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Articles by G Hu
Total Records ( 8 ) for G Hu
  Z Tian , T Ye , X Zhang , E Liu , W Wang , P Wang , G Liu , X Yang , G Hu and Z. Yu
 

Objective  To investigate the association between sleep duration and risk of hyperglycemia among preschool Chinese children.

Design  A population-based cross-sectional study.

Setting  Seventy-one randomly selected kindergartens in Tianjin, China.

Participants  Six hundred nineteen obese (body mass index z score ≥1.65) and 617 nonobese (body mass index z score <1.65) children aged 3 to 6 years were recruited and matched by age.

Main Exposure  Sleep duration.

Main Outcome Measures  Hyperglycemia, defined as a fasting glucose level of 100 mg/dL or higher.

Results  Obese children were more likely to have shorter sleep duration (≤8 hours) compared with their nonobese counterparts (P < .001). Compared with those who slept for 9 or 10 hours per night, those who slept for 8 hours or less had a significantly higher likelihood of having hyperglycemia, controlling for age and sex (odds ratio [OR], 1.65; 95% confidence interval [CI], 1.12-2.45). After further adjustment for other potential confounders, the association still remained statistically significant (OR, 1.64; 95% CI, 1.09-2.46). In the stratified multivariable analyses, those who were obese and slept for 8 hours or less had an increased risk of having hyperglycemia (OR, 2.12; 95% CI, 1.06-4.21) compared with those who were nonobese and slept for 9 hours or more.

Conclusions  Shorter sleep duration is associated with an increased risk of having hyperglycemia among preschool Chinese children. Whether adequate sleep may help maintain euglycemia among children, especially for those who are overweight or obese, warrants further investigation.

  Y Sun , G Hu , X Zhang and R. D. Minshall
 

Rationale: Oxidants are important signaling molecules known to increase endothelial permeability, although the mechanisms underlying permeability regulation are not clear.

Objective: To define the role of caveolin-1 in the mechanism of oxidant-induced pulmonary vascular hyperpermeability and edema formation.

Methods and Results: Using genetic approaches, we show that phosphorylation of caveolin-1 Tyr14 is required for increased pulmonary microvessel permeability induced by hydrogen peroxide (H2O2). Caveolin-1–deficient mice (cav-1–/–) were resistant to H2O2-induced pulmonary vascular albumin hyperpermeability and edema formation. Furthermore, the vascular hyperpermeability response to H2O2 was completely rescued by expression of caveolin-1 in cav-1–/– mouse lung microvessels but was not restored by the phosphorylation-defective caveolin-1 mutant. The increase in caveolin-1 phosphorylation induced by H2O2 was dose-dependently coupled to both increased 125I-albumin transcytosis and decreased transendothelial electric resistance in pulmonary endothelial cells. Phosphorylation of caveolin-1 following H2O2 exposure resulted in the dissociation of vascular endothelial cadherin/β-catenin complexes and resultant endothelial barrier disruption.

Conclusions: Caveolin-1 phosphorylation–dependent signaling plays a crucial role in oxidative stress-induced pulmonary vascular hyperpermeability via transcellular and paracellular pathways. Thus, caveolin-1 phosphorylation may be an important therapeutic target for limiting oxidant-mediated vascular hyperpermeability, protein-rich edema formation, and acute lung injury.

  X Lu , Q Wang , G Hu , C Van Poznak , M Fleisher , M Reiss , J Massague and Y. Kang
 

Bone metastasis is mediated by complex interactions between tumor cells and resident stromal cells in the bone microenvironment. The functions of metalloproteinases in organ-specific metastasis remain poorly defined despite their well-appreciated role in matrix degradation and tumor invasion. Here, we show a mechanism whereby two distinct metalloproteinases, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS1) and matrix metalloproteinase-1 (MMP1), orchestrate a paracrine signaling cascade to modulate the bone microenvironment in favor of osteoclastogenesis and bone metastasis. Proteolytic release of membrane-bound epidermal growth factor (EGF)-like growth factors, including Amphiregulin (AREG), heparin-binding EGF (HB-EGF), and transforming growth factor (TGF) from tumor cells suppress the expression of osteoprotegerin (OPG) in osteoblasts and subsequently potentiate osteoclast differentiation. EGF receptor (EGFR) inhibitors block osteolytic bone metastasis by targeting EGFR signaling in bone stromal cells. Furthermore, elevated MMP1 and ADAMTS1 expression is associated with increased risk of bone metastasis in breast cancer patients. This study established MMP1 and ADAMTS1 in tumor cells, as well as EGFR signaling in osteoblasts, as promising therapeutic targets for inhibiting bone metastasis of breast cancer.

  G Hu , P Jousilahti , J Tuomilehto , R Antikainen , J Sundvall and V. Salomaa
 

Objective: Our objective was to assess whether the association of serum C-reactive protein (CRP) with type 2 diabetes risk is modified by sex.

Design and Subjects: We prospectively followed 12,861 Finnish men and women who were 35–74 yr of age, and free of diabetes, coronary heart disease, stroke, and cancer at baseline. Hazard ratios of type 2 diabetes were estimated for different levels of serum CRP.

Results: During the follow-up, 208 men and 113 women developed diabetes. The multivariable-adjusted (age, physical activity, education, smoking, alcohol and coffee drinking, family history of diabetes, use of antihypertensive drugs, cholesterol-lowering agents, and hormone replacement therapy in women, systolic blood pressure, serum high-density lipoprotein cholesterol, serum triglycerides, and body mass index) hazard ratios of diabetes at three different levels of CRP (0.05–0.99, 1.0–2.99, and ≥3.0 mg/liter) based on the recommendation by Centers for Disease Control and the American Heart Association were 1.00, 1.46, and 1.85 (P for trend = 0.006) in men, and 1.00, 3.83, and 8.37 (P for trend <0.001) in women, respectively. CRP had a stronger association with diabetes risk in women than men (P for interaction: 2 = 6.42; 1 df; P < 0.025). This positive association between CRP and diabetes risk did not change when participants were stratified by age group, smoking status, level of obesity, alcohol drinking habit, or family history of diabetes.

Conclusions: High baseline level of serum CRP was associated with an increased risk of diabetes among both men and women, but this association was stronger in women than men.

  J Xue , P. B Thippegowda , G Hu , K Bachmaier , J. W Christman , A. B Malik and C. Tiruppathi
 

Activation of NF-B is essential for protease-activated receptor-1 (PAR-1)-mediated ICAM-1 expression in endothelial cells. Here we show that PAR-1 activation induces binding of both p65/RelA and NFATc1 to the NF-B binding site localized in intron-1 of the ICAM-1 gene to initiate transcription in endothelial cells. We discovered the presence of two NF-B binding sites in intron-1 (+70, NF-B site 1; +611, NF-B site 2) of the human ICAM-1 gene. Chromatin immunoprecipitation results showed that thrombin induced binding of p65/RelA and of NFATc1 specifically to intronic NF-B site 1 of the ICAM-1 gene. Electrophoretic mobility shift and supershift assays confirmed the binding of p65/RelA and NFATc1 to the intronic NF-B site 1 in thrombin-stimulated cells. Thrombin increased the expression of ICAM-1-promoter-intron 1-reporter (–1,385 to +234) construct ~25-fold and mutation of intronic NF-B site 1 markedly reduced thrombin-induced reporter expression. Moreover, inhibition of calcineurin, knockdown of either NFATc1 or p65/RelA with siRNA significantly reduced thrombin-induced ICAM-1 expression and polymorphonuclear leukocyte adhesion to endothelial cells. In contrast, NFATc1 knockdown had no effect on TNF--induced ICAM-1 expression. Thus these results suggest that p65/RelA and NFATc1 bind to the intronic NF-B site 1 sequence to induce optimal transcription of the ICAM-1 gene in response to thrombin in endothelial cells.

  T. J Chemmanur , G Hu and J. Huang
 

In this article, we use a large sample of transaction-level institutional trading data to analyze the role of institutional investors in initial public offerings (IPOs). The theoretical literature on IPOs has long argued that institutional investors possess private information about IPOs and that underpricing is a mechanism for compensating them to reveal this private information. We study whether institutions indeed have private information about IPOs, retain their information advantage in post-IPO trading, and are able to realize significant profits from their participation in IPOs. We also study institutional IPO allocations and allocation sales to analyze whether institutions play an important role in supporting IPOs in the aftermarket and are rewarded by underwriters for playing such a role. We find that institutions sell 70.2% of their IPO allocations in the first year, fully realize the "money left on the table," and do not dissipate these profits in post-IPO trading. Further, institutions hold allocations in IPOs with weaker post-issue demand for a longer period, and they are rewarded for this by underwriters with more IPO allocations. Finally, institutional trading has predictive power for long-run IPO performance, especially in IPOs in which they received allocations; however, this predictive power decays over time. Overall, our results suggest that institutional investors possess significant private information about IPOs, play an important supportive role in the IPO aftermarket, and receive considerable compensation for their participation in IPOs.

  F Ye , G Hu , D Taylor , B Ratnikov , A. A Bobkov , M. A McLean , S. G Sligar , K. A Taylor and M. H. Ginsberg
 

In vitro analysis confirms talin binding is sufficient for activation and extension of membrane-embedded integrin.

 
 
 
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