More and more studies have found that EBV infection is closely related to the occurrence, development, treatment and prognosis of lymphoma. The treatment of EBV-positive lymphoma bases mainly on combined chemo-radiotherapy together with ganciclovir, acyclovir and other antiviral drugs. Also there are novel ways to treat EBV positive- lymphoma including CD70 monoclonal antibody, butyrate, etc. The only way to prevent EBV infection is to inoculate anti-viral vaccine. The criterion of treating EBV positive-lymphoma remains to be further investigated.

Objective:To study the relationships of portal hypertensions to vasoactive substances-angiotensin(AT-Ⅱ)in cirrhosis patients.Methods:48 patients with liver cirrhosis(LC)(including 18 patients with compensated LC and 30 patients with decompensated LC) and 32 normal controls(NC) were studied. Color duplex doppler ultrasonography was used to study portal venous and splenic venous blood flow(PVBF and SVBF).Also,the blood concentration of AT-Ⅱ was detected.Then,analyze the correlation between PVBF and SVBF to AT-Ⅱ.Results:Portal hyperdynamic exists in cirrhosis patients from beginning to the end. Low level of AT-Ⅱ in compensated LC patient has no relation with portal hyperdynamic, high level of AT-Ⅱ in decompensated LC has positive relation with portal hyperdynamic.Conclusion:This study has directed significance of clinical treatment and diagnosis.

Objective To explore the effect of HIPK2 on apoptosis of human kidney tubular epithelial cells (HKC) induced by cisplatin.Methods Apoptosis of HKC cells was induced by cisplatin and the expression of HIPK2 was detected by RT-qPCR and Western blot.Two HIPK2 siRNAs were designed according to gene sequence of HIPK2 and cell lines with HIPK2 knockdown were established through transfecting the HIPK2 siRNAs into HKC cells by liposome.The expression of HIPK2 mRNA and protein was detected by RT-qPCR and Western blot after induced by cisplatin.Then cell apoptosis was detected by Annexin V/PI after the HIPK2-knockdown cells were treated with cisplatin.Moreover,the expression of pro-apoptotic protein bax was detected by Western blot after HIPK2 was knockdown.Results The expression of HIPK2 mRNA and protein was down-regulated obviously on the process of HKC apoptosis which induced by dose-dependent cisplatin (P＜0.05).The transfection of siRNA could significantly reduce the expression of HIPK2 mRNA and protein in HKC (P＜0.05),which promotes the HKC cells apoptosis induced by cisplatin.Conclusions HIPK2 can suppress the HKC cells apoptosis induced by cisplatin.

ObjectiveTo study the effects of rehabilitation training on the expression of brain derived neurotrophic factor(BDNF) around the cerebral infarcted area of rats.Methods60 SD rats were randomly divided into rehabilitation group and immobilization group 24 hours after cerebral infarction.The rehabilitation group were given water maze training,rotating bar and rolling cage exercises everyday while the immobilization group were fixed in cages. Histochemistry was used to detect the BDNF expression around the cerebral infarcted area at the 1st,3rd,7th,10th and 14th day after infarction respectively.ResultsAt 1st day after the infarction, the expression of BDNF increased obviously around the infarcted area in both group. More BDNF positive neurons were found in the rehabilitation group than that in the immobilization group at 3rd day (P<0.01). BDNF positive astrocytes showed obvious increasing in both group. BDNF positive neurons decreased with time going, and the color became lighter at the same time .At the 7th day after infarction, there were only a few positive neurons, and seldom obvious positive neurons could be seen around the infarcted area at 10th and 14th day. Great deal of BDNF positive astrocytes were found at 3rd,7th,10th and 14th day, and the rehabilitation group showed more expression than that of the immobilization group(P<0.01).ConclusionsThe rehabilitation training may increase the expression of BDNF which might take an active part in the recovery of the central nervous system injury and the rebuilding of its function.

Objective To investigate the incidence of AKI and its relationship to mortality of inpatients by analyzing the changes of serum creatinine(SCr). Methods We collected the data of SCr in Peking Union Medical College Hospital through Jun 2006 to May 2007 and then selected the patients who were subjected to SCr determination more than one time. The relationship between the frequency of SCr determination and gender, age was analyzed. The relationship of increased SCr to gender, age, frequency of determination was also analyzed. The risk stratification based on SCr was investigated. In our study, we investigated the incidence of AKI in different diagnostic groups. The relationship between AKI and mortality in ICU and MICU unit was analyzed. Results There were 36 855 patients in one year, 16 934 patients were subjected to SCr determination only one time, 15 233 patients were subjected to SCr determination at least two times. Elder men were subjected to SCr determination more frequently (P<0.01). Along with the increase of SCr concentration, the frequency of SCr determination were increased significantly (P<0.01). Using the increasing of SCr exceeding 50% as the criteria for diagnosis of AKI, the incidence of hospital-acquired AKI was 8.46%, and it was higher in patients with injury and poisoning (16.7%), infection (16.0%), hematological system diseases (16.1%), neoplasms (12.7%). The incidence of AKI was 27.7% and 55.2% in ICU and MICU, respectively. Mortality of patients in MICU was increased along with the increasing of SCr level Mortality of patients with AKI in ICU was 23.3%, that was significant higher than patients without AKI, the adjust OR was 2.7 (P<0.01). Conclusions The incidence of AKI evaluated by analyzing SCr changing is significantly higher than that using experienced clinical diagnosis. This method is convenient in clinic for early diagnosis of AKI.

Objective To understand the changes of cardiac systolic and diastolic function in human immunodeficiency virus (HIV)-infected patients without evidence of cardiac disease in China.Methods Forty-two HIV-infected patients who were followed up in the Department of Infectious Diseases at Peking Union Medical College Hospital without cardiac involvement were recruited.All the HIV-infected patients had received highly active antiroviral therapy (HAART) for more than 12 months with viral suppression.And 30 age and sex matched healthy subjects without cardiac disease manifestations were enrolled as controls.Every group members underwent transthoracic echocardiography evaluation.The indexes of cardiac systolic and diastolic function between HIV-infected patients and healthy controls were compared.Results Diastolic abnormality occurred in 20 cases in HIV-infected group and 6 cases in control group, with statistically significant difference (χ2=5.79, P=0.007).The E wave deceleration time (EDT) in HIV-infected patients were significantly decreased than healthy controls ([161.87±21.64] ms vs.[190.34±37.22], t=-3.20, P=0.002).There were no significant differences of E/A ratio ([1.16±0.35] vs.[1.19±0.26]), E/Ea ratio ([5.43±1.99] vs.[5.78±0.91]), isovolumic relaxation time (IVRT), ([93.18±20.34] ms vs.[93.57±18.55]ms), Ea ([10.18±2.80] cm/s vs.[11.45±2.75] cm/s) between HIV-infected patients and controls (t=1.13,1.53,0.67 and 0.29, respectively, all P>0.05).Among cardiac systolic function markers, left ventricular ejection fractions in HIV-infected patients and control group were (66.7±6.4)% and (68.7±4.2)%, respectively.And left ventricular shortening rates were (37.08±4.79)% and (38.17±3.96)%, respectively.Both showed no significant difference between the two groups (t=-1.51 and-1.00, respectively, both P>0.05).Conclusions Compared with control group, subclinical cardiac diastolic dysfunction is more frequently observed in HIV-infected patients.However, there are no significant differences of cardiac systolic function markers between HIV-infected patients and controls.

Objective To investigate the activation of nuclear factor-κB(NF-κB),which was stimulated by angiotensin-Ⅱ(AngⅡ)through classical pathway in human pulmonary microvascular endothehal cells(HPMEC).Method The experiment was divided into two groups:in Ang Ⅱ group,HPMECS were incubated with 10-6mol/L AngⅡ for 0,0.5,1,2 and 4 hours,respectively;in losartan group,HPMEC was pretreated with 10-6mol/L losartan(inhibitor of AngⅡ type 1 receptor)for 1 hour,and then stimulated with 10-6mol/L AngⅡ for 2 hours,and the nucleax protein and the cell plasma protein were prepared by lysis and centrifugation.Electrophoretic mobility shift assay(EMSA)was used to detect the NF-κB DNA binding activity.The inhibitor of κBa(IκBα)was detected by Western blotting.The data were expressed as(x±s)and analyzed with one way analysis of variance.A P value less than 0.05 indicated significant difference.Results Compared with the activity of NF-κB at 0 h (100.0±25.1)after AngⅡstimalation,the activity increased significantly at 0.5 hour(144.5±16.1,P＜0.05),and reached peak value at 2 hours(270.1±27.2,P＜0.05).The concentration of IκBα at 0 hours was 44.4%±2.1%,decreased markedly at 0.5 hours(38.9%±3.6%,P＜0.05),and to the lowest level at 2hours(32.6%±2.3%,P＜0.05).The activity of NF-κB(115.4±10.7)and the concentration of IκBα(43.6%±3.7%)in losartan group had ilo significant difference with AngⅡ group at 0 h(P＞0.05).The activity of NF-κB and the concentration of IκBα in losartan group had significant difference with AngⅡ group at 2hours.Conclusions NF-κB can be activated through classical pathway,which stimulated by AngⅡ in HPMEC.

AIM: To study the effects of Ginkgo biloba extract (GbE) on cerebral ischemia-reperfusion injury. METHODS: Cerebral ischemia-reperfusion injury was produced by 10 min or 20 min occlusion of bilateral carotid arteries followed by 5 d or 1 d reperfusion in gerbils. Ninety-five gerbils were divided into 4 groups: sham-operation, ischemia-reperfusion, GbE 50 mg*kg-1 and GbE 100 mg*kg-1 groups. Drugs were given intragastrically 2 d prior to ischemia and during reperfusion. The effects of GbE on the contents of calcium, sodium, water in cortex, and lipid peroxide(LPO) in brain hemispheres, as well as the density of neuron in hippocampal CA1 sector were observed. RESULTS: GbE could reduce the increase of calcium, sodium, water content in a manner of dose-depedance. The dosage of GbE 100 mg*kg-1 could decrease the content of LPO and the mortality, increase the density of neuron in hippocampal CA1 sector. CONCLUSION: GbE has protective effects on cerebral ischemia reperfusion injury.

Animals ; Beer ; adverse effects ; Blood Glucose ; metabolism ; Diabetes Mellitus, Experimental ; metabolism ; Lipid Metabolism ; Male ; Physical Conditioning, Animal ; physiology ; Rats ; Rats, Wistar

Objective To construct a eukaryotic vector of chicken-derived Wnt3a tagged with EGFP (pCAG-MCs-Wnt3a-EGFP) and investigate the influence to the proliferation and axonal formation of neural precursor cells when Wnt3a was overexpressed during the development of chick embryonic spinal cord. Methods Wnt3a gene was amplified from the total RNA obtained from chick embryonic spinal cord using molecular techniques, then connected with pCAG-MCs-EGFP to construct pCAG-MCs-Wnt3a-EGFP, which was identified by digestion and genetic sequencing. At embryonic day (E) 2.5-3.0, pCAG-MCs-Wnt3a-EGFP (experimental group) and pCAG-MCs-EGFP (control group) were transfected into the chick embryonic spinal cord using in vivo electroporation, respectively. Samples were collected at E4 (5 simples of each groups) and then conducted frozen section. The immunofluorescent staining was performed to detect the expression of Wnt3a and proliferating cell nuclear actigen (PCNA) for analyzing the relationship between Wnt3a and cell proliferation, and observe the axonal formation of neural precursor according to the green fluorescence of Wnt3a protein. Results pCAG-MCs-Wnt3a-EGFP was obtained and its gene sequencing was identical with the Gene bank. Green fluorescence was observed at E4 after pCAG-MCs-Wnt3a-EGFP transformed to chick spinal cord. In transversal section of chick embryonic spinal cord, the results of immunofluorescent staining showed Wnt3a was successfully overexpressed. Meanwhile, the amount of neurons projecting axons was dramatically decreased (n=3, P < 0.01), compared to the control group, concomitant with the significant elevation of PCNA level (n =3, P < 0.01). Conclusion pCAG-MCs-Wnt3a-EGFP is successfully constructed and our study confirmed that Wnt3a plays a vital role in the proliferation and axonal formation of neural precursor cells in the developing chick spinal cord.