2
40
328
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Text
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<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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NEOMED College
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Department of Integrative Medical Sciences
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Title
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Acute alcohol intoxication impairs sonic hedgehog-GLI1 signaling and activation of primitive hematopoietic precursor cells in the early stage of host response to bacteremia.
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Alcoholism, Clinical And Experimental Research
Date
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2020
2020-08-09
Subject
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Alcohol; Bacteremia; Hematopoietic Stem Cells; Host Response; Sonic Hedgehog
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Shi X;Simms KJ;Zhang P
Description
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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.)
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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
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
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<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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Department of Integrative Medical Sciences
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Title
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Acute alcohol intoxication impairs SHH-GLI1 signaling and activation of primitive hematopoietic precursor cells in the early stage of host response to bacteremia.
Publisher
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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
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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.
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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
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<a href="http://doi.org/10.1038/s41590-020-0750-1" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/s41590-020-0750-1</a>
ISSN
1529-2916 1529-2908
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August 2020 List
NEOMED College
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Department of Integrative Medical Sciences
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IL-1 induces mitochondrial translocation of IRAK2 to suppress oxidative metabolism in adipocytes.
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Nature Immunology
Date
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2020
2020-08-10
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Zhou H; Wang H; Yu M; Schugar RC; Qian W; Tang F; Liu W; Yang H; McDowell RE; Zhao J; Gao J; Dongre A; Carman JA; Yin M; Drazba JA; Dent R; Hine C; Chen Y; Smith JD; Fox PL; Brown JM; Li X
Description
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Chronic inflammation is a common feature of obesity, with elevated cytokines such as interleukin-1 (IL-1) in the circulation and tissues. Here, we report an unconventional IL-1R-MyD88-IRAK2-PHB/OPA1 signaling axis that reprograms mitochondrial metabolism in adipocytes to exacerbate obesity. IL-1 induced recruitment of IRAK2 Myddosome to mitochondria outer membranes via recognition by TOM20, followed by TIMM50-guided translocation of IRAK2 into mitochondria inner membranes, to suppress oxidative phosphorylation and fatty acid oxidation, thereby attenuating energy expenditure. Adipocyte-specific MyD88 or IRAK2 deficiency reduced high-fat-diet-induced weight gain, increased energy expenditure and ameliorated insulin resistance, associated with a smaller adipocyte size and increased cristae formation. IRAK2 kinase inactivation also reduced high-fat diet-induced metabolic diseases. Mechanistically, IRAK2 suppressed respiratory super-complex formation via interaction with PHB1 and OPA1 upon stimulation of IL-1. Taken together, our results suggest that the IRAK2 Myddosome functions as a critical link between inflammation and metabolism, representing a novel therapeutic target for patients with obesity.
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<a href="http://doi.org/10.1038/s41590-020-0750-1" target="_blank" rel="noreferrer noopener">10.1038/s41590-020-0750-1</a>
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journalArticle
2020
August 2020 List
Brown JM
Carman JA
Chen Y
Dent R
Department of Integrative Medical Sciences
Dongre A
Drazba JA
Fox PL
Gao J
Hine C
journalArticle
Li X
Liu W
McDowell RE
Nature Immunology
NEOMED College of Medicine
Qian W
Schugar RC
Smith JD
Tang F
Wang H
Yang H
Yin M
Yu M
Zhao J
Zhou H
-
Text
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<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
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July 2020 List
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Department of Integrative Medical Sciences
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The C1q/TNF-related proteins (CTRPS) in pathogenesis of obesity-related metabolic disorders: Focus on type 2 diabetes and cardiovascular diseases.
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Life Sciences
Date
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2020
2020-06
Subject
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Obesity; Type 2 diabetes; Cardiovascular diseases; C1q/TNF-related proteins (CTRPs)
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Shanaki M; Shabani P; Goudarzi A; Omidifar A; Bashash D; Emamgholipour S
Description
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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.
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<a href="http://doi.org/10.1016/j.lfs.2020.117913" target="_blank" rel="noreferrer noopener">10.1016/j.lfs.2020.117913</a>
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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
-
Text
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<a href="http://doi.org/10.1038/s41598-020-66617-2" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/s41598-020-66617-2</a>
Pages
9827
Issue
1
Volume
10
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July 2020 List
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Department of Integrative Medical Sciences
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Title
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Transient receptor potential vanilloid channel regulates fibroblast differentiation and airway remodeling by modulating redox signals through NADPH oxidase 4.
Publisher
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Scientific Reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-06
Subject
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ASTHMA; CAPSAICIN receptors; GROWTH factors; NICOTINAMIDE adenine dinucleotide phosphate; OXIDATION-reduction reaction; TRP channels
Creator
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Al-Azzam N; Teegala LR; Pokhrel S; Ghebreigziabher S; Chachkovskyy T; Thodeti S; Gavilanes I; Covington K; Thodeti CK; Paruchuri S
Description
An account of the resource
Asthma is characterized by pathological airway remodeling resulting from persistent myofibroblast activation. Although transforming growth factor beta 1 (TGFβ1), mechanical signals, and reactive oxygen species (ROS) are implicated in fibroblast differentiation, their integration is still elusive. We identified that Transient Receptor Potential Vanilloid 4 (TRPV4), a mechanosensitive ion channel mediates lung fibroblast (LF) differentiation and D. farinae-induced airway remodeling via a novel
Identifier
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<a href="http://doi.org/10.1038/s41598-020-66617-2" target="_blank" rel="noreferrer noopener">10.1038/s41598-020-66617-2</a>
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journalArticle
2020
Al-Azzam N
asthma
CAPSAICIN receptors
Chachkovskyy T
Covington K
Department of Integrative Medical Sciences
Gavilanes I
Ghebreigziabher S
growth factors
journalArticle
July 2020 List
NEOMED College of Medicine
NEOMED College of Medicine Student
NEOMED Student Publications
NICOTINAMIDE adenine dinucleotide phosphate
OXIDATION-reduction reaction
Paruchuri S
Pokhrel S
Scientific reports
Teegala LR
Thodeti CK
Thodeti S
TRP channels
-
Text
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URL Address
<a href="http://doi.org/10.1212/WNL.0000000000009525" target="_blank" rel="noreferrer noopener">http://doi.org/10.1212/WNL.0000000000009525</a>
ISSN
1526-632X 0028-3878
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Update Year & Number
June 2020 Update II
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Pediatrics
Department of Integrative Medical Sciences
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Title
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Quality improvement in neurology: Neurology Outcomes Quality Measurement Set.
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Neurology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-05-12
Creator
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Sico Jason J; Sarwal Aarti; Benish Sarah M; Busis Neil A; Cohen Bruce H; Das Rohit R; Finsilver Shari; Halperin John J; Kelly Adam G; Meunier Lisa; Phipps Michael S; Thirumala Parthasarathy D; Villanueva Raissa; von Gaudecker Jane; Bennett Amy; Shenoy Anant M
Identifier
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<a href="http://doi.org/10.1212/WNL.0000000000009525" target="_blank" rel="noreferrer noopener">10.1212/WNL.0000000000009525</a>
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journalArticle
2020
Benish Sarah M
Bennett Amy
Busis Neil A
Cohen Bruce H
Das Rohit R
Department of Integrative Medical Sciences
Department of Pediatrics
Finsilver Shari
Halperin John J
journalArticle
June 2020 Update II
Kelly Adam G
Meunier Lisa
NEOMED College of Medicine
Neurology
Phipps Michael S
Sarwal Aarti
Shenoy Anant M
Sico Jason J
Thirumala Parthasarathy D
Villanueva Raissa
von Gaudecker Jane
-
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.ebiom.2020.102754" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ebiom.2020.102754</a>
Pages
102754
Volume
55
ISSN
2352-3964 2352-3964
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June 2020 Update II
NEOMED College
NEOMED College of Medicine
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Department of Integrative Medical Sciences
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Targeting the gut microbiota for treating colitis: Is FGF19 a magic bullet?
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EBioMedicine
Date
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2020
2020-05
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Chiang John Y L; Ferrell Jessica M
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<a href="http://doi.org/10.1016/j.ebiom.2020.102754" target="_blank" rel="noreferrer noopener">10.1016/j.ebiom.2020.102754</a>
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journalArticle
2020
Chiang John Y L
Department of Integrative Medical Sciences
EBioMedicine
Ferrell Jessica M
journalArticle
June 2020 Update II
NEOMED College of Medicine
-
Text
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URL Address
<a href="http://doi.org/10.1016/j.ijcard.2020.04.074" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ijcard.2020.04.074</a>
ISSN
1874-1754 0167-5273
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June 2020 Update II
NEOMED College
NEOMED College of Medicine
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Department of Integrative Medical Sciences
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Title
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Myocardial ischemia: From disease to syndrome.
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
2020
2020-04-26
Subject
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Angina; Chronic coronary syndromes; Coronary artery disease; Ischemic heart disease; Microvascular dysfunction
Creator
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Marzilli Mario; Crea Filippo; Morrone Doralisa; Bonow Robert O; Brown David L; Camici Paolo G; Chilian William M; DeMaria Anthony; Guarini Giacinta; Huqi Alda; Merz C Noel Bairey; Pepine Carl; Scali Maria Chiara; Weintraub William S; Boden William E
Description
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Although current guidelines on the management of stable coronary artery disease acknowledge that multiple mechanisms may precipitate myocardial ischemia, recommended diagnostic, prognostic and therapeutic algorithms are still focused on obstructive epicardial atherosclerotic lesions, and little progress has been made in identifying management strategies for non-atherosclerotic causes of myocardial ischemia. The purpose of this consensus paper is three-fold: 1) to marshal scientific evidence that obstructive atherosclerosis can co-exist with other mechanisms of ischemic heart disease (IHD); 2) to explore how the awareness of multiple precipitating mechanisms could impact on pre-test probability, provocative test results and treatment strategies; and 3) to stimulate a more comprehensive approach to chronic myocardial ischemic syndromes, consistent with the new understanding of this condition.
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<a href="http://doi.org/10.1016/j.ijcard.2020.04.074" target="_blank" rel="noreferrer noopener">10.1016/j.ijcard.2020.04.074</a>
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journalArticle
2020
Angina
Boden William E
Bonow Robert O
Brown David L
Camici Paolo G
Chilian William M
Chronic coronary syndromes
Coronary Artery Disease
Crea Filippo
DeMaria Anthony
Department of Integrative Medical Sciences
Guarini Giacinta
Huqi Alda
International journal of cardiology
Ischemic heart disease
journalArticle
June 2020 Update II
Marzilli Mario
Merz C Noel Bairey
Microvascular dysfunction
Morrone Doralisa
NEOMED College of Medicine
Pepine Carl
Scali Maria Chiara
Weintraub William S
-
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/hep4.1487" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1487</a>
Pages
527-539
Issue
4
Volume
4
ISSN
2471-254X 2471-254X
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Update Year & Number
June 2020 Update I
NEOMED College
NEOMED College of Medicine; NEOMED College of Graduate Studies
NEOMED Department
Department of Integrative Medical Sciences; NEOMED Postdoc Publications
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
Hepatocyte-Specific Expression of Human Carboxylesterase 1 Attenuates Diet-Induced Steatohepatitis and Hyperlipidemia in Mice.
Publisher
An entity responsible for making the resource available
Hepatology communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
Subject
The topic of the resource
decreases blood-lipids; deficiency; dyslipidemia; hepatic steatosis; lipotoxicity; Liver; protects; receptor-alpha; reduces atherosclerosis; transgenic expression
Creator
An entity primarily responsible for making the resource
Xu Yanyong; Zhu Yingdong; Bawa Fathima Cassim; Hu Shuwei; Pan Xiaoli; Yin Liya; Zhang Yanqiao
Description
An account of the resource
Rodents have at least five carboxylesterase 1 (Ces1) genes, whereas there is only one CES1 gene in humans, raising the question as to whether human CES1 and mouse Ces1 genes share the same functions. In this study, we investigate the role of human CES1 in the development of steatohepatitis or dyslipidemia in C57BL/6 mice. Hepatocyte-specific expression of human CES1 prevented Western diet or alcohol-induced steatohepatitis and hyperlipidemia. Mechanistically, human CES1 induced lipolysis and fatty acid oxidation, leading to a reduction in hepatic triglyceride and free fatty acid levels. Human CES1 also reduced hepatic-free cholesterol levels and induced low-density lipoprotein receptor. In addition, human CES1 induced hepatic lipoprotein lipase and apolipoprotein C-II expression. Conclusion: Hepatocyte-specific overexpression of human CES1 attenuates diet-induced steatohepatitis and hyperlipidemia.
Identifier
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<a href="http://doi.org/10.1002/hep4.1487" target="_blank" rel="noreferrer noopener">10.1002/hep4.1487</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
Bawa Fathima Cassim
decreases blood-lipids
deficiency
Department of Integrative Medical Sciences
dyslipidemia
hepatic steatosis
Hepatology communications
Hu Shuwei
Journal Article
journalArticle
June 2020 Update I
lipotoxicity
Liver
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
Pan Xiaoli
protects
receptor-alpha
reduces atherosclerosis
transgenic expression
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong
-
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/10.1212/NXG.0000000000000402" target="_blank" rel="noreferrer noopener">http://doi.org/10.1212/NXG.0000000000000402</a>
Pages
e402
Issue
2
Volume
6
ISSN
2376-7839 2376-7839
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<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
June 2020 Update I
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Pediatrics; Department of Integrative Medical Sciences
Affiliated Hospital
Akron Children's Hospital
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
Mitochondrial diseases in North America: An analysis of the NAMDC Registry.
Publisher
An entity responsible for making the resource available
Neurology. Genetics
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
Subject
The topic of the resource
criteria; dna; melas; merrf; natural-history; nuclear; prevalence
Creator
An entity primarily responsible for making the resource
Barca Emanuele; Long Yuelin; Cooley Victoria; Schoenaker Robert; Emmanuele Valentina; DiMauro Salvatore; Cohen Bruce H; Karaa Amel; Vladutiu Georgirene D; Haas Richard; Van Hove Johan L K; Scaglia Fernando; Parikh Sumit; Bedoyan Jirair K; DeBrosse Susanne D; Gavrilova Ralitza H; Saneto Russell P; Enns Gregory M; Stacpoole Peter W; Ganesh Jaya; Larson Austin; Zolkipli-Cunningham Zarazuela; Falk Marni J; Goldstein Amy C; Tarnopolsky Mark; Gropman Andrea; Camp Kathryn; Krotoski Danuta; Engelstad Kristin; Rosales Xiomara Q; Kriger Joshua; Grier Johnston; Buchsbaum Richard; Thompson John L P; Hirano Michio
Description
An account of the resource
Objective: To describe clinical, biochemical, and genetic features of participants with mitochondrial diseases (MtDs) enrolled in the North American Mitochondrial Disease Consortium (NAMDC) Registry. Methods: This cross-sectional, multicenter, retrospective database analysis evaluates the phenotypic and molecular characteristics of participants enrolled in the NAMDC Registry from September 2011 to December 2018. The NAMDC is a network of 17 centers with expertise in MtDs and includes both adult and pediatric specialists. Results: One thousand four hundred ten of 1,553 participants had sufficient clinical data for analysis. For this study, we included only participants with molecular genetic diagnoses (n = 666). Age at onset ranged from infancy to adulthood. The most common diagnosis was multisystemic disorder (113 participants), and only a minority of participants were diagnosed with a classical mitochondrial syndrome. The most frequent classical syndromes were Leigh syndrome (97 individuals) and mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (71 individuals). Pathogenic variants in the mitochondrial DNA were more frequently observed (414 participants) than pathogenic nuclear gene variants (252 participants). Pathogenic variants in 65 nuclear genes were identified, with POLG1 and PDHA1 being the most commonly affected. Pathogenic variants in 38 genes were reported only in single participants. Conclusions: The NAMDC Registry data confirm the high variability of clinical, biochemical, and genetic features of participants with MtDs. This study serves as an important resource for future enhancement of MtD research and clinical care by providing the first comprehensive description of participant with MtD in North America.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1212/NXG.0000000000000402" target="_blank" rel="noreferrer noopener">10.1212/NXG.0000000000000402</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
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journalArticle
2020
Akron Children's Hospital
Barca Emanuele
Bedoyan Jirair K
Buchsbaum Richard
Camp Kathryn
Cohen Bruce H
Cooley Victoria
criteria
DeBrosse Susanne D
Department of Integrative Medical Sciences
Department of Pediatrics
DiMauro Salvatore
DNA
Emmanuele Valentina
Engelstad Kristin
Enns Gregory M
Falk Marni J
Ganesh Jaya
Gavrilova Ralitza H
Goldstein Amy C
Grier Johnston
Gropman Andrea
Haas Richard
Hirano Michio
Journal Article
journalArticle
June 2020 Update I
Karaa Amel
Kriger Joshua
Krotoski Danuta
Larson Austin
Long Yuelin
melas
merrf
natural-history
NEOMED College of Medicine
Neurology. Genetics
nuclear
Parikh Sumit
Prevalence
Rosales Xiomara Q
Saneto Russell P
Scaglia Fernando
Schoenaker Robert
Stacpoole Peter W
Tarnopolsky Mark
Thompson John L P
Van Hove Johan L K
Vladutiu Georgirene D
Zolkipli-Cunningham Zarazuela
-
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/10.21037/hbsn.2019.09.03" target="_blank" rel="noreferrer noopener">http://doi.org/10.21037/hbsn.2019.09.03</a>
Pages
152-169
Issue
2
Volume
9
ISSN
2304-3881 2304-3881
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.21037/hbsn.2019.09.03" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.21037/hbsn.2019.09.03</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
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
A name given to the resource
Bile acid-based therapies for non-alcoholic steatohepatitis and alcoholic liver disease.
Publisher
An entity responsible for making the resource available
Hepatobiliary surgery and nutrition
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
Subject
The topic of the resource
alcoholic liver disease (ALD); bacterial translocation; Bile acid; binding protein; farnesoid X receptor (FXR); farnesoid-x-receptor; fatty liver; glucagon-like peptide-1; growth-factor 19; gut microbiota; microbiota; molecular-cloning; non-alcoholic steatohepatitis (NASH); non-alcoholic steatohepatitis (NASH); nuclear receptor; solute transporter-alpha
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chiang John Y L
Description
An account of the resource
Bile acids are synthesized from cholesterol only in hepatocytes. Bile acids circulating in the enterohepatic system act as physiological detergent molecules to help solubilize biliary cholesterol and emulsify dietary lipids and fat-soluble vitamins in small intestine. Bile acids are signaling molecules that activate nuclear receptor farnesoid X receptor (FXR) and cell surface G protein-coupled receptor TGR5. FXR critically regulates bile acid homeostasis by mediating bile acid feedback inhibition of hepatic bile acid synthesis. In addition, bile acid-activated cellular signaling pathways regulate metabolic homeostasis, immunity, and cell proliferation in various metabolically active organs. In the small and large intestine, gut bacterial enzymes modify primary bile acids to generate secondary bile acids to help shape the bile acid pool composition and subsequent biological effects. In turn, bile acids exhibit anti-microbial properties and modulate gut microbiota to influence host metabolism and immunity. Currently, bile acid-based therapies including systemic and intestine-restricted FXR agonists, TGR5 agonists, fibroblast growth factor 19 analogue, intestine FXR antagonists, and intestine apical sodium-bile acid transporter (ASBT) inhibitors have been developed as promising treatments for non-alcoholic steatohepatitis (NASH). These pharmacological agents improved metabolic and inflammatory disorders via distinct mechanisms of action that are subjects of extensive research interest. More recently, human and experimental alcoholic liver disease (ALD) has been associated with disrupted bile acid homeostasis. In additional, new findings showed that targeting bile acid metabolism and signaling may be promising therapeutic approaches for treating ALD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.21037/hbsn.2019.09.03" target="_blank" rel="noreferrer noopener">10.21037/hbsn.2019.09.03</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
journalArticle
2020
alcoholic liver disease (ALD)
Bacterial Translocation
bile acid
binding protein
Chiang John Y L
Department of Integrative Medical Sciences
farnesoid X receptor (FXR)
farnesoid-x-receptor
Fatty Liver
glucagon-like peptide-1
growth-factor 19
gut microbiota
Hepatobiliary surgery and nutrition
Journal Article
journalArticle
June 2020 Update I
Li Tiangang
Microbiota
molecular-cloning
NEOMED College of Medicine
non-alcoholic steatohepatitis (NASH)
Nuclear Receptor
solute transporter-alpha
-
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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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1002/cld.861" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1002/cld.861</a>
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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
A name given to the resource
Bile Acid Biology, Pathophysiology, and Therapeutics.
Publisher
An entity responsible for making the resource available
Clinical liver disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-03
Creator
An entity primarily responsible for making the resource
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
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
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
-
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/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-020-0775-5</a>
Pages
14-14
Issue
2
Volume
115
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1007/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1007/s00395-020-0775-5</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 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
TRPV4 deletion protects heart from myocardial infarction-induced adverse remodeling via modulation of cardiac fibroblast differentiation.
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
2020
2020-01
Subject
The topic of the resource
Mechanotransduction; TRPV4; Myocardial infarction; Myocardial infarction; TGF-beta1; Rho/Rho kinase; Mechanotransduction; TGF-β1; Myocardial infarction; EXTRACELLULAR matrix; HEART failure; HEART fibrosis; HEART; Cardiac fibroblast; Cardiac fibrosis; Rho/Rho kinase; TRPV4; Cardiac fibroblast; Cardiac fibrosis; DELETION mutation
Creator
An entity primarily responsible for making the resource
Adapala Ravi K; Kanugula Anantha K; Paruchuri Sailaja; Chilian William M; Thodeti Charles K
Description
An account of the resource
Cardiac fibrosis caused by adverse cardiac remodeling following myocardial infarction can eventually lead to heart failure. Although the role of soluble factors such as TGF-beta is well studied in cardiac fibrosis following myocardial injury, the physiological role of mechanotransduction is not fully understood. Here, we investigated the molecular mechanism and functional role of TRPV4 mechanotransduction in cardiac fibrosis. TRPV4KO mice, 8 weeks following myocardial infarction (MI), exhibited preserved cardiac function compared to WT mice. Histological analysis demonstrated reduced cardiac fibrosis in TRPV4KO mice. We found that WT CF exhibited hypotonicity-induced calcium influx and extracellular matrix (ECM)-stiffness-dependent differentiation in response to
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">10.1007/s00395-020-0775-5</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).
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2020
Adapala Ravi K
Basic research in cardiology
cardiac fibroblast
Cardiac fibrosis
Chilian William M
DELETION mutation
Department of Integrative Medical Sciences
Extracellular Matrix
heart
Heart failure
HEART fibrosis
Kanugula Anantha K
Mechanotransduction
myocardial infarction
NEOMED College of Medicine
NEOMED Postdoc Publications
Paruchuri Sailaja
Rho/Rho kinase
TGF-beta1
TGF-β1
Thodeti Charles K
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/10.1093/cvr/cvaa002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/cvr/cvaa002</a>
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1093/cvr/cvaa002" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1093/cvr/cvaa002</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 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
Experimental animal models of coronary microvascular dysfunction.
Publisher
An entity responsible for making the resource available
Cardiovascular research
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-01
Creator
An entity primarily responsible for making the resource
Sorop Oana; van de Wouw Jens; Chandler Selena; Ohanyan Vahagn; Tune Johnathan D; Chilian William M; Merkus Daphne; Bender Shawn B; Duncker Dirk J
Description
An account of the resource
Coronary microvascular dysfunction (CMD) is commonly present in patients with metabolic derangements and is increasingly recognized as an important contributor to myocardial ischemia, both in the presence and absence of epicardial coronary atherosclerosis. The latter condition is termed 'ischemia with non-obstructive coronary arteries' (INOCA). Notwithstanding the high prevalence of INOCA, effective treatment remains elusive. Although to date there is no animal model for INOCA, animal models of CMD, one of the hallmarks of INOCA, offer excellent test models for enhancing our understanding of the pathophysiology of CMD and for investigating novel therapies. This article presents an overview of currently available experimental models of CMD - with an emphasis on metabolic derangements as risk factors - in dogs, swine, rabbits, rats and mice. In all the available animal models, metabolic derangements are most often induced by a high fat diet and/or diabetes mellitus via injection of alloxan or streptozotocin, but there is also a wide variety of spontaneous as well as transgenic animal models which develop metabolic derangements. Depending on number, severity and duration of exposure to risk factors - all these animal models show perturbations in coronary microvascular (endothelial) function and structure, similar to what has been observed in patients with INOCA and co-morbid conditions. The use of these animal models will be instrumental in identifying novel therapeutic targets and for the subsequent development and testing of novel therapeutic interventions to combat ischemic heart disease, the number one cause of death worldwide.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/cvr/cvaa002" target="_blank" rel="noreferrer noopener">10.1093/cvr/cvaa002</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).
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2020
Bender Shawn B
Cardiovascular research
Chandler Selena
Chilian William M
Department of Integrative Medical Sciences
Duncker Dirk J
Merkus Daphne
NEOMED College of Medicine Student
NEOMED Student Publications
Ohanyan Vahagn
Sorop Oana
Tune Johnathan D
van de Wouw Jens
-
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/ajpgi.00223.2019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpgi.00223.2019</a>
Pages
G554-G573
Issue
3
Volume
318
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Update Year & Number
March 2020 Update
NEOMED College
NEOMED College of Medicine; NEOMED College of Graduate Studies
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
Bile acid receptors FXR and TGR5 signaling in fatty liver diseases and therapy.
Publisher
An entity responsible for making the resource available
American journal of physiology. Gastrointestinal and liver physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-03
Subject
The topic of the resource
bile acid metabolism; liver diseases; farnesoid X receptor; alcoholic and nonalcoholic fatty; bile acid therapies; Takeda G protein-coupled receptor 5
Creator
An entity primarily responsible for making the resource
Chiang John Y L; Ferrell Jessica M
Description
An account of the resource
Bile acid synthesis is the most significant pathway for catabolism of cholesterol and for maintenance of whole body cholesterol homeostasis. Bile acids are physiological detergents that absorb, distribute, metabolize, and excrete nutrients, drugs, and xenobiotics. Bile acids also are signal molecules and metabolic integrators that activate nuclear farnesoid X receptor (FXR) and membrane Takeda G protein-coupled receptor 5 (TGR5; i.e., G protein-coupled bile acid receptor 1) to regulate glucose, lipid, and energy metabolism. The gut-to-liver axis plays a critical role in the transformation of primary bile acids to secondary bile acids, in the regulation of bile acid synthesis to maintain composition within the bile acid pool, and in the regulation of metabolic homeostasis to prevent hyperglycemia, dyslipidemia, obesity, and diabetes. High-fat and high-calorie diets, dysbiosis, alcohol, drugs, and disruption of sleep and circadian rhythms cause metabolic diseases, including alcoholic and nonalcoholic fatty liver diseases, obesity, diabetes, and cardiovascular disease. Bile acid-based drugs that target bile acid receptors are being developed for the treatment of metabolic diseases of the liver.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpgi.00223.2019" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00223.2019</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).
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2020
alcoholic and nonalcoholic fatty
American journal of physiology. Gastrointestinal and liver physiology
Bile acid metabolism
bile acid therapies
Chiang John Y L
Department of Integrative Medical Sciences
Farnesoid X receptor
Ferrell Jessica M
Liver Diseases
NEOMED College of Graduate Studies
NEOMED College of Medicine
Takeda G protein-coupled receptor 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/10.1161/ATVBAHA.120.313811" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.120.313811</a>
Pages
498-499
Issue
3
Volume
40
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1161/ATVBAHA.120.313811" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1161/ATVBAHA.120.313811</a>
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Update Year & Number
March 2020 Update
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
Step by Step: Advancing the Understanding of Local Vascular Control.
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
2020
2020-03
Subject
The topic of the resource
Editorials; vasodilation; hypoxia; dilation; endothelium; arterial pressure
Creator
An entity primarily responsible for making the resource
Chilian William M; Yin Liya; Ohanyan Vahagn
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.120.313811" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.120.313811</a>
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Journal Article
2020
and vascular biology
Arterial Pressure
Arteriosclerosis
Arteriosclerosis, thrombosis, and vascular biology
Chilian William M
Department of Integrative Medical Sciences
dilation
Editorials
Endothelium
hypoxia
NEOMED College of Medicine
Ohanyan Vahagn
Thrombosis
vasodilation
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/10.1194/jlr.C120000621" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.C120000621</a>
Pages
269-271
Issue
3
Volume
61
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Update Year & Number
March 2020 Update
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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Is CYP2C70 the key to new mouse models to understand bile acids in humans?
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
2020
2020-03
Creator
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Guo Grace L; Chiang John Y L
Identifier
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<a href="http://doi.org/10.1194/jlr.C120000621" target="_blank" rel="noreferrer noopener">10.1194/jlr.C120000621</a>
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Journal Article
2020
Chiang John Y L
Department of Integrative Medical Sciences
Guo Grace L
Journal of lipid research
NEOMED College of 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/10.3389/fimmu.2020.00092" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fimmu.2020.00092</a>
Pages
92-92
Volume
11
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Update Year & Number
March 2020 Update
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
Intravital Microscopy of the Beating Murine Heart to Understand Cardiac Leukocyte Dynamics.
Publisher
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Frontiers in immunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
1905-07
Subject
The topic of the resource
HEART; cardiovascular; leukocyte; intravital microscopy; multiphoton microscopy
Creator
An entity primarily responsible for making the resource
Allan-Rahill Nathaniel H; Lamont Michael R E; Chilian William M; Nishimura Nozomi; Small David M
Description
An account of the resource
Cardiovascular disease is the leading cause of worldwide mortality. Intravital microscopy has provided unprecedented insight into leukocyte biology by enabling the visualization of dynamic responses within living organ systems at the cell-scale. The heart presents a uniquely dynamic microenvironment driven by periodic, synchronous electrical conduction leading to rhythmic contractions of cardiomyocytes, and phasic coronary blood flow. In addition to functions shared throughout the body, immune cells have specific functions in the heart including tissue-resident macrophage-facilitated electrical conduction and rapid monocyte infiltration upon injury. Leukocyte responses to cardiac pathologies, including myocardial infarction and heart failure, have been well-studied using standard techniques, however, certain questions related to spatiotemporal relationships remain unanswered. Intravital imaging techniques could greatly benefit our understanding of the complexities of in vivo leukocyte behavior within cardiac tissue, but these techniques have been challenging to apply. Different approaches have been developed including high frame rate imaging of the beating heart, explantation models, micro-endoscopy, and mechanical stabilization coupled with various acquisition schemes to overcome challenges specific to the heart. The field of cardiac science has only begun to benefit from intravital microscopy techniques. The current focused review presents an overview of leukocyte responses in the heart, recent developments in intravital microscopy for the murine heart, and a discussion of future developments and applications for cardiovascular immunology.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3389/fimmu.2020.00092" target="_blank" rel="noreferrer noopener">10.3389/fimmu.2020.00092</a>
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Journal Article
2020
Allan-Rahill Nathaniel H
Cardiovascular
Chilian William M
Department of Integrative Medical Sciences
Frontiers in immunology
heart
intravital microscopy
Lamont Michael R E
leukocyte
multiphoton microscopy
NEOMED College of Medicine
Nishimura Nozomi
Small David 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="https://www.fasebj.org/doi/abs/10.1096/fasebj.2019.33.1_supplement.689.4#:~:text=">https://www.fasebj.org/doi/abs/10.1096/fasebj.2019.33.1_supplement.689.4#:~:text=</a>
Volume
33
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Update Year & Number
March 2020 Update
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
The Role of Kv1.2 Channels in Coronary Metabolic Dilation
Publisher
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Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-04
Creator
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Ohanyan Vahagn; Hakobyan Tatevik; Enrick Molly; Shockling Lindsay; Yin Liya; Kolz Christopher L; Chilian William
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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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Journal Article
2019
Chilian William
Department of Integrative Medical Sciences
Enrick Molly
Faseb Journal
Hakobyan Tatevik
Kolz Christopher L
NEOMED College of Medicine
Ohanyan Vahagn
Shockling Lindsay
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/10.1161/RES.0000000000000311" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/RES.0000000000000311</a>
Pages
E106-E106
Issue
12
Volume
125
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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
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/RES.0000000000000311" target="_blank" rel="noreferrer noopener">10.1161/RES.0000000000000311</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).
Format
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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/10.1161/res.125.suppl_1.592" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/res.125.suppl_1.592</a>
Volume
125
Search for Full-text
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Update Year & Number
March 2020 Update
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences; NEOMED Student Publications; NEOMED Postdoc Publications
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
Cardioprotection During Ischemia by Induced Coronary Collateral Growth
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
2019-08
Creator
An entity primarily responsible for making the resource
Jamaiyar Anurag; Juguilon Cody; Cumpston Devan; Weiguo Wan; Wang Tao; Zhiyuan Wang; Gadd James; Enrick Molly; Chinchilla Sofia; McCabe Caige; Pu Autumn Y; Chilian William; Yin Liya
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/res.125.suppl_1.592" target="_blank" rel="noreferrer noopener">10.1161/res.125.suppl_1.592</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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Journal Article
2019
Chilian William
Chinchilla Sofia
Circulation research
Cumpston Devan
Department of Integrative Medical Sciences
Enrick Molly
Gadd James
Jamaiyar Anurag
Juguilon Cody
McCabe Caige
NEOMED College of Graduate Studies Student
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED College of Medicine Student
NEOMED Postdoc Publications
NEOMED Student Publications
Pu Autumn Y
Wang Tao
Weiguo Wan
Yin Liya
Zhiyuan Wang
-
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="https://www.fasebj.org/doi/abs/10.1096/fasebj.2019.33.1_supplement.685.14" target="_blank" rel="noreferrer noopener">https://www.fasebj.org/doi/abs/10.1096/fasebj.2019.33.1_supplement.685.14</a>
Volume
33
Search for Full-text
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Update Year & Number
March 2020 Update
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
Doxorubicin-induced cardiomyopathy: Prevention and treatment by a coronary specific vasodilator
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
2019
2019-04
Creator
An entity primarily responsible for making the resource
Gyulkhasyan Tigran; Hakobyan Tatevik; Parikh Ankur; Peketi Punita; Enrick Molly; Shockling Lindsay; Kolz Christopher L; Chilian William; Ohanyan Vahagn
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
Journal Article
2019
Chilian William
Department of Integrative Medical Sciences
Enrick Molly
Faseb Journal
Gyulkhasyan Tigran
Hakobyan Tatevik
Kolz Christopher L
NEOMED College of Medicine
NEOMED College of Medicine Student
NEOMED Student Publications
Ohanyan Vahagn
Parikh Ankur
Peketi Punita
Shockling Lindsay
-
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/10.1093/neuonc/noz175.767" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/neuonc/noz175.767</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
S57-S58
Issue
4, SI
Volume
66
ISSN
1545-5009
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1093/neuonc/noz175.767" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1093/neuonc/noz175.767</a>
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Dublin Core
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Title
A name given to the resource
Chemotherapy Strategies for Young Children Newly-Diagnosed with Medulloblastoma up to the Era of Molecular Profiling - A Comparative Outcomes Analysis
Publisher
An entity responsible for making the resource available
Pediatric Blood & Cancer
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
Finlay J; Mynarek M; Dhall G; Lafay-Cousin L; Mazewski C M; Ashley D; Cohen B H; von Bueren A O; Gerber N; Leary S; Geyer J R; Tait D; Gajjar A; Rutkowski S
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/neuonc/noz175.767" target="_blank" rel="noreferrer noopener">10.1093/neuonc/noz175.767</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Akron Children's Hospital
Ashley D
Cohen B H
Department of Integrative Medical Sciences
Department of Pediatrics
Dhall G
Finlay J
Gajjar A
Gerber N
Geyer J R
Journal Article
Lafay-Cousin L
Leary S
Mazewski C M
Mynarek M
NEOMED College of Medicine
November 2019 Update
Pediatric blood & cancer
Rutkowski S
Tait D
von Bueren A O
-
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
1378A
Issue
1
Volume
70
ISSN
0270-9139
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Dublin Core
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Title
A name given to the resource
BILE ACID RECEPTORS FXR AND TGR IN LIVER FIBROSIS AND INFLAMMATION: STUDY OF FXR/TGR5 DOUBLE KNOCKOUT MICE
Publisher
An entity responsible for making the resource available
Hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Boehme Shannon; Gilliland Tricia; Chiang John Y L
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
2019
Boehme Shannon
Chiang John Y L
Department of Integrative Medical Sciences
Ferrell Jessica M
Gilliland Tricia
Hepatology
Journal Article
NEOMED College of Medicine
November 2019 Update
-
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/10.1007/978-3-030-22254-3_6" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/978-3-030-22254-3_6</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
73
ISSN
3-030-22254-3
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Title
A name given to the resource
Contributing Roles of CYP2E1 and Other Cytochrome P450 Isoforms in Alcohol-Related Tissue Injury and Carcinogenesis
Publisher
An entity responsible for making the resource available
Human Cell Transformation : Advances In Cell Models For The Study Of Cancer And Aging
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
inflammation; Oxidative stress; Cancer; CYP2E1; Cell Biology; Oncology; Alcohol; Acetaldehyde; Biomedical and Life Sciences; Cancer Research; DNA mutation; Life Sciences
Creator
An entity primarily responsible for making the resource
Byoung-Joon Song; Mohamed A Abdelmegeed; Young-Eun Cho; Mohammed Akbar; Johng S Rhim; Min-Kyung Song; James P Hardwick
Description
An account of the resource
The purpose of this review is to briefly summarize the roles of alcohol (ethanol) and related compounds in promoting cancer and inflammatory injury in many tissues. Long-term chronic heavy alcohol exposure is known to increase the chances of inflammation, oxidative DNA damage, and cancer development in many organs. The rates of alcohol-mediated organ damage and cancer risks are significantly elevated in the presence of co-morbidity factors such as poor nutrition, unhealthy diets, smoking, infection with bacteria or viruses, and exposure to pro-carcinogens. Chronic ingestion of alcohol and its metabolite acetaldehyde may initiate and/or promote the development of cancer in the liver, oral cavity, esophagus, stomach, gastrointestinal tract, pancreas, prostate, and female breast. In this chapter, we summarize the important roles of ethanol/acetaldehyde in promoting inflammatory injury and carcinogenesis in several tissues. We also review the updated roles of the ethanol-inducible cytochrome P450-2E1 (CYP2E1) and other cytochrome P450 isozymes in the metabolism of various potentially toxic substrates, and consequent toxicities, including carcinogenesis in different tissues. We also briefly describe the potential implications of endogenous ethanol produced by gut bacteria, as frequently observed in the experimental models and patients of nonalcoholic fatty liver disease, in promoting DNA mutation and cancer development in the liver and other tissues, including the gastrointestinal tract.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/978-3-030-22254-3_6" target="_blank" rel="noreferrer noopener">10.1007/978-3-030-22254-3_6</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
acetaldehyde
Alcohol
Biomedical and Life Sciences
Byoung-Joon Song
Cancer
Cancer Research
Cell Biology
CYP2E1
Department of Integrative Medical Sciences
DNA mutation
Human Cell Transformation : Advances In Cell Models For The Study Of Cancer And Aging
Inflammation
James P Hardwick
Johng S Rhim
Journal Article
Life sciences
Min-Kyung Song
Mohamed A Abdelmegeed
Mohammed Akbar
NEOMED College of Medicine
November 2019 Update
oncology
Oxidative Stress
Young-Eun Cho
-
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
36P-37P
Issue
43
ISSN
17496187
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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
Is heart failure a coronary microvascular disorder?
Publisher
An entity responsible for making the resource available
Proceedings Of The Physiological Society
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-01
Subject
The topic of the resource
HEART failure; MICROCIRCULATION disorders; COMPRESSIVE force; ENDOTHELIUM diseases
Creator
An entity primarily responsible for making the resource
Ohanyan V; Hakobyan T; Shockling L; Gyulkhasyan T; Enrick M; Kolz C L; 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
2019
Chilian W M
COMPRESSIVE force
Department of Integrative Medical Sciences
ENDOTHELIUM diseases
Enrick M
Gyulkhasyan T
Hakobyan T
Heart failure
Journal Article
Kolz C L
MICROCIRCULATION disorders
NEOMED College of Medicine
November 2019 Update
Ohanyan V
Proceedings Of The Physiological Society
Shockling 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/10.1016/j.ymthe.2019.09.008" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ymthe.2019.09.008</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
1525-0016
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.ymthe.2019.09.008" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.ymthe.2019.09.008</a>
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Dublin Core
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Title
A name given to the resource
Macrophage miR-34a Is a Key Regulator of Cholesterol Efflux and Atherosclerosis
Publisher
An entity responsible for making the resource available
Molecular Therapy
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-01-01
Subject
The topic of the resource
atherosclerosis; inflammation; cholesterol efflux; ABCA1; ABCG1; LXR; miR-34a
Creator
An entity primarily responsible for making the resource
Xu Yanyong; Xu Yang; Zhu Yingdong; Sun Huihui; Juguilon Cody; Li Feng; Fan Daping; Yin Liya; Zhang Yanqiao
Description
An account of the resource
Macrophages play a crucial role in the pathogenesis of atherosclerosis, but the molecular mechanisms remain poorly understood. Here we show that microRNA-34a (miR-34a) is a key regulator of macrophage cholesterol efflux and reverse cholesterol transport by modulating ATP-binding cassette transporters ATP-binding cassette subfamily A member 1 (ABCA1) and ATP-binding cassette subfamily G member 1 (ABCG1). miR-34a also regulates M1 and M2 macrophage polarization via liver X receptor α. Furthermore, global loss of miR-34a reduces intestinal cholesterol or fat absorption by inhibiting cytochrome P450 enzymes CYP7A1 and sterol 12α-hydroxylase (CYP8B1). Consistent with these findings, macrophage-selective or global ablation of miR-34a markedly inhibits the development of atherosclerosis. Finally, therapeutic inhibition of miR-34a promotes atherosclerosis regression and reverses diet-induced metabolic disorders. Our studies outline a central role of miR-34a in regulating macrophage cholesterol efflux, inflammation, and atherosclerosis, suggesting that miR-34a is a promising target for treatment of cardiometabolic diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ymthe.2019.09.008" target="_blank" rel="noreferrer noopener">10.1016/j.ymthe.2019.09.008</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
ABCA1
ABCG1
Atherosclerosis
cholesterol efflux
Department of Integrative Medical Sciences
Fan Daping
Inflammation
Journal Article
Juguilon Cody
Li Feng
LXR
miR-34a
Molecular Therapy
NEOMED College of Graduate Studies Student
NEOMED College of Medicine
November 2019 Update
Sun Huihui
Xu Yang
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong
-
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/s41598-019-51614-x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/s41598-019-51614-x</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
15087
Issue
1
Volume
9
ISSN
2045-2322
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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
Procyanidin A1 Alleviates Inflammatory Response induced by LPS through NF-κB, MAPK, and Nrf2/HO-1 Pathways in RAW264.7 cells
Publisher
An entity responsible for making the resource available
Scientific Reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10-21
Creator
An entity primarily responsible for making the resource
Han Shan; Gao Hongwei; Chen Shaoru; Wang Qinqin; Li Xinxing; Du Li-Jun; Li Jun; Luo Ying-Ying; Li Jun-Xiu; Zhao Li-Chun; Feng Jianfang; Yang Shilin
Description
An account of the resource
Inflammation is a complex physiological process that poses a serious threat to people's health. However, the potential molecular mechanisms of inflammation are still not clear. Moreover, there is lack of effective anti-inflammatory drugs that meet the clinical requirement. Procyanidin A1 (PCA1) is a monomer component isolated from Procyanidin and shows various pharmacological activities. This study further demonstrated the regulatory role of PCA1 on lipopolysaccharide (LPS)-stimulated inflammatory response and oxidative stress in RAW264.7 cells. Our data showed that PCA1 dramatically attenuated the production of pro-inflammatory cytokines such as NO, iNOS, IL-6, and TNF-α in RAW264.7 cells administrated with LPS. PCA1 blocked IκB-α degradation, inhibited IKKα/β and IκBα phosphorylation, and suppressed nuclear translocation of p65 in RAW264.7 cells induced by LPS. PCA1 also suppressed the phosphorylation of JNK1/2, p38, and ERK1/2 in LPS-stimulated RAW264.7 cells. In addition, PCA1 increased the expression of HO-1, reduced the expression of Keap1, and promoted Nrf2 into the nuclear in LPS-stimulated RAW264.7 cells. Cellular thermal shift assay indicated that PCA1 bond to TLR4. Meanwhile, PCA1 inhibited the production of intracellular ROS and alleviated the depletion of mitochondrial membrane potential in vitro. Collectively, our data indicated that PCA1 exhibited a significant anti-inflammatory effect, suggesting that it is a potential agent for the treatment of inflammatory diseases.
Identifier
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<a href="http://doi.org/10.1038/s41598-019-51614-x" target="_blank" rel="noreferrer noopener">10.1038/s41598-019-51614-x</a>
PMID: 31636354 PMCID: PMC6803657
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Chen Shaoru
Department of Integrative Medical Sciences
Du Li-Jun
Feng Jianfang
Gao Hongwei
Han Shan
Journal Article
Li Jun
Li Jun-Xiu
Li Xinxing
Luo Ying-Ying
NEOMED College of Medicine
November 2019 Update
Scientific reports
Wang Qinqin
Yang Shilin
Zhao Li-Chun
-
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
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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
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
An unambiguous reference to the resource within a given context
<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/10.1002/hep4.1341" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1341</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
763-775
Issue
6
Volume
3
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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
Lipocalin‐2 Protects Against Diet‐Induced Nonalcoholic Fatty Liver Disease by Targeting Hepatocytes.
Publisher
An entity responsible for making the resource available
Hepatology Communications
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
FATTY liver; LIPOCALIN; LIVER disease treatment
Creator
An entity primarily responsible for making the resource
Xu Yanyong; Zhu Yingdong; Jadhav Kavita; Li Yuanyuan; Sun Huihui; Yin Liya; Kasumov Takhar; Chen Xiaoli; Zhang Yanqiao
Description
An account of the resource
Hepatocytes are the major source of hepatic lipocalin‐2 (LCN2), which is up‐regulated in response to inflammation, injury, or metabolic stress. So far, the role of hepatocyte‐derived LCN2 in the development of nonalcoholic fatty liver disease (NAFLD) remains unknown. Herein we show that overexpression of human LCN2 in hepatocytes protects against high fat/high cholesterol/high fructose (HFCF) diet–induced liver steatosis and nonalcoholic steatohepatitis by promoting lipolysis and fatty acid oxidation (FAO) and inhibiting de novo lipogenesis (DNL), lipid peroxidation, and apoptosis. LCN2 fails to reduce triglyceride accumulation in hepatocytes lacking sterol regulatory element‐binding protein 1. In contrast, Lcn2−/− mice have defective lipolysis, increased lipid peroxidation and apoptosis, and exacerbated NAFLD after being fed an HFCF diet. In primary hepatocytes, Lcn2 deficiency stimulates de novo lipogenesis but inhibits FAO. Conclusion: The current study indicates that hepatocyte LCN2 protects against diet‐induced NAFLD by regulating lipolysis, FAO, DNL, lipid peroxidation, and apoptosis. Targeting hepatocyte LCN2 may be useful for treatment of NAFLD. [ABSTRACT FROM AUTHOR]
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep4.1341" target="_blank" rel="noreferrer noopener">10.1002/hep4.1341</a>
2019
Chen Xiaoli
Department of Integrative Medical Sciences
Fatty Liver
Hepatology communications
Jadhav Kavita
Kasumov Takhar
Li Yuanyuan
LIPOCALIN
LIVER disease treatment
NEOMED College of Medicine
September 2019 Update
Sun Huihui
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong
-
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="https://e-dmj.org/Synapse/Data/PDFData/2004DMJ/dmj-43-257.pdf" target="_blank" rel="noreferrer noopener">http://doi.org/10.4093/dmj.2019.0043</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
257-272
Issue
3
Volume
43
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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
Understanding Bile Acid Signaling in Diabetes: From Pathophysiology to Therapeutic Targets.
Publisher
An entity responsible for making the resource available
Diabetes & Metabolism Journal
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
BILE acids; Bile acids and salts; cholesterol 7-alpha-hydroxylase; Cytoplasmic and Nuclear; Endocrinology & Metabolism; FARNESOID X receptor; farnesoid-x-receptor; FATTY liver; fatty liver-disease; G protein coupled receptors; G-protein-coupled; Gastrointestinal microbiome; growth-factor 19; gut microbiota; hepatic steatosis; improves insulin sensitivity; liver disease; metabolic; Non-alcoholic fatty; Non-alcoholic Fatty Liver Disease; nuclear; receptor; Receptors; serum fgf21 levels; syndrome
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Chiang John Y L
Description
An account of the resource
Diabetes and obesity have reached an epidemic status worldwide. Diabetes increases the risk for cardiovascular disease and nonalcoholic fatty liver disease. Primary bile acids are synthesized in hepatocytes and are transformed to secondary bile acids in the intestine by gut bacteria. Bile acids are nutrient sensors and metabolic integrators that regulate lipid, glucose, and energy homeostasis by activating nuclear farnesoid X receptor and membrane Takeda G protein-coupled receptor 5. Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Gut bacteria, in turn, control circulating bile acid composition and pool size. Dysregulation of bile acid homeostasis and dysbiosis causes diabetes and obesity. Targeting bile acid signaling and the gut microbiome have therapeutic potential for treating diabetes, obesity, and non-alcoholic fatty liver disease. [ABSTRACT FROM AUTHOR]
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.4093/dmj.2019.0043" target="_blank" rel="noreferrer noopener">10.4093/dmj.2019.0043</a>
2019
BILE acids
Bile Acids and Salts
Chiang John Y L
cholesterol 7-alpha-hydroxylase
Cytoplasmic and Nuclear
Department of Integrative Medical Sciences
Diabetes & Metabolism Journal
Endocrinology & Metabolism
Farnesoid X receptor
farnesoid-x-receptor
Fatty Liver
fatty liver-disease
Ferrell Jessica M
G protein coupled receptors
G-protein-coupled
Gastrointestinal Microbiome
growth-factor 19
gut microbiota
hepatic steatosis
improves insulin sensitivity
Liver disease
Metabolic
NEOMED College of Medicine
Non-alcoholic fatty
Non-alcoholic Fatty Liver Disease
nuclear
Receptor
Receptors
September 2019 Update
serum fgf21 levels
Syndrome
-
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="https://www.omicsonline.org/open-access/why-donrsquot-we-have-a-vaccine-against-autoimmune-diseases--a-review.pdf" target="_blank" rel="noreferrer noopener">http://doi.org/10.4172/2155-9899.1000574</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).
Issue
1
Volume
10
Search for Full-text
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Dublin Core
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Title
A name given to the resource
Why Don't We Have a Vaccine Against Autoimmune Diseases? - A Review
Publisher
An entity responsible for making the resource available
Journal of Clinical & Cellular Immunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019
Subject
The topic of the resource
Autoimmune; Immunotherapy; Multiple sclerosis; Rheumatoid arthritis; Type 1 diabetes; Vaccine
Creator
An entity primarily responsible for making the resource
Rosenthal Ken S; Carambula Roy; Zimmerman Daniel H
Description
An account of the resource
This review examines some of the reasons why we don't have a vaccine against autoimmune diseases and highlights the progress that has been made. Many autoimmune diseases, such as rheumatoid arthritis (RA), multiple sclerosis (MS) and type 1 diabetes (T1D), are driven by autoimmune T cell responses. Unlike vaccines for most infectious diseases, which elicit antibody responses, are intended for immuno-naive individuals and considered preventative, a vaccine for an autoimmune disease must be therapeutic and resolve or control the on-going autoimmune response and condition in the diseased host. Despite these differences, many of the same considerations for infectious disease vaccines must also be addressed to develop a therapeutic vaccine for autoimmune diseases. The disease initiator/triggers, antigens and autoantigens, nature of the immunopathogenic and protective/therapeutic immune response will be compared for infectious and autoimmune diseases as will approaches for developing vaccines including formulations, animal models and indicators of success. The rationale for a therapeutic vaccine for RA will be discussed in greater detail with a relatively limited discussion of T1D, MS and other autoimmune diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.4172/2155-9899.1000574" target="_blank" rel="noreferrer noopener">10.4172/2155-9899.1000574</a>
2019
Autoimmune
Carambula Roy
Department of Integrative Medical Sciences
immunotherapy
Journal of clinical & cellular immunology
Multiple sclerosis
NEOMED College of Medicine
Rheumatoid arthritis
Rosenthal Ken S
September 2019 Update
Type 1 diabetes
Vaccine
Zimmerman Daniel H
-
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.119.312610" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.119.312610</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
1574-1587
Issue
8
Volume
39
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Title
A name given to the resource
Hepatic Forkhead Box Protein A3 Regulates ApoA-I (Apolipoprotein A-I) Expression, Cholesterol Efflux, and Atherogenesis
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
2019
2019-08
Subject
The topic of the resource
activation; Atherosclerosis; Cardiovascular System & Cardiology; cholesterol efflux; fatty-acids; FOXA3; FOXA3; gene; Hematology; high-density-lipoprotein; increased; Liver; Macrophages; mice lacking; nuclear factor 3-gamma; transport
Creator
An entity primarily responsible for making the resource
Li Yuanyuan; Xu Yanyong; Jadhav Kavita; Zhu Yingdong; Yin Liya; Zhang Yanqiao
Description
An account of the resource
OBJECTIVE: To determine the role of hepatic FOXA3 (forkhead box A3) in lipid metabolism and atherosclerosis. Approach and Results: Hepatic FOXA3 expression was reduced in diabetic or high fat diet-fed mice or patients with nonalcoholic steatohepatitis. We then used adenoviruses to overexpress or knock down hepatic FOXA3 expression. Overexpression of FOXA3 in the liver increased hepatic ApoA-I (apolipoprotein A-I) expression, plasma HDL-C (high-density lipoprotein cholesterol) level, macrophage cholesterol efflux, and macrophage reverse cholesterol transport. In contrast, knockdown of hepatic FOXA3 expression had opposite effects. We further showed that FOXA3 directly bound to the promoter of the Apoa1 gene to regulate its transcription. Finally, AAV8 (adeno-associated virus serotype 8)-mediated overexpression of human FOXA3 in the hepatocytes of Apoe-/- (apolipoprotein E-deficient) mice raised plasma HDL-C levels and significantly reduced atherosclerotic lesions. CONCLUSIONS: Hepatocyte FOXA3 protects against atherosclerosis by inducing ApoA-I and macrophage reverse cholesterol transport.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.119.312610" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.119.312610</a>
2019
activation
and vascular biology
Arteriosclerosis
Arteriosclerosis, thrombosis, and vascular biology
Atherosclerosis
Cardiovascular System & Cardiology
cholesterol efflux
Department of Integrative Medical Sciences
fatty-acids
FOXA3
gene
Hematology
high-density-lipoprotein
increased
Jadhav Kavita
Li Yuanyuan
Liver
Macrophages
mice lacking
NEOMED College of Medicine
nuclear factor 3-gamma
September 2019 Update
Thrombosis
transport
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong
-
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.00247.2019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00247.2019</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).
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<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
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
Exosomes derived from Induced Vascular Progenitor Cells Promote Angiogenesis in vitro and in an in vivo Rat Hindlimb Ischemia Model
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
2019
2019-08
Subject
The topic of the resource
angiogenesis; endothelial cell; exosome; microRNA; progenitor cell
Creator
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Johnson Takerra K; Zhao Lina; Zhu Dihan; Wang Yang; Xiao Yan; Oguljahan Babayewa; Zhao Xueying; Kirlin Ward G; Yin Liya; Chilian William M; Liu Dong
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Induced vascular progenitor cells (iVPCs) were created as an ideal cell type for regenerative medicine and have been reported to positively promote collateral blood flow and improve cardiac function in a rat model of myocardial ischemia. Exosomes have emerged as a novel biomedicine that mimics the function of the donor cells. We investigated the angiogenic activity of exosomes from induced vascular progenitor cells (iVPC-Exo) as a cell-free therapeutic approach for ischemia. Exosomes from iVPCs and rat aortic endothelial cells (RAECs) were isolated using a combination of ultrafiltration and size-exclusion chromatography. Nanoparticle tracking analysis revealed that exosome isolates fell within the exosomal diameter (<150 nm). These exosomes contained known markers Alix and TSG101, and their morphology was validated using transmission electron microscopy. Compared to RAECs, iVPCs significantly increased the secretion of exosomes. Cardiac microvascular endothelial cells and aortic ring explants were pretreated with RAEC-Exo or iVPC-Exo, and basal medium was used as a control. iVPC-Exo exerted an in vitro angiogenic effect on the proliferation, tube formation, and migration of endothelial cells and stimulated microvessel sprouting in an ex vivo aortic ring assay. Additionally, iVPC-Exo increased blood perfusion in a hindlimb ischemia model. Proangiogenic proteins (pentraxin-3 and insulin-like growth factor-binding protein-3) and microRNAs (-143-3p, -291b, and -20b-5p) were found to be enriched in iVPC-Exo, which may mediate iVPC-Exo induced vascular growth. Our findings demonstrate that treatment with iVPC-Exo promotes angiogenesis in vitro, ex vivo, and in vivo. Collectively, these findings indicate a novel cell-free approach for therapeutic angiogenesis.
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<a href="http://doi.org/10.1152/ajpheart.00247.2019" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00247.2019</a>
2019
American journal of physiology. Heart and circulatory physiology
angiogenesis
Chilian William M
Department of Integrative Medical Sciences
endothelial cell
exosome
Johnson Takerra K
Kirlin Ward G
Liu Dong
MicroRNA
NEOMED College of Medicine
Oguljahan Babayewa
progenitor cell
September 2019 Update
Wang Yang
Xiao Yan
Yin Liya
Zhao Lina
Zhao Xueying
Zhu Dihan
-
Text
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<a href="http://doi.org/10.1002/jcb.29326" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcb.29326</a>
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N-end rule pathway inhibitor sensitizes cancer cells to antineoplastic agents by regulating XIAP and RAD21 protein expression
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Journal of Cellular Biochemistry
Date
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2019
2019-08
Subject
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apoptosis; Biochemistry & Molecular Biology; cancer; Cell Biology; cleavage; cyclin; degradation; drug sensitivity; hdm2; heterovalent inhibitors; mechanisms; N-end rule; oncoprotein; RAD21; reaper; substrate; UBR1; XIAP
Creator
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Pore Subrata K; Ganguly Anirban; Sau Samaresh; Godeshala Sudhakar; Kanugula Anantha K; Ummanni Ramesh; Kotamraju Srigiridhar; Banerjee Rajkumar
Description
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Anticancer drugs exert their effects on cancer cells by deregulating many pathways linked to cell cycle, apoptosis, etc. but cancer cells gradually become resistive against anticancer drugs, thereby necessitating the development of newer generation anticancer molecules. N-end rule pathway has been shown to be involved in the degradation of many cell cycle and apoptosis-related proteins. However, the involvements of this pathway in cancer are not well established. Recently, we developed a non-peptide-based N-end rule pathway inhibitor, RF-C11 for type 1 and 2 recognition domains of E3 ubiquitin ligases. The inhibitor significantly increased the half-life of potential N-degrons leading to significant physiological changes in vivo. We hypothesized RF-C11 may be used to decipher the N-end rule pathway's role in cancer towards the development of anticancer therapeutics. In this study, we showed that RF-C11, barring noncancer cells, significantly sensitizes cancer cells towards different anticancer agents tested. We further find that the profound cellular sensitization to anticancer drugs was affected by (a) downregulation of X-linked inhibitor of apoptosis protein, an antiapoptotic protein and (b) by stabilization of RAD21, and thereby inhibiting metaphase to anaphase promotion. The study shows that RF-C11 or its analogs may be used as a novel additive in combination therapy against cancer.
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<a href="http://doi.org/10.1002/jcb.29326" target="_blank" rel="noreferrer noopener">10.1002/jcb.29326</a>
2019
Apoptosis
Banerjee Rajkumar
Biochemistry & Molecular Biology
Cancer
Cell Biology
cleavage
cyclin
degradation
Department of Integrative Medical Sciences
drug sensitivity
Ganguly Anirban
Godeshala Sudhakar
hdm2
heterovalent inhibitors
Journal of cellular biochemistry
Kanugula Anantha K
Kotamraju Srigiridhar
mechanisms
N-end rule
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
oncoprotein
Pore Subrata K
RAD21
reaper
Sau Samaresh
September 2019 Update
substrate
UBR1
Ummanni Ramesh
XIAP
-
Text
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URL Address
<a href="http://doi.org/10.1097/SHK.0000000000001374" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/SHK.0000000000001374</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).
Pages
133-134
Issue
6
Volume
51
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Title
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THE BONE MARROW ENDOTHELIAL PROGENITOR CELL RESPONSE TO SEPTIC INFECTION
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Shock
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
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& Cardiology; Cardiovascular System; General & Internal Medicine; Hematology; Surgery
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Shi X; Simms K J; Ewing T J; Zhang P
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<a href="http://doi.org/10.1097/SHK.0000000000001374" target="_blank" rel="noreferrer noopener">10.1097/SHK.0000000000001374</a>
& Cardiology
2019
Cardiovascular System
Department of Integrative Medical Sciences
Ewing T J
General & Internal Medicine
Hematology
NEOMED College of Medicine
September 2019 Update
Shi X
Shock
Simms K J
Surgery
Zhang P
-
Text
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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
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ALCOHOL INHIBITS UPREGULATION OF GBP7 EXPRESSION BY HEMATOPOIETIC STEM/PROGENITOR CELLS DURING THE GRANULOPOIETIC RESPONSE TO SEPTIC INFECTION
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Alcoholism-Clinical and Experimental Research
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2019
2019-06
Subject
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Substance Abuse
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Shi X; Simms K J; Ewing T J; Zhang P
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<a href="http://doi.org/10.1111/acer.14059">http://doi.org/10.1111/acer.14059</a>
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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
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.jsxm.2019.01.194" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jsxm.2019.01.194</a>
Pages
S92–S92
Issue
4
Volume
16
ISSN
1743-6095
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IMPACT OF RHOGDI GENE TRANSFECTION OF BLADDER SMOOTH MUSCLE CONTRACTILITY IN A VALIDATED EX-VIVO MURINE MODEL
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Journal of Sexual Medicine
Date
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2019
2019-04
Subject
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Urology & Nephrology
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Joice G; Bell J M; La Favor J; Yoshida T; Torga G; Harris K; Liu X; Kiedrowski M; Penn M; Bivalacqua T
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<a href="http://doi.org/10.1016/j.jsxm.2019.01.194" target="_blank" rel="noreferrer noopener">10.1016/j.jsxm.2019.01.194</a>
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19th Annual Fall Scientific Meeting of SMSNA
Introduction Plasmid-based gene therapy is an intriguing option for treating malignant and bladder pathologies. The RhoA pathway is involved in bladder smooth muscle regulation, cancer invasion and metastasis. Rho GDP-dissociation inhibitor (RhoGDI) is an inhibitor of the RhoA pathway. We validated ex-vivo bladder gene transfer to facilitate assessment of gene targets for treating bladder pathology. Methods Basic Local Alignment Search Tool was used to identify human RhoGDI coding sequences and to compare between rats and humans, which were cloned into a eCMV-based expression vector. NBTII rat bladder cancer cell lines were transfected using FuGENE (Promega, USA) and human protein expression and interaction with endogenous RhoA were tested using flow cytometry, immunofluorescence, and RNA expression analysis. Bladders were harvested from female Lewis Rats (∼250g) and sectioned and cultured for 72-hours following transfection with RhoGDI and FuGENE. Transfected bladder tissues were analyzed as described above. Non-transfected cultured bladder segments were analyzed using myography for viability and intact smooth muscle physiology in response to 120 mM KCl and 30uM carbachol. Results Human and rodent RhoGDI protein homology is 96%. Human RhoGDI was successfully detected exclusively in transfected NBTII cells with a top efficiency of 26%. qPCR analysis demonstrated rodent RhoA and RhoGDI levels were not impacted but ROCK1 and ROCK2 mRNA were significantly decreased by 23.6% (p=0.034) and 40.0% (p=0.015), respectively following human RhoGDI transfection. Human RhoGDI was detected in transfected ex-vivo cultured bladder segments in both FuGENE and microinjection experiments. Similar to NBTII cells, qPCR analysis demonstrated rodent RhoA and RhoGDI levels were not impacted but ROCK1 and ROCK2 mRNA were significantly decreased by 15.0% (p=0.035) and 22.4% (p=0.010) after FuGENE transfection and 20.5% (p=0.024) and 21.4% (p=0.015) after microinjections. Ex-vivo cultured bladder strips successfully contracted to KCl (mean 0.88+/-0.48 mN/mg tissue) and carbachol (1.82+/-0.97 mN/mg tissue) stimulation. After microinjection, RhoGDI caused a significant reduction in KCl mediated constriction although this was not observed in FuGENE experiments. Conclusion Ex-vivo bladder culture, transfection, and physiological assessment are feasible and may provide a high-throughput method to test novel gene transfer technologies before in-vivo testing. RhoGDI plasmid microinjection transfection appears to decrease contractility of ex-vivo bladder smooth muscle.
2019
Bell J M
Bivalacqua T
Department of Integrative Medical Sciences
Harris K
Joice G
Journal of Sexual Medicine
June 2019 Update
Kiedrowski M
La Favor J
Liu X
NEOMED College of Medicine
Penn M
Torga G
Urology & Nephrology
Yoshida T
-
Text
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URL Address
<a href="http://doi.org/10.1093/cvr/cvy286" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/cvr/cvy286</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).
Pages
1143-1155
Issue
7
Volume
115
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Title
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coronary circulation in acute myocardial ischaemia/reperfusion injury: a target for cardioprotection.
Publisher
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Cardiovascular Research
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
acute coronary syndromes; blood capillaries; cardiac myocytes; cardiac vasculature; Cardioprotection; Coronary circulation; Coronary circulation; CYTOLOGY; edema; endothelium; erythrocytes; HEMORRHAGE; infarction; Ischaemia; ischemia; ischemia; ISCHEMIC preconditioning; leukocytes; MEDICAL sciences; Microvascular obstruction; midventricular obstruction; MYOCARDIAL reperfusion; personal integrity; pharmacology; physiologic reperfusion; PRASUGREL; Reperfusion; reperfusion injury; reperfusion injury; reperfusion therapy
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Hausenloy Derek J; Chilian William; Crea Filippo; Davidson Sean M; Ferdinandy Peter; Garcia-Dorado David; van Royen Niels; Schulz Rainer; Heusch Gerd
Description
An account of the resource
The coronary circulation is both culprit and victim of acute myocardial infarction. The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolization of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leucocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction (MVO), and intramyocardial haemorrhage (IMH). Therefore, the coronary circulation is a valid target for cardioprotection, beyond protection of the cardiomyocyte. Virtually all of the above deleterious endpoints have been demonstrated to be favourably influenced by one or the other mechanical or pharmacological cardioprotective intervention. However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. MVO and IMH can be diagnosed by modern imaging technologies, but still await an effective therapy. The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.
Identifier
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<a href="http://doi.org/10.1093/cvr/cvy286" target="_blank" rel="noreferrer noopener">10.1093/cvr/cvy286</a>
2019
acute coronary syndromes
blood capillaries
cardiac myocytes
cardiac vasculature
cardioprotection
Cardiovascular research
Chilian William
Coronary Circulation
Crea Filippo
CYTOLOGY
Davidson Sean M
Department of Integrative Medical Sciences
Edema
Endothelium
erythrocytes
Ferdinandy Peter
Garcia-Dorado David
Hausenloy Derek J
Hemorrhage
Heusch Gerd
Infarction
Ischaemia
ischemia
Ischemic Preconditioning
June 2019 Update
LEUKOCYTES
MEDICAL sciences
Microvascular obstruction
midventricular obstruction
Myocardial Reperfusion
NEOMED College of Medicine
personal integrity
pharmacology
physiologic reperfusion
PRASUGREL
Reperfusion
Reperfusion Injury
reperfusion therapy
Schulz Rainer
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/10.4093/dmj.2019.0043" target="_blank" rel="noreferrer noopener">http://doi.org/10.4093/dmj.2019.0043</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).
Pages
257-272
Issue
3
Volume
43
Dublin Core
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Title
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Understanding Bile Acid Signaling in Diabetes: From Pathophysiology to Therapeutic Targets
Publisher
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Diabetes & Metabolism Journal
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
Bile acids and salts; cytoplasmic and nuclear; G-protein-coupled; Gastrointestinal microbiome; Non-alcoholic fatty liver disease; Receptors
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Chiang John Y L
Description
An account of the resource
Diabetes and obesity have reached an epidemic status worldwide. Diabetes increases the risk for cardiovascular disease and non-alcoholic fatty liver disease. Primary bile acids are synthesized in hepatocytes and are transformed to secondary bile acids in the intestine by gut bacteria. Bile acids are nutrient sensors and metabolic integrators that regulate lipid, glucose, and energy homeostasis by activating nuclear farnesoid X receptor and membrane Takeda G protein-coupled receptor 5. Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Gut bacteria, in turn, control circulating bile acid composition and pool size. Dysregulation of bile acid homeostasis and dysbiosis causes diabetes and obesity. Targeting bile acid signaling and the gut microbiome have therapeutic potential for treating diabetes, obesity, and non-alcoholic fatty liver disease.
Identifier
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<a href="http://doi.org/10.4093/dmj.2019.0043" target="_blank" rel="noreferrer noopener">10.4093/dmj.2019.0043</a>
2019
Bile Acids and Salts
Chiang John Y L
Cytoplasmic and Nuclear
Department of Integrative Medical Sciences
Diabetes & Metabolism Journal
Ferrell Jessica M
G-protein-coupled
Gastrointestinal Microbiome
June 2019 Update
NEOMED College of Medicine
Non-alcoholic Fatty Liver Disease
Receptors