Objective To investigate the relationship of D-dimer(DD) and fibrinogen levels in blood plasma and diabetic nephropathy(DN).Methods According to the results of urinary albumin excretion rate (UAER), 98 cases of type 2 diabetas were divided into simple diabetic mellitus ( SDM), early diabetic nephropathy ( EDN) and clinical diabetic nephropathy (CDN); other 45 healthy persons were employed as control. Plasma levels of DD and the fibrinogen of all groups were examined.Results There was significant difference of DD and fibrinogen levels in all groups as compared with control group (P

Objective To investigate the diagnostic value of biexponential model of DWI in nontypical hippocampal sclerosis (HS) of the youth.Methods DWI with multiple b values were performed on 75 youths with right temporal lobe epilepsy and 20 healthy youths(control group).There were no abnormalities in hippocampus on conventional MRI.11 of 75 patients were proved right HS by surgery and pathology (HS group).Compare the volume of the right hippocampus and their D,D? and f values in HS group and control group.Results There were statistical differences in D and f values between HS group and control group (Z=-3.08,Z=-2.23,P<0.05). There were no statistical differences in the volume of hippocampus and D? values between two groups (Z=1.77,Z=-0.19,P>0.05). Conclusion When HS does not have typical appearances on conventional MRI,D and f values can provide help from diffusion and the perfusion of microcirculation aspects.

Lower urinary tract symptoms due to benign prostatic hyperplasia is of great prevalence among ageing males,and it can markedly affect patients' quality of life.Personalized drug therapy according to genetic characteristics is the ideal choice for this problem.Here we summarized the latest research findings on the associations of gene polymorphisms with drug efficacy and adverse reaction in the treatment of benign prostatic hyperplasia/urinary tract symptoms.

The membrane fluidity of mitochondria isolated from langendorff perfused rat hearts was studied with ESR spin labeling technique and TBA method was used to detect the content of lipid peroxide. After total ischemia for 40min followed by a 20min reperfusion the 10-DSA region of the mitochondrial membrane showed significantly increased S (0.1(?)2?0.006) and ?_c(7.13?0.09?10~(10)sec) values (i. e. a decrease of membrane fluidity)in comparison with aerobic control (S=0.103?0.007); ?_c=6.86?0.20?10~(-10) sec) (P0.05). In addition, we found that DS182 could remove O_2~? produced by O_2~? generating system. Our results have showed that DS-182 is a potent scavenger of superoxide. The protective effect of DS-182 on mitochondria during ischemia/reperfusion might be due to its antioxidative activity。

This study was performed on rabbits to examine the changes of calmodulin (CAM) and cAMP in the myocardium during ischemia and reperfusion by radioimmunoassay method. The result showed the levels of CaM and cAMP increased at 20 min of ischemia. Although these two parmeters were unchanged at 40 min of ischemia as compared with the changes at 20 min, they were changed during reperfusion at different times of ischemia. At 20 min ischemia following 10 min reperfusion, the content of CaM decreased, the content of cAMP increased. On the basis of 40 min ischemia, reperfusion induced opposite changes: CaM increased, cAMP decreased. The possible mechanism of these changes was discussed.

We studied the protective effects of redix salviae miltiorrhizae (RSM) on the ischemic and post-ischemic reperfusion injury which was made by ligating and reopening of the left ventricular branch of the coronary artery of the open-chest anaethetised rabbits under the supervision of ECG. There were 14 rabbits in each group, 7 of them for the measurement of myocardial lipid peroxide level (MLPL) by the thiobarbituric acid method (Hiroshi Ohkawa, 1979), and the other 7 for measuring distribution of regional myocardial blood flow (RMBF) by the biological radionuclidelabeled particle method (Wang Jingxian, 1985). With increasing duration of ischemia, MLPL increased significantly in the ischemic and post-ischemic reperfusion injured heart. In the case of 60 mins ischemia followed by 30 mins reperfusion, MLPL was much higher than that without reperfusion. However, which compared with that of 90 mins ischemia, no significant difference was found. The recovery of RMBF was only 53.2% after 30 mins of reperfusion following 60 mins of ischemia. The occurance of post-ischemic reperfusion injury was dependent on the duration and severity of ischemia. The injury of reperfusion after long period (60 mins) of ischemia is similar to that of increasing duration of ischemia. No-reflow phenomenon was observed in ischemic zones during reperfusion after 60 mins of ischemia. In the RSM (2g/kg body wt) protected reperfusion group. MLPL was reduced by 56.0% and the recovery of RMBF was increased by 32.0%.

The time-dependent changes in myocardio membrane system during ischemia/reperfusion injury were studied with ligature of the left ventricular branch of coronary artery in rabbit. The permeability of cardiac membrane system being tested by using lanthanum tracer technique and stereological methods. Lanthanum granules were observed in the sarplacosma and sarccpiasmic tubes especially at ischemia for 20min. The pecmeability of membrane system for La~(+++) was more marked when hearts were reperfused for 20min. With the increase in time of ischemia, the changes became more and more serious. A lot of lanthanum granules were entered into mitochondria when the hearts were reperfused after 40min ischemia. There were neither intact mitichondria nor lanthanum granules in mitochondria observed when the hearts were reperfused after 60min ischemia. The structural changes were irreversible at this stage of reperfusion The results of our study indicated that the changes of permeability of cardiac cell for La~(+++) in ischcmia/reperfusion are time-dependent, 40min ischemia is the demarcation line between the reversible and irreversible injury during reperfusion. On the basis of our experiment, we like to propose a new conception of reversible and irreversible injury of reperfusion.

Objective To summarize the experience on bronchiallavage to cure pulmonary atelectasis and pulmonary infection after thoracotomy.Methods 48 patients were selected and treated by bronchiallavage under monitoring,and antibiotics was used according to sputum culture and drug sensitive test.The out come was analyzed and evaluated.Results All patients of the pulmonary atelectasis were cured and those with pulmonary infection were controled.There was no serious complication.Conclusion Bronchiallavage is applied to treat pulmonary atelectasis and pulmonary infection after thoracotomy,the curative rate is significant.The appliance of antibiotics is guided by drug sensitivity.It is such a safe and feasible therapeutic tool that the bronchofibroscope is applied to cure pulmonary atelectasis and pulmonary infection after thoracotomy.

Objective To investigate the receptor involved in the TNF?induced HO-1 expression and the related signal transduction mechanisms in the brain microvessel endothelial cells.Methods TNF? receptor 1(TNFR1)knockout murine brain microvessel endothelial cells(BMVECs)in vitro culture were stimulated respectively by TNF?(5ng/ml).After 24 hours,the level of HO-1 gene mRNA were detected by semi-quantitative RT-PCR,the effect of TNF?on JNK 、ERK or transcription factor AP-1 were analyzed by Western blot,while ERK inhibitor(PD98059)or JNK inhibitor(SP600125)were used.Results Exposure of wild-type BMVECs and TNFR1(p55)knockout BMVECs [BVEC/TNF-RI(-/-)] to TNF?(5ng/ml,24 h)caused a marked increase in HO-1 mRNA expression.Furthermore,TNF? stimulation also lead to the activation of JNK,ERK and the transcription factor AP-1 in the BVEC/TNF-RI(-/-),However,incubation with the JNK inhibitor SP600125 but not the ERK inhibitor PD98095 attenuated the TNF?-induction of HO-1 in the BVEC/TNF-RI(-/-).Conclusions TNFR2 and JNK activation but not TNFR1 might be essential for mediating the TNF?-induction of the HO-1 in the endothelial cells.

Objective To detect the expression of TrkA in the brain of the Wistar rats during the embryonic phase.Methods Adult Wistar rats were fed in one cage.It was E0 day when sepermia were found in vaginal suppository and vaginal smear.The expressions of TrkA in the brain of Wistar rats during various brain regions were observed by immunohistochemistry on E13,E15,E17,E19 and E21 day. Results On E13 day no obvious expression of TrkA was observed in the embryonic brain.The expression of TrkA had an obviously increasing tendency in the cortex of telencephalon from E15 day to E17 day.And on E17 day,the positive rate of the expression of TrkA reached the second peak.While on E19 day,the expression of TrkA had a temporary decreasing.Then on E21 day the expression of TrkA reached the highest peak.The striatum and hippocampus developed later than the telencephalon till E17 day,and the expressions of TrkA during these stages were same as the cerebrum.Conclusion From E15 to E17 day,obvious expressions of TrkA are observed in the embryonic telencephalon,and it accords with embryonic induction.