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Articles by Degang Wang
Total Records ( 2 ) for Degang Wang
  Salim S. Virani , Degang Wang , LeChauncy D. Woodard , Supicha S. Chitwood , Cassie R. Landrum , Franklin J. Zieve , Christie M. Ballantyne and Laura A. Petersen


The Adult Treatment Panel III guidelines established non-high-density lipoprotein cholesterol (non-HDL-C) as a secondary treatment target. However, non-HDL-C levels are not reported on standard lipid panels by many hospital-based and/or commercial biochemical laboratories.


We determined whether reporting non-HDL-C was associated with improved non-HDL-C goal attainment.


We identified patients with cardiovascular disease (CVD) and/or diabetes receiving care within the Veterans Health Administration. We matched a facility that reported non-HDL-C levels on lipid panels (3994 CVD and 5108 diabetes patients) to a facility with similar size, patient complexity, and academic mission that did not report non-HDL-C (4269 CVD and 6591 diabetes patients). We performed patient-level analysis to assess differences in non-HDL-C from baseline to the most recent lipid panel at these facilities.


Baseline non-HDL-C levels for CVD patients were 114 mg/dL and 107 mg/dL at the reporting and nonreporting facilities, respectively. At 2.3-year follow-up, non-HDL-C levels decreased at both facilities but by a greater amount at the reporting facility (−11 mg/dL vs −3 mg/dL at the nonreporting facility, P < .001). Results remained significant (P < .001) after we adjusted for patient's age, race, gender, illness burden, history of diabetes, hypertension, medication adherence, statin use, number of lipid panels, and number of primary care visits between baseline and follow-up. Reductions were greater among CVD patients with triglycerides ≥200 mg/dL (−25 mg/dL vs −16 mg/dL at the respective facilities, P = .004). Results were similar in diabetes patients. Reporting was also associated with greater proportions of patients meeting non-HDL-C treatment goal of <130 mg/dL.


Non-HDL-C reporting could improve non-HDL-C goal attainment.

  Stephanie A. Pangas , Xiaohui Li , Lieve Umans , An Zwijsen , Danny Huylebroeck , Carolina Gutierrez , Degang Wang , James F. Martin , Soazik P. Jamin , Richard R. Behringer , Elizabeth J. Robertson and Martin M. Matzuk
  The transforming growth factor β (TGFβ) family has critical roles in the regulation of fertility. In addition, the pathogenesis of some human cancers is attributed to misregulation of TGFβ function and SMAD2 or SMAD4 mutations. There are limited mouse models for the BMP signaling SMADs (BR-SMADs) 1, 5, and 8 because of embryonic lethality and suspected genetic redundancy. Using tissue-specific ablation in mice, we deleted the BR-SMADs from somatic cells of ovaries and testes. Single conditional knockouts for Smad1 or Smad5 or mice homozygous null for Smad8 are viable and fertile. Female double Smad1 Smad5 and triple Smad1 Smad5 Smad8 conditional knockout mice become infertile and develop metastatic granulosa cell tumors. Male double Smad1 Smad5 conditional knockout mice are fertile but demonstrate metastatic testicular tumor development. Microarray analysis indicated significant alterations in expression of genes related to the TGFβ pathway, as well as genes involved in infertility and extracellular matrix production. These data strongly implicate the BR-SMADs as part of a critical developmental pathway in ovaries and testis that, when disrupted, leads to malignant transformation.
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