- Mechanical Circulatory Support Devices
- Inflammatory mediators and NSAID effects
- Fuel Cells and Related Materials
- Cardiac Structural Anomalies and Repair
- Liver physiology and pathology
- Neonatal Respiratory Health Research
- Pulmonary Hypertension Research and Treatments
- MicroRNA in disease regulation
- Tissue Engineering and Regenerative Medicine
- Eicosanoids and Hypertension Pharmacology
- Pancreatic function and diabetes
- Pluripotent Stem Cells Research
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Biomarkers in Disease Mechanisms
- Circular RNAs in diseases
- Organ Transplantation Techniques and Outcomes
- Fibroblast Growth Factor Research
- Cardiovascular Function and Risk Factors
- Extracellular vesicles in disease
- Cancer-related molecular mechanisms research
- Cardiac Ischemia and Reperfusion
- Adipose Tissue and Metabolism
- Protease and Inhibitor Mechanisms
- Peptidase Inhibition and Analysis
- Cytomegalovirus and herpesvirus research
University of Nebraska Medical Center
2010-2024
University of Pittsburgh
2021
SleepMed
2010
Pulmonary and Critical Care Associates
2010
University of Tennessee Health Science Center
1999-2000
The relatedness of group A streptococcal (GAS) strains isolated from 35 Canadian patients with invasive disease different severity was investigated by a variety molecular methods. All were infected M1T1 and, based on clinical criteria, classified as severe (n = 21) and nonsevere 14) GAS infection cases. the M1 studied had emm1.0 allele same pyrogenic exotoxin (Spe) genotype, speA(+) speB(+) speC speF(+) speG(+) speH smeZ(+) ssa. isolates speA allotype, speA2. randomly amplified polymorphic...
Persistent inflammation plays a major role in chronic obstructive pulmonary disease (COPD) pathogenesis, but its mechanisms are incompletely defined. Overproduction of the inflammatory mediator prostaglandin (PG) E₂ by COPD fibroblasts contributes to reduced repair function.The present study determined if from subjects with overproduce PGE₂ after stimulation cytokines IL-1β and tumor necrosis factor-α, further defined mechanism for overproduction.Fibroblasts were isolated parenchymal tissue...
α1-Antitrypsin deficiency is an inherited condition that causes liver disease and emphysema. The normal function of this protein, which synthesized by the liver, to inhibit neutrophil elastase, a protease degrades connective tissue lung. In classical form disease, inefficient secretion mutant α1-antitrypsin protein (AAT-Z) results in its accumulation within hepatocytes reduced inhibitor activity, resulting injury pulmonary Because increases hepatocyte cell stress, we investigated whether...
Vitamin D insufficiency has been increasingly recognized in the general population worldwide and associated with several lung diseases, including asthma, chronic obstructive pulmonary disease (COPD), respiratory tract infections. Fibroblasts play a critical role tissue repair remodeling, which is key feature of COPD asthma. modulate by producing modifying extracellular matrix components releasing mediators that act as autocrine or paracrine modulators remodeling. The current study was...
In advanced cirrhosis, impaired function is caused by intrinsic damage to the native liver cells and from abnormal microenvironment in which reside. The extent each plays a role failure regeneration unknown. To examine this issue, hepatocytes cirrhotic age-matched control rats were isolated, characterized, transplanted into livers of noncirrhotic hosts whose permit extensive repopulation with donor cells. Primary derived cirrhosis compensated maintained metabolic activity ability secrete...
This study assessed the effect of extended exposure to cigarette smoke extract (CSE) on tissue repair functions in lung fibroblasts. Human fetal (HFL-1) and adult fibroblasts were exposed CSE for 14 days. Senescence-associated β-galactosidase (SA β-gal) expression, cell proliferation, including chemotaxis gel contraction assessed. HFL-1 proliferation was inhibited by nearly half CSE-exposed cells SA β-gal positive after days exposure, whereas 33% response 10% exposure. The β-gal-positive did...
Myocardial recovery with left ventricular assist device (LVAD) therapy is highly variable and difficult to predict. Next generation ribonucleic acid (RNA) sequencing an innovative, rapid, quantitative approach gene expression profiling in small amounts of tissue. Our primary goal was identify baseline transcriptional profiles non-ischemic cardiomyopathies that predict myocardial response LVAD therapy. We also sought verify differences between failing non-failing human hearts.RNA isolated...
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Tumor necrosis factor (TNF)-α can alter tissue repair functions in a variety of cells including endothelial cells. However, the mechanism by which TNF-α mediates these functional changes has not fully been studied. We investigated role mitogen-activated protein kinases (MAPKs) on mediating regulatory effect human pulmonary artery (HPAECs). protected HPAECs from undergoing apoptosis induced serum and growth deprivation, augmented collagen gel contraction, stimulated wound closure. activated...
The mechanisms for persistent and progressive loss of myocardial function in advanced heart failure (HF) remain incompletely characterized. In the current study, we sought to determine impact TGF-β on fibroblasts transcriptional profiles assess if exosomes from treated could induce a phenotype co-cultured cardiomyocytes.Normal were with final conc. 2.5 ng/ml serum free media. HF also obtained patients undergoing implantation left ventricular assist devices. Exosomes collected using...
Fibroblasts are heterogeneous mesenchymal cells that play important roles in the production and maintenance of extracellular matrix. Although their heterogeneity is recognized, progenitor progeny relationships among fibroblasts factors control fibroblast differentiation poorly defined. The current study was designed to develop a reliable method would permit vitro fibroblast-like from human murine embryonic stem (ESCs). Undifferentiated ESCs were differentiated into embryoid bodies (EBs) with...
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Cigarette smoking is an important risk factor for cardiac diseases. In the current study, we sought to assess effect of electronic cigarette extract (ECE) and conventional smoke (CSE) on cardiomyocytes.iPSCs-derived cardiomyocytes were used in study evaluate cellular toxicities. Cells exposed either ECE or CSE two consecutive days as acute exposure every other day 14 days. Concentration nicotine both measured by Mass-Spectrometry Q-Exactive-HF was identify ingredients extracts. Fluorescent...