Objective To investigate the role of nitric oxide synthase (NOS) in neurotoxic mechanisms of beta amyloid (A?) and the pathogenesis of Alzheimer′s disease (AD). Methods 35 adult rats were divided into 3 groups: normal control,saline injection,and A? 1 40 injection groups A? 1 40 was initially solubilized in saline (10?g/?l) and incubated for at least 1 week before use 1?l incubated A? 1 40 or saline were injected into dorsal blade of dentate gyrus in right hippocampus of rats Immunohistochemical assay of neuronal NOS (nNOS) and inducible NOS (iNOS) was performed at the 2 nd,10 th,and 30 th day after A? 1 40 or saline injection. Results The nNOS like immunoreactivity (nNOSLIR) neurons were found in different brain regions such as cortex,striatum and hippocampus of normal rats,and the number of neurons in dentate gyrus was 8 96?0 31 The number and configuration of nNOSLIR neurons were found without changes after saline injection (8 97?0 29) At 2,10,and 30 d after A? 1 40 injection,the number of nNOS neurons at the site around injection was significantly reduced (3 13?0 27,2 89?0 19 and 2 91?0 25 respectively),but there were no notable differences at these three experimental time points iNOS like immunoreactivity (iNOSLIR) cells were not found in any brain region of normal or saline injected rats After A? 1 40 injection,a large percentage of glia (mainly were astrocytes) had an activated morphological change and showed a strong iNOSLIR around the injection site The responded areas with these cells were 0 905?0 082,0 962?0 161 and 0 935?0 125 mm 2 respectively at 2,10 and 30 day after A? 1 40 injection,but there appeared no significant differences among them. Conclusions The results demonstrate that intrahippocampal injection of A? 1 40 may result in a significant loss of nNOS neurons and induce a considerable expression of iNOS in astrocytes,indicating that NOS may play an important role in neurotoxic mechanisms of A? and the pathogenesis of AD

To examine the effect of Gankang Suppository on duck hepatitis B virus (DHBV), the serum biochemistry and hepatic histology in an animal model of DHBV infection, a model of DHBV infection was established by infecting 1-day-old Yingtaogu ducklings with DHBV-positive serum. The successful model was confirmed by PCR assay and 48 ducklings infected with DHBV were randomly divided into 3 groups: a Gankang Suppository treatment group, an acyclovir (ACV) group and a DHBV model group (control), with each group having 16 animals. All the animals were given the medicines for 4 weeks in a row. The serum of the animals was taken 14 and 28 days after the medication and 7 days after drug discontinuation. Real-time PCR was performed to detect the copy numbers of DHBV DNA in the serum. ALT and AST were dynamically monitored. The ducklings were sacrificed on the 7th day after the discontinuation of the treatment and livers were harvested and examined for inflammation and degeneration of liver cells by using HE staining. The results showed that on day 14, 28 after the treatment and day 7 after the withdrawal, the logarithmic values (log) of DHBV DNA copy numbers in ducklings of Gankang Suppository treatment group were significantly lower than that before the treatment (P=0.0092, P=0.0070, P=0.0080, respectively). Compared with DHBV model control group, the ALT level was significantly decreased (P=0.0020, P=0.0019, respectively) on day 28 after the treatment and on day 7 after the withdrawal. The AST level was also reduced on day 14 after the treatment (P=0.0298). Compared with the ACV control group, the level of ALT was lower on day 7 after the withdrawal (P=0.0016). Histologically, the hepatocyte swelling, vacuolous degeneration and acidophilic degeneration in Gankang Suppository treatment group were alleviated 7 days after the withdrawal as compared with model control group (P=0.0282, P=0.0084, P=0.0195, respectively). It is concluded that Gankang Suppository can effectively suppress DHBV replication, reduce the levels of serum ALT and AST and improve hepatic histology.

Objective To find out whether the benefits entitled to peasants have increased since NRCM is in place in Beijing, and to analyze the extent of such benefit increase if any. Methods The first is to calculate changes to the reimbursement ratio of hospitalization charges for the peasants covered by NRCM; the second is to calculate the role played by NRCM for alleviating the catastrophic health expenditure of peasants. Results The reimbursement ratio of hospitalization charges for peasants covered by NRCM rose from 32.4% in 2004 to 45.4% in 2007. Survey data from districts and counties in the sampling test indicate that NRCM has gained an ever growing power in alleviating the catastrophic expenditure of peasants. Conclusion Recent years have witnessed a marked growth in medical charges, peasants' income, and peasants' demand for medical services. Against such a background, NRCM can still sharply downsize their catastrophic health expenditure, and its role keeps intensifying. This proves that the fund raising speed of NRCM has greatly outpaced the growth of medical charges and peasants' demand for medical services, and NRCM is playing a more effective role in alleviating the peasants from poverty caused by diseases.

Objective To study the distance of MRI in the practice of correct diagnosed meningioma.Methods 152 cases which have been diagnosed meningioma from MRI scan compared to operation and pathology.16 cases which do not fit the diagnosis from them were analysed.Results There were 10 cases which were misdiagnosed other tumour(6.5%).Other tumour misdiagnosed meningioma were 6 cases(4%).The general misdiagnostic rate was 10.5%.Conclusion Because of complexity in histological structural,equipment function and scan technology,it is inevitable to misdiagnose.If we can pay more attention to the typical character and study the plain film and medical history taking carefully,we could increase correct diagnostic rate of meningioma.

Objective To investigate the correlation of vitamin D with essential hypertension and its target organ damages in the elderly.Methods In the retrospective study,365 elderly participants aged ≥ 60 years hospitalized in our department during January 2013 to February 2014 were involved,including 247 patients with confirmed essential hypertension(HT)and 118 patients without HT.Serum 25-hydroxy vitamin D[25(OH)D]levels were measured and compared between HT and non-HT group,and binary regression analysis was used to discuss potential influencing factors of HT.The damage index of vitamin D target organ was compared between vitamin D deficiency group(n=198)and vitamin D non deficiency group(n=49).Results The median serum 25(OH)D level of participants is 35.3 nmol/L,77.5%(283 cases)were in the insufficient vitamin D status.The level of 25(OH)D was significantly lower in HT group than in non-HT group(34.0 vs.38.7 nmol/L,P<0.05).There were not statistically significant differences between vitamin D insufficient group and sufficient group(P>0.05)in albumin/creatinine ratio,serum creatinine,estimated glomerular filtration rate,ankle-brachial index,pulse wave velocity,intima media thickness of carotid artery,Sokolow-Lyon index,cornell index and left ventricular mass index.The serum 25(OH)D level was significantly lower in CHD plus HT group than non-CHD(P<0.05).The 25(OH)D level was negatively correlated with coronary heart disease(B=-0.021,P=0.019).The serum 25(OH)D level was significantly lower in groups with double-and triple-vessel coronary artery disease than in non-CHD group(P<0.01).Conclusions Vitamin D insufficiency is common in the elderly.The serum 25(OH)D level is significantly lower in old patients with HT especially with stage 3 HT than in non-HT ones.The 25(OH)D level is lower in HT patients with comorbid CHD,and more obvious in HT patients with multi-vessel coronary artery disease.An insufficient vitamin D status is not correlated with hypertensive target organ damages including kidney,peripheral vascular and left ventricular cardiac structure.

Objective To evaluate the effect of sevoflurane postconditioning on the expression of Pim-1 kinase during myocardial ischemia-reperfusion (I/R) in rats.Methods Male Sprague-Dawley rats,weighing 250-300 g,were used in this study.After the animals were anesthetized,their hearts were immediately removed and retrogradely perfused with an oxygenated K-H solution at 37 ℃ in a Langendorff apparatus.Thirty-six isolated rat hearts were assigned into 3 groups (n=12 each) using a random number table:control group (group C),group I/R and sevoflurane postconditioning group (group SP).The hearts were subjected to ischemia for 30 min followed by 120 min of reperfusion to establish the model of myocardial I/R injury.In group SP,the hearts were perfused with K-H solution saturated with 3％ sevoflurane for 15 min starting from the beginning of reperfusion.Heart rate (HR),left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP) and the maximum rate of increase and decrease of left ventricular pressure (±dp/dtmax)were recorded at the end of equilibration and 30,60,90and 120 min of reperfusion.Myocardial tissues were obtained at T2 for determination of the expression of Pim-1 kinase,Bcl-2 and cytochrome c (Cyt c) in cytoplasm and mitochondria by Western blot.The hearts were selected at T4 for determination of myocardial infarct size (by TTC staining) and for examination of mitochondrial ultrastructure (with transmission electron microscope).Results Compared with group C,HR,LVDP and ±dp/dtmax were significantly decreased,and LVEDP was increased at T1-4,the myocardial infarct size was enlarged,the expression of Pim-1 and Bcl-2 in cytoplasm and mitochondria was down-regulated,the expression of Cyt c in cytoplasm was up-regulated,and the expression of Cyt c in mitochondria was down-regulated in group I/R (P＜0.05).Compared with group I/R,HR,LVDP and ±dp/ dtmax were significantly increased,and LVEDP was decreased at T1-4,the myocardial infarct size was decreased,the expression of Pim-1 kinase and Bcl-2 in cytoplasm and mitochondria was up-regulated,the expression of Cyt c in cytoplasm was down-regulated,and the expression of Cyt c in mitochondria was upregulated in group SP (P＜0.05).The damage to mitochondria was significantly attenuated in group SP as compared with group I/R,and was aggravated as compared with group C.Conclusion The mechanism by which sevoflurane postconditioning attenuates myocardial I/R may be related to up-regulation of Pim-1 kinase expression in rats.

Background and purpose:Chemotherapy is the important way of breast cancer treatment, but the drug-resistance has attracted special attention. The emergence of drug resistance is closely related to the abnormal enhancement of DNA-damage repair. Both Kif4A and PARP-1 are important molecules of DNA repair. The research investigated the function of Kif4A in epirubicin up-regulating the activity of PARP-1 in breast cancer cells and possible significance. Methods:Western blot was used to detect the expression of Kif4A and PARP-1 after treatment with epirubicin in MDA-MB-231 and MCF-7 cells; the expression of PARP-1 and its activity were detected after high expression of Kif4A and treatment with epirubicin;FCM was used to detect cell apoptosis after treatment with epirubicin combined with PARP-1 inhibitor 3-ABA. Results:Epirubicin up-regulated PARP-1 activity and induced low expression of Kif4A in breast cancer cells, both of them showed dose-dependent and time-dependent. After high expression of Kif4A, the activity of PARP-1 was inhibited and the apoptosis of cells increased, epirubicin partially reversed the activity of PARP-1 inhibited by high Kif4A expression. Both of epirubicin and 3-ABA induced cell apoptosis, combination of them further increased cell apoptosis compared with alone used (P<0.05). The results also showed the apoptosis rate of MDA-MB-231 cells induced by epirubicin, PARP-1 inhibitor 3-ABA and high expression Kif4A was higher than that of MCF-7 cells (P<0.05). Conclusion:Epirubicin increases the activity of PARP-1 dependent on the low expression of Kif4A in breast cancer cells. Kif4A might become a novel target for overcoming resistance of epirubicin.

ObjectiveTo investigate the effect ofpinacidil hyperpolarizaed arrest on p38 mitogen-activited protein kinase (p38MAPK) during myocardial ischemia-reperfusion (I/R) in isolated rat hearts.MethodsFortyeight male SD rats weighting 250-300 g were randomly divided into 6 groups( n =8 each): natural arrest group (group A) ; St.Thomas group (group B) ; pinacidil hyperpolarization arrest group (group C) ;5-hydroxydecanoate (5-HD) group (group D);HMR-1098 group(group E) and 5-HD + HMR-1098 group(group F).Langendorff reperfusion model was established and K-H solution was retrogradely perfused for 15 min.In group A the hearts were arrested naturally afar perfusion was stopped; in group B St.Thomas solution was perfused; in group C pinacidil hyperpolarization solution was perfused; in the other three groups,K-H solution was perfused to isolated rat hearts for 10 min followed by 5 min 5-HD (group D) or HMR-1098(group E) or 5-HD and HMR-1098(group F) perfusion,then hyperpolarization arrest solution was given in each group.Each hearts suffered 60 min ischemia after arrest followed by 30 min K-H solution reperfusion.Coronary flow(CF),HR,left ventricular developed pressure( LVDP),left ventricular systolic pressure(LVSP) and the maximum rate of pressure rise (dp/dtmax) were measured at the end of 15 min K-H solution perfusion and at 20 min of reperfusion.Myocardial phosphatic and nonphosphatic p38MAPK expression was determined by Western blot at 30 min of reperfusion.ResultsCompared with group C,CF,HR,LVDP,LVSP and dp/dtmax were significantly decreased at 20 min of reperfusion and phosphatic p38MAPK expression was down-regulated,non-phosphatic p38MAPK expression was up-regulated at 30 min of reperfusion in groups A,B,D,E and F (P ＜ 0.05).Compared with group E,CF,HR,LVDP,LVSP and dp/ dtmax were significantly decreased at 20 min of reperfusion and phosphatic p38MAPK expression was down-regulated,non-phosphatic p38MAPK expression was up-regulated at 30 min of reperfusion in groups D and F ( P ＜0.05).ConclusionHyperpolarized arrest induced by pinacidil can improve cardiac function following myocardial I/R injury by up-regulating phosphatic p38MAPK expression,down-regulating non-phosphatic p38 MAPK expression and mitochondrial potassium channel is more important than membranous one during the regulation of phosphatic p38MAPK expression.

Objective To observe the imaging features of intraosseous ganglion of the wrist. Methods The radiographs (6 cases), CT (4 cases), and MR (1 case) in 6 cases (7 lesions) of surgically confirmed intraosseous ganglion were retrospectively reviewed. Results Typical intraosseous ganglion was seen as sharp margined and cystic lesion with the size of approximately 0.5 cm in diameter. All but one lesion showed no communication with joint. No degenerative changes were seen in the joints nearby. CT was able to depict the lesions better than radiographs in 4 cases. Intraosseous ganglion was seen as slight low signal on T 1WI and slight high signal on T 2WI MR images. Conclusion Intraosseous ganglion was typically seen as sharp-margined and cystic lesion on radiographs, and it could be better demonstrated with CT and MR. With typical imaging appearance, a suggestion to the diagnosis of intraosseous ganglion could be made.

Aim To investigate the effect of nicotinyl salicylic acid(NSA) on rabbit platelet aggregation induced by Collagen,ADP and AA.Methods Platelet aggregation induced by collagen,adenosine diphosphate(ADP) or arachidonic acid(AA) was studied with turbidimetry in rabbtis blood,in vitro and vivo.Results NSA significantly inhibited the platelet aggregation induced by Collagen and ADP,in vitro and vivo.The inhibition by NSA was dose-dependent.NSA had no effect on the platelet aggregation induced by AA.Conclusion NSA can inhibit rabbit platelet aggregation induced by Collagen and ADP.