Background:Dexamethasone can protect mice against the acute inflammatory liver injury by inhibiting innate immune cell function. However,the roles of T cell in this protective effect remain unknown. Aims:To investigate the regulatory effect of dexamethasone on T cell immune response in acute inflammatory liver injury. Methods:Six male C57BL/ 6J mice were randomly divided into 2 groups. One hour before induction of acute inflammatory liver injury by lipopolysaccharide, dexamethasone 5 mg/ kg and PBS were given intraperitoneally in experimental group and model group,respectively. All the mice were sacrificed 12 hours after model construction. The clinical score and liver function parameters were assessed;splenic mononuclear cells were isolated for measurements of T cell activation,as well as cytokine expression,secretion, and transcriptional factor expression for different T-cell subsets. Results:Clinical score and serum levels of transaminase were significantly lower in experimental group when compared with the model group. Meanwhile,percentage of CD44 +CD62L - T cells(i. e. activated or memory T cells)from spleen was significantly decreased in experimental group. Among splenic T cell population,expression and secretion of IFN-γ,a Th1-type cytokine,was decreased;expression and secretion of IL-4,a Th2-type cytokine,percentage of regulatory T cells(Treg cells),and ratios of Th2 / Th1 and Treg/ Th1 were increased;transcriptional factor specific for Th1 cells was down-regulated,and those for Th2 and Treg cells were up-regulated. Conclusions:Dexamethasone inhibits T cell activation and directs the reciprocal T cell lineage differentiation (repressing Th1 cell differentiation,promoting Th2 and Treg cell differentiation),which may contribute to the protection against acute inflammatory liver injury.

Objective To investigate the significance of renal tubular dysfunction in patients with refractoriness nephrotic syndrome(RNS)and the effect of interference treatment of Valsartan (VAL).Methods 79 cases of RNS and 68 healthy controls were recruited into the study. The 79 patients of RNS were divided randomly into the VAL group and the dipyridam group. On the basis of routine therapy, the VAL group was given VAL(80mg/d),and the dipyridam group taken dipyridam (150mg/d)orally for 12 weeks The glomerular tubular function(u-RBP,α1-MG,β2-MG,mAlb,NAG)were detected and the pathologic changes of tubukinterstitium were observed by using the methods of ELISA, biochemistry and scoring of the pathologic damage of tubulointerstitium before and after 12 weeks of VAL treatment in all of the cases. Results Urinary RBP,α1-MG,β2-MG,mAlb and NAG in all patients with RNS was evidently higher than that in healthy controls(P＜0.01).Those had positive correlations with damages of tubulointerstitium(r=0.436,0.626,0.499,0.668,0.657,P＜0.01).The interference outcome displayed that the excretion rates of urinary series of protein after oral use VAL in treatment group were markedly lower, while the control group had no distinct change. Conclusion There were various injury of tubulointerstitium and the disfiguration of renal tubular function in all cases with RNS. Damages of renal tubular function had positive correlation with tubulointemtitium injury and renal globular injury. Interference treatment with ARB in patients with RNS could improve renal tubular function, which is of great significance in delaying the progress of RNS.

Objective To explore the molecular mechanisms of hepatic stimulator substance (HSS) gene knockout in promoting the development and progression of nonalcoholic steatohepatitis (NASH).Methods NASH model mice (n=20) with HSS wild-type (HSS+/+) or HSS gene knockout (HSS-/-) were constructed using modified choline-deficient diet (CD-diet),untreated C57BL6-HSS-/-and C57BL6-HSS+/+ mice (n=20) were considered as control.Ten mice of each group were killed at month 1 and 2,respectively.The levels of triglyceride (TG) and total cholesterol (TC) in liver were measured using ELISA method.Histopathology and collagen deposition in liver tissue were observed using HE staining and Masson staining,respectively.Lipid content in liver tissue was observed and calculated using oil red O staining.The levels of mRNA and proteins of peroxisome proliferators activated receptor gama coactivator 1 alpha (PGC-1α),mitochondrial transcription factor A (TFAM),transcription factor-E2 related factor α (Nrf2),[-loop,dynamin-related protein 1 (Drp1),mitochondrial fission 1 protein (Fis1),mitofusins 1 (Mfn1),autophagy related gene 3 (Atg3) in liver tissue were detected using Real-time PCR and Western blot,respectively.Content of malonaldehyde (MDA),cyclooxygenase Ⅳ (COX Ⅳ) and adenosine tirphosphate (ATP) were measured using kits,and the activity of respiratory chain complex Ⅴ and cytochrome C oxidase in liver tissue were measured using spectrophotometry.the comparison between groups was done by t test.Results The levels of HSS mRNA and protein in mice-HSS-/-were 0.154± 0.04 and 0.08± 0.01,respectively,which were both significantly lower than those in mice-HSS+/+ (0.952 ± 0.08 and 1.362±-0.130,respectively),and t he differences had statistical significance (t =10.244 and 10.375,respectively,both P＜0.05).One month and 2 months after NASH modeled,TC contents in mice-HSS-/ were (248.6±21.5) μmol/g and (217.4±18.0) μmol/g,respectively,which were both remarkably higher than those in mice-HSS+/+ [(153.5 ± 11.2) μmol/g and (140.8 ±7.5) μmol/g,respectively],and the differences had statistical significance (t=15.270 and 10.524,respectively,both P＜0.05).The results form HE staining,oil red O staining and Masson staining indicated that fat deposition,collage deposition and inflammation in liver tissues of mice-HSS-/-were severer than those in mice-HSS+/+.One month after NASH modeled,protein levels of Drp1,Fis1,Mfn1 and Atg3 in liver tissues of mice-HSS-/ were all significantly decreased compared with those in mice-HSS+/+,and the differences had statistical significance (t=10.705,24.072,9.892 and 17.540,respectively,all P＜ 0.05).Two months after NASH modeled,protein levels of Drp1,Fis1,Mfn1and Atg3 in liver tissues of mice-HSS-/ were all significantly decreased compared with those in mice-HSS+/+,and the differences had statistical significance (t=125.378,15.926,34.330 and 13.437,respectively,all P＜0.05).One month after NASH modeled,mRNA levels of Drp1,Fis1,Mfn1 and Atg3 in liver tissues of mice-HSS-/-were all significantly decreased compared with those in mice-HSS+/+,the differences had statistical significance (t=36.337,40.825,33.508 and 28.104,respectively,all P＜0.05).Two months after NASH modeled,mRNA levels of Drp1,Fis1,Mfn1 and Atg3 in liver tissues of mice-HSS-/-were all significantly decreased compared with those in mice-HSS+/+,and the differences had statistical significance (t=35.210,42.375,27.753 and 20.560,respectively,all P＜0.05).The protein levels of PGC-1α,TFAM,Nrf2 and D-loop in liver of C57BL6-HSS-/-group were lower than those in liver of C57BL6-HSS+/+ group,and the differences had statistical significance (one month:t=20.548,31.036,19.445 and 10.974,respectively;two months:t=9.887,13.330,22.375 and 18.903,respectively,all P＜0.05).The mRNA levels of PGC-1α,TFAM,Nrf2 and D-loop in liver of C57BL6-HSS-/-group were all lower than those in C57BL6-HSS+/+ group,and the differences had statistical significance (one month:t=9.087,12.582,21.451 and 7.774,respectively;two months:t=23.758,17.924,9.924 and 15.209,respectively,all P＜0.05).One month and 2 months after NASH modeled,the levels of ATP mRNA in liver of C57BL6-HSS / group were both significantly lower than those in C57BL6-HSS+/+,and the differences had statistical significance 0=43.775 and 28.375,respectively,both P＜0.05);the levels of COXⅣ mRNA in liver of C57BL6-HSS / group were 0.142 ± 0.06 and 0.068± 0.001,respectively,which were both significantly lower than those in C57BL6-HSS+/+ group (0.255± 0.08 and 0.172 ±0.06,respectively),and the differences had statistical significance (t=28.337 and 19.782,respectively,both P＜0.05);the levels of MDA mRNA in liver of C57BL6-HSS-/-group were 0.973 ±0.112 and 1.253±0.054,respectively,which were both significantly lower than those in C57BL6-HSS+/+ group (0.366±0.02 and 0.872±0.05,respectively),and the differences had statistical significance (t=8.357 and 6.582,respectively,both P＜0.05).Conclusion Deletion of HSS accelerates NASH progression via inhibiting mitochondrial fusion,which leads to dysfunction of mitochondrial respiratory chain and inhibition of fatty acid oxidation.

Objective? To? explore? the? clinical? significance? of? early? oral? intervention? measures? in? the?prognosis?of?premature?infants.? Methods? 151?preterm?infants?admitted?to?neonatal?intensive?care?unit?(NICU)?of?Liaocheng?People's?Hospital?from?January?2015?to?January?2017?were?enrolled.?Premature?infants?were?divided?into?intervention?group?and?control?group?according?to?random?number?table?method?and?with?the?consent?of?legal?guardian.?Both?groups?received?routine?treatment?of?preterm?infants?after?stable?vital?signs.?The?intervention?group?received?the?oral?massage?method?adopted?by?none-nutritive?sucking,?stimulating?swallowing?function?and?SandraFucile?on?the?basis?of?routine?treatment,?once?a?day?for?14?consecutive?days.?Both?groups?were?followed?up?for?6?months.?The?oral?feeding?ability?of?premature?infants?was?evaluated?by?the?proficiency?(PRO),?rate?of?transfer?(RT),?feeding?process?and??non-nutritive?suction?(NNS).?At?40?weeks?of?postmenstrual?age?(PMA),?neonatal?behavioral?neurological?(NBNA)?was?used?to?assess?neonatal?brain?development;?Infanib?was?used?for?early?motor?development?evaluation?at?3?months?and??6?months?after?birth.? Results? Finally,?151?premature?infants?were?enrolled,?including?78?in?the?intervention?group?and?73?in?the?control?group.?The?time?to?complete?oral?feeding?of?the?intervention?group?was?significantly?shorter?than?that?of?the?control?group?(days:?18.1±3.7?vs.?23.4±5.8,?P??0.05).?Infanib?evaluation?at?3?months?of?age?showed?that?the?proportion?of?normal?children?in?the?intervention?group?was?significantly?higher?than?that?in?the?control?group?[67.95%?(53/78)?vs.?49.31%?(36/73),?P?

IL-22 is a member of IL-10 cytokine family. In recent years, increasing evidence has shown that IL-22 is closely related to the immunity in female reproductive tract, and its role in disease development is two-sided. It can not only maintain the balance of microbiota, enhance the resistance to pathogens and reduce the tissue damage caused by infection, but also promote the development and progression of malignant diseases via various signaling pathways. More studies on the biological characteristics and functions of IL-22 are needed for clarifying the pathogenic mechanism and providing new insight into the diagnosis and treatment of female reproductive tract diseases.