Objective; To study the role of nucleocapsid protein in virus replication and cell signaling passway ,and to observe the cellular localization of SARS - CoV nucleocapsid protein. Methods; The sequence of SARS - CoV nucleocapsid protein was analyzed by protein analysis programs to identify nuclear localization signals ( NLS); 293 cells were transfected by the pECFP - C1 recombinant plasmids which expressed fusion protein of enhanced green fluorescence protein(EGFP) and nucleocapsid protein. At 24, 48, 72 hours post transfection (p. t. ) ,the Green Fluorescent Proteins (GFP) were observed by fluorescence microscope. Results; By using PROS-ITE, we identified a nuclear localization signal sequence from amino acids 373 to 389 or from amino acids 374 to 390 in the nucleocapsid protein sequence. However, the analysis of PredictNLS server revealed that the nuclear localization signal region was located between amino acids 36 and 44. N1 protein( 1 - 187aa) was located in both cytoplasm and cell nucleu;N protein(1 -422aa) and N2 protein( 161 -422aa) were located in cytoplasms . Conclusion; The nuclear localization signal is likely to be located between amino acids 36 and 44 in SARS - CoV nucleocapsid protein.

Viral infection begins with the entry of the virus into the host target cell and initiates replication.For this reason,the virus entry machinery is an excellent target for antiviral therapeutics.In general,a virus life cycle includes several major steps: cell-surface attachment,entry,replication,assembly,and egress,while some viruses involve another stage called latency.The early steps of the virus life cycle include virus attachment,receptor binding,and entry.These steps involve the initial interactions between a virus and the host cell and thus are major determinants of the tropism of the virus infection,the nature of the virus replication,and the diseases resulting from the infection.Owing to the pathological importance of these early steps in the progress of viral infectious diseases,the development of inhibitors against these steps has been the focus of the pharmaceutical industry.In this review,Herpes Simplex Virus(HSV),Hepatitis C Virus(HCV),and Human Enterovirus 71(EV71)were used as representatives of enveloped DNA,enveloped RNA,and non-enveloped viruses,respectively.The current mechanistic understanding of their attachment and entry,and the strategies for antagonist screenings are summarized herein.

Objective To summarize the clinical features of Budd-Chiari syndrome.Methods A total of 151 Budd-Chiari syndrome admitted in Peking University People's Hospital from 1996 to 2012 were analyzed retrospectively.Results Abdominal distension was the most common complaint,with 62.9％ (95/151)of lower extremity edema,53.0％ (80/151)of typical bottom-up flow of the abdominal wall longitudinal varicose veins and 60.9％ (92/151) with ascites.Laboratory tests results showed median of alanine aminotransferase (ALT) was 21.5 (15.0,30.0) U/L,aspartate aminotransferase (AST) was 30.0 (23.8,42.0) U/L,total bilirubin was 31.1 (23.3,47.8) μmol/L,blood albumin 37.5 was (31.8,41.5) g/L,prothrombin activity was 71％ (61％,84％).WBC was 5.2 (3.5,7.5) × 109/L,hemoglobin concentration was 126.5 (108.8,144.2) g/L,and platelet count was 117.0 (85.5,155.5) × 109/L.Abdominal B-ultrasound examination showed hepatomegaly existed in 68.9％ (104/151) patients.Intraoperative angiography and surgical exploration showed that 41.1％ (62/151) patients were simple inferior vena cava obstruction or stenosis,15.9％ (24/151)were simple hepatic vein obstruction or stenosis and 43.0％ (65/151) suffered from the inferior vena cava combined with hepatic vein stenosis or obstruction.Surgically confirmation of the lesions showed that inferior vena cava membrane-like structure combined with thrombosis was in 59.6％ (90/151) cases.Conclusions Liver congestion,inferior vena cava congestion and portal hypertension are the main clinical manifestations of Budd-Chiari syndrome.With slightly liver function injury,liver dysfunction of Budd-Chiari syndrome isn't parallel with its portal hypertension.

Objective Toinvestigatetheeffectofwhetherposteriorcommunicatingartery(PCoA) patent or not on hemodynamics of extracranial internal carotid artery (EICA)in patients with moyamoya disease.Methods Atotalof103consecutivepatientswithmoyamoyadisease(unilaterallesion) detected by transcranial color Doppler ultrasonography (TCD)and Color Doppler flow imagining (CDFI), and confirmed by digital subtraction angiography (DSA)from August 2008 to April 2014 were enrolled. According to the patency of PCoA showed by DSA,the patients were divided into either a PCoA non-patent group (n=83)and a PCoA patent group (n=20). Eighty healthy subjects screened by TCD and CDFI in the same period were used as a control group. CDFI and TCD were used to detect the peak systolic velocity (PSV),end diastolic velocity (EDV),vascular resistance index (RI)and/or pulsatility index (PI)of EICA,and posterior cerebral artery (PCA)in subjects of both groups. Results (1 )There were significant differences in PSV,EDV and RI among the three groups (F=5. 76,12. 24,and 8. 10,respectively;all P<0. 05). The PSV of vascular EICA (42 ± 15 cm/s)and EDV (14 ± 7 cm/s)on the lesion sites in patients of the PCoA non-patent group were all lower than those in the control group (92 ± 24 and 38 ± 11 cm/s). The differences were statistically significant (all P<0. 05). The PSV of vascular EICA on the lesion sites in patients of the PCoA patent group was lower than that of the control group (P<0. 05),but EDV was higher than the control group (P<0. 05). (2)Compared with the control group,the RI value was increased in the PCoA non-patent group (P<0. 01)and that was decreased in the PCoA patent group (P<0. 01). (3)PSV and EDV of PCA in the moyamoya disease group were higher than those of the control group (P<0.05),andthePIvaluewaslowerthanthatofthecontrolgroup(P<0.01).Conclusion Whether PCoA patent or not in patients with moyamoya disease have different influences on hemodynamic parameters of EICA. PSV and EDV of the patients with PCoA non-patent are lower than those of the healthy subjects and their RI values are increased. EICA of the patent group is lower than PSV and RI of the control group, and their EDV is increased.

Eukaryotic elongation factor 1 alpha 2(eEF1 A2),which plays a role in the translational elongation process,is normally expressed only in the heart,brain and skeletal musle,but recent studies found it is highly expressed in a variety of tumors and closely related to the oncogenesis and development of tumor.As the signal transduction mechanism is clarified,eEF1A2 is likely to become a novel target for tumor therapy.

Objective To study the relationship between coagulation and inflammatory in 2,4,6- trinitrobenzenesulfonate (TNBS) induced colitis model as well as the therapeutic effect of warfarin.Methods Forty SD-rats were divided into 4 groups, including normal control group (received 0.9% HCI solution), colitis group, warfarin treated group (240 ng/kg daily) and salieylazosulfapyridine (SASP) treated group (100 mg/kg daily). The animal model was induced by injection with 20 mg TNBS. The blood and colon of the rats were removed and the rats was sacrificed at the 14th day. The index of coagulation such as prothrombin time (PT), activated partial thromboplastin time (APTT) and the activity of antithrombins (AT) and the level of tumor necrosis factor-α (TNF-α) were tested.The damage and inflammatory state of the colitis were evaluated by macroscopical score and histological score . The value of disease activity index (DAI) and the platelet counts were alsomeasured. Results The value of DAI was lower in warfarin (1.20±0.45) and SASP (1.78±0.90) treated groups as compared with colitis group (2. 25 ± 0. 89) with no difference (P>0. 05). The macroscopical score was lower in warfarin (1.40 ± 0.55) and SASP (3.14± 1.46) treated grouos as compared with colitis group (4.75 ± 1.66, P<0.01 ). The histological score in warfarin (4. 00± 1.41 ) and SASP (4.28 ± 1.49) treated groups were lower than that in colitis group (7. 75± 1.04, P<0.01). The level of TNF-α was lowest in normal control group (P<0. 01 ), and highest in colitis group. (P<0.01). The PT and APTT were shorter and the aetivity of AT was lower in colitis groupin comparison with warfarin treated group and normal control group (P<0.01). The platelet counts was highest in colitis group. P<0.01). Conclusion The abnormal coagulation in TNBS induced colitis can be effectively treated with warfarin.

Objective To study the relationship between coagulation abnormal and inflammatory in the TNBS induced rats colitis model as well as the therapeutic effect of heparin on this model Methods Forty SD-rats were separated into 4 groups randomly, including normal control group, colitis group, heparin group and SASP group. PT, APTT and the activity of antithrombin (AT)were chosen as indexs of coagulation. The level of damage ancl inflammatory state of the colitis rats were assessed by macroscopical score, histological score and the level of TNFα in each group. Results Compared with normal control group, TNBS induced colitis group has a shorter PT [(14.83±0.45)s vs(16.68±1.08 )s, P < 0.05] and APTT[(12.49±1.30)s vs(29.06±1.60) s, P<0.05] and a lower activity level of AT [(111.33± 8.50)% vs(122.13±3.52)%,P<0.05]. In heparin group, PT, APTT were prolonged [PT: (17.83± 0.78)s vs (14.83±0.45)s,P<0.05, APTT:(53.34±9.49)s vs (12.49±1.30)s,P<0.05] and AT activity was higher than colitis group [(131.67±6.92)% vs (111.33±8.50) %, P < 0.05]. SASP group has a similar data in PT, APTT compared with colitis group and no statistical significance(P>0.05). The activity of AT in SASP group is higher than in colitis group [(122. 33±5.82)% vs (111.33±8.50)%,P <0.05]. The heparin therapy group showed lower macroscopical score(2.50±0.55 vs 4.75±1.16, P< 0.05), histological scores(3.83±0.41 vs 7.75±1.04, P<0.05) and the level of TNFα[(84.75± 18.03) ng/L vs (149.93±23.52)ng/L, P < 0.05] compared with the colitis group. Conclusion Coagulation was abnormality in the rat colitis model induced by TNBS; heparin therapy is effective in the colitis model It seemed that the abnormality of coagulation plays an important role in the pathogenesis of the rat colitis model.

Community health service institutions are the basic tentacles of medical services which directly indicates their relation to the quality and experience of health service.This paper focuses on the behavioral logic of community health service institutions under the background of new medical reform, and looks forward to a perspective on the grassroots practice caused by the reform of medical system through the behavioral analysis of the community health service institutions.The behavioral logic features of the community health service institutions were constructed based on the interview data Nanjing City using the grounded theory.It was found that the realization of public welfare orientation of the aforesaid institutions needs to be completed under the internal and external coordination.The degree of coordination among the interests, orientation, incentives and resource elements will determine the behavior orientation and basic operational practices in the community health service institutions.This study will provide a reference value for the cognition and optimization of healthcare reform policies.

Objective To investigate the clinical features of ulcerative colitis(UC).Methods Based on typical clinical manifestation,enteroscopy and pathological results,138 in-hospital patients were diagnosed UC during 1998 to 2006.Their clinical features were analyzed in this report.ResultsUC was more commonly seen in people aged 20～60(n=108,78.3％).Nearly forty-six percent of the patients (n=63,45.7％)had the disease less than one year.More patients(n=100,72.4％)showed mild or moderate UC.Bloody stool was the most common manifestation.erythrocyte sedimentation rate,hemoglobin,albumin and α1 or α2 globulin levels were closely related with the condition.The mean value of platelet counting was in the upper limit of the normal value.Enteroscopy found more lesion located in the whole colon (n=78,56.5％).Pathological results showed infiltration of inflammatory cells,especially in patients with chronic inflammation.Salieylazosulfapyridine(SASP)and/or 5-Aminosalicyclic(5-ASA)were effective in most UC patients(n=70,50.7％).ConclusionsChinese patients usually had mild to moderate UC,and their courses were often shorter than abroad.The disease was closely related with α1 and α2 globulin levels.Most of the patients had response to SASP and/or 5-ASA.

The effects of high-intensity pulsed electromagnetic stimulation (HIPEMS) on proliferation and differentiation of neonatal rat neural stem cells in vitro were investigated. Neural stem cells derived from neonatal rats were exposed to 0.1 Hz, 0.5-10 Tesla (T) [8 groups of B-I, respectively], 5 stimuli of HIPEMF. The sham exposure controls were correspondingly established. Inverted phase contrast microscope was used to observe the cultured cells, MTT assay to detect the viability of the cells as expressed by absorbance (A) value, and flow cytometry to measure differentiation of neural stem cells. The results showed that A values of neural stem cells in both 3.0 T and 4.0 T groups were significantly higher than the other groups 24 to 168 h post HPEMS, indicating a strong promotion of the growth of neural stem cells (P<0.05). The A values of neural stem cells in the 6.0 T, 8.0 T, and 10.0 T groups were lower than the sham exposure control group, indicating a restraint of the growth of neural stem cells. The rate of neuron-specific enolase-positive neurons revealed by flow cytometry in HPEMS groups was the same as that in control group (P>0.05). It was suggested that 0.1 Hz, 5 pulses stimulation of HPEMS within certain scale of intensity (0.5-10.0 T), significantly promoted the growth of neural stem cells with the rational intensity being 4.0 T.