This article reports a patient with hepatic coma who underwent artificial liver support therapy and liver transplantation successfully， and the patient recovered well in the later stage after active treatment. This article also discusses the timing of liver transplantation.

The standardized training system for physicians has been implemented for many years in China. Based on the current situation of neurosurgery specialist training and the sub-professional development, the study discusses the specific plan and direction of glioma sub-professional physicians training from the aspects of glioma sub-professional physicians training outline, training content, requirements of glioma sub-professional training base, training assessment methods and training management. It provided reference for the training of neurosurgical glioma professionals in China, so as to make glioma receive comprehensive and standardized treatment.

Purpose: Isocitrate dehydrogenase 1 (IDH1) mutations are the most common genetic abnormalities in low-grade gliomas and secondary glioblastomas. Glioma patients with these mutations had better clinical outcomes. However, the effect of IDH1 mutation on drug sensitivity is still under debate. Materials and Methods: IDH1-R132H mutant cells were established by lentivirus. IDH1-R132H protein expression was confirmed by western blot. The expression of ataxia telangiectasia mutated (ATM) signaling pathway and apoptosis-related proteins were detected by immunofluorescence and western blot. Temozolomide (TMZ) induced cell apoptosis was detected by flow cytometry. Tumor cell proliferation was detected by Cell Counting Kit-8. In vivo nude mice were used to confirm the in vitro roles of IDH1 mutation. Results: We established glioma cell lines that expressed IDH1-R132H mutation stably. We found that TMZ inhibited glioma cells proliferation more significantly in IDH1 mutant cells compared to wild type. The IC50 of TMZ in IDH1-R132H mutant group was less than half that of wild-type group (p < 0.01). TMZ significantly induced more DNA damage (quantification of γH2AX expression in IDH1 mutation vs. wild type, p < 0.05) and apoptosis (quantification of AnnexinV+propidium iodide–cells in IDH1 mutation versus wild type, p < 0.01) in IDH1 mutant gliomas compared to wild-type gliomas. The ATM-associated DNA repair signal was impaired in IDH1 mutant cells. Inhibiting the ATM/checkpoint kinase 2DNA repair pathway further sensitized IDH1 mutant glioma cells to chemotherapy. We found that IDH1 mutation significantly inhibited tumor growth in vivo (the tumor size was analyzed statistically, p < 0.05). Moreover, we confirmed that gliomas with IDH1 mutation were more sensitive to TMZ in vivo compared to wild type significantly and the results were consistent with the in vitro experiment. Conclusion These results provide evidence that combination of TMZ and ATM inhibitor enhances the antitumor effect in IDH1 mutant gliomas.

Purpose: Isocitrate dehydrogenase 1 (IDH1) mutations are the most common genetic abnormalities in low-grade gliomas and secondary glioblastomas. Glioma patients with these mutations had better clinical outcomes. However, the effect of IDH1 mutation on drug sensitivity is still under debate. Materials and Methods: IDH1-R132H mutant cells were established by lentivirus. IDH1-R132H protein expression was confirmed by western blot. The expression of ataxia telangiectasia mutated (ATM) signaling pathway and apoptosis-related proteins were detected by immunofluorescence and western blot. Temozolomide (TMZ) induced cell apoptosis was detected by flow cytometry. Tumor cell proliferation was detected by Cell Counting Kit-8. In vivo nude mice were used to confirm the in vitro roles of IDH1 mutation. Results: We established glioma cell lines that expressed IDH1-R132H mutation stably. We found that TMZ inhibited glioma cells proliferation more significantly in IDH1 mutant cells compared to wild type. The IC50 of TMZ in IDH1-R132H mutant group was less than half that of wild-type group (p < 0.01). TMZ significantly induced more DNA damage (quantification of γH2AX expression in IDH1 mutation vs. wild type, p < 0.05) and apoptosis (quantification of AnnexinV+propidium iodide–cells in IDH1 mutation versus wild type, p < 0.01) in IDH1 mutant gliomas compared to wild-type gliomas. The ATM-associated DNA repair signal was impaired in IDH1 mutant cells. Inhibiting the ATM/checkpoint kinase 2DNA repair pathway further sensitized IDH1 mutant glioma cells to chemotherapy. We found that IDH1 mutation significantly inhibited tumor growth in vivo (the tumor size was analyzed statistically, p < 0.05). Moreover, we confirmed that gliomas with IDH1 mutation were more sensitive to TMZ in vivo compared to wild type significantly and the results were consistent with the in vitro experiment. Conclusion These results provide evidence that combination of TMZ and ATM inhibitor enhances the antitumor effect in IDH1 mutant gliomas.

OBJECTIVE: To investigate the molecular mechanism underlying the inhibitory effect of propofol on pyroptosis of macrophages. METHODS: Macrophages derived from bone marrow were extracted and divided into three groups: control group, LPS+ATP group and propofol+LPS+ATP group. The control group was not given any treatment; LPS+ATP group was given LPS 1 μg/mL stimulation for 4 h, then ATP 4 mM stimulation for 1 h; Propofol+LPS+ATP group was given propofol+LPS 1 μg/mL stimulation for 4 h, then ATP stimulation for 1 h. After treatment, the supernatant and cells of cell culture were collected. the cell activity was detected by CCK8 and flow cytometry. The inflammatory cytokines IL-1βand IL-18 were detected by Elisa. Western blot was used to detect the expression of caspase-1 protein and TLR4 on cell membran Immunohistochemical fluorescence was used to detect apoptosis of cells. RESULTS: LPS+ATP significantly decreased the viability of the macrophages and increased the cellular production of IL-1β and IL-18, activation of caspase-1 protein and the expression of TLR-4 on the cell membrane ( < 0.05). Treatment with propofol obviously reversed the changes induced by LPS+ATP. CONCLUSIONS LPS+ATP can induce pyroptosis of mouse bone marrow-derived macrophages, and propofol effectively inhibits such cell death, suggesting that propofol anesthesia is beneficial during operation and helps to regulate the immune function of in patients with sepsis.
Animals ; Caspase 1 ; Lipopolysaccharides ; Macrophages ; Mice ; Propofol ; Pyroptosis

Objective To investigate the efficacy and safety of mesenchymalstem cells (MSCs)in improving the renal transplantation functional recovery of donation after citizens death (DCD)derived renal donors.Methods A retrospective analysis of 97 cases of DCD renal transplantation was performed in our center from July 2011 to December 2016.Among them,50 cases were treated with MSCs (the treatment group) and 47 cases without MSCs (the control group).In the treatment group,the umbilical cord stem cell suspension (50 mL,approximately 1 106/kg weight) was infused before vascular patency and 1 week,2 weeks,and 3 weeks after renal transplantation.Postoperative renal function within 3 months of recovery,delayed graft function (DGF) incidence and duration,the incidence of pulmonary infection,acute rejection and surgical complications were analyzed.Resuts The incidence rate of DGF and duration in the treatment group were 16.0％ and (14.42 ± 3.95) days,and those in the control group were 27.7％ and (17.85 ± 6.25) days respectively,and there were statistically significant difference.The incidence of acute rejection in the treatment group and the control group was 12.0 and 21.3％ respectively with the difference being statistically significant.The incidence rate of pulmonary infection in the treatment group and control group was 10％ and 12.7％respectively with the different being not statistically significant.Comparison of eGFR at 1st,1st month and 3rd month after operation showed that the eGFR in the control group was statistically significantly lower than that in the treatment group at 1st and 3rd month,but there was no significant difference in eGFR at 1st week between the two groups.There was no significant difference in the surgical complications between the two groups.Conclusion In the treatment group,the incidence rate of DGF was lower,and DGF duration was shorter than in the control group.The acute rejection rate in the control group increased significantly,but there was no significant difference in pulmonary infection and surgical complications between two groups.The recovery trend of renal function in the treatment group was better than that in the control group.

Objective To assess the association between the concentration of the air pollutant PM2.5 and daily outpatient visits for respiratory disease. Methods All records of daily outpatient visits to three hospitals in Shenzhen from January 1 to December 31, 2013 were collected. Daily air pollution monitoring and meteorology data from the same period were also collected in Shenzhen. The data were analyzed using a semiparametric generalized additive model with Poisson distribution of time series analysis controlling for long-term and seasonal trends, flu, DOW, public holidays, and meteorological factors. The excess risk (ER) of respiratory disease and its 95%CI value were calculated, along with the incremental increase of 10 μg/m3 in PM2.5 concentration. Results Number of outpatient visits for respiratory diseases totaled 1 428 672 (daily range:1 790-5 228). The annual average PM2.5 concentration was 40.2μg/m3 (daily range:7.2-137.1μg/m3). The lag1 factor had the most significant impact on the lag effect. We estimated that a 10 μg/m3 increase in day-before PM2.5 concentration was associated with a 1.809% (95% CI:1.709%-1.909%) ER of visits for respiratory disease. After controlling for other pollutants (NO2, CO, and O3), the effect remained stable. When NO2, CO, and O3 were introduced separately, for every 10μg/m3 rise in PM2.5 concentration, the excess risk of daily outpatient visits for respiratory disease was 1.814% (95% CI:1.706%-1.923%), 2.780% (95% CI: 2.668%-2.892%), and 1.513% (95% CI: 1.403%-1.624%), respectively. With simultaneous control of NO2 and O3, NO2 and CO, and CO and O3, for every 10μg/m3 rise in PM2.5 concentration, the excess risk of respiratory disease was 1.369% (95% CI: 1.242%-1.497%), 2.709% (95% CI: 2.590%- 2.828% ), and 2.577% (95% CI: 2.452%- 2.702% ), respectively. With simultaneous control of NO2, CO, and O3, for every 10μg/m3 rise in PM2.5 concentration, the excess risk of respiratory disease was 2.370% (95% CI: 2.231%-2.509%). Conclusions PM2.5 can increase the risk of outpatient visits for respiratory disease in Shenzhen.

Objective To assess the association between the concentration of the air pollutant PM2.5 and daily outpatient visits for respiratory disease. Methods All records of daily outpatient visits to three hospitals in Shenzhen from January 1 to December 31, 2013 were collected. Daily air pollution monitoring and meteorology data from the same period were also collected in Shenzhen. The data were analyzed using a semiparametric generalized additive model with Poisson distribution of time series analysis controlling for long-term and seasonal trends, flu, DOW, public holidays, and meteorological factors. The excess risk (ER) of respiratory disease and its 95%CI value were calculated, along with the incremental increase of 10 μg/m3 in PM2.5 concentration. Results Number of outpatient visits for respiratory diseases totaled 1 428 672 (daily range:1 790-5 228). The annual average PM2.5 concentration was 40.2μg/m3 (daily range:7.2-137.1μg/m3). The lag1 factor had the most significant impact on the lag effect. We estimated that a 10 μg/m3 increase in day-before PM2.5 concentration was associated with a 1.809% (95% CI:1.709%-1.909%) ER of visits for respiratory disease. After controlling for other pollutants (NO2, CO, and O3), the effect remained stable. When NO2, CO, and O3 were introduced separately, for every 10μg/m3 rise in PM2.5 concentration, the excess risk of daily outpatient visits for respiratory disease was 1.814% (95% CI:1.706%-1.923%), 2.780% (95% CI: 2.668%-2.892%), and 1.513% (95% CI: 1.403%-1.624%), respectively. With simultaneous control of NO2 and O3, NO2 and CO, and CO and O3, for every 10μg/m3 rise in PM2.5 concentration, the excess risk of respiratory disease was 1.369% (95% CI: 1.242%-1.497%), 2.709% (95% CI: 2.590%- 2.828% ), and 2.577% (95% CI: 2.452%- 2.702% ), respectively. With simultaneous control of NO2, CO, and O3, for every 10μg/m3 rise in PM2.5 concentration, the excess risk of respiratory disease was 2.370% (95% CI: 2.231%-2.509%). Conclusions PM2.5 can increase the risk of outpatient visits for respiratory disease in Shenzhen.

BACKGROUND:Bone mesenchymal stem cells have immunological regulation function both in vitro and in vivo, while the effect of bone marrow mesenchymal stem cells on CD4+T cellimmune function in patients receiving kidney transplantation remains unclear. OBJECTIVE:To explore the monitoring significance of CD4+T-cellimmune function by ImmuKnow assay and to determine the effect of induction therapy with bone marrow mesenchymal stem cells on cellimmune function in patients receiving kidney transplantation. METHODS:From January 2011 to June 2013, 24 patients receiving al ograft renal transplantation with autologous bone marrow mesenchymal stem cells were included and another 48 patients receiving al ograft renal transplantation and Simulect induction therapy with various matched preoperative characters served as controls. In both groups, adenosine triphosphate levels in CD4+T cells in the peripheral blood were determined by the ImmuKnow assay preoperatively and at 14, 30, 60, 90, 180 days postoperatively, as wel as during acute rejection and infection episodes. RESULTS AND CONCLUSION:During the 180 days postoperatively, fewer patients in the bone marrow mesenchymal stem cellgroup had acute rejection and injection than the Simulect group, but no significant differences were observed. Postoperative adenosine triphosphate levels in CD4+T cells were significantly lower than those determined preoperatively in both groups (P<0.05), while no significant differences were observed between the two groups. A total of 12 patients in the bone marrow mesenchymal stem cellgroup and 26 patients in the Simulect group had infection episodes, and the adenosine triphosphate levels in CD4+T cells during the infection episodes were lower than clinical stable patients in both groups (P<0.01). For patients receiving renal transplantation, induction therapy with bone marrow mesenchymal stem cells can effectively decrease the cellimmune function, which can be reflected by the adenosine triphosphate levels in CD4+T cells in the peripheral blood determined by the ImmuKnow assay.

Objective To evaluate the values of cell-mediated immune function in elderly renal allograft recipients.Method The levels of immuknowTM ATP was sequentially monitored by means of Cylex immuknowTM assay in 52 elderly renal allograft recipients including 11 with infection and 8 with acute rejection.Results No statistically significant difference was found between stable allograt function and uremia (P＞0.05).The levels of immuknowTM ATP during infection was significantly lower than those with stable allograft function with acute rejection (P ＜ 0.01).The levels of immuknowTM ATP during acute rejection was significantly higher than those with stable allograft function with infection (P＜0.01).Conclusion Sequential monitoring of immuknowTM ATP is helpful for elderly renal allograft recipients in individualized immunosuppression therapy.Cylex immuknowTM assay can be used as a potent tool for assessment of high risk in infection and rejection.