Objective To verify the dynamic changes of ANP during the diastolic heart failure and the protective effect of amlodipine. Methods Male SD rats underwent the abdominal aorta ligation. Four weeks after Surgery, 40 rats were divided into 4 groups: hypertension model group (group B), low-dose group (group C), mid-dose group (group D), high-dose group (group E). Another 10 healthy male SD rats were used as sham group (group A). During the experiment, different drugs were gavaged to different groups and the normal saline was used for control group. Results After 12 weeks, ANP levels increased in group B much more than in group A, while lower in group C(P < 0.05); LVSP and dp/dt max decreased in group B significantly than in group A, while higher in group C than in group B (P < 0.05); LVEDP and -dp/dt max had no statistically significant (P >0.05); HW/BW and LW/BW decreased in group B than in group A, while higher in group C than in group B (P < 0.05); The extent of myocardial necrosis and fibrosis in group C were much lower than in group B. But there was no Significant differences (P > 0.05). Conclusion ANP level gradually increased accompanying with the aggravation of heart failure, which is related with the dose of the drug within limits. Amlodipine can inhibit cardiomyocyte remodeling by interfering ANP secretion.

Objective To reveal the role of PDK1 in vascular endothelial cells. Methods PDK1 was knocked out in endothelial cells by recombinase-mediated Cre to observe it′s effects on vascular endothelial cells. Results Abnormality of vascular development in rats could be found as a result of endothelial PDK1 deletion. Meanwhile, vascular leakage and bleeding phenotype were observed, and tissue analysis showed vascular endothelial cells abnormalities. Conclusions PDK1 plays an important role in the functioning and integrity of vascular endothelial cells, which made tentative explanation for PDK1-Akt signal path and laid basis for further research.

Objective To investigate the effect of di-( 2-ethylhexyl ) phthalate (DEHP) on pregnant rat and the protection of zinc.Methods Fifty rats were randomized equally into 5 groups consisting of blank (given 1 ml 0.9％ sodium chloride),corn oil (given 1 ml corn oil),zinc (given 1 ml zinc gluconate including 1.2 mg zinc),DEHP (given 50 mg · kg-1 · d-1 DEHP)and DEHP + zinc (given 50 mg· kg-1 · d-1 DEHP + zinc gluconate ).At the beginning of the experiment (about 7 d before pregnancy),the female rats were administered with corresponding drugs everyday.The pregnant rats were killed and the fetal rats were removed on 19th day.The following results in each group were recorded:the body weight and the organic weight of the female rats,the number and the weight of fetus rats and the placental weight.Results The weight and the coefficient of female rats' kidney/body,spleen/body,brain/ body,and heart/body in DEHP group compared with other groups were not statistical significance (all P ＞0.05).The coefficient of female rats' liver/body,uterus/body,and ovary/body of blank group were (4.4 ± 0.7 ) ％,( 1.26 ± 0.09 ) ％,( 0.083 ± 0.009 ) ％ respectively,corn oil group were (4.5 ± 0.6 ) ％,( 1.29 ±0.10)％,(0.084 ±0.008)％,zinc group were (4.4 ±0.4)％,( 1.26 ±0.08)％,(0.084 ± 0.009 ) ％,DEHP group were ( 5.4 ± 1.0 ) ％,( 1.11 ± 0.08 ) ％,( 0.074 ± 0.012 ) ％,and DEHP + zinc group were (4.4 ± 1.0)％,( 1.28 ± 0.10)％,(0.082 ± 0.007)％ ; in DEHP group the coefficient of female rats' liver/body,uterus/body,and ovary/body compared with other groups was statistical significance ( P ＜ 0.05 ).The fetal quantity,fetal weight and placental weight of female rats of blank group were 12.8 ± 2.7,(6.03 ±0.16) g,( 1.00 ±0.03) g respectively,corn oil group were 13.6 ±3.1,(6.07 ±0.20) g,(1.00±0.04) g,zinc group were 13.3 ±3.1,(6.16 ±0.18) g,( 1.00 ±0.05) g,DEHP group were 9.2±4.1,(4.03 ±0.09) g,(0.95 ±0.03) g,and zinc +DEHP group were 12.1 ±2.9,(6.09 ± 0.17 ) g,(0.99 ±0.03 ) g.In DEHP group the fetal quantity,fetal weight and placental weight of female rats compared with other groups were statistical significance ( P ＜ 0.05 ).Conclusion DEHP can damage female rats and fetal rats in gestation period.Zinc supplied before pregnancy can relieve the influence by DEHP.

Objective:To investigate the mechanism of liver and lung injury in mouse septic models.Methods:Twenty-four male Kunming mice were subjected to cecal ligation and puncture(CLP)or sham operation.The permeability of microvasculature,water contents,activities of myeloperoxidase(MPO)and the apoptosis of microvascular endothelial cells in lung microvasculature and liver sinus were examined 3 h and 12 h after operation.Results:Both the liver and lung showed a significant increase in microvessel permeability at 12 h in CLP group compared with sham operation group.MPO activity and water content in CLP group were obviously higher than those in the sham operation group.The apoptosis of lung microvascular endothelial cells at 12 h in CLP group(5.03?0.92)% was significantly higher than that of control group(3.48?1.21)%(P

Abstracting and Indexing as Topic ; Neoplasms ; Periodicals as Topic

AIM:To investigate the effects of 17-AAG on apoptosis and cell cycle of HCT-15 cells and to clar-ify the related mechanisms .METHODS: MTT method was employed to evaluate the inhibitory effects of 17-AAG with Aifferent time and different doses on the proliferation of HCT-15 cells.The cells were stained with Annexin V-FITC/propid-iumiodide and measured by flow cytometry .The expression of STAT3, cyclin D1, Cyt C, caspase 9 and caspase 3 at mR-NA and protein levels was determined by RT-PCR and Western blotting .RESULTS:Treatment with 17-AAG at concentra-tion of 1.25~20 mg/L for 24 h and 48 h significantly inhibited the activity of HCT-15 cells at both time-and concentra-tion-dependent manners .Treatment with 17-AAG at concentrations of 0.425, 0.85 and 1.7 mg/L for 48 h significantly in-duced apoptosis and cell cycle arrest of HCT-15 cells.The exposure of 17-AAG at concentrations of 0.425, 0.85 and 1.7 mg/L for 48 h to the HCT-15 cells significantly down-regulated the expression of STAT 3 and cyclin D1 at mRNA and pro-tein levels, but up-regulated Cyt C, caspase 9 and caspase 3 mRNA and protein in a concentration-dependent manner . CONCLUSION:17-AAG inhibits the cell activity , induces apoptosis and G 1 arrest by down-regulating the expression of cyclin D1, and promoting the mitochondria apoptosis through STAT 3 pathway.

Objective To investigate the causes of severe H1N1 Flu with multiple organ dysfunction, and measures to reduce mortality. Method The data of the patient, who was diagnosed as severe H1N1 Flu and mul-tiple organ dysfunction syndrome in First People's Hospital Affiliated to Shanghai Jiaotong University in September 2009, were retrospectively analyzed. The patient was male, 35 year-old, obese, high fever, sore throat, cough, progressive dyspnea, severe hypoxemia and hypotension. Effective measures were carried out, including protective lung ventilation, recruitment maneuver, vasopressor support, limited fluid resuscitation, appropriate corticosteroid, anfiviral plasma, anticoagulafion and antiviral medicine (Oseltamivir)in early stage and full dose. Results After one-month intensive care, clinical symptoms was improved obviously, oxygen pressure reached 74 mmHg without oxygen supply, CT scan showed diffused interstitial ehange. Neuromyopathy developed at approximately 3 weeks after the onset of H1N1. Conclusions H1N1 Flu can develop in healthy adults, and obesity is one of the inde-pendent risk factors. Effective measures should be taken as soon as possible to reduce the mortality.

There were significant increase in urine protein excretion,raised malondialdehyde(MDA) level and expressions of NF-?B,p22phox and p47phox in renal tissue,and significant decrease in reduced glutathione,superoxide dismutase,vitamin C and E levels in type 2 diabetic Goto-Kakisaki rats after 12 weeks. There was obvious histomorphologic change in the kidneys.All the above indices were improved by intraperitoneal injection of?-lipoic acid(35 mg/kg q.o.d).Besides,significant positive correlations were found of MDA level to p22phox,p47phox and NF-?B in the renal tissue,?-lipoic acid seems to protect the diabetic kidney in this diabetic rat model via antioxidative effects.

Objective: To explore therapeutic effect of in-hospital intravenous alprostadil injection on patients with acute myocardial infarction (AMI) complicated diabetic nephropathy (DN) undergoing percutaneous coronary intervention (PCI), and evaluate their long-term prognosis.Methods: A total of 80 AMI + DN patients undergoing PCI were selected from our hospital.They were randomly divided into alprostadil group (n=40) and routine treatment group (n=40).Renal function after PCI, cardiac function during hospitalization, serum creatinine (Scr) level on 72h after PCI and incidence of major adverse cardiovascular events (MACE) within one-year follow-up were compared between two groups.Results: Compared with routine treatment group on 72h after PCI, there was significant reduction in Scr level [(126.92±35.28) μmol/L vs.(104.32±22.91) μmol/L], and significant rise in estimated glomerular filtration rate [eGFR, (55.23±31.48) ml·min-1·1.73m-2 vs.(62.14±36.23) ml·min-1·1.73m-2] in alprostadil group, P<0.05 both.Postoperative one-year follow-up indicated that there were no significant difference in incidence rate of MACE and percentage of kidney replacement therapy between two groups, P>0.05 all.Conclusion: Intravenous alprostadil injection based on routine treatment possesses significant therapeutic effect on renal function in AMI + DN patients after PCI, and it's safe

Heat shock protein 27 ( HSP27 ) is an endogenous protein that plays an important role in a great variety of physio-logical and pathological processes. It can express a large number under body stress conditions. Recent studies have shown estro-gen upregulates the expression of HSP27 through a number of ways, playing a perfect “triple protection” role. In the early stage of atherosclerosis, estrogen induces the phosphorylation of HSP27 via PI3K/Akt signaling pathway. Phosphorylation of HSP27 can resist the injury of vascular endothelial cells( VECs) through an antioxidant and anti-apoptotic pathway as well as the inhibition of cytochrome C. In the stage of forming foam cells, estrogen induces the expression and release of HSP27 from mac-rophages by stimulating the estrogen receptor β ( ERβ) , then HSP27 inhibits the LDL uptake and the release of proinflammato-ry cytokine by binding scavenger receptor A ( SR-A) . During the proliferation and migration of vascular smooth muscle cells ( VSMCs) , estrogen induces estrogen receptor α ( ERα) and protein phosphatase 2 ( PP2A) to form a complex that enhances the activity of PP2A, then it can lead to the dephosphorylation of HSP27 and finally inhibit cells proliferation and migration. In summary, the anti-atherosclerotic effect of estrogen is closely re-lated to the role of HSP27. Given the side effects of estrogen re-placement therapy( MHT) , regulating HSP27 may provide a no-vel therapy for the prevention and treatment of cardiovascular dis-eases in menopausal women clinically.