Objective To explore the prophylaxis and treatment strategies for psychic syndrome in patients after piggyback liver transplantation.Methods The data on the etiology,treatment outcome and prognosis of psychic syndrome occurring in 45 of 235 patients who had piggyback liver transplantation were retrospectively analyzed.Results The incidence of psychic syndrome complication was 19.1%(45/235),22 cases presented as mania(48.9%),5 cases as tristimania(11.1%),3 cases as hallucinosis(6.7%),1 case as suicidal tendency(2.2%),1 case as metamorphopsia(2.2%),8 cases as angst insomnia(17.8%),2 cases as maladjusted disturbance(4.4%),3 cases as affective disturbance(6.7%),and the majority presented as delirious alienation.All the cases were cured,except 1 case of coma,who was confirmed by CT to have intracranial hemorrage,died after failure of resuscitation.Conclusions The incidence of psychic syndrome in patients after piggyback liver transplantation is relatively high.However,most cases have mild symptoms and the prognosis is fine.When the patients have psychogenic symptoms,the prognosis of patients can be improved by some symptomatic treatment strategies directed to their different clinical manifestations.

Objective To observe the curative effect of continuous gastrointestinal decompression after gastric lavage with edible oil on saving patients with oral aluminum phosphide poisoning.Methods Seventy-eight patients with oral aluminum phosphide admitted to the Department of Internal Emergency of the Second People's Hospital of Yunnan Province from October 2009 to October 2016 were divided into a mild poisoning group (39 cases), a moderate poisoning group (26 cases) and a severe poisoning group (13 cases) according to clinical manifestations and laboratory examinations, all the patients were treated with continuous gastrointestinal decompression after early gastric lavage with edible oil, including scavenging toxicant, correcting intracellular oxygen intake and metabolic disturbance, and inhibiting and eliminating inflammatory mediators. The difference of remission times of clinical symptoms, recovery times of abnormal indexes and hospitalization times were compared among patients with different disease severities. Results With the aggravation of disease, the remission times of clinical symptoms (hours: from mild to severe were 24±12, 54±18, 84±12), recovery times of abnormal indexes (hours: from mild to severe were 18±6, 72±0, 108±12) and hospitalization times (hours: from mild to severe 48±24, 120±24, 144±24) were all gradually extended. Of the 13 patients with severe poisoning, 2 patients died of multiple organ functional failure (MOF) after 28 hours of treatment because they were incapable of cooperating with continuous gastrointestinal decompression. There were 76 patients were clinically cured, the cure rate being 97.4%. In the follow-ups at 1 month and 6 months after the treatment, no abnormalities were seen.Conclusion Continuous gastrointestinal decompression after early gastric lavage with edible oil for saving patients with oral aluminum phosphide poisoning is an effective therapy worthwhile to be popularized.

Objective To investigate expression of histone deacetylase 5 (HDAC5) in normal and colorectal cancer (CRC) tissues and its mechanism.Methods Immunohistochemistry was used to detect the expression of HDAC5 in CRC tissues.The relationship between HDAC5 expression content and survival prognosis was analyzed.Proliferation,immigration and apoptosis changes were observed after knockdown of HDAC5.Results Positive expression of HDAC5 in tumor tissue was related with poor prognosis of CRC patients,and HDAC5 could inhibit the LS174T cell proliferation by regulating the SIX1 expression.Conclusion Our results reveal that HDAC5 expression is variant in CRC tissues,and it is correlated with prognosis of colorectal cancer,and can affect cell proliferation by regulating the SIX1 expression.

Objective To investigate expression of histone deacetylase 5 (HDAC5) in normal and colorectal cancer (CRC) tissues and its mechanism.Methods Immunohistochemistry was used to detect the expression of HDAC5 in CRC tissues.The relationship between HDAC5 expression content and survival prognosis was analyzed.Proliferation,immigration and apoptosis changes were observed after knockdown of HDAC5.Results Positive expression of HDAC5 in tumor tissue was related with poor prognosis of CRC patients,and HDAC5 could inhibit the LS174T cell proliferation by regulating the SIX1 expression.Conclusion Our results reveal that HDAC5 expression is variant in CRC tissues,and it is correlated with prognosis of colorectal cancer,and can affect cell proliferation by regulating the SIX1 expression.

Objective Recent studies have indicated that early brain injury is the leading cause of death in patients with subarachnoid hemorrhage ( SAH) .Our study investigated the role of aminoguanidine ( AG) in early brain injury after SAH . Methods Sixty-eight male SD rats were equally randomized into four groups of equal number :control, sham, SAH, and AG.The animals in the sham group were injected with isotonic saline solution , while those of the latter two groups with femoral artery blood ( FAB) and FAB+AG, respectively, into the pre-chiasmatic cistern to induce SAH. At 24 hours after modeling , all the rats were killed for HE staining , obtainment of behavioral neurological assessment ( BNA ) scores by Garcia, measurement of the apoptosis of neurons by TUNEL , and de-termination of the expressions of the iNOS and NSE proteins by West-ern blot. Results The results of HE staining showed the presence of more red blood cells in the subarachnoid cavity of the rats in the SAH group, with a significantly decreased BNA score ( 14.47 ± 0.62) as compared with those in the control (17.94 ±0.24), sham (17.59 ±0.51), and AG group (15.71 ±0.47) (P<0.05). The rate of positive cells was remarkably higher in the SAH group ([42.38 ±2.38]%) than in the control ([6.35 ±0.94]%), sham ([6.85 ±0.69]%), and AG group ([30.48 ±2.89]%) ( P<0.01), with significant differences among the latter three groups (P<0.05).The expressions of iNOS and NSE were markedly higher in the SAH group ([3.86 ±0.07] and [1.59 ±0.06]) than in the control (0 and[0.35 ±0.09]), sham ([2.96 ±0.34] and [0.38 ±0.08]), and AG group ([3.41 ±0.04] and [0.70 ±0.12]) ( P<0.05).Both the expression levels of iNOS and NSE were positively correlated with the rate of positive cells (r=0 .879 and 0.935, P<0.01). Conclusion AG can alleviate early brain injury after SAH in SD rats by improving the neuro-ethologic function , suppressing the apoptosis of neurons , and reducing the expressions of iNOS and NSE .

This study performed to observe the effect of Yiqi Jianpi Shengjin recipe on Tfr/Tfh cell balance and autophagy expression in primary Sj?gren's syndrome(pSS)patients,and to explore the intervention mechanism of Yiqi Jianpi Shengjin recipe in treating pSS.We collected 60 cases of pSS with deficiency of both qi and yin from the Department of Rheumatology and Immunology of Anhui Provincial Hospital of TCM and randomly grouped them into experimental group and control group,with each group consisting of 30 cases.The control group was given a dose of hydroxychloroquine sulphate 0.2 g bid,the experimental group received an additional oral dose of Yiqi Jianpi Shengjin formula on top of the control group's treatment,and both continued to take it for 12 weeks.IL-10,IL-21 and IL-6 levels were measured by enzyme-linked immunosorbent assay,Tfh and Tfr cells ratios were measured by Flow cytometry,Western blot was used to detect the protein expression of Atg5,Beclin1 and LC3-Ⅱ/Ⅰ,and qPCR was used to detect the RNA expression of Atg5,Beclin1 and LC3.The indexes of inflammation,dryness,ESSPRI,ESSDAI and TCM syndrome integral before and after treatment were statistically analyzed.Data showed that the scores of corneal fluorescence stainin g in the experimental group were significantly lower and the static saliva flow rate was significantly higher compared with the control group.The experimental group showed a marked reduction in TCM,ESSPRI and ESSDAI score after treatment compared to control group.The expression of IL-21,IL-10 and IgG in the experimental group was markedly lower compa red with the control group.Tfr cells were significantly lower in the experimental group as compared to the control group.T he expression and ratio of autophagy protein and mRNA in the experimental group were significantly lower compared with t he control group.In conclusion,Yiqi Jianpi Shengjin recipe can effectively reestablish the balance of Tfr/Tfh cells,regulate cytokines,inhibit autophagy and activity,relieve clinical symptoms,delay disease activity,and improve the secretion of lacrimal gland and salivary gland.

The aim of this study is to investigate the mechanism by which triptolide(TP)ameliorates inflammation in adjuvant arthritis(AA)rats by inhibiting pyroptosis through the lncRNA GAS5/miR-21/TLR4 signaling axis.Rats were divided into 4 groups:normal control group(NC),model control group(MC),triptolide group(TP)and methotrexate group(MTX),with 6 rats in each group.The AA rat model was established,and the general state,right foot-plantar swelling and arthritis index were observed;HE staining was used to detect the histopathological morphology of synovial joints of rats in each group;ELISA was used to detect the levels of inflammatory factors IL-1β,IL-6,IL-18 and TNF-α;fluorescence quantitative PCR was used to detect the mRNA expression levels of Caspase-1,IL-1β,NLRP3,GSDMD,GAS5,TLR4,NF-κB and miR-21;and Western blot was used to detect the expression levels of Caspase-1,NLRP3,GSDMD,NF-κB,Caspase-4 and TLR4 proteins.Compared with the NC group,rats in the MC group showed significantly higher levels of swelling,arthritis index(P<0.05)and inflammatory cell infiltration;compared with the MC group,the levels of IL-1β,IL-6,IL-18 and TNF-α were decreased in the TP and MTX groups(P<0.05),and the levels of Caspase-1,IL-1β,NLRP3,GSDMD,TLR4,NF-κB,miR-21 mRNA expression decreased,GAS5 mRNA expression increased(P<0.05),and the protein levels of Caspase-1,NLRP3,GSDMD,NF-κB,Caspase-4 and TLR4 decreased(P<0.05);compared with the MTX group,the TP group showed lower levels of IL-1β,IL-6,IL-18,TNF-α(P<0.05),and lower expression levels of Caspase-1,IL-1β,NLRP3,GSDMD,TLR4,NF-κB and miR-21 mRNA(P<0.05).In conclusion,triptolide may inhibit the production of pro-inflammatory factors and inhibit pyroptosis through the lncRNA GAS5/miR-21/TLR4 signaling axis,thus ameliorate inflammation in AA rats.

Objective To explore the mechanism underlying the protective effect of α2-macroglobulin (A2M) against glucocorticoid-induced femoral head necrosis. Methods In a human umbilical vein endothelial cell (HUVEC) model with injuries induced by gradient concentrations of dexamethasone (DEX;10-8-10-5 mol/L), the protective effects of A2M at 0.05 and 0.1 mg/mL were assessed by examining the changes in cell viability, migration, and capacity of angiogenesis using CCK-8 assay, Transwell and scratch healing assays and angiogenesis assay. The expressions of CD31 and VEGF-A proteins in the treated cells were detected using Western blotting. In BALB/c mouse models of avascular necrosis of the femoral head induced by intramuscular injections of methylprednisolone, the effects of intervention with A2M on femoral trabecular structure, histopathological characteristics, and CD31 expression were examined with Micro-CT, HE staining and immunohistochemical staining. Results In cultured HUVECs, DEX treatment significantly reduced cell viability, migration and angiogenic ability in a concentration- and time-dependent manner (P<0.05), and these changes were obviously reversed by treatment with A2M in positive correlation with A2M concentration (P<0.05). DEX significantly reduced the expression of CD31 and VEGF-A proteins in HUVECs, while treatment with A2M restored CD31 and VEGF-A expressions in the cells (P<0.05). The mouse models of femoral head necrosis showed obvious trabecular damages in the femoral head, where a large number of empty lacunae and hypertrophic fat cells could be seen and CD31 expression was significantly decreased (P<0.05). A2M treatment of the mouse models significantly improved trabecular damages, maintained normal bone tissue structures, and increased CD31 expression in the femoral head (P<0.05). Conclusion A2M promotes proliferation, migration, and angiogenesis of DEX-treated HUVECs and alleviates methylprednisolone-induced femoral head necrosis by improving microcirculation damages and maintaining microcirculation stability in the femoral head.

Objective To explore the mechanism underlying the protective effect of α2-macroglobulin (A2M) against glucocorticoid-induced femoral head necrosis. Methods In a human umbilical vein endothelial cell (HUVEC) model with injuries induced by gradient concentrations of dexamethasone (DEX;10-8-10-5 mol/L), the protective effects of A2M at 0.05 and 0.1 mg/mL were assessed by examining the changes in cell viability, migration, and capacity of angiogenesis using CCK-8 assay, Transwell and scratch healing assays and angiogenesis assay. The expressions of CD31 and VEGF-A proteins in the treated cells were detected using Western blotting. In BALB/c mouse models of avascular necrosis of the femoral head induced by intramuscular injections of methylprednisolone, the effects of intervention with A2M on femoral trabecular structure, histopathological characteristics, and CD31 expression were examined with Micro-CT, HE staining and immunohistochemical staining. Results In cultured HUVECs, DEX treatment significantly reduced cell viability, migration and angiogenic ability in a concentration- and time-dependent manner (P<0.05), and these changes were obviously reversed by treatment with A2M in positive correlation with A2M concentration (P<0.05). DEX significantly reduced the expression of CD31 and VEGF-A proteins in HUVECs, while treatment with A2M restored CD31 and VEGF-A expressions in the cells (P<0.05). The mouse models of femoral head necrosis showed obvious trabecular damages in the femoral head, where a large number of empty lacunae and hypertrophic fat cells could be seen and CD31 expression was significantly decreased (P<0.05). A2M treatment of the mouse models significantly improved trabecular damages, maintained normal bone tissue structures, and increased CD31 expression in the femoral head (P<0.05). Conclusion A2M promotes proliferation, migration, and angiogenesis of DEX-treated HUVECs and alleviates methylprednisolone-induced femoral head necrosis by improving microcirculation damages and maintaining microcirculation stability in the femoral head.

Objective To improve the performance of auto-segmentation of prostate target area and organs-at-risk in online magnetic resonance image and enhance the efficiency of magnetic resonance imaging-guided adaptive radiotherapy(MRIgART)for prostate cancer.Methods A retrospective study was conducted on 40 patients who underwent MRIgART for prostate cancer,including 25 in the training set,5 in the validation set,and 10 in the test set.The planning CT images and corresponding contours,along with online MR images,were registered and input into a deep learning network for online MR image auto-segmentation.The proposed method was compared with deformable image registration(DIR)method and single-MR-input deep learning(SIDL)method.Results The overall accuracy of the proposed method for auto-segmentation was superior to those of DIR and SIDL methods,with average Dice similarity coefficients of 0.896 for clinical target volume,0.941 for bladder,0.840 for rectum,0.943 for left femoral head and 0.940 for right femoral head,respectively.Conclusion The proposed method can effectively improve the accuracy and efficiency of auto-segmentation in MRIgART for prostate cancer.