Objective To investigate the effect of pantoprazole (proton pump inhibitor, PPI) and gefarnate (gastric mucosa protectant) on the prevention of upper gastrointestinal bleeding in patients undergoing post-percutaneous coronary intervention (PCI) dual anti-platelet therapy.Methods This research included 1263 patients taking enteric aspirin and clopidogrel after PCI.The cases were divided into 4 groups: routine treatment group (n=332), PPI group (n=318), gastric mucosa protectant group (n=299), and PPI+gastric mucosa protectant group (n=314).A follow-up for 6 months was observed including gastrointestinal symptoms, upper gastrointestinal bleeding, major adverse cardiac events (MACE), and adverse reactions.Results There were 52 cases of upper gastrointestinal bleeding within 6 months, including 21 cases from routine treatment group, 9 from PPI group, 15 from gastric mucosa protectant group, and 7 from PPI+gastric mucosa protectant group.The incidence of upper gastrointestinal bleeding among the 4 groups within 6 months was statistically different (X2=8.883, P=0.031).The routine treatment group had significant higher rate than the PPI group and the gastric mucosa protectant group (P<0.05), while among other groups there was no significant difference (P>0.05).The upper gastrointestinal bleeding occurred within 3 postoperative months in 34 out of 52 cases (65.4%).There was no statistical significance among the four groups in regard to bleeding occurrence time (X2=4.212,P=0.648).Conclusions Patients undergoing post-PCI dual anti-platelet treatment can reduce the incidence of gastrointestinal bleeding by taking pantoprazole or combined with gefarnate.Intervention against upper gastrointestinal bleeding should start on the first day after PCI and last for a minimum of 3-6 months.

To ascertain whether heat shock gene expression could protect pulmonaryendothelial cell from hydrogen peroxide(H2O2)一indueed injury,the protective effect of HSPgene expression induced by pretreatment of bovine pulmonary endothelial eells(BPAECs)by heat shock (42 ℃, 2h)against lethal dose(lmmol?L(-1),45min) of H2O2一induced cyt-otoxieity was observed in vitro.It was found that BPAECs heat一shocked prior to exposureto H2O2(Immol?L(-1) 45min)showed significant decrease in H2O2一mediated incrementof LDH rdlease and TBARS production and had an obvious alleviation of H2O2一induccddecreased activities of catalase and superoxide dismutase. Further study showed thatcycloheximide, a protein synthesis inhibitor and Actinomycin D,a mRNA transcriptioninhibitor blocked the expression of HSP 70 and HSP 70 mRNA respectively.Both agentsprevented the cytoprotective effect of heat shock pretreatment against H2O2一mediatedBPAECs injury. The results suggested that HSP70 gene selectively translated after heat shockwas invoived in enhancement of eellular antioxidant mechanism and protected BPAECsagainst H2O2一induced injury

HSF1 is the major heat shock transcription factor that binds heat shock element (HSE) in the promoter of heat shock proteins (HSPs) and controls rapid HSP induction in cells subjected to various stresses such as elevated temperature, chemicals, or exposure to toxins. Although at least four members of the vertebrate HSF have been cloned, details of their individual physiological roles remain relatively obscure. To clarify the exact in vivo functions of HSF1 and assess whether HSF1 exhibits redundant or unique roles, we have created homozygous Hsf1-/- mice using standard gene targeting techniques and isolated Hsf1-/- embryonic fibroblasts. Here we demonstrate that heat shock response (HSR) was not attainable in Hsf1-/- embryonic fibroblasts, and this response was required for thermotolerance and protection against heat-induced apoptosis, and that homozygous Hsf1-/- mice, which survived to adulthood according to genetic background, exhibited multiple phenotypes including: (1) placental defects that reduced embryonic viability after late midgestation (day 13.5); (2) growth retardation; (3) female infertility caused by preimplantation lethality, and (4) increased mortality (+/+ vs -/-, P＜0.05) and exaggerated production of proinflammatory cytokine, TNF α (+/-　vs -/-, P＜0.05) after endotoxin challenge. Interestingly, although Hsf1-/- mice exhibited placental defects and embryonic death, basal HSP expression is not appreciably altered during embryonic development by the HSF1 null mutation, suggesting this factor might be involved in regulating some non-HSP genes or signaling pathways which may be important for development. Taken together, our results established direct causal effects for the HSF1 transactivator in regulating diverse physiological and pathophysiological conditions such as developnent, growth, reproduction, apoptosis and sepsis. The present work also provided a useful mammalian model for further investigating the implications of Hsf1 and its target genes (HSPs and other possible non-HSP genes) in various physiological and pathophysiological processes.