Alport syndrome is a hereditary glomerular basement membrane disease.Hematuria,sensorineural deafness and progressive renal function impairment is the main clinical symptoms.Alport syndrome can be associated with ocular abnormalities,and a few of patients were complicated with diffuse leiomyoma.The incidence of Alport syndrome with diffuse leiomyoma is low,and it mainly invades esophagus,the trachea and female genital tract,et al.Patients with Alport syndrome and diffuse leiomyoma have difficulty in swallowing and postprandial vomiting,recurrent bronchitis symptoms and dyspnea.Diffuse leiomyoma is commonly seen in the esophagus.Alport syndrome with huge esophageal and gastric leiomyoma is rarely seen in clinical practice.In this article,the imaging manifestations of Alport syndrome combined with huge esophageal and gastric leiomyoma is summarized to improve the understanding and diagnostic accuracy of this disease.

Objective　To study the effect of the combined use of aminoguanidine (AG) and cyclosporine A (CsA) on acute rejection following cardiac allograft. Methods　Except the control group, all other three groups were respectively treated by AG 600mg/kg every day subcutaneously 0 to 7 days after transplantation, low-dose CsA 2mg/kg every day i.m 0 to 7 days after transplantation, and low-dose CsA plus AG. Inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production during acute allograft rejection were detected at 4th day after operation, and the graft survival was observed.Results　Compared with the control group, iNOS expression and NO production were significantly inhibited in the AG-treated group (P＜0.05)，the progression of acute rejection was slightly attenuated and allografted heart survival prolonged. The inhibitory effects of iNOS activity and NO production in the recipients receiving the combined treatment of low-dose CsA plus AG were higher than those receiving low-dose CsA alone. Compared with the low-dose CsA group, low-dose CsA plus AG could significantly reduce the histologic grade of acute rejection (P＜0.01) and prolong the graft survival (P＜0.05). Conclusion　The combined use of low-dose CsA and AG could synergistically suppress iNOS activity and NO production, and significantly prolong allografted heart survival.

Objective To explore expression of IL -33 and IL -33 mRNA in peripheral blood of patients with ankylosing spondylitis,and analyze the clinical significance,so as to provide scientific reference for the treatment and prognosis of the disease.Methods From February 201 4 to May 201 6,32 patients with ankylosing spondylitis were included as study group,30 healthy persons were selected as control group.Real -time quantitative PCR and enzyme -linked immunosorbent assay were used to detect IL -33 mRNA level in peripheral blood and IL -33 level in plasma of subjects.Results Compared with the control group (1 .23 ±0.58),IL -33 mRNA in peripheral blood of patients in the study group was higher(1 .74 ±0.75),and the difference was statistically significant (t =2.981 , P =0.004).ELISA results showed that IL -33 level in plasma of the study group was higher (227.30 ±45.67)pg/mL than the the control group (1 1 4.70 ±39.58)pg/mL,the difference was statistically significant (t =1 0.344,P <0.01 ).Compared with the control group,the ESR,CRP and PLT of the study group were significantly higher[(47.80 ± 4.73)mm/h,(42.60 ±3.38)mg/L,(329.60 ±48.39)×1 09 /L](t =42.542,54.722,1 4.040,all P <0.01 ).IL -33 in plasma and IL -33 mRNA in peripheral blood of ankylosing spondylitis patients were positively correlated with BASDAI(r =0.472,0.457,all P <0.05),CRP(r =0.71 3,0.687,all P <0.05).Conclusion IL -33 and IL -33 mRNA in patients with ankylosing spondylitis significantly increase,indicates that they should play important role in the occurrence and development of ankylosing spondylitis.

Objective To investigate the expression of T help cell 1(Th1),T help cell 2(Th2)and related cytokines interleukin 12 (IL -12)and interleukin 4 (IL -4)in the lumbar disc herniation and their clinical significance. Methods 30 postoperative patients with lumbar disc herniation were included as observation group.The control group included 10 patients with lumbar fracture.Flow cytometry was used to distinguish the Th1 and Th2 cells.ELISA was used to measure the expression of interferon γ(IFN -γ),IL -12(the cytokines secreted by Th1 cells)and IL -4 (the cytokine secreted by Th2 cells).RT -PCR was used to detect the mRNA levels of STAT4 and STAT6.Results The distribution of Th1 /Th2 cells was higher in patients with lumbar disc herniation compared to the control group [(6.24 ±2.89)vs (25.12 ±3.20),t =16.26,P <0.05;(2.68 ±0.58)vs (8.16 ±1.20),t =3.84,P <0.05]. The levels of IFN -γand IL -12 in the study group were significantly higher than the control group,the differences were statistically significant[(23.47 ±5.61)vs (7.65 ±3.21),t =8.422,P <0.05;(1.52 ±0.87)vs (5.34 ± 1.39),t =8.135,P <0.05].The level of IL -4 was undetectable in the control group,however,IL -4 expressed in the study group.The expressions of IL -12,IFN -γand IL -4 in the study group were negatively correlated by Spearman correlation analysis (r =-0.57,P <0.05;r =-0.23,P <0.05).In addition,the mRNA level of STAT4 was higher in patients with lumbar disc herniation compared to the control group[(3.21 ±0.49)vs (1.12 ±0.24), t =13.15,P <0.05].Conclusion The expressions of Th1 cells,Th2 cells and related cytokines were participated in the pathogenesis of lumbar disc herniation.

OBJECTIVE To investigate the distribution and drug resistance of nosocomial infection pathogens in ICU from 2005 to 2008.METHODS Antimicrobial susceptibility test of 850 clinical isolates were carried out by means of K-B method.RESULTS Among 850 isolates,Gram-negative bacilli,Gram-positive cocci and fungi accounted for 68.9%,15.8% and 15.3%,respectively.ESBLs-producing strains accounted for 50% and 55.4% in E.coli and Klebsiella spp.MRS was detected in 82.7% of Staphylococcus.Imipenem and meropenem were the most active agents against strains of Enterobacteriaceae,Acinetobacter spp and Pseudomonas aeruginosa.No VRE or VRS strains were detected.CONCLUSIONS Gram-negative bacilli are the most frequent organisms in ICU.It is necessary to conduct drug resistance supervision of nosocomial infection pathogens in ICU and take measures to control nosocomial infection spread.

0.05).(4) There was significant correlation between CD62p and CD63 ( P 0.05). Conclusions Patients with cerebral infarction show evidence of enhanced platelet activation and increasment of MPV and MAR,which may relate to the pathological process of cerebral infarction. Moreover MPV and MAR can reflect the clinical severity of cerebral infarction better than PLT. Anti-platelet aggregation treatment should be further taken in patients with cerebral infarction.

OBJECTIVETo investigate the injury stress responses caused by ischemia reperfusion and its effects on the salivary secretory function of rat submandibular glands.

METHODSAn in situ ischemia reperfusion experimental model of rat submandibular glands was developed. The rat submandibular glands were subjected to 90 min of ischemia without denervation followed by reperfusion for 1, 12, 24, and 72 h. Salivary secretion, histological changes, reactive oxygen species (ROS) levels, and cellular apoptosis of the involved submandibular glands were detected after reperfusion.

RESULTSThe secretory function of the glands decreased at 1 and 12 h, and the saliva secretion gradually had the same value as that of the control sample 72 h after reperfusion. Increasing inflammatory cells infiltration, cellular atrophy, and tissue edema were observed especially after reperfusion for 12 h. The level of ROS and the number of apoptotic cells exhibited the same tendency, and higher ROS levels and more apoptosis cells 1 and 12 h after reperfusion were observed.

CONCLUSIONOur study suggests that ischemia reperfusion can cause a series of injury stress responses in submandibular glands, which might have an important function in the early phase dysfunction of transplanted submandibular glands.

Immunoprecipitation and Western-blot were performed to detect the expression of LGR8 in the testes in wild type (Wt) and Insl3-knockout ( KO ) mice.Testis were harvested from WT and KO mice on embryonic day 18 (E18) and on postnatal(P) 1,3,7,14,17,20,23,51,and 90 days.LGR8 staining in Leydig cells was stronger in all Wt mice than that in KO mice( all P＜0.05 ).LGR8 expression on spermatocytes varies with age.Strong stain on P1 Wt and postpubertal mice was concentrated in the developing and mature acrosome of spermatids

The influenza A virus (IAV) belongs to the family Influenza Virus and subfamily Orthomyxoviridae. The IAV can cause acute infections of the lower respiratory in human and animals. Recently, many studies have been performed to reveal the lung CD4+ T cells, CD8+ T cells and Tregs via multiple effector and regulatory mechanisms to against IAV. In this paper, we review the state of progress with regards to various strategies of IAV escape from T cell responses, T cells and innate T cells immunity against influenza virus, which will provide a useful reference tool for future related reseach.
Animals ; Humans ; Influenza A virus ; immunology ; physiology ; Lung ; immunology ; virology ; T-Lymphocytes ; immunology

Background Anti-VEGF drugs are generally applied in the treatment of ocular neovascular diseases.However,the therapy effect is unsatisfactory in some patients.Studing the effect of hypoxia-inducible factor-1 (HIF-1),a upstream regulatory gene of VEGF,and its limiting enzyme prolyl-4-hydroxylase domain proteins (PHDs) is of important clinical significance.Objective This study was to investigate the negtive regulation of exogeneous PHDs on HIF-1 pathway in human RPE cells.Methods pFLAG-PHD1,pFLAG-PHD2 and pFLAG-PHD3 plasmids were constructed by extracting RNA from Hela cell line and coloning PHD1,PHD2 and PHD3 using reverse transcription PCR with restriction enzyme.The plasmids were identified by gene sequencing.ARPE-19 cells were cultured at 21％ O2 (normoxia group),1％ O2 (hypoxia group),or in hypoxia-mimicking agents (CoCl2,anoxia group),respectively,and then were transfected with plasmids encoding FLAG-tagged PHD1,PHD2,PHD3 and pFLAGCMV2 transfected cells served as blank control.The expressional intensities of PHD1,PHD2 and PHD3 in the cells were detected and compared among different groups by using Western blot assay.The transcriptional activity of HIF-1 in the cells was evaluated with dual luciierase reporter assay.Results Western blot assay showed that PHD1,PHD2 and PHD3 all were expressed in ARPE-19 cells in the normoxia group,hypoxia group and anoxia group.The expression was strong in PHD2 protein and was weak in PHD3 protein,a statistically significant difference was found between PHD2 protein expression and PHD1 or PHD3 expressions (all at P＜0.05).Endogenous HIF-1 activity was elevated in pFLAG-CMX transfected cells in the hypoxia group and anoxia group than that in the normoxia group.Compared with pFLAG-CMX transfected cells,no obvious change was seen in the endogenous HIF-1 activity in the normoxia group,however,HIF-1 activity was declined in the hypoxia group and anoxia group after pFLAG-PHD1,pFLAG-PHD2 or pFLAG-PHD3 transfection.Under the same oxygen environment,HIF-1 activity was lower in the pFLAG-PHD2 transfected cells than that in the pFLAG-PHD1 or pFLAG-PHD3 transfected cells (both at P＜0.05).Conclusions PHDs play a negative regulation to HIF-1 activating pathway in human RPE cells,especially in hypoxia and anoxia cells.Among PHDs proteins,PHD2 presents the strongest inhibition on HIF-1 activating pathway.