protein of Sp1 family transcription factors known to regulate many cytochrome P450 genes. Electrophoretic mobility shift assays have identified a basic transcription element (BTE) in BARE-II and a Sp1 binding site located in the nt -100/-82 region of the CYP7A promoter. Transient transfection assays have confirmed that BTEB was able to transactivate the CYP7A promoter/luciferase chimergic gene.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1006/bbrc.1998.9759" target="_blank" rel="noreferrer noopener">10.1006/bbrc.1998.9759</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
1998
Animals
Bile Acids and Salts/genetics
Binding Sites/genetics
Biochemical and biophysical research communications
Carcinoma
Chiang J Y
Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism
Complementary/analysis
Cultured
Department of Integrative Medical Sciences
DNA
DNA-Binding Proteins/metabolism/*physiology
Electrophoresis
Enzyme Activation/genetics
Foti D
Genetic
Hepatocellular
Humans
Kruppel-Like Transcription Factors
Liver/enzymology
NEOMED College of Medicine
Podophyllin/analogs & derivatives/metabolism
Podophyllotoxin/analogs & derivatives
Polyacrylamide Gel
Promoter Regions
Protein Binding/genetics
Rats
Stroup D
Transcription Factors/metabolism/*physiology
Tumor Cells
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.bcp.2014.03.012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bcp.2014.03.012</a>
Pages
490–502
Issue
4
Volume
89
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
BCNU-induced gR2 defect mediates S-glutathionylation of Complex I and respiratory uncoupling in myocardium.
Publisher
An entity responsible for making the resource available
Biochemical pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-06
Subject
The topic of the resource
Alkylating/*adverse effects/pharmacology; Animals; Antineoplastic Agents; Cardiotoxins/adverse effects/pharmacology; Carmustine/*adverse effects/pharmacology; Cattle; Cell Line; Complex I; Electron Transport Complex I/chemistry/*metabolism; Fatty Acids; Glutathione reductase; Glutathione Reductase/*antagonists & inhibitors/metabolism; Glutathione/*metabolism; Heart Ventricles/drug effects/metabolism/physiopathology; Heart/*drug effects/metabolism; Ion Channels/metabolism; Left/*chemically induced/metabolism/physiopathology; Male; Mice; Mitochondria; Mitochondrial Proteins/metabolism; Nonesterified/metabolism; Oxidative stress; Oxidative Stress/drug effects; Post-Translational/drug effects; Protein Processing; Rats; S-Glutathionylation; Sprague-Dawley; Superoxide Dismutase/genetics/metabolism; Systolic dysfunction; Transgenic; Uncoupling Protein 3; Ventricular Dysfunction
Creator
An entity primarily responsible for making the resource
Kang Patrick T; Chen Chwen-Lih; Ren Pei; Guarini Giacinta; Chen Yeong-Renn
Description
An account of the resource
A deficiency of mitochondrial glutathione reductase (or GR2) is capable of adversely affecting the reduction of GSSG and increasing mitochondrial oxidative stress. BCNU [1,3-bis (2-chloroethyl)-1-nitrosourea] is an anticancer agent and known inhibitor of cytosolic GR ex vivo and in vivo. Here we tested the hypothesis that a BCNU-induced GR2 defect contributes to mitochondrial dysfunction and subsequent impairment of heart function. Intraperitoneal administration of BCNU (40 mg/kg) specifically inhibited GR2 activity by 79.8 +/- 2.7% in the mitochondria of rat heart. However, BCNU treatment modestly enhanced the activities of mitochondrial Complex I and other ETC components. The cardiac function of BCNU-treated rats was analyzed by echocardiography, revealing a systolic dysfunction associated with decreased ejection fraction, decreased cardiac output, and an increase in left ventricular internal dimension and left ventricular volume in systole. The respiratory control index of isolated mitochondria from the myocardium was moderately decreased after BCNU treatment, whereas NADH-linked uncoupling of oxygen consumption was significantly enhanced. Extracellular flux analysis to measure the fatty acid oxidation of myocytes indicated a 20% enhancement after BCNU treatment. When the mitochondria were immunoblotted with antibodies against GSH and UCP3, both protein
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bcp.2014.03.012" target="_blank" rel="noreferrer noopener">10.1016/j.bcp.2014.03.012</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Alkylating/*adverse effects/pharmacology
Animals
Antineoplastic Agents
Biochemical pharmacology
Cardiotoxins/adverse effects/pharmacology
Carmustine/*adverse effects/pharmacology
Cattle
Cell Line
Chen Chwen-Lih
Chen Yeong-Renn
Complex I
Department of Integrative Medical Sciences
Electron Transport Complex I/chemistry/*metabolism
Fatty Acids
Glutathione reductase
Glutathione Reductase/*antagonists & inhibitors/metabolism
Glutathione/*metabolism
Guarini Giacinta
Heart Ventricles/drug effects/metabolism/physiopathology
Heart/*drug effects/metabolism
Ion Channels/metabolism
Kang Patrick T
Left/*chemically induced/metabolism/physiopathology
Male
Mice
Mitochondria
Mitochondrial Proteins/metabolism
NEOMED College of Medicine
Nonesterified/metabolism
Oxidative Stress
Oxidative Stress/drug effects
Post-Translational/drug effects
Protein Processing
Rats
Ren Pei
S-Glutathionylation
Sprague-Dawley
Superoxide Dismutase/genetics/metabolism
Systolic dysfunction
Transgenic
Uncoupling Protein 3
Ventricular Dysfunction
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajplung.90629.2008" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.90629.2008</a>
Pages
L487–495
Issue
3
Volume
297
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Beta-adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure.
Publisher
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American journal of physiology. Lung cellular and molecular physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-09
Subject
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Adrenergic; Animals; beta/*metabolism; Body Fluids/*metabolism; Epithelial Cells/drug effects/metabolism/pathology; Gene Expression Regulation/drug effects; Heart Failure/blood/diagnostic imaging/*metabolism/*pathology; Hormones/blood; Hyperplasia; Ion Channels/genetics/metabolism; Male; Messenger/genetics/metabolism; Myocardial Infarction/blood/diagnostic imaging/pathology; Pulmonary Alveoli/drug effects/*pathology; Rats; Receptors; RNA; Sprague-Dawley; Terbutaline/pharmacology; Ultrasonography
Creator
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Maron Michael B; Luther Daniel J; Pilati Charles F; Ohanyan Vahagn; Li Tianbo; Koshy Shyny; Horne Walter I; Meszaros J Gary; Walro Jon M; Folkesson Hans G
Description
An account of the resource
The alveolar epithelium plays a critical role in resolving pulmonary edema. We thus hypothesized that its function might be upregulated in rats with heart failure, a condition that severely challenges the lung's ability to maintain fluid balance. Heart failure was induced by left coronary artery ligation. Echocardiographic and cardiovascular hemodynamics confirmed its development at 16 wk postligation. At that time, alveolar fluid clearance was measured by an increase in protein concentration over 1 h of a 5% albumin solution instilled into the lungs. Baseline alveolar fluid clearance was similar in heart failure and age-matched control rats. Terbutaline was added to the instillate to determine whether heart failure rats responded to beta-adrenoceptor stimulation. Alveolar fluid clearance in heart failure rats was increased by 194% after terbutaline stimulation compared with a 153% increase by terbutaline in control rats. To determine the mechanisms responsible for this accelerated alveolar fluid clearance, we measured ion transporter expression (ENaC, Na-K- ATPase, CFTR). No significant upregulation was observed for these ion transporters in the heart failure rats. Lung morphology showed significant alveolar epithelial type II cell hyperplasia in heart failure rats. Thus, alveolar epithelial type II cell hyperplasia is the likely explanation for the increased terbutaline-stimulated alveolar fluid clearance in heart failure rats. These data provide evidence for previously unrecognized mechanisms that can protect against or hasten resolution of alveolar edema in heart failure.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajplung.90629.2008" target="_blank" rel="noreferrer noopener">10.1152/ajplung.90629.2008</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2009
Adrenergic
American journal of physiology. Lung cellular and molecular physiology
Animals
beta/*metabolism
Body Fluids/*metabolism
Department of Integrative Medical Sciences
Epithelial Cells/drug effects/metabolism/pathology
Folkesson Hans G
Gene Expression Regulation/drug effects
Heart Failure/blood/diagnostic imaging/*metabolism/*pathology
Hormones/blood
Horne Walter I
Hyperplasia
Ion Channels/genetics/metabolism
Koshy Shyny
Li Tianbo
Luther Daniel J
Male
Maron Michael B
Messenger/genetics/metabolism
Meszaros J Gary
Myocardial Infarction/blood/diagnostic imaging/pathology
NEOMED College of Medicine
Ohanyan Vahagn
Pilati Charles F
Pulmonary Alveoli/drug effects/*pathology
Rats
Receptors
RNA
Sprague-Dawley
Terbutaline/pharmacology
Ultrasonography
Walro Jon M
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/cld.861" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/cld.861</a>
Pages
91-94
Issue
3
Volume
15
ISSN
2046-2484 2046-2484
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Update Year & Number
June 2020 Update I
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Bile Acid Biology, Pathophysiology, and Therapeutics.
Publisher
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Clinical liver disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-03
Creator
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Chiang John Y L; Ferrell Jessica M
Description
An account of the resource
http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/vide o/15-3-reading-chiang a video presentation of this article http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/vide o/15-3-interview-chiang an interview with the author.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/cld.861" target="_blank" rel="noreferrer noopener">10.1002/cld.861</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
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journalArticle
2020
Chiang John Y L
Clinical liver disease
Department of Integrative Medical Sciences
Ferrell Jessica M
Journal Article
journalArticle
June 2020 Update I
NEOMED College of Graduate Studies
NEOMED College of Medicine