Objective To examine the association of pro-hepcidin with iron metabolism and inflammation in maintenance hemodialysis (MHD) patients with erythropoietin (EPO) resistance.Methods Forty MHD patients and twenty healthy controls were enrolled in the study.Among MHD patients,20 were hyporesponsive to EPO therapy and 20 were normal responsive to EPO therapy.Complete blood red cell count (RBC),Hb concentration,hematocrit (Hct),reticulocyte count (Ret),and serum ferritin (SF),serum iron (Fe),total ironbinding capacity (TIBC),saturation rate of transferrin (TSAT),transferrin (TF),hyper-sensitive C-reactive protein (hs-CRP),pro-hepcidin were measured in all the patients and controls.Differences were compared between groups.Influencing factors were analyzed by Pearson correlation.Predicting value of pro-hepcidin was investigated by ROC curve.Results Serum levels of SF,pro-hepcidin and hs-CRP were significantly higher in MHD patients than those in healthy controls (P＜0.01),while serum TF was lower in MHD patients (P＜0.05).Serum levels of SF,pro-hepcidin and hs-CRP were significantly higher in EPO resistant patients as compared to normal responsive cases (P＜0.01).Serum prohepcidin level was positively correlated with SF (r=0.843,P=0.000) and hs-CRP (r=0.695,P=0.001).In predicting EPO resistance,area under ROC curve of pro-hepcidin,SF and hs-CRP was 0.713,0.769 and 0.958 respectively.Conclusions EPO resistance is correlated with inflammation and iron metabolism.Serum pro-hepcidin,SF and hs-CRP may be used as markers of EPO resistance in MHD patients.

Objective To investigate the risk factors of trauma induced coagulopathy and its effect on the outcome of ICU patients with severe trauma.Methods Totally 223 severe trauma patients admitted to emergency ICU within 24h after injuring between June,2008 and September,2009 were retrospectively analyzed.Injury severity score (ISS),APACHE Ⅱ score,coagulation function,routine blood test,biochemical test,and blood gas assay were completed for each patient. Hypoperfusion was defined as vasoactive agents usage,or base deficit (BD) ≥ 6 or shock index ≥ 1. Patients were divided into coagulopathy group and non-coagulopathy (control) group according to coagulation function.ISS,APACHE Ⅱ score,the occurrence of hypothermia and hypoperfusion were compared between the two groups.The risk factors of trauma induced coagulopathy were analyzed,and the multivariate logistic regression equation was formulated.Coagulation function and incidence of trauma induced coagulopathy were compared between nonsurvival and survival group.Results Fifty-two of 223 (23.3 ％ ) patients met the criteria of trauma induced coagulopathy.Mortality rate in this group was significantly higher than that in non-coagulopathy group (36.5％ vs 9.4％, P ＜ 0.01 ). Patients in both groups had the comparability in age,sex, injury mechanism and time after trauma.ISS,the incidence of hypothermia,hypoperfusion and severe traumatic brain injury in coagulopathy group were higher than those in non-coagulopathy group ( P ＜ 0.01 ).GCS,hemoglobin,hematocrit,and platelet counts in coagulopathy group were significantly lower than that in noncoagulopathy group (P＜ 0.01).Base deficit ≥6,GCS ≤ 8,and platelet counts were considered as the independent risk factors involved in trauma- induced coagulopathy according to logistic regression in this study.Coagulation function of non-survivors also remarkably attenuated when compared with survival group.Conclusions The incidence rate of trauma induced coagulopathy is high in severe trauma patients admitted to ICU within 24h. Trauma induced coagulopathy correlates well with ISS core,severe traumatic brain injury,shock and hypothermia,and results in high mortality.

ObjectiveToevaluateourrevisedsyndromicalgorithmforthemanagementinpatientswithvaginaldischargeanddetermineitssensitivity,specificity,andpositivepredictivevalue(PPV).MethodsPatientswithvaginaldischargesyndromewereselectedintheirfirstvisitstotwoSTDclinicsinShanghaiandSichuan.Theyweremanagedaccordingtorevisedsyndromicflowcharts.Theetiologyofthesyndromewasdetectedbylaboratorytesting.ThedatawereanalyzedusingEPIINFOV5.0software.ResultsTherewere27(8.1%)patientswithgonorrhea,57(17.1%)withchlamydialinfection,and18(5.4%)withbothinfectionsin334patientswithvaginaldischarge.Thesensitivitywas70.6%,specificity54.7%,PPV40.7%,andnegativepredictivevalue(NPV)80.9%forthediagnosisofgonorrheaand/orchlamydialinfectionbysyndromicapproach.ConclusionThespecificityandPPVforsyndromicmanagementofvaginaldischargearenotsatisfied.Furthervalidationandrevisionareneededforsyndromicapproachesofvaginaldischarge.

Objective To observe the release of glutamate (Glu)and γ-amino butyric acid (GABA) from PC 12 cells induced by aconitine,and to study the intervention of Shuanghuanglian on the injury of these cells. Methods The cell proliferation test agent in cell counting kit(CCK-8)was applied to assay the aconitine toxicity to PC12 cells and to establish the PC12 cell injury model induced by aconitine. The PC12 cells during logarithmic growing phase were randomly divided into the following groups:blank control group(complete medium containing 0.1% dimethyl sulfoxide was added), Shuanghuanglian control group (complete medium containing 50 μg/mL Shuanghuanglian),baicalin control group(complete medium containing 20 μmol/L baicalin),aconitine toxic group(complete medium containing 100 μmol/L aconitine),Shuanghuanglian intervention group(complete medium containing 100μmol/L aconitine and 50μg/mL Shuanghuanglian)and baicalin intervention group(complete medium containing 100 μmol/L aconitine and 20 μmol/L baicalin). The cells in all groups were incubated for 24 hours respectively. The changes of PC12 cell absorbance(A)values were detected by CCK-8 assay before and after intervention by Shuanghuanglian and baicalin. The PC12 cell apoptosis was determined by flow cytometry. Glu and GABA contents in cell culture medium were determined by chromatometry and enzyme-linked immunosorbent assay (ELISA). Results Compared with blank control group,after the PC12 cells treated with 100 μmol/L aconitine for 24 hours,their cytoactivity was decreased markedly(A value:1.003±0.042 vs. 1.685±0.030,P<0.05),then afterwards in the experiment,the incubation of 100 μmol/L aconitine with PC12 cells for 24 hours was considered as the intervention concentration. In blank control group,the normal PC12 cells accounted for 95.89%,while in the aconitine toxic group,the rate of injured PC12 cells reached 64.27% and early apoptosis rate reached 45.46%, and in Shuanghuanglian intervention group and baicalin intervention group,the early apoptosis rate was decreased to 33.24% and 28.22% respectively. Compared with blank control group,there were no significant differences in cytoactivities and the contents of Glu and GABA released by PC12 cells in Shuanghuanglian control group and baicalin control group(all P<0.05),while in the aconitine toxic group,the cytoactivity was significantly decreased(A value:1.056±0.039 vs. 1.722±0.083),and the contents of Glu and GABA were significantly increased〔Glu(μmol/L):5.295±0.137 vs. 3.433±0.138;GABA(μmol/L):0.769±0.020 vs. 0.528±0.012,both P<0.05〕. Compared with aconitine toxic group,the cytoactivities of PC12 were significantly elevated(1.202±0.059 and 1.180±0.032),the levels of Glu were significantly reduced(4.055±0.086 and 3.984±0.057),and the contents of GABA were obviously increased(0.809±0.016 and 0.930±0.021)in the cell culture medium of the Shuanghuanglian intervention group and baicalin intervention group(all P<0.05). The increase of cytoactivity in Shuanghuanglian intervention group was more marked than that of baicalin intervention group(P<0.05). There were no statistical significant differences in contents of Glu and GABA between Shuanghuanglian intervention group and baicalin intervention group(both P>0.05). Conclusions The changes of Glu and GABA may be one of the mechanisms of neural toxic effect of aconitine. Shuanghuanglian possibly can decrease Glu level and increase GABA content by way of its main component baicalin to antagonize the aconitine neurotoxicity.

Objective To investigate the effects of trimebutine maleate (TM) on the expression of large conductance calcium-activated potassium channel (BKCa) and ryanodine receptors (RyR)channels at mRNA and protein level in colonic smooth muscle cell of cold restraint stress(CRS)induced rats.Methods A total of 24 Wistar rats were divided into CRS group,CRS with TM group and control group equally.The rats of CRS group were gavaged with 0.9％NaCl (6 ml/kg) daily; the rats of CRS with TM group were gavaged with 15 g/L TM (6 ml/kg) daily and activity was restricted in wire cage at 4 ℃ for two hours,continuously for five days.The rats of control group were gavaged with 0.9 ％ NaCl (6 ml/kg) once without CRS.The amount and characteristics of stool of rats in each group were observed.The colonic smooth muscle was isolated to detect the expression of BKCa and RyR at mRNA and protein level by reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot.Results The median of rats defecation particles of CRS group was six,control group was one and CRS with TM group was five.Compared with control group,the defecation appearance of CRS group and CRS with TM group was looser and wetter observed by naked eyes.Compared with control group,there was no obvious pathological changes in CRS and CRS with TM group.There was no significant difference in the mRNA expression of BKCa and RyR channels between control group and CRS group.Compared with control group,the BKCa expression at mRNA level of CRS with TM group increased 1.45 fold.Compared with control group,the RyR2 expression at mRNA level of CRS with TM group increased 1.32 fold.Compared with control group,the BKCa expression at protein level of CRS with TM group increased 1.39 fold,and there was no RyR2 expression band at protein level.Conclusion TM might affect colonic smooth muscle contraction through the upregulation of BKCa expression at mRNA and protein level and RyR expression at mRNA level.

Objective To investigate the interference effect of baicalin on acute brain injury induced by aconitine in rats and its mechanism. Methods A total of 200 Sprague-Dawley(SD)rats were randomly divided into five groups:normal control,baicalin control,aconitine poisoning,baicalin 15 mg/kg intervention and baicalin 30 mg/kg intervention groups(each,n=40). Aconitine(20μg/kg)was given via tail vein in aconitine poisoning group. The rats in the normal control group and baicalin control group were respectively injected with saline 2 mL/kg and baicalin 30 mg/kg via tail vein. The aconitine poisoning rats were given with baicalin at the dose of 15 mg/kg and 30 mg/kg respectively in the low and high dose baicalin intervention groups within 2-3 minutes after injection of aconitine. Rats in all groups in the study were anesthetized and sacrificed at 1,6,12,24 hours after various agents were respectively given in the groups,the rat cerebral cortex samples were collected,the histological changes in normal and baicalin control groups and pathological changes of the aconitine poisoning rats were observed,the levels of glutamate(Glu),aspartate(Asp),γ-aminobutyric acid(GABA),glycine(Gly)were detected and the apoptotic cells were determined at the above time points. Results Compared with the normal control group,the aconitine poisoning group had significantly higher levels of excitatory amino acids Glu and Asp and the number of apoptotic neurons. After exposure to aconitine for 1 hour, the levels of inhibitory amino acids of GABA and Gly were markedly decreased in the rat cortex in the poisoning group compared to the normal control group(both P<0.05),at 6 hours and 12 hours they were significantly increased and after 24 h,they began to decline,but still maintained at relatively high levels. Compared with the aconitine poisoning group, after baicalin intervention for 1 hour,in the 15 mg/kg and 30 mg/kg baicalin intervention groups,the levels of Glu and Asp were markedly decreased〔Glu(μmol/L):309.39±14.59,307.22±23.69 vs. 370.46±40.31,Asp(μmol/L):143.43±8.36,129.12±4.86 vs. 222.97±6.26〕,while the levels of GABA and Gly were increased〔GABA(μmol/L):55.91±4.76,59.61±13.11 vs. 32.05±2.20,Gly(μmol/L):32.33±1.85,33.90±0.66 vs. 21.96±4.75〕,and the number of neuronal apoptosis was obviously decreased(cell/mm2:18.65±4.10,14.80±1.89 vs. 58.15±3.68,both P<0.05). Under microscope and electron microscope,the pathological and ultrastructural changes indicated that the aconitine poisoning group had the most marked cerebral cortex damage at 12 hours after poisoning,while the two baicalin intervention groups showed milder damage than that in aconitine poisoning group. Conclusions The neural toxic effect of aconitine in rats may be related to the imbalance between the neurotransmitter contents of excitatory Glu. Asp and inhibitory GABA,Gly in the cerebral cortex. Baicalin can decrease the contents of excitatory amino acid and elevate the inhibitory amino acid,therefore it may ameliorate the cerebral injury of acute aconitine intoxication in rats.

Objective:To explore the prognostic factors of patients with Vibrio vulnificus sepsis. Methods:The clinical data of 67 patients with Vibrio vulnificus sepsis from January 2008 to December 2019 in the First Affiliated Hospital of Wenzhou Medical University were retrospectively analyzed. Univariate analysis was used to compare the differences in general information, clinical manifestations, admission laboratory indicators, antibiotics and surgery between the death group and the cured group. Then the factors with significant difference in univariate analysis were included in multivariate analysis, and the factors of prognosis were obtained. Results:Univariate analysis showed that there were significant difference in liver disease, admission with hypotension shock, multiple limb injuries; admission leukocytes, platelets, pH value, albumin, lactic acid, aspartate aminotransferase, creatinine, procalcitonin, creatine kinase, activated partial thromboplastin time, prothrombin time between the death group and the cured group (all P <0.05). Multivariate analysis showed that admission lactate ( OR=0.628, 95% CI: 0.461-0.855, P=0.003), albumin ( OR=1.330, 95% CI:1.062-1.667, P=0.013), creatine kinase ( OR=0.999, 95% CI: 0.998-1.000, P=0.016) and admission surgery time ( OR=0.118, 95% CI: 0.015-0.938, P=0.043) were risk factors of the prognosis. Patients with high lactate, creatine kinase and low albumin at admission indicate poor prognosis; patients with admission surgery time≤ 12 h have better prognosis. Conclusion:For the treatment of patients with Vibrio vulnificus sepsis, medical staff should dynamically evaluate these prognostic factors in the early stage, and early surgical treatment should be adopted to improve the prognosis of patients.

Objective To investigate the change in NF-κB activity in astrocytes in spinal dorsal horn in a rat model of neuropathic pain and the underlying mechanism. Methods Sixteen male SD rats aged 2-3 months weighing 220-280 g were randomly divided into 2 groups ( n = 8 each) : sham operation group (group S) and CCI group. Neuropathic pain was induced by chronic constrictive injury (CCI) . Right sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 chromic catgut. In group S the right sciatic nerve was exposed but not ligated. The paw withdrawal threshold (PWT) to von Frey filament stimulation and paw withdrawal latency (PWL) to radiant heat stimulation were measured at 1 d before (baseline) and 7 d after operation. The animals were then killed and the lumbar segment of the spinal cord (L_(4-6)) was removed. The expression of NF-κB in the astrocytes in spinal dorsal horn was determined by immuno-histochemistry. Results PWT and PWL to mechanical and thermal stimuli were significantly decreased after operation as compared with the baseline before operation in group CCI. The number of NF-κBp65 immunoreaction positive cells in the spinal dorsal horn on the operated side was significantly larger in group CCI than in group S. Conclusion NF-κB signal transduction pathway in the astrocytes in the spinal dorsal hom may be involved in neuropathic pain.

Objective To investigate the relationship between Klotho and autophagy in sepsisinduced acute kidney injury mice model.Methods The male healthy Balb/c mice were used to establish the model of sepsis-induced acute kidney injury by using cecal ligation and puncture (CLP).Mice were sacrificed at 3 h,6 h,12 h,1 d,2 d,3 d,and 5 d after CLP (n =12 for each interval) and on 1 d 6 mice in sham group as well as 6 mice in normal group were sacrificed at the same time.Scr and BUN in the blood serum were detected.The HE and PAS staining were employed for observation on the histopathological changes in kidney tissues under light microscope.The autophagosomes were observed under transmission electron microscope (TEM).The renal protein of Klotho,LC3 and P62 were detected by using Western blot and Immunohistochemistry.Statistical analyses were performed using Student's t-test by SPSS 23.0.software.Results Scr and BUN increased significantly after CLP,especially on 1 d,respectively (165.64 ± 20.56) μmol/L and (45.51 ± 4.05) mmol/L.HE and PAS staining showed renal tissue was damaged obviously 1 d after CLP,as indicated by desquamation of the brush border of proximal tubular epithelial cells,appearance of bare basement membrane,and interstitial inflammatory cell infiltration.Under TEM,autophagosomes and phagocytosis were observed.Compared with sham group,the expression of Klotho protein decreased gradually from 3 h to 1 d and dropped to the trough at 1 d (t =51.851,P ＜0.01),then resumed gradually from 2 d to 5 d.On the contrary,the activation of autophagy increased as indicated by the expression of LC3-Ⅱ/L3-Ⅰ and p62.Autophagy was induced gradually from 3 h to 1 d and reached peak at 1 d,then declined gradually from 2 d to 5 d (P ＜ 0.01).The protein of Klotho and LC3-Ⅱ mainly distributed in renal tubular cytoplasm,and Klotho was reduced significantly (t =-8.371,P ＜ 0.01) and LC3-Ⅱ appeared in high density remarkably (t =4.995,P =0.001) on 1 d after CLP.Conclusions Klotho protein reduction and autophagy protein increase were observed in sepsis-induced acute kidney injury,and the expressions of Klotho and autophagy acted out in certain extent of time dependence.

Objective To discuss the feasibility,safety and efficacy of robot-assisted laparoscopic buccal mucosal ureteroplasty in the treatment of long segment upper ureteral stricture.Methods Five patients with complex ureteral strictures were treated with robot-assisted laparoscopic buccal mucosa ureteroplasty (5 males;right side,2 cases;left side,3 cases) in our hospital from March to July of 2017.The patients aged 25-40 years with median of 35 years old.The median body mass index was 23.5 kg/m2 (19-29 kg/m2).Data of surgical conditions,postoperative complications,and follow-up were collected.Results All patients were treated with robot-assisted laparoscopic buccal mucosa ureteroplasty and the operations were uneventful.The median length of stricture of upper ureter were 3 cm (2-6 cm).The median operation time was 360 min (200-400 min),median blood loss was 100 ml (50-200 ml),drainage tube retained time was 5 d(2-9 d),post-operative hospital stay was 11 d(7-12 d),and the median creatinine value was 85 μmol/L (76-98 μmol/L).No urine leakage,infection,buccal mucosa necrosis or other serious complications occurred after surgery.Five patients' CT examnation showed improved hydronephrosis 3 weeks post-operatively.DJ stent was removed 3 months after surgery in 2 patients,and 1 patient presented with no hydronephrosis,another one with mild hydronephrosis.DJ stent was removed 6 months after surgery in the other 3 patients with improved hydronephrosis.Conclusions Robot-assisted laparoscopic buccal mucosal ureteroplasty for the treatment of long segment upper ureteral stricture is a safe and feasible procedure,with a good short-term effectiveness and without severe complications.