Internists, Endocrinologist (diabetes, hormones)
7 years of experience

Accepting new patients
Strong
University of Rochester Medical Center, N.Y.
601 Elmwood Ave
Rochester, NY 14642
585-275-8762
Locations and availability (3)

Education ?

Medical School Score Rankings
Columbia University (2003)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Associations
American Board of Internal Medicine

Affiliations ?

Dr. Hsiao is affiliated with 3 hospitals.

Hospital Affilations

Score

Rankings

  • University of Michigan Hospitals & Health Centers
    1500 E Medical Center Dr, Ann Arbor, MI 48109
    • Currently 4 of 4 crosses
    Top 25%
  • Strong Memorial Hospital
    601 Elmwood Ave, Rochester, NY 14642
    • Currently 2 of 4 crosses
  • University of Rochester Medical Center, N.Y.
    601 Elmwood Ave, Rochester, NY 14642
  • Publications & Research

    Dr. Hsiao has contributed to 5 publications.
    Title Thiazolidinediones and Fractures: Evidence from Translating Research into Action for Diabetes.
    Date November 2010
    Journal The Journal of Clinical Endocrinology and Metabolism
    Excerpt

    Thiazolidinedione (TZD) treatment has been associated with fractures. The purpose of this study was to examine the association between TZD treatment and fractures in type 2 diabetic patients.

    Title Thiazolidinediones, Cardiovascular Disease and Cardiovascular Mortality: Translating Research into Action for Diabetes (triad).
    Date October 2010
    Journal Pharmacoepidemiology and Drug Safety
    Excerpt

    Studies have associated thiazolidinedione (TZD) treatment with cardiovascular disease (CVD) and questioned whether the two available TZDs, rosiglitazone and pioglitazone, have different CVD risks. We compared CVD incidence, cardiovascular (CV), and all-cause mortality in type 2 diabetic patients treated with rosiglitazone or pioglitazone as their only TZD.

    Title Effect of a Managed Care Disease Management Program on Diabetes Care.
    Date September 2010
    Journal The American Journal of Managed Care
    Excerpt

    To determine if processes and outcomes of diabetes care improved between 2000 and 2006 in a managed care health plan with a comprehensive diabetes disease management program.

    Title Alexander-disease Mutation of Gfap Causes Filament Disorganization and Decreased Solubility of Gfap.
    Date September 2005
    Journal Journal of Cell Science
    Excerpt

    Alexander disease is a fatal neurological illness characterized by white-matter degeneration and the formation of astrocytic cytoplasmic inclusions called Rosenthal fibers, which contain the intermediate filament glial fibrillary acidic protein (GFAP), the small heat-shock proteins HSP27 and alphaB-crystallin, and ubiquitin. Many Alexander-disease patients are heterozygous for one of a set of point mutations in the GFAP gene, all of which result in amino acid substitutions. The biological effects of the most common alteration, R239C, were tested by expressing the mutated protein in cultured cells by transient transfection. In primary rat astrocytes and Cos-7 cells, the mutant GFAP was incorporated into filament networks along with the endogenous GFAP and vimentin, respectively. In SW13Vim(-) cells, which have no endogenous cytoplasmic intermediate filaments, wild-type human GFAP frequently formed filamentous bundles, whereas the R239C GFAP formed 'diffuse' and irregular patterns. Filamentous bundles of R239C GFAP were sometimes formed in SW13Vim(-) cells when wild-type GFAP was co-transfected. Although the presence of a suitable coassembly partner (vimentin or GFAP) reduced the potential negative effects of the R239C mutation on GFAP network formation, the mutation affected the stability of GFAP in cells in a dominant fashion. Extraction of transfected SW13Vim(-) cells with Triton-X-100-containing buffers showed that the mutant GFAP was more resistant to solubilization at elevated KCl concentrations. Both wild-type and R239C GFAP assembled into 10 nm filaments with similar morphology in vitro. Thus, although the R239C mutation does not appear to affect filament formation per se, the mutation alters the normal solubility and organization of GFAP networks.

    Title Antecedent Hyperglycemia is Associated with an Increased Risk of Neutropenic Infections During Bone Marrow Transplantation.
    Date
    Journal Diabetes Care
    Excerpt

    OBJECTIVE: To use bone marrow transplantation (BMT) as a model for testing the association between hyperglycemia and infection. RESEARCH DESIGN AND METHODS: This cohort study included 382 adults (6.5% with diabetes) who had no evidence of infection before neutropenia during BMT. Mean glucose was calculated from central laboratory and bedside measurements taken before neutropenia; the primary outcome was neutropenic infections. RESULTS: Eighty-four patients (22%) developed at least one neutropenic infection, including 51 patients (13%) with bloodstream infections. In patients who did not receive glucocorticoids during neutropenia, each 10 mg/dl increase in mean preneutropenia glucose was associated with an odds ratio of 1.08 (95% CI 0.98-1.19) (P = 0.14) for any infection and 1.15 (1.03-1.28) (P = 0.01) for bloodstream infections, after adjusting for age, sex, race, year, cancer diagnosis, transplant type, and total glucocorticoid dose before neutropenia. In those who received glucocorticoids during neutropenia (n = 71), the adjusted odds ratio associated with a 10 mg/dl increase in mean glucose was 1.21 (1.09-1.34) (P < 0.0001) for any infection and 1.24 (1.11-1.38) (P < 0.0001) for bloodstream infections. There was no association between mean glycemia and long length of hospital stay, critical status designation, or mortality. CONCLUSIONS: In a BMT population highly susceptible to infection, there was a continuous positive association between mean antecedent glycemia and later infection risk, particularly in patients who received glucocorticoids while neutropenic. Tight glycemic control during BMT and glucocorticoid treatment may reduce infections.


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