1
40
5
-
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.apsb.2015.01.003" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.apsb.2015.01.003</a>
Pages
113–122
Issue
2
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
Circadian rhythms in liver metabolism and disease.
Publisher
An entity responsible for making the resource available
Acta pharmaceutica Sinica. B
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-03
Subject
The topic of the resource
ARC; arcuate nucleus; BMAL1; brain and muscle ARNT-like 1; CAR; cholesterol 7alpha-hydroxylase; circadian locomotor output cycles kaput; Circadian rhythm; CLOCK; constitutive androstane receptor; CRY; cryptochrome; CYP7A1; CYPs; cytochrome P450 enzymes; D-site binding protein; DBP; E-box; emergency medical technician; EMT; enhance box; FAA; familial advanced sleep-phase syndrome; farnesoid-X receptor; FASPS; FEO; food anticipatory activity; food entrainable oscillator; forkhead box O3; FOXO3; FXR; G protein-coupled bile acid receptor; glucose transporter 2; GLUT2; HDAC3; hepatic leukemia factor; HIP; histone deacetylase 3; HLF; hypoxia inducing protein; LDL; Liver; liver receptor homolog 1; low-density lipoprotein; LRH1; Metabolic syndrome; NAD+; nicotinamide adenine dinucleotide; PER; period; retinohypothalamic tract; retinoid-related orphan receptor alpha; RHT; ROR-response element; RORalpha; RORE; SCN; SHP; SIRT1; sirtuin 1; small heterodimer partner; suprachiasmatic nucleus; TEF; TGR5; thyrotroph embryonic factor; transcriptional translational feedback loop; TTFL; Type 2 diabetes
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Chiang John Y L
Description
An account of the resource
Mounting research evidence demonstrates a significant negative impact of circadian disruption on human health. Shift work, chronic jet lag and sleep disturbances are associated with increased incidence of metabolic syndrome, and consequently result in obesity, type 2 diabetes and dyslipidemia. Here, these associations are reviewed with respect to liver metabolism and disease.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.apsb.2015.01.003" target="_blank" rel="noreferrer noopener">10.1016/j.apsb.2015.01.003</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
Acta pharmaceutica Sinica. B
ARC
arcuate nucleus
BMAL1
brain and muscle ARNT-like 1
CAR
Chiang John Y L
cholesterol 7alpha-hydroxylase
circadian locomotor output cycles kaput
Circadian Rhythm
CLOCK
constitutive androstane receptor
CRY
cryptochrome
CYP7A1
CYPs
cytochrome P450 enzymes
D-site binding protein
DBP
Department of Integrative Medical Sciences
E-box
emergency medical technician
EMT
enhance box
FAA
familial advanced sleep-phase syndrome
farnesoid-X receptor
FASPS
FEO
Ferrell Jessica M
food anticipatory activity
food entrainable oscillator
forkhead box O3
FOXO3
FXR
G protein-coupled bile acid receptor
glucose transporter 2
GLUT2
HDAC3
hepatic leukemia factor
Hip
histone deacetylase 3
HLF
hypoxia inducing protein
LDL
Liver
liver receptor homolog 1
Low-density lipoprotein
LRH1
Metabolic syndrome
NAD+
NEOMED College of Medicine
nicotinamide adenine dinucleotide
PER
period
retinohypothalamic tract
retinoid-related orphan receptor alpha
RHT
ROR-response element
RORalpha
RORE
SCN
SHP
SIRT1
sirtuin 1
small heterodimer partner
suprachiasmatic nucleus
TEF
TGR5
thyrotroph embryonic factor
transcriptional translational feedback loop
TTFL
Type 2 diabetes
-
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.00888.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00888.2009</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
H1182-H1189
Issue
4
Volume
298
Search for Full-text
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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
Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation
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
2010
2010-04
Subject
The topic of the resource
potassium channels; exercise; Physiology; Cardiovascular System & Cardiology; blood flow; activation; smooth-muscle-cells; heart; adenosine; adenosine triphosphate-dependent; arterioles; calcium-activated potassium channels; cardiovascular-disease mortality; coronary reactive hyperemia; myocardial reactive hyperemia; Ossabaw miniature swine; sensitive potassium channels; type 2 diabetes; voltage-activated potassium channels
Creator
An entity primarily responsible for making the resource
Borbouse L; Dick G M; Payne G A; Berwick Z C; Neeb Z P; Alloosh M; Bratz I N; Sturek M; Tune J D
Description
An account of the resource
Borbouse L, Dick GM, Payne GA, Berwick ZC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation. Am J Physiol Heart Circ Physiol 298: H1182-H1189, 2010. First published January 29, 2010; doi: 10.1152/ajpheart.00888.2009.-This investigation tested the hypothesis that metabolic syndrome decreases the relative contribution of specific K+ channels to coronary reactive hyperemia. Ca2+-activated (BKCa), voltage-activated (K-V), and ATP-dependent (K-ATP) K+ channels were investigated. Studies were conducted in anesthetized miniature Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) for 20 wk. The latter diet induces metabolic syndrome, increasing body weight, fasting glucose, total cholesterol, and triglyceride levels. Ischemic vasodilation was determined by the coronary flow response to a 15-s occlusion before and after cumulative administration of antagonists for BKCa (penitrem A; 10 mu g/kg iv), K-V (4-aminopyridine; 0.3 mg/kg iv) and K-ATP (glibenclamide; 1 mg/kg iv) channels. Coronary reactive hyperemia was diminished by metabolic syndrome as the repayment of flow debt was reduced similar to 30% compared with lean swine. Inhibition of BKCa channels had no effect on reactive hyperemia in either lean or metabolic syndrome swine. Subsequent inhibition of KV channels significantly reduced the repayment of flow debt (similar to 25%) in both lean and metabolic syndrome swine. Additional blockade of K-ATP channels further diminished (similar to 45%) the repayment of flow debt in lean but not metabolic syndrome swine. These data indicate that the metabolic syndrome impairs coronary vasodilation in response to cardiac ischemia via reductions in the contribution of K+ channels to reactive hyperemia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00888.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00888.2009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
activation
adenosine
adenosine triphosphate-dependent
Alloosh M
American Journal of Physiology-Heart and Circulatory Physiology
Arterioles
Berwick Z C
blood flow
Borbouse L
Bratz I N
calcium-activated potassium channels
Cardiovascular System & Cardiology
cardiovascular-disease mortality
coronary reactive hyperemia
Dick G M
Exercise
heart
Journal Article or Conference Abstract Publication
myocardial reactive hyperemia
Neeb Z P
Ossabaw miniature swine
Payne G A
Physiology
Potassium Channels
sensitive potassium channels
smooth-muscle-cells
Sturek M
Tune J D
Type 2 diabetes
voltage-activated potassium channels
-
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
n/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
2-2
Issue
21
Volume
124
Search for Full-text
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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
Targeting Mitochondrial Dna To Reduce Consequences Of Oxidative Stress: Role In The Prevention Of The Diabetic Cardiomyopathy
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
2011
2011-11
Subject
The topic of the resource
arrhythmias; Cardiovascular System & Cardiology; Coronary circulation; Coronary microcirculation; heart failure; Mitochondrial energetics; oxidative stress; Type 2 Diabetes
Creator
An entity primarily responsible for making the resource
Guarini G; Kolz C L; Pung Y F; Ohanyan V A; Yin L Y; Bratz I N; Marzilli M; Chilian W M
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
Arrhythmias
Bratz I N
Cardiovascular System & Cardiology
Chilian W M
Circulation
Coronary Circulation
Coronary microcirculation
Guarini G
Heart failure
Journal Article or Conference Abstract Publication
Kolz C L
Marzilli M
Mitochondrial energetics
Ohanyan V A
Oxidative Stress
Pung Y F
Type 2 diabetes
Yin L Y
-
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/10.3390/biom10040520" target="_blank" rel="noreferrer noopener">http://doi.org/10.3390/biom10040520</a>
Issue
4
Volume
10
ISSN
2218-273X 2218-273X
Search for Full-text
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.3390/biom10040520" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.3390/biom10040520</a>
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Update Year & Number
June 2020 Update I
NEOMED College
NEOMED College of Pharmacy
NEOMED Department
Department of Pharmaceutical 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
Temporal Dynamics of High-Density Lipoprotein Proteome in Diet-Controlled Subjects with Type 2 Diabetes.
Publisher
An entity responsible for making the resource available
Biomolecules
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-03-30
Subject
The topic of the resource
apolipoproteins; HDL dysfunction; heavy water; proteomics; type 2 diabetes
Creator
An entity primarily responsible for making the resource
Kheniser Karim G; Osme Abdullah; Kim Chunki; Ilchenko Serguei; Kasumov Takhar; Kashyap Sangeeta R
Description
An account of the resource
We examined the effect of mild hyperglycemia on high-density lipoprotein (HDL) metabolism and kinetics in diet-controlled subjects with type 2 diabetes (T2D). (2)H2O-labeling coupled with mass spectrometry was applied to quantify HDL cholesterol turnover and HDL proteome dynamics in subjects with T2D (n = 9) and age- and BMI-matched healthy controls (n = 8). The activities of lecithin-cholesterol acyltransferase (LCAT), cholesterol ester transfer protein (CETP), and the proinflammatory index of HDL were quantified. Plasma adiponectin levels were reduced in subjects with T2D, which was directly associated with suppressed ABCA1-dependent cholesterol efflux capacity of HDL. The fractional catabolic rates of HDL cholesterol, apolipoprotein A-II (ApoA-II), ApoJ, ApoA-IV, transthyretin, complement C3, and vitamin D-binding protein (all p < 0.05) were increased in subjects with T2D. Despite increased HDL flux of acute-phase HDL proteins, there was no change in the proinflammatory index of HDL. Although LCAT and CETP activities were not affected in subjects with T2D, LCAT was inversely associated with blood glucose and CETP was inversely associated with plasma adiponectin. The degradation rates of ApoA-II and ApoA-IV were correlated with hemoglobin A1c. In conclusion, there were in vivo impairments in HDL proteome dynamics and HDL metabolism in diet-controlled patients with T2D.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3390/biom10040520" target="_blank" rel="noreferrer noopener">10.3390/biom10040520</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
Apolipoproteins
Biomolecules
Department of Pharmaceutical Sciences
HDL dysfunction
Heavy water
Ilchenko Serguei
Journal Article
journalArticle
June 2020 Update I
Kashyap Sangeeta R
Kasumov Takhar
Kheniser Karim G
Kim Chunki
NEOMED College of Pharmacy
Osme Abdullah
proteomics
Type 2 diabetes
-
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.lfs.2020.117913" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.lfs.2020.117913</a>
Pages
117913
Volume
256
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/10.1016/j.lfs.2020.117913" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.lfs.2020.117913</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
July 2020 List
NEOMED College
NEOMED College of Medicine Postdoc
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
The C1q/TNF-related proteins (CTRPS) in pathogenesis of obesity-related metabolic disorders: Focus on type 2 diabetes and cardiovascular diseases.
Publisher
An entity responsible for making the resource available
Life Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-06
Subject
The topic of the resource
Obesity; Type 2 diabetes; Cardiovascular diseases; C1q/TNF-related proteins (CTRPs)
Creator
An entity primarily responsible for making the resource
Shanaki M; Shabani P; Goudarzi A; Omidifar A; Bashash D; Emamgholipour S
Description
An account of the resource
The growing evidence has been tried to explain and characterize C1q/TNF- related proteins (CTRPs) family as the potential diagnostic or therapeutic targets of obesity-related metabolic disorders such as insulin resistance, type 2 diabetes (T2D), and cardiovascular disorders. However, the underlying mechanism is still obscure. Unraveling the signaling pathways downstream of CTRP family members is of great interest and could certainly be beneficial for finding new insights into therapeutic strategies for improving metabolic abnormalities. This review focused on the role of CTRP members in the initiation and development of obesity-related metabolic disorders with a focus on T2D and cardiovascular diseases. Here we summarize and discuss the role of CTRPs in the regulation of insulin signaling, inflammatory pathways, and energy metabolism, and other signaling pathways pertinent to the pathogenesis of T2D and cardiovascular diseases. We also review available clinical studies to better elucidate the roles of these potential molecules in the initiation and development of the afore-mentioned disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.lfs.2020.117913" target="_blank" rel="noreferrer noopener">10.1016/j.lfs.2020.117913</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
Bashash D
C1q/TNF-related proteins (CTRPs)
CARDIOVASCULAR diseases
Department of Integrative Medical Sciences
Emamgholipour S
Goudarzi A
journalArticle
July 2020 List
Life sciences
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
Obesity
Omidifar A
Shabani P
Shanaki M
Type 2 diabetes