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 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 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

Objective To investigate the effect of once yearly zoledronic acid of 5 mg on postmenopausal women with osteoporosis of different causes. MethodsFrom October 2009 to December 2009,a total of 89 postmenopausal women with osteoporosis were enrolled and assigned into 2 groups.There were 45 cases of primary postmenopausal osteoporosis,including 27 cases of fresh fracture,in group A.They were aged from 47 to 83 years,with an average of 63.7 years.There were 44 cases of secondary postmenopausal osteoporosis,including 28 cases of fresh fracture,in group B.All patients were given a.single 30-minute intravenous injection of zoledronic acid (5 mg),supplemented by 1,25-dihydroxyvitamin D of 0.25 μg and calcium of 600 mg with VitD125 IU daily.At pre-intervention and 12 months after intervention respectively,bone mineral density (BMD) was measured by dual-X-ray absorptiometry (DXA) at the lumbar spine and hip,and a balance test(Sunlight Tetrax- Ⅱ) was performed to evaluate the risk of falling.Intervention compliance of the patients and adverse events related to zoledronic acid infusion were observed. Results All cases of fresh fracture healed well at 3-month follow-up.At 12 months,43 subjects in group A and 42 subjects in group B completed the follow-up.In group A,BMD increased by 5.8％ at the lumbar spine,by 2.9％ at the femoral neck,by 5.2％ at the Words area,by 5.3％ at the greater trochanter and by 3.9％ at the total hip while the risk of falling decreased by 26.1％; in group B,BMD increased by by 3.4％ at the lumbar spine,by 2.1％ at the femoral neck,by 3.2％ at the Words area,by 3.0％ at the greater trochanter and by 2.5％ at the total hip while the risk of falling decreased by 21.8％.The differences between pre-intervention and post-intervention were significant in both groups ( P ＜ 0.05).No intolerable adverse events occurred in both groups except that one new fracture happened in each group but responded to conservative treatment.ConclusionA once-yearly infusion of zoledronic acid of 5 mg is a convenient and effective therapy for treatment of osteoporosis in postmenopausal women.

Objective To study the effects of YinlingⅠon expelling lead and the improvement of the ability of learning memory in lead poisoned mice.Methods Poisoning model of lead was prepared by drinking water with lead acetate,and the administration of YinlingⅠor EDTA-Na_2Ca to lead poisoned mice was performed.Lead content was detected in blood, brain and bone.The ability of lear- ning and memory of mice was measured monthly by Y-water maze test. Ultrastructure of CA3 cell in hippocampus was observed with transmission electron microscope.Results After administration of YinlingⅠ,the lead content in blood, brain and bone decreased remarkably, the ability of learning and memory increased,and the ultrastructure changes of CA3 cell in hippocampus markedly dimi- nished.Conclutions YinlingⅠ may expel lead of the mice with lead poisoning and improve their ability of learning and memory.

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 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.

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.

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.