Objective To prevent the prevalence of drug resistance viruses,we analyzed drug resistance mutations of HIV-1 among HIV-1 infected individuals in seven provinces of China.Methods We acquired 718 HIV-1 infected patients' treatment and compliance from questionnaires,amplified HIV-1 pol genes by RT-PCR and nest-PCR,sequenced RT and protease regions and run clustal with the subtype B consensus amino acid sequence in Stanford HIV drug resistance sequence database.Results The viral load in treated patients was obviously lower than that in untreated patients(P

BACKGROUND:Arthroscopic treatment of tibial eminence fracture requires tiny wire,induces less epiphyseal plate damage during operations,obtains strong fixations,alows early movement postoperatively,obviously attenuate the injuries,facilitate wound healing,and reduce complications.OBJECTIVE:To investigate the biocompatibility of arthroscopic reduction and wire fixation in treatment of fresh and old tibial eminence fractures.METHODS:Twenty-five patients with fresh and old tibial eminence fractures were treated with arthroscopic reduction and wire fixation from January 2010 to April 2012 in the Second People's Hospital of Yichang City.The postoperative fracture healing time and knee function improvement in the two groups were observed.RESULTS AND CONCLUSION: Compared with the fresh fracture patients,the fracture healing time was longer,Lachman test positive rate was higher in the old fracture patients than (P＜0.05),knee flexion and extension activity and Lysholm score were lower (P＜0.05).Experimental findings indicate that,arthroscopic reduction and wire fixation is a feasible clinical treatment of fresh and old tibial intercondylar eminence fractures.

Objective To evaluate the protective effect of epigallocatechin gallate (EGCG) against interleukin (IL)-17-induced injury to keratinocytes,and to explore its mechanism.Methods Some cultured HaCaT cells were divided into 3 groups to be treated with IL-17 alone at concentrations of 50,70,90 μg/L,respectively,with those receiving no treatment as the blank control group.Some HaCaT cells were divided into 5 groups:IL-17 group treated with 90 μg/L IL-17 alone,IL-17 + EGCG group treated with 90 μg/L IL-17 and 60 μmol/L EGCG,IL-17 + SP600125 group treated with 90 μg/L IL-17 and SP600125 (a JAK signaling pathway inhibitor),IL-17+ EGCG + anisomycin group treated with 90μg/L IL-17,60xmol/L EGCG and anisomycin (a Janus kinase signaling pathway activator),and blank control group receiving no treatment.After different durations of treatment,CCK-8 assay was performed to evaluate cellular proliferative activity,flow cytometry to detect cell apoptosis,enzyme-linked immunosorbent assay (ELISA) to measure expression levels of IL-6,IL-23 and IL-8,and Western-blot analysis to determine protein expressions of c-Jun N-terminal kinase (JNK) and phosphorylated JNK (P-JNK).Results IL-17 promoted cellular proliferation of HaCaT cells,and the proliferation rate,which was correlated with the concentration of IL-17,reached the maximum in the 90-μg/L IL-17 group (P ＜ 0.05).EGCG at 60 μmol/L significantly inhibited cellular proliferation of,promoted apoptosis in,and reduced IL-6,IL-23 and IL-8 expressions in,HaCaT cells induced by 90 μg/L IL-17 (all P ＜ 0.05).Compared with the IL-17 group,the IL-17 + EGCG group and IL-17 + SP600125 group both showed significantly decreased P-JNK expression,cell proliferation rate and IL-6,IL-23 and IL-8 expression levels (all P ＜ 0.05).However,compared with the IL-17 + EGCG group,the IL-17 + EGCG + anisomycin group showed significantly increased protein expression of P-JNK,cell proliferation rate and IL-6,IL-23 and IL-8 expression levels (all P ＜ 0.05).Conclusion EGCG protected against IL-17-induced injury to HaCaT cells,such as abnormal cell proliferation,apoptosis and inflammatory response,likely by inhibiting the JNK signaling pathway.

Study the infect of child anorexia granule on serum ghrelin and leptin of anorexia children and its clinical efficacy. Selected 81 cases of anorexia children aged 1-6 years old into treatment group (42 cases) and control group (39 cases), in addition, 30 case healthy children as healthy control group. The control group children were treated with domperidone suspension 0.3 mg x kg(-1) x d(-1), tid, orally 30 minutes before meals. Treatment group were treated with child anorexia granule, 1-3 years 1 package, bid; 4-6 years 1 package, tid; po, 4 weeks as a course of treatment. Study the change of serum ghrelin and leptin before and after therapy. The study demonstrates that before treatment, the serum ghrelin level of disease group was lower than healthy group (P < 0.01), and the serum leptin level was higher than healthy group (P < 0.01). After treatment, the serum ghrelin level both increase, and the serum leptin decline. And the change of treatment group was significantly different with control group (P < 0.01). And the clinical effective rate are 95.23% and 74.35% (P < 0.01). After 6 months of follow-up visit, the children weight significantly increase in treatment group (P < 0.01). Results indicate that child anorexia granule can facilitate secretion of ghrelin, and inhibit secretion of leptin, so as to work up an appetite. And the molecular mechanism is its infect on serum ghrelin, leptin.
Anorexia ; drug therapy ; metabolism ; physiopathology ; Appetite Regulation ; drug effects ; Body Weight ; drug effects ; Child ; Child, Preschool ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Ghrelin ; metabolism ; Humans ; Infant ; Leptin ; metabolism ; Male

Adult ; Humans ; Lipids ; blood ; Male ; Occupational Exposure ; Vanadium ; toxicity

ObjectiveTo investigate the action mechanism of CD20 lymphocyte infiltration in the renal allograft biopsy with chronic allograft nephropathy (CAN).MethodsCAN cases confirmed by renal biopsy within 2 years after renal transplantation served as study subjects. By using immunohistochemistry,the deposition of C4d and the CD20-positive lymphocytes infiltration in the renal grafts were examined.The clinical follow-up data were analyzed.ResultsForty-four cases of CAN were enrolled in the study, including 13 cases (29.5％ ) of CD20-positive lymphocytes infiltration,and 31cases (70.5％ )of CD20-negative lymphocytes infiltration. CD20-positive lymphocytes in biopsy showed nodular and scattered lymphocytes infiltration.There were 5 (26.3％)cases of CAN Ⅰ,4 cases (25.0％) of CAN Ⅱ,and 4 (44.4％) of CAN Ⅲ in CD20-positive group.There was no statistically significant difference between the only CAN group and CAN with AR group in CD20-positive rate.Immunohistochemical staining showed there were 12 cases (27.3％) with C4d linear deposition in peritubular capillary endothelial cells (PTC).C4d positive rate had no significant difference among the CAN classifications. There was no significant relationship between C4d deposition and CD20-positive lymphocytic infiltration.The average serum creatinine in CD20-negtive group and CD20-posigtive group was 140.8 ± 22.0 and 183.5 ± 25.5μmol/L before biopsy,and 165.6 ± 37.6 and 242.2 ± 59.1 μmol/L one year after biopsy.The average serum creatinine level in CD20-positive group was higher than in CD20-negtive group before and after biopsy.ConclusionProgressive chronic humoral immunity is high risk in the process of CAN. The CD20-positive lymphocyte infiltration has no relevance with CAN grade and C4d deposition in PTC,but is associated with circulating antibody PRA and allograft long-term outcome. Pathogenetic mechanism may not contribute to chronic humoral immune,but B cells presenting donor antigens,are recognized and activated by T cells as antigen-presenting cells.

BACKGROUND: It has reported that the combination of Tacrolimus and Wuzhi capsules can increase the peak concentration and area under curve of Tacrolimus recipients, however, the effects of this combination on recipients is poorly understood. OBJECTIVE: To investigate the effects of Wuzhicapsules on the blood concentration of Tacrolimus recipients. METHODS: A total of 38 renal transplantation recipients receiving triple therapy regime (Tacrolimus+mycophenolate +Prednisolone) were involved in the study and were divided into the experimental group (n=21) and control group (n=17). Recipients in the experimental group were taking Wuzhi capsules simultaneously, and those in the control group were not taking Wuzhicapsules. The Tacrolimus dosage to therapeutic concentration window and renal function were compared between the two groups at months 1,3 and 6 after transplantation. The incidence rates of acute rejection and diabetes mellitus, and renal and liver functions were observed at 6 months after transplantation. RESULTS AND CONCLUSION: The Tacrolimus dosage to therapeutic concentration window of the experimental group was significantly smaller than that of the control group (P < 0.05). However, incidence rate of acute rejection, diabetes mellitus, and renal and liver functions had no dramatically difference in 2 groups (P > 0.05). Results suggest that Wuzhi capsules may improve the immunosuppressive efficacy of Tacrolimus in renal recipients, therefore, can decrease the toxic effect of Tacrolimus with reduction dosage.

Objective To investigate the effects of colchicine on the proliferation and apoptosis of human Tenon's capsule fibroblasts (HTCFs) in vitro.Methods HTCFs were cultured in vitro,and the subcultured cells were identified.MTS assay was used to observe the inhibitory actions of colchicine on HTCFs at different concentrations.The apoptotic rates of the cells were detected by flow cytometry.The apoptosisrelated proteins,including PARP,Caspase-9,Caspase-3 and active-Caspase-3,were detected by Western blot.Results MTS assay showed that colchicine inhibited the proliferation of HTCFs in a dose-and time-dependent manner.Flow cytometry showed that colchicine induced a dose-dependent apoptosis of HTCFs for 48 hours,the apoptotic rates of 5 μmol · L-1,10 μmol · L-1 and 20 μmol · L-1 were (18.37 ±4.26)％,(33.80 ±5.02)％ and (52.00 ± 2.00)％,respectively,there were significant differences compared with the control (F =91.59,P ＜ 0.001).Western blot showed the activation of Caspase-3 and PARP followed by colchicine treatment.Conclusion Colchicine significantly inhibits the proliferation of HTCFs in vitro,and induced apoptosis,which may be associated with the activation of mitochondrial apoptotic pathways.

This article brought forward the adverse vocational education model-organizing lower level of undergraduates to participate in the work of public health specialty. This model enhanced their understanding of this work and urged more students to devote themselves in this area. Besides, questionnaires were used to know how alumni performed and what was needed for a future professional of public health.

Objective To evaluate effects of ursolic acid (UA) on interleukin?33 (IL?33) expression in HaCaT cells induced by interferon?γ(IFN?γ), and to explore their mechanism. Methods Some HaCaT cells were treated with UA at different concentrations(0, 0.1, 1, 5, 10, 20, 40 and 80μmol/L)for 24, 48 and 72 hours separately. Then, methyl thiazolyl tetrazolium(MTT)assay was conducted to evaluate cell proliferative activity. A cell model of inflammation was established by culture of HaCaT cells with the presence of 200μg/L IFN?γ. Some HaCaT cells were classified into several groups to be treated with IFN?γ(200μg/L)and UA(10 and 15μmol/L)alone or in combination (firstly treated with IFN?γ followed by UA treatment), and those receiving no treatment served as the blank control group. Reverse transcription PCR (RT?PCR) was performed to detect mRNA expressions of IL?6 and IL?33, and Western?blot analysis to measure IL?33 protein expression after 12?hour culture. The expressions of extracelluar signal?regulated kinase 1/2(ERK1/2)and phosphorylated ERK1/2(p?ERK1/2)were also measured by Western?blot analysis after 5?and 60?minute treatments with IFN?γand UA alone or in combination. Results MTT assay showed that the treatments with 5-20μmol/L UA for 24 hours had no effects on cell proliferative activity, while 40-80μmol/L UA could significantly inhibit it at 24, 48 and 72 hours (all P < 0.05). Thus, 10 and 15 μmol/L were chosen as the concentrations of UA for further study. After the treatment with 200μg/L IFN?γ, there was a significant increase in the expressions of IL?33 mRNA(0.812 ± 0.036 vs. 0.412 ± 0.021), IL?6 mRNA(0.947 ± 0.091 vs. 0.595 ± 0.030)and IL?33 protein(1.317 ± 0.119 vs. 0.147 ± 0.036)in HaCaT cells compared with the blank control group(all P<0.05). Compared with the IFN?γgroup, the IFN?γ+10?μmol/L UA group and IFN?γ+15?μmol/L UA group both showed significantly decreased expressions of IL?33 mRNA(0.447 ± 0.042 and 0.438 ± 0.028 respectively, both P<0.05), IL?6 mRNA(0.437 ± 0.099 and 0.350 ± 0.075 respectively, both P<0.05)and IL?33 protein(0.923 ± 0.058 and 0.564 ± 0.113 respectively, both P<0.05). There were no significant differences in IL?33 mRNA expression between the IFN?γ+10?or 15?μmol/L UA group and blank control group(P>0.05), while IL?33 protein expression was significantly lower in the IFN?γ+15?μmol/L UA group than in the IFN?γ+10?μmol/L UA group(P<0.05). The p?ERK1/2 protein expression significantly increased in HaCaT cells treated with IFN?γ for 5 and 60 minutes compared with the blank control group, but significantly decreased in the IFN?γ+15?μmol/L UA group compared with the IFN?γgroup(0.458 ± 0.053 vs. 0.941 ± 0.042 at 5 minutes, 0.302 ± 0.054 vs. 0.509 ± 0.032 at 60 minutes, both P < 0.05). However, no significant differences were observed in the total ERK1/2 protein expression between the IFN?γ+15?μmol/L UA group and IFN?γgroup at 5 or 60 minutes. Conclusion UA can suppress IL?33 expression in HaCaT cells induced by IFN?γ, likely by regulating expressions of the ERK signaling pathway?related proteins.