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Articles by W Pan
Total Records ( 3 ) for W Pan
  W. R Lewis , A. G Ellrodt , E Peterson , A. F Hernandez , K. A LaBresh , C. P Cannon , W Pan and G. C. Fonarow
 

Background— Significant disparities have been reported in the application of evidence-based guidelines in the treatment of coronary artery disease (CAD) in women and the elderly. We hypothesized that participation in a quality-improvement program could improve care for all patients and thus narrow treatment gaps over time.

Methods and Results— Treatment of 237 225 patients hospitalized with CAD was evaluated in the Get With the Guidelines–CAD program from 2002 to 2007. Six quality measures were evaluated in eligible patients without contraindications: aspirin on admission and discharge, β-blockers use at discharge, angiotensin-converting enzyme inhibitor or angiotensin receptor antagonist use, lipid-lowering medication use, and tobacco cessation counseling along with other care metrics. Over time, composite adherence on these 6 measures increased from 86.5% to 97.4% (+10.9%) in men and 84.8% to 96.2% (+11.4%) in women. There was a slight difference in composite adherence by sex that remained significant over time (P<0.0001), but this was confined to patients <75 years. Composite adherence in younger patients (<75 years) increased from 87.1% to 97.7% (+10.6%) and from 83.0% to 95.1% (+12.1%) in the elderly (≥75 years) over time.

Conclusions— Among hospitals participating in Get With the Guidelines–CAD, guideline adherence has improved substantially over time for both women and men and younger and older CAD patients, with only slight age and sex differences in some measures persisting.

  Y Li , W Pan , W Xu , N He , X Chen , H Liu , L Darryl Quarles , H Zhou and Z. Xiao
 

Cleidocranial dysplasia (CCD) is an autosomal dominant bone disease in humans caused by haploinsufficiency of the RUNX2 gene. The RUNX2 has two major isoforms derived from P1 and P2 promoters. Over 90 mutations of RUNX2 have been reported associated with CCD. In our study, DNA samples of nine individuals from three unrelated CCD families were collected and screened for all exons of RUNX2 and 2 kb of P1 and P2 promoters. We identified two point mutations in the RUNX2 gene in Case 1, including a nonsense mutation (c.577C>T) that has been reported previously and a silent substitution (c.240G>A). In vitro studies demonstrated that c.577C>T mutation led to truncated RUNX2 protein production and diminished stimulating effects on mouse osteocalcin promoter activity when compared with full-length Runx2-II and Runx2-I isoforms. These results confirm that loss of function RUNX2 mutation (c.577C>T) in Case 1 family is responsible for its CCD phenotype.

  S Zhu , W Pan , P Shi , H Gao , F Zhao , X Song , Y Liu , L Zhao , X Li , Y Shi and Y. Qian
 

Interleukin 17 (IL-17) plays critical roles in the pathogenesis of various autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE). How the signals triggered by this powerful inflammatory cytokine are controlled to avoid abnormal inflammatory responses is not well understood. In this study, we report that TRAF3 is a receptor proximal negative regulator of IL-17 receptor (IL-17R) signaling. TRAF3 greatly suppressed IL-17–induced NF-B and mitogen-activated protein kinase activation and subsequent production of inflammatory cytokines and chemokines. Mechanistically, the binding of TRAF3 to IL-17R interfered with the formation of the receptor signaling activation complex IL-17R–Act1–TRAF6, resulting in suppression of downstream signaling. TRAF3 markedly inhibited IL-17–induced expression of inflammatory cytokine and chemokine genes in vivo and consequently delayed the onset and greatly reduced the incidence and severity of EAE. Thus, TRAF3 is a negative regulator of IL-17R proximal signaling.

 
 
 
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