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.

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 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 observe the expression of the G-protein-coupled-receptor 14 (GPR14), urotensinⅡreceptor, in the cardiovascular system and brain of SD rats. Methods: Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the GPR14 mRNA. Results: In cardiovascular system, GPR14 mRNA was detected in the left ventricle, left atrium, thoratic aorta and carotid aorta. The highest level of expression was found in the left ventricle. In the brain, GPR14 mRNA was detected in cortex, hippocampus, hypothalamus and cerebellum, and higher level of expression was found in the cerebellum. Conclusion: GPR14 mRNA expression is found in the cardiovascular and neural tissues of tested rat, suggesting that urotensinⅡ may play an important role in cardiovasculature and central nervous activity.

Objective To investigate the association between arsenic(+3 oxidation state) methyltransferase (AS3MT) genetic polymorphism and susceptibility to endemic arsenism.Methods Polymerase chain reactionrestriction fragment length polymorphism-single strand conformation polymorphism(PCR-RFLP-SSCP) technology was performed to detect mutations of AS3MT gene intron 8 and exon 9 in genome DNA of the 79 cases and 110 controls.PCR products with abnormal band forms were further sequenced to find the types and sites of mutation.Chi-square test and multivariate Logistic analyses were conducted.Results The incidence of the 9149 base mutation(A→C) in AS3MT gene intron 8(AS3MT-9149) in case group(19.0％,15/79) was lower than that in control group (23.6％,26/110).The incidence of the codon 287 mutation(ATG→AT/CG) in AS3MT gene exon 9(AS3MT-287)in case group(10.1％,8/79) was lower than that in control group (11.8％,13/110).However,statistical analysis indicated no significant difference in both mutations between two groups[AS3MT-9149:odds ratio(OR) =0.59,95％ confidence interval(CI):0.26-1.31,P =0.195; AS3MT-287:OR =0.85,95％ CI:0.32-230,P =0.751].Conclusions There are no significant association between the genetic polymorphisms of AS3MT-9149,AS3MT-287 and the susceptibility to endemic arsenism.Similarly,due to small sample amount,we can not exclude the possibility that these gene polymorphisms are related to susceptibility to endemic arsenism.

Objective To observe the changing levels of serum sFas before and after intravenous i mmunoglobulin (IVIG) treatment of incomplete Kawasaki disease (IKD),to explore the roles of sFas in the pathogenesis of IKD and IVIG treatment mechanism.Methods Thirty eight cases of IKD children were selected as experimental group and 20 examples of the same age of children as the control group.The IKD children were treated by IVIG in combination with aspirin (ASP) ; and blood test was performed before treatment,3 days after treatment,and 14 days after treatment,respectively.Dual-resistant sandwich enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of serum sFas,plasma Fibrinogen (PT-D),d-dimer (D-D),and c-reactive protein (CRP).Results The levels of serum sFas,PT-D,D-D,and CRP were significantly higher than the control group for IKD children before treatment[(0.55 ± 0.14)ng/L vs (0.24 ±0.04) ng/L,(552.3 ± 147.2) mg/dl vs (277.3 ±82.5)mg/dl,(649.0 ±201.6) μg/L vs (315.4 ±91.8)μg/L,and(72.2 ±28.7)mg/L vs (7.2 ±2.9)mg/L; t' =12.41,9.11,8.64,13.82;All P ＜ 0.05] ;3 days after treatment,compared with those before treatment and control group,the sFas level of IKD children at the third day after treatment was significantly decreased compared to that before treatment and control groups,respectively [(0.43 ± 0.09) ng/L vs (0.55 ± 0.14) ng/L,(0.24 ± 0.04) ng/L,F =47.624,All P ＜0.05] ;For the level of sFas at the 14th day after treatment,no statistical significance was found between IKD children and the control group[(0.24 ±0.05) ng/L vs (0.24 ±0.04) ng/L,t =0.596,P ＞ 0.05].Conclusions The abnormally increased serum sFas level before IVIG treatment suggests that dysfunction of apoptosis be involved in the pathogenesis of the IKD.Intravenous immunoglobulin treatment may be involved in the apoptosis process.

Purpose To explore the relationship between the mutations of epidermal growth factor receptor ( EGFR) and KRAS genes and clinicopathological characteristics in patients with non-small cell lung cancers (NSCLC). Methods Clinical samples from 431 NSCLC patients were obtained for EGFR and KRAS gene analysis. PCR based direct DNA sequencing was used to investigate mutations in exon 18-21 of EGFR gene and codon 12 and 13 of exon 2 of KRAS gene. Results The overall EGFR mutation rate of primary NSCLC was 53. 6% (231/431) in this study cohort and eight cases showed double EGFR mutations. Mutation rates in female and male were 65. 2% (122/187) and 46. 9% (98/209), respectively. The mutation rate was higher in patients with non-smokers and adeno-carcinoma and adenosquamous carcinoma subtypes than in their counterparts (P<0. 05), with the percentage of 57. 2% (124/216), 60. 3% (199/330), 42. 9% (6/14), respectively. In squamous cell carcinomas and other subtypes, EGFR mutation rates were 11. 6% (5/43) and 11. 1% (1/9), respectively. The EGFR mutation types included exon 18 point mutations (4. 0%, 9/227), exon 19 deletion mutations (4. 5%, 101/227), exon 20 insert or point mutations (9. 7%, 22/227) and exon 21 point mutations (41. 4%, 94/227). Activating mutations of KRAS gene were detected in 7. 8%(31/396) of NSCLC. Twenty-eight patients showed codon 12 mutations ( G>T, G>A, G>C) , and three patients had codon 13 mutations ( G>A, G>T) . Most of these mutations were G to T transversion (64. 5%, 20/31). Conclusion Polymerase chain reaction-direct sequencing is a reliable and effective method for the detection of the EGFR and KRAS gene mutation in NSCLC patients. The mutation rate of EGFR is higher in Chinese patients, especial-ly in non-smoking female patients with adenocarcinoma.