OBJECTIVE:To observe the effect of Bilobalide on ischemical reperfusion injury in orthotopic liver transplantation model rats and to discuss its protective effect on ischemical reperfusion injury of rats undergoing liver transplantation.METHODS:The model of orthotopic liver transplantation was established by in rats by setting up the bridge between portal vein and left renal vein and building blood bypass by inlaying of canal in the inferior vena,after modeling,the rats were treated with Bilobalide,then levels of NO(active medium of blood vessel)and ET1 before ischemia and at 10 min,30min and 2h after reperfusion were determined by nitratase reduction method;serum levels of ALT,AST,ALP,LDH enzymology,ATP and MDA in the liver tissues were determined as well.The hepatic tissue sample was taken at 2h and fixed with formalin to be made into specimen for observation of the ultrastructure of liver cells and hepatic lobules under electron microscope.RESULTS:After being treated by Bilobalide,serum NO level was elevated and the pathological elevated levels of ALT,AST and LDH were brought down,the microcirculation in ischemical reperfusion injury rats was improved and the extent of damage in the ultrastructure of liver cells was lessened in rats.CONCLUSION:Bypass of portal vein and inferior vena cava prior liver transplantation is helpful for the prevention of ischemical reperfusion injury of liver.The balance of NO/ET1 is possibly a factor influencing the blood flow in the microcirculation of transplanted liver.Bilobalide was proved to be of protective effect on ischemical reperfusion injury in rats.

Objective To analyse the effect of octreotide combined with compound coenzyme on Th17/CD4 +CD25 +Foxp3 + regulatory T cells imbalance in patients with purulent appendicitis.Methods 150 patients with acute suppurative appendicitis were randomly divided into experimental group and control group, 75 cases in each group.Patients of two groups underwent appendicitis laparoscopic resection, then the control group were given conventional treatment and experimental group were given subcutaneous injection of octreotide on the basis of conventional treatment.Th17, CD4 +CD25 +Foxp3 +regulation T cells ( Treg) , and Th17 /Treg balance were analyzed.ResuIts Compared with control group, Th17/Treg imbalance of experimental group recovered better: the proportion of Th17, Treg, and Th17/Treg ratio decreased (P<0.05); the expression levels of related transcription factor, RORγt and Foxp3 mRNA decreased (P<0.05); serum cytokine (IL-4, IL-6, IL-10, IL-17, IL-23 and TGF beta) and C-reactive protein (CRP) content decreased (P<0.05);serum interferon gamma (IFN-gamma) content increased (P<0.05).ConcIusion Octreotide combined with compound coenzyme could correct Th17/Treg imbalance in suppurative appendicitis patients, improve the immune function of patients and affect the prognosis of patients.

Objective To analyze health status and characters of health service demand and utilization among farmers and herdsmen in Kangxiwa and Saitula border areas from the altitude of 3700m to 4300m for offered scientific advices to the health management institutions for optimizing the allocation of health resources.Methods A total of 51 families in the Kangxiwa and Saitula areas in Karakorum-Kunlun Mountains were randomly chosen with stratified sampling method for the family health survey.Physical and biochemical examination were carried out for each herdsman.Results Among the participants,the most disease the two-week medical consultation rate was 1.74％.the hospitalization rate was 0.98％.The two-week medical consultation and hospitalization rate of herds were lower than the national and Xinjiang level for rural area.Herdsmen's doctor poor accessibility and low-income may be the main reasons for the underutilization of health services ;The difficult situation of herdsmen has been initially improved after participating in the new rural cooperative medical care.Conclusion The health status of native herdsmen in Kara Kunlun mountains was poor,and the provision of health services cannot meet the demand for health service of native herdsmen.It's necessary to improve efficiency of utilization of health service and optimize the allocation of health resources.

This study explored the possibility that the components in melanoma cytoplasm induce murine BMSCs transformation and expression of Melan-A by morphologically observing the changes of BMSCs and immunocytochemically detecting Melan-A in the cells after culturing BMSCs in medium containing melanoma cytoplasm components (MCC). MCC of B16 melanoma cells was prepared and BMSCs were cultured and induced by adding the MCC into culture medium. The cells were morphologically observed and Melan-A was immunohistochemically detected to confirm BMSCs transformation. MCC-induced BMSCs underwent morphological changes. A number of melanin granules appeared in the cytoplasm of the cells and some were released into surrounding areas. Several cells that might come from one cell formed a cluster, and their granules, together with those secreted by other induced BMSCs, formed a so-called "sphere-formed structure". The induced BMSCs expressed Melan-A. We are led to conclude that there might be some factors in the cytoplasm of melanoma cells that might induce BMSCs transformation toward melanogenic cell, or even melanoma.

OBJECTIVE: To investigate the mutation characteristics of common deafness gene from 127 non-syndromic hearing loss patients in Guangxi province. METHOD: Deafness-related gene mutations detection kit was used to detect 15 mutation sites in four deafness-associated genes, and a total of 127 hearing impaired patients were tested. The samples that could not be diagnosed with DNA microarray were subjected to PCR and sequenced to detect other mutations. RESULT Among the 127 patients with non-syndromic deafness, the total mutation rate is 8.66% (11/127), including GJB2 235delC homozygous in 3 cases (2.36%), 235delC single heterozygous mutation in 2 cases (1.57%), GJB2 235delC and 109 A > G mutations in 2 cases (1.57%); SLC26A4 1229C > T homozygous in 1 case (0.79%), IVS7-2A > G, IVS11 + 47T > C and 15448insC mutaion in 2 cases (1.57%); mitochondrial 12S rRNA gene mutations were not detected. The result indicates that GJB2 and SLC26A4 were the main genes in this study, and the mutation rate is significantly lower than the national average level. Three new mutations (SLC26A4 IVS11 + 47T > C,1548insC and GJB2 109A > G) were found. There may be rare mutations among sites or genes associated with deafness in Guangxi.
China ; Connexin 26 ; Connexins ; genetics ; DNA Mutational Analysis ; Deafness ; genetics ; Heterozygote ; Homozygote ; Humans ; Membrane Transport Proteins ; genetics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction ; RNA, Ribosomal ; genetics ; Sulfate Transporters

This study explored the possibility that the components in melanoma cytoplasm induce murine BMSCs transformation and expression of Melan-A by morphologically observing the changes of BMSCs and immunocytochemically detecting Melan-A in the cells after culturing BMSCs in medium containing melanoma cytoplasm components (MCC).MCC of B16 melanoma cells was prepared and BMSCs were cultured and induced by adding the MCC into culture medium.The cells were morphologically observed and Melan-A was immunohistochemically detected to confirm BMSCs transformation.MCC-induced BMSCs underwent morphological changes.A number of melanin granules appeared in the cytoplasm of the cells and some were released into surrounding areas.Several cells that might come from one cell formed a cluster,and their granules,together with those secreted by other induced BMSCs,formed a so-called “sphere-formed structure”.The induced BMSCs expressed Melan-A.We are led to conclude that there might be some factors in the cytoplasm of melanoma cells that might induce BMSCs transformation toward melanogenic cell,or even melanoma.

Glutamate serves as a major excitatory neurotransmitter in the mammalian central nervous system and is stored in synaptic deft by an uptake system that is dependent on the high-affinity glutamate transporters (ETTAs),which locate in the plasma membrane of glial cells and neurons.ETTAs can rapidly terminate the action of glutamate and maintain its normal physiological functions.If the content or function of glutamate transporters is abnormal,it can result in many physiological dysfunctions.Studies have demonstrated that high-affinity glutamate transporters play an important role in the development of chronic pain,which might be a new therapeutic target for the pain.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.