Chemotherapy-induced amenorrhea(CIA) is a objective process,the reason is clear basically,for patients with hormonal receptor positive will improve disease free survival and overall survival when develop CIA,so we can prevent ovarian function for patients have lower risk and intend to keep bearing ability;and further treatment inhibit ovarian function for improving outcome in patients with high risk and poor prognosis without CIA developed;CIA is an objective and simply observed factor.

Objective To observe the effects of selective α2-adrenergic receptor agonist alpha-Methylnore-pinephrine(α-MNE) as a vasopressin agent on hemodynamics, troponin T(cTnT) and myocardium in the rabbit cardiopulmonary resuscitation. Method Eighteen health rabbits, weighing 2.5 - 3.5 kg, both male and female,were provided by Lanzhou institute of veterinary medicine. After setting up rabbit model of cardiopulmonary resuscitation, 18 rabbits were randomly divided into three groups. The rabbits in group A as a operation-control group were processed with anesthesia, endotracheal intubation, and surgery without ventricular fibrillation induced. The rabbits in group B as a epinephrine group were administered with 30 ug/kg epinephrineduring CPR. The rabbits in group C as a MNE group were administered with 100 ug/kg α-MNE during CPR. The left ventrictdar end-diastolic pressure(LVEDP), left ventricular pressure rise and fall rate(± dp/dt) and serum concentrations of BNP were measured. Statistic package of SPSS 10.0 was used for the data analysis and significant differences between means were evaluated by ANOVA analysis. Results Compared with group A, LVEDP of other two groups gradually increased respectively(P < 0. 01), and peak ± dp/dt decreased in other two groups(P<0.01). Increase in LVEDP in group C was less than that in group B(P<0.05), whereas peak ± dp/dt in group C were higher than that in group B(P<0.05), at the same stage. Compared with group A, the cTnT of the remaining two groups increased(P<0.01, respectively),and reached peak at 30 minutes. In group C, the elevation of cTnT was less than that in group B(P<0.05) during the same period. In group B and C, myocardial injury was seen under a light microscope, but the injury in group C was lighter than that in group B. Conclusion The methylnorepinephrine can lessen the myocardial dysfunction after CPR.

The changes in the tau protein phosphorylation and expression of bcl-2, and bax in rat parietal cortex neurons after focal cerebral ischemia-reperfusion (I/R) were explored, and the relationship between the tau protein phosphorylation and the expression of bax or apoptosis was clarified in order to elucidate the relationship between cerebral infarction and Alzheimer's disease. The rat focal cerebral I/R model was induced by occlusion of the right middle cerebral artery using the intraluminal suture method. The level of tau protein phosphorylation at Ser396, Ser404, Tyr231, Ser199/202 sites and the expression of bcl-2, bax and total tau 5 in rat parietal cortex during focal cerebral ischemia/reperfusion were detected by Western blot. The relationship between the tau protein phosphorylation and the expression of bax, or apoptosis was examined by TUNEL method and double-labeling immunofluorenscence method. The results showed that the level of tau hyperphosphorylation at Ser199 / 202, Ser396, Ser404, Tyr231 sites and the expression levels of bcl-2, and bax were significantly higher in I/R group than in the sham group, but the ratio of bcl-2/bax was decreased. Neuronal apoptosis, bax expression and the tau protein hyperphosphorylation were co-localized. It is suggested that Alzheimer's disease-like pathological changes occur after cerebral I/R. The highly abnormal phosphorylation of tau protein plays a key role in cerebral I/R-induced apoptosis. The cerebral infarction may contribute to Alzheimer's disease occurrence and development.

The changes in the tau protein phosphorylation and expression of bcl-2,and bax in rat parietal cortex neurons after focal cerebral ischemia-reperfusion(I/R)were explored,and the relationship between the tau protein phosphorylation and the expression of bax or apoptosis was clarified in order to elucidate the relationship between cerebral infarction and Alzheimer's disease.The rat focal cerebral I/R model was induced by occlusion of the right middle cerebral artery using the intraluminal suture method.The level of tau protein phosphorylation at Ser396,Ser404,Tyr231,Ser199/202 sites and the expression of bcl-2,bax and total tau 5 in rat parietal cortex during focal cerebral ischemia/reperfusion were detected by Western blot.The relationship between the tau protein phosphorylation and the expression of bax,or apoptosis was examined by TUNEL method and double-labeling immunofluorenscence method.The results showed that the level of tau hyperphosphorylation at Ser199/202,Ser396,Ser404,Tyr231 sites and the expression levels of bcl-2,and bax were significantly higher in I/R group than in the sham group,bat the ratio of bcl-2/bax was decreased.Neuronal apoptosis,bax expression and the tau protein hyperphosphorylation were co-localized.It is suggested that Alzheimer's disease-like pathological changes occur after cerebral I/R.The highly abnormal phosphorylation of tau protein plays a key role in cerebral I/R-induced apoptosis.The cerebral infarction may contribute to Alzheimer's disease occurrence and development.