Topics (16) View all

Education

  • Sep 2004–
    May 2006
    Johns Hopkins Bloomberg School of Public Health
    Health Policy and Management · MHS
    USA · Baltimore
  • Sep 1977–
    Jun 1981
    Wayne State University
    Medicine · MD
    USA · Detroit
  • Sep 1973–
    May 1977
    Stanford University
    Biological Sciences · BS
    USA · Palo Alto

Other

  • Scientific Memberships
    National Academy of Sciences Institute of Medicine

Questions and Answers (1) View all

Publications (168) View all

  • Source
    Dataset: Distinct expression of synaptic NR2A and NR2B in the central nervous system 2008 (Final)
  • Source
    Dataset: Distinct expression of synaptic NR2A and NR2B in the central nervous system 2008 (Final)
  • Article: Hypoxia-induced mitogenic factor (HIMF/FIZZ1/RELMalpha) in chronic hypoxia- and antigen-mediated pulmonary vascular remodeling.
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    ABSTRACT: BACKGROUND: Both chronic hypoxia and allergic inflammation induce vascular remodeling in the lung, but only chronic hypoxia appears to cause PH. We investigate the nature of the vascular remodeling and the expression and role of hypoxia-induced mitogenic factor (HIMF/FIZZ1/RELMalpha) in explaining this differential response. METHODS: We induced pulmonary vascular remodeling through either chronic hypoxia or antigen sensitization and challenge. Mice were evaluated for markers of PH and pulmonary vascular remodeling throughout the lung vascular bed as well as HIMF expression and genomic analysis of whole lung. RESULTS: Chronic hypoxia increased both mean pulmonary artery pressure (mPAP) and right ventricular (RV) hypertrophy; these changes were associated with increased muscularization and thickening of small pulmonary vessels throughout the lung vascular bed. Allergic inflammation, by contrast, had minimal effect on mPAP and produced no RV hypertrophy. Only peribronchial vessels were significantly thickened, and vessels within the lung periphery did not become muscularized. Genomic analysis revealed that HIMF was the most consistently upregulated gene in the lungs following both chronic hypoxia and antigen challenge. HIMF was upregulated in the airway epithelial and inflammatory cells in both models, but only chronic hypoxia induced HIMF upregulation in vascular tissue. CONCLUSIONS: The results show that pulmonary vascular remodeling in mice induced by chronic hypoxia or antigen challenge is associated with marked increases in HIMF expression. The lack of HIMF expression in the vasculature of the lung and no vascular remodeling in the peripheral resistance vessels of the lung is likely to account for the failure to develop PH in the allergic inflammation model.
    Respiratory research 01/2013; 14(1):1. · 3.36 Impact Factor
  • Article: Epigenetics as a new therapeutic target for postoperative cognitive dysfunction.
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    ABSTRACT: Persistent memory and learning disabilities may occur postoperatively and may be related to neurodegenerative processes. Epigenetic dysregulation has been implicated to abnormal brain function and neurodegenerative diseases. Some risk factors contributing to postoperative cognitive disorder (POCD) have been identified, including exposure to general anesthesia, hypotension, hypoxia, psychoactive drugs, hippocampal inflammation induced by the surgical intervention, etc. The current evidence supports these risk factors might induce epigenetic dysfunction in the brain. It is possible that epigenetic regulation might be the common downstream pathway of these risk factors, since the chromatin remodeling is necessary for the memory-associated gene transcription and expression. Here, we present our hypothesis that the epigenetic dysregulation might be a critical mechanism underlying POCD. Our hypothesis may lead to a new therapeutic strategy of epigenetic intervention for POCD.
    Medical Hypotheses 12/2012; · 1.39 Impact Factor
  • Article: Clinical outcomes after bariatric surgery: a five-year matched cohort analysis in seven US states.
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    ABSTRACT: Bariatric surgery is the most effective weight loss treatment, yet few studies have reported on short- and long-term outcomes postsurgery. Using claims data from seven Blue Cross/Blue Shield health plans serving seven states, we conducted a non-concurrent, matched cohort study. We followed 22,693 persons who underwent bariatric surgery during 2003-2007 and were enrolled at least 6 months before and after surgery. Using logistic regression, we compared serious and less serious adverse clinical outcomes, hospitalizations, planned procedures, and obesity-related co-morbidities between groups for up to 5 years. Relative to controls, surgery patients were more likely to experience a serious [odds ratio (OR) 1.9; 95% confidence interval (CI) 1.8-2.0] or less serious (OR 2.5, CI 2.4-2.7) adverse clinical outcome or hospitalization (OR 1.3, CI 1.3-1.4) at 1 year postsurgery. The risk remained elevated until 4 years postsurgery for serious events and 5 years for less serious outcomes and hospitalizations. Some complication rates were lower for patients undergoing laparoscopic surgery. Planned procedures, such as skin reduction, peaked in postsurgery year 2 but remained elevated through year 5. Surgery patients had a 55% decreased risk of obesity-related co-morbidities, such as type 2 diabetes, in the first year postsurgery, which remained low throughout the study (year 5: OR 0.4, CI 0.4-0.5). While bariatric surgery is associated with a higher risk of adverse clinical outcomes compared to controls, it also substantially decreased obesity-related co-morbidities during the 5-year follow-up.
    Obesity Surgery 01/2012; 22(5):749-63. · 3.29 Impact Factor

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