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  1. Article ; Online: Understanding Perceived Appreciation to Create a Culture of Wellness.

    Nadkarni, Ashwini / Harry, Elizabeth / Rozenblum, Ronen / Kimberly, Heidi H / Schissel, Scott L / DeOliveira, Maria C / Jackson, Amy B / Giess, Catherine S / Ashley, Stanley W / Dudley, Jessica C

    Academic psychiatry : the journal of the American Association of Directors of Psychiatric Residency Training and the Association for Academic Psychiatry

    2021  Volume 46, Issue 2, Page(s) 228–232

    Abstract: Objective: To fully address physician burnout, academic medical centers need cultures that promote well-being. One observed driver of a culture of wellness is perceived appreciation. The authors identified several contributors to perceived appreciation ... ...

    Abstract Objective: To fully address physician burnout, academic medical centers need cultures that promote well-being. One observed driver of a culture of wellness is perceived appreciation. The authors identified several contributors to perceived appreciation among faculty at a large, metropolitan academic institution through use of a novel survey.
    Methods: The authors surveyed clinical faculty in five departments: psychiatry, emergency medicine, internal medicine, thoracic surgery, and radiology. Two open-ended response questions assessed sources of perceived and lack of perceived appreciation in narrative form. The authors also collected data on gender and department identity. Grounded theory methodology was used to analyze the narrative responses and design thinking to brainstorm specific recommendations based on the main themes identified.
    Results: A total of 179 faculty respondents filled out the survey for an overall response rate of 29%. Major drivers of perceived appreciation were patient and families (42%); physician, trainee and non-physician colleagues (32.7%); chairs (10%); and compensation (3.3%). Major drivers of perceived lack of appreciation were disrespect for time and skill level, including inadequate staffing (30%); devaluation by a physician colleague, chief of one's service or the chair (29%); poor communication and transparency (13%); and patient and family anger (6%).
    Conclusions: Opportunities to improve perceived appreciation include structured communication of patient gratitude, community building programs, top of licensure initiatives and accountability for physician wellness, and inclusivity efforts from organizational leaders.
    MeSH term(s) Burnout, Professional/psychology ; Faculty ; Humans ; Internal Medicine ; Physicians/psychology ; Surveys and Questionnaires
    Language English
    Publishing date 2021-05-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1045331-3
    ISSN 1545-7230 ; 1042-9670
    ISSN (online) 1545-7230
    ISSN 1042-9670
    DOI 10.1007/s40596-021-01489-w
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  2. Article: Telomerase, myofibroblasts, and pulmonary fibrosis.

    Schissel, Scott L / Layne, Matthew D

    American journal of respiratory cell and molecular biology

    2006  Volume 34, Issue 5, Page(s) 520–522

    MeSH term(s) Animals ; Cell Differentiation ; Fibroblasts/cytology ; Muscle Cells/cytology ; Pulmonary Fibrosis/enzymology ; Pulmonary Fibrosis/pathology ; Telomerase/metabolism
    Chemical Substances Telomerase (EC 2.7.7.49)
    Language English
    Publishing date 2006-05
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.F312
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  3. Article ; Online: Virtual Care Team Guided Management of Patients With Heart Failure During Hospitalization.

    Bhatt, Ankeet S / Varshney, Anubodh S / Moscone, Alea / Claggett, Brian L / Miao, Zi Michael / Chatur, Safia / Lopes, Mathew S / Ostrominski, John W / Pabon, Maria A / Unlu, Ozan / Wang, Xiaowen / Bernier, Thomas D / Buckley, Leo F / Cook, Bryan / Eaton, Rachael / Fiene, Jillian / Kanaan, Dareen / Kelly, Julie / Knowles, Danielle M /
    Lupi, Kenneth / Matta, Lina S / Pimentel, Liriany Y / Rhoten, Megan N / Malloy, Rhynn / Ting, Clara / Chhor, Rosette / Guerin, Joshua R / Schissel, Scott L / Hoa, Brenda / Lio, Connie H / Milewski, Kristina / Espinosa, Michelle E / Liu, Zhenzhen / McHatton, Ralph / Cunningham, Jonathan W / Jering, Karola S / Bertot, John H / Kaur, Gurleen / Ahmad, Adeel / Akash, Muhammad / Davoudi, Farideh / Hinrichsen, Mona Z / Rabin, David L / Gordan, Patrick L / Roberts, David J / Urma, Daniela / McElrath, Erin E / Hinchey, Emily D / Choudhry, Niteesh K / Nekoui, Mahan / Solomon, Scott D / Adler, Dale S / Vaduganathan, Muthiah

    Journal of the American College of Cardiology

    2023  Volume 81, Issue 17, Page(s) 1680–1693

    Abstract: Background: Scalable and safe approaches for heart failure guideline-directed medical therapy (GDMT) optimization are needed.: Objectives: The authors assessed the safety and effectiveness of a virtual care team guided strategy on GDMT optimization ... ...

    Abstract Background: Scalable and safe approaches for heart failure guideline-directed medical therapy (GDMT) optimization are needed.
    Objectives: The authors assessed the safety and effectiveness of a virtual care team guided strategy on GDMT optimization in hospitalized patients with heart failure with reduced ejection fraction (HFrEF).
    Methods: In a multicenter implementation trial, we allocated 252 hospital encounters in patients with left ventricular ejection fraction ≤40% to a virtual care team guided strategy (107 encounters among 83 patients) or usual care (145 encounters among 115 patients) across 3 centers in an integrated health system. In the virtual care team group, clinicians received up to 1 daily GDMT optimization suggestion from a physician-pharmacist team. The primary effectiveness outcome was in-hospital change in GDMT optimization score (+2 initiations, +1 dose up-titrations, -1 dose down-titrations, -2 discontinuations summed across classes). In-hospital safety outcomes were adjudicated by an independent clinical events committee.
    Results: Among 252 encounters, the mean age was 69 ± 14 years, 85 (34%) were women, 35 (14%) were Black, and 43 (17%) were Hispanic. The virtual care team strategy significantly improved GDMT optimization scores vs usual care (adjusted difference: +1.2; 95% CI: 0.7-1.8; P < 0.001). New initiations (44% vs 23%; absolute difference: +21%; P = 0.001) and net intensifications (44% vs 24%; absolute difference: +20%; P = 0.002) during hospitalization were higher in the virtual care team group, translating to a number needed to intervene of 5 encounters. Overall, 23 (21%) in the virtual care team group and 40 (28%) in usual care experienced 1 or more adverse events (P = 0.30). Acute kidney injury, bradycardia, hypotension, hyperkalemia, and hospital length of stay were similar between groups.
    Conclusions: Among patients hospitalized with HFrEF, a virtual care team guided strategy for GDMT optimization was safe and improved GDMT across multiple hospitals in an integrated health system. Virtual teams represent a centralized and scalable approach to optimize GDMT.
    MeSH term(s) Humans ; Female ; Middle Aged ; Aged ; Aged, 80 and over ; Male ; Heart Failure ; Stroke Volume ; Ventricular Function, Left ; Hospitalization ; Patient Care Team
    Language English
    Publishing date 2023-03-06
    Publishing country United States
    Document type Multicenter Study ; Journal Article
    ZDB-ID 605507-2
    ISSN 1558-3597 ; 0735-1097
    ISSN (online) 1558-3597
    ISSN 0735-1097
    DOI 10.1016/j.jacc.2023.02.029
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  4. Article ; Online: Frontline Science: Targeted expression of a dominant-negative high mobility group A1 transgene improves outcome in sepsis.

    Baron, Rebecca M / Kwon, Min-Young / Castano, Ana P / Ghanta, Sailaja / Riascos-Bernal, Dario F / Lopez-Guzman, Silvia / Macias, Alvaro Andres / Ith, Bonna / Schissel, Scott L / Lederer, James A / Reeves, Raymond / Yet, Shaw-Fang / Layne, Matthew D / Liu, Xiaoli / Perrella, Mark A

    Journal of leukocyte biology

    2018  Volume 104, Issue 4, Page(s) 677–689

    Abstract: High mobility group (HMG) proteins are a family of architectural transcription factors, with HMGA1 playing a role in the regulation of genes involved in promoting systemic inflammatory responses. We speculated that blocking HMGA1-mediated pathways might ... ...

    Abstract High mobility group (HMG) proteins are a family of architectural transcription factors, with HMGA1 playing a role in the regulation of genes involved in promoting systemic inflammatory responses. We speculated that blocking HMGA1-mediated pathways might improve outcomes from sepsis. To investigate HMGA1 further, we developed genetically modified mice expressing a dominant negative (dn) form of HMGA1 targeted to the vasculature. In dnHMGA1 transgenic (Tg) mice, endogenous HMGA1 is present, but its function is decreased due to the mutant transgene. These mice allowed us to specifically study the importance of HMGA1 not only during a purely pro-inflammatory insult of endotoxemia, but also during microbial sepsis induced by implantation of a bacterial-laden fibrin clot into the peritoneum. We found that the dnHMGA1 transgene was only present in Tg and not wild-type (WT) littermate mice, and the mutant transgene was able to interact with transcription factors (such as NF-κB), but was not able to bind DNA. Tg mice exhibited a blunted hypotensive response to endotoxemia, and less mortality in microbial sepsis. Moreover, Tg mice had a reduced inflammatory response during sepsis, with decreased macrophage and neutrophil infiltration into tissues, which was associated with reduced expression of monocyte chemotactic protein-1 and macrophage inflammatory protein-2. Collectively, these data suggest that targeted expression of a dnHMGA1 transgene is able to improve outcomes in models of endotoxin exposure and microbial sepsis, in part by modulating the immune response and suggest a novel modifiable pathway to target therapeutics in sepsis.
    MeSH term(s) Animals ; Blood Vessels/metabolism ; Cells, Cultured ; Cytokines/blood ; Endotoxemia/physiopathology ; Endotoxemia/therapy ; Escherichia coli Infections/genetics ; Gene Expression Regulation ; Genes, Dominant ; Genetic Therapy ; HMGA1a Protein/genetics ; Hypotension/etiology ; Inflammation ; Interleukin-1beta/pharmacology ; Lipopolysaccharides/pharmacology ; Mice ; Mice, Transgenic ; Myocytes, Smooth Muscle/metabolism ; NF-kappa B/metabolism ; Phagocytosis ; Recombinant Proteins/pharmacology ; Sepsis/therapy ; Treatment Outcome ; Tumor Necrosis Factor-alpha/pharmacology
    Chemical Substances Cytokines ; Interleukin-1beta ; Lipopolysaccharides ; NF-kappa B ; Recombinant Proteins ; Tumor Necrosis Factor-alpha ; lipopolysaccharide, E. coli O26-B6 ; HMGA1a Protein (124544-67-8)
    Language English
    Publishing date 2018-07-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1002/JLB.4HI0817-333RR
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  5. Article ; Online: Aortic carboxypeptidase-like protein is expressed in fibrotic human lung and its absence protects against bleomycin-induced lung fibrosis.

    Schissel, Scott L / Dunsmore, Sarah E / Liu, Xiaoli / Shine, Robert W / Perrella, Mark A / Layne, Matthew D

    The American journal of pathology

    2009  Volume 174, Issue 3, Page(s) 818–828

    Abstract: The pathological hallmarks of idiopathic pulmonary fibrosis include proliferating fibroblasts and myofibroblasts, as well as excessive collagen matrix deposition. In addition, both myofibroblast contraction and remodeling of the collagen-rich matrix ... ...

    Abstract The pathological hallmarks of idiopathic pulmonary fibrosis include proliferating fibroblasts and myofibroblasts, as well as excessive collagen matrix deposition. In addition, both myofibroblast contraction and remodeling of the collagen-rich matrix contribute to the abnormal structure and function of the fibrotic lung. Little is known, however, about collagen-associated proteins that promote fibroblast and myofibroblast retention, as well as the proliferation of these cells on the extracellular matrix. In this study, we demonstrate that aortic carboxypeptidase-like protein (ACLP), a collagen-associated protein with a discoidin-like domain, is expressed at high levels in human fibrotic lung tissue and human fibroblasts, and that its expression increases markedly in the lungs of bleomycin-injured mice. Importantly, ACLP-deficient mice accumulated significantly fewer myofibroblasts and less collagen in the lung after bleomycin injury, as compared with wild-type controls, despite equivalent levels of bleomycin-induced inflammation. ACLP that is secreted by lung fibroblasts was retained on fibrillar collagen, and ACLP-deficient lung fibroblasts that were cultured on collagen exhibited changes in cell spreading, proliferation, and contraction of the collagen matrix. Finally, the addition of recombinant discoidin-like domain of ACLP to cultured ACLP-deficient lung fibroblasts restored cell spreading and increased the contraction of collagen gels. Therefore, both ACLP and its discoidin-like domain may be novel targets for anti-myofibroblast-based therapies for the treatment of pulmonary fibrosis.
    MeSH term(s) Animals ; Aorta/enzymology ; Bleomycin/toxicity ; Carboxypeptidases/deficiency ; Carboxypeptidases/genetics ; Cell Adhesion ; Collagen/pharmacology ; Female ; Fibroblasts/cytology ; Fibroblasts/pathology ; Gene Expression Regulation, Enzymologic ; Humans ; Lung/enzymology ; Lung/pathology ; Lung Transplantation ; Male ; Mice ; Mice, Knockout ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/enzymology ; Pulmonary Fibrosis/pathology ; Pulmonary Fibrosis/prevention & control ; Repressor Proteins/genetics
    Chemical Substances AEBP1 protein, human ; Aebp1 protein, mouse ; Repressor Proteins ; Bleomycin (11056-06-7) ; Collagen (9007-34-5) ; Carboxypeptidases (EC 3.4.-)
    Language English
    Publishing date 2009-01-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.2353/ajpath.2009.080856
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  6. Article ; Online: Absence of cyclooxygenase-2 exacerbates hypoxia-induced pulmonary hypertension and enhances contractility of vascular smooth muscle cells.

    Fredenburgh, Laura E / Liang, Olin D / Macias, Alvaro A / Polte, Thomas R / Liu, Xiaoli / Riascos, Dario F / Chung, Su Wol / Schissel, Scott L / Ingber, Donald E / Mitsialis, S Alex / Kourembanas, Stella / Perrella, Mark A

    Circulation

    2008  Volume 117, Issue 16, Page(s) 2114–2122

    Abstract: Background: Cyclooxygenase-2 (COX-2) is upregulated in pulmonary artery smooth muscle cells (PASMCs) during hypoxia and may play a protective role in the response of the lung to hypoxia. Selective COX-2 inhibition may have detrimental pulmonary vascular ...

    Abstract Background: Cyclooxygenase-2 (COX-2) is upregulated in pulmonary artery smooth muscle cells (PASMCs) during hypoxia and may play a protective role in the response of the lung to hypoxia. Selective COX-2 inhibition may have detrimental pulmonary vascular consequences during hypoxia.
    Methods and results: To investigate the role of COX-2 in the pulmonary vascular response to hypoxia, we subjected wild-type and COX-2-deficient mice to a model of chronic normobaric hypoxia. COX-2-null mice developed severe pulmonary hypertension with exaggerated elevation of right ventricular systolic pressure, significant right ventricular hypertrophy, and striking vascular remodeling after hypoxia. Pulmonary vascular remodeling in COX-2-deficient mice was characterized by PASMC hypertrophy but not increased proliferation. Furthermore, COX-2-deficient mice had significant upregulation of the endothelin-1 receptor (ET(A)) in the lung after hypoxia. Similarly, selective pharmacological inhibition of COX-2 in wild-type mice exacerbated hypoxia-induced pulmonary hypertension and resulted in PASMC hypertrophy and increased ET(A) receptor expression in pulmonary arterioles. The absence of COX-2 in vascular smooth muscle cells during hypoxia in vitro augmented traction forces and enhanced contractility of an extracellular matrix. Treatment of COX-2-deficient PASMCs with iloprost, a prostaglandin I(2) analog, and prostaglandin E(2) abrogated the potent contractile response to hypoxia and restored the wild-type phenotype.
    Conclusions: Our findings reveal that hypoxia-induced pulmonary hypertension and vascular remodeling are exacerbated in the absence of COX-2 with enhanced ET(A) receptor expression and increased PASMC hypertrophy. COX-2-deficient PASMCs have a maladaptive response to hypoxia manifested by exaggerated contractility, which may be rescued by either COX-2-derived prostaglandin I(2) or prostaglandin E(2).
    MeSH term(s) Animals ; Blood Pressure/physiology ; Cells, Cultured ; Chronic Disease ; Collagen ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Dinoprostone/pharmacology ; Endothelin-1/pharmacology ; Gels ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/physiopathology ; Hypertrophy, Right Ventricular/metabolism ; Hypertrophy, Right Ventricular/physiopathology ; Hypoxia/metabolism ; Hypoxia/physiopathology ; Iloprost/pharmacology ; Mice ; Mice, Mutant Strains ; Muscle Contraction/drug effects ; Muscle Contraction/physiology ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/enzymology ; Pulmonary Artery/cytology ; Pulmonary Artery/physiology ; Receptor, Endothelin A/genetics ; Traction ; Vasoconstriction/drug effects ; Vasoconstriction/physiology ; Vasodilator Agents/pharmacology
    Chemical Substances Endothelin-1 ; Gels ; Receptor, Endothelin A ; Vasodilator Agents ; Collagen (9007-34-5) ; Ptgs2 protein, mouse (EC 1.14.99.-) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Iloprost (JED5K35YGL) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2008-04-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.107.716241
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  7. Article ; Online: Disruption of striated preferentially expressed gene locus leads to dilated cardiomyopathy in mice.

    Liu, Xiaoli / Ramjiganesh, Tripurasundari / Chen, Yen-Hsu / Chung, Su Wol / Hall, Sean R / Schissel, Scott L / Padera, Robert F / Liao, Ronglih / Ackerman, Kate G / Kajstura, Jan / Leri, Annarosa / Anversa, Piero / Yet, Shaw-Fang / Layne, Matthew D / Perrella, Mark A

    Circulation

    2008  Volume 119, Issue 2, Page(s) 261–268

    Abstract: Background: The striated preferentially expressed gene (Speg) generates 4 different isoforms through alternative promoter use and tissue-specific splicing. Depending on the cell type, Speg isoforms may serve as markers of striated or smooth muscle ... ...

    Abstract Background: The striated preferentially expressed gene (Speg) generates 4 different isoforms through alternative promoter use and tissue-specific splicing. Depending on the cell type, Speg isoforms may serve as markers of striated or smooth muscle differentiation.
    Methods and results: To elucidate function of Speg gene isoforms, we disrupted the Speg gene locus in mice by replacing common exons 8, 9, and 10 with a lacZ gene. beta-Galactosidase activity was detected in cardiomyocytes of the developing heart starting at day 11.5 days post coitum (dpc). beta-Galactosidase activity in other cell types, including vascular smooth muscle cells, did not begin until 18.5 dpc. In the developing heart, protein expression of only Spegalpha and Spegbeta isoforms was present in cardiomyocytes. Homozygous Speg mutant hearts began to enlarge by 16.5 dpc, and by 18.5 dpc, they demonstrated dilation of right and left atria and ventricles. These cardiac abnormalities in the absence of Speg were associated with a cellular hypertrophic response, myofibril degeneration, and a marked decrease in cardiac function. Moreover, Speg mutant mice exhibited significant neonatal mortality, with increased death occurring by 2 days after birth.
    Conclusions: These findings demonstrate that mutation of the Speg locus leads to cardiac dysfunction and a phenotype consistent with a dilated cardiomyopathy.
    MeSH term(s) Animals ; Animals, Newborn ; Cardiomyopathy, Dilated/enzymology ; Cardiomyopathy, Dilated/etiology ; Cardiomyopathy, Dilated/genetics ; Gene Targeting ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Muscle Proteins/biosynthesis ; Muscle Proteins/deficiency ; Muscle Proteins/genetics ; Mutagenesis, Site-Directed ; Myosin-Light-Chain Kinase/biosynthesis ; Myosin-Light-Chain Kinase/deficiency ; Myosin-Light-Chain Kinase/genetics
    Chemical Substances Muscle Proteins ; Speg protein, mouse (EC 2.7.11.1) ; Myosin-Light-Chain Kinase (EC 2.7.11.18)
    Language English
    Publishing date 2008-12-31
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.108.799536
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