Antibodies, Viral ; blood ; Enzyme-Linked Immunosorbent Assay ; Humans ; Immunoglobulin G ; blood ; Metapneumovirus ; genetics ; immunology ; Paramyxoviridae Infections ; complications ; diagnosis ; Respiratory Tract Infections ; blood ; etiology ; pathology ; Reverse Transcriptase Polymerase Chain Reaction

Objective To observe the effect of ciclosporin(CsA) treatment on children with refractory nephrotic syndrome(NS).Met-hods Combination treatment of CsA[3-5 mg/(kg?d)] and prednisone were given 55 cases with refractory NS,in which including steroid-dependent NS(SDNS) 3 cases,steroid-resistant NS(SRNS) 22 cases,frequent-relapses NS(FRNS) 30 cases.Concentration of CsA was maintained 100-200 ng/L.Course of treatment was 10 months,the dose was tapered gradually in 4 months.Scr,BUN,Alb,ALT,Ccr,Chol,24 hours urine protein quantitation was measured before and after CsA treatment.Side effect of CsA was observed at the same time.SPSS 13.0 software was used to analyze the data.Results Forty-one cases(74.5%) were complete remission,6 cases(10.9%) were partial remission,total effective rate was 85.5%.Remission rate was 97.6% in simple type NS,50.0% in nephritis type NS,100% in SDNS and FRNS groups,63.6% in SRNS group.In group minimal change disease(MCD),the remission rate was 100.0%,while 60.0% in group mesangial prolife-rative glomerulonephritis(MsPGN),and 42.9% in group focal segmental glomerulosclerosis(FSGS).Fifteen cases(31.9%) relapsed when the dose of CsA was tapering.The adverse effects included hairiness(55 cases),gum hypertrophy(16 cases),hypertension(9 cases),gastroi-ntestinal tract reaction(8 cases),but no obvious nephric adverse effects were observed during the treatment process.Conclusion CsA is safe and effective on refractory NS children,especially to those with SDNS,FRNS and MCD.

Adenocarcinoma, Mucinous ; pathology ; Breast Neoplasms ; pathology ; Carcinoma, Ductal, Breast ; pathology ; Carcinoma, Renal Cell ; pathology ; Carcinoma, Squamous Cell ; pathology ; Cystadenocarcinoma, Mucinous ; pathology ; Cystadenoma, Mucinous ; pathology ; Female ; Giant Cells ; pathology ; Humans ; Osteoclasts ; pathology ; Ovarian Neoplasms ; pathology ; Pancreatic Neoplasms ; pathology ; Thyroid Carcinoma, Anaplastic ; Thyroid Neoplasms ; pathology ; Tongue Neoplasms ; pathology ; Urologic Neoplasms ; pathology

Objective To study the distribution of IL-10 and TNF gene polymorphisms in patients with gastroduodenal diseases in Hubei Han ethnic and their association with Helicobacter pylori (Hp) infection. Methods Six hundred and five patients with gastroduedenal diseases (196 chronic gastritis, 189 gastroduodenal ulcer and 220 gastric cancer) as well as 624 healthy controls were genotyped with PCR-RFLP method for IL-10-1082,-819,-592 and TNFα-308, lymphotoxin-α (LTα) Nco Ⅰ and AspH Ⅰ gene polymorphisms. Hp infection status was determined with ELLS& Results (1) There was significant difference of IL-10-1082 AG + GG genotype among the gastric cancer group with the non-malignant gastric diseases groups and healthy control group (P <0. 05). There was no significant difference of IL-10-592 and -819 gene polymorphisms among gastric cancer patients,non-malignant gastric disease patients and healthy controls (P>0. 05). The genotype frequencies of IL-10-819 were the same as those of IL-10-592. (2) Frequency of IL-10-1082 AG + GG genotype in gastric cancer patients with positive Hp was significantly higher than that in the other three groups (P < 0. 05). (3) Frequency of LTα Nco I AG genotype in gastric cancer patients with Hp infection was signiilcandy higher than that in Hp positive healthy controls (P < 0. 05). There were no other associations between TNFα-308, LTα Nco Ⅰ and AspH Ⅰ gene polymorphisms and Hp infection in gastroduodenal diseases. Conclusions (1) Allele AG + GG of IL-10-1082 was associated with gastric cancer in Han nationality of Hubei province. (2) IL-10-1082 AG + GG,LTct Nco ⅠAG heterozygous genotype may be associated with Hp infection in patients with gastric cancer in Han nationality of Hubei province.

AIDS-Related Opportunistic Infections ; complications ; microbiology ; Acquired Immunodeficiency Syndrome ; complications ; microbiology ; Adult ; Humans ; Male ; Penicillium ; pathogenicity ; Pharyngeal Neoplasms ; complications ; microbiology ; Pharynx ; microbiology ; pathology

OBJECTIVE:To provide reference for further formulation of the rational use of vancomycin. METHODS:Retro-spective analysis was conducted on the related information of discharged patients who intravenously used vancomycin from Jun. 2013 to Dec. 2014. RESULTS:178 patients were enrolled,with average age of 59.6 and 73.60% male,who were mainly with lung infectious(74.72%). Support examinations were sufficient before using of vancomycin. 66.29% patients were empirically giv-en vancomycin with pathogenic detection rate of 85.39%. 71.91% patients were conducted therapeutic drug monitoring with only 47.54% of first blood samples achieved the target range. CONCLUSIONS:Vancomycin application is generally rational in our hos-pital. However,issues like duration of empirical therapy,rational therapeutic monitoring,and individualized start dosing still need to be noticed.

AIM:To investigate the role of high glucose in primary hepatocytes of mice fed with a high fat di-et.METHODS:Male C57BL/6J mice were fed a high fat (45%of calories) diet ad libitum for 6 weeks to induce hepatic steatosis.Primary hepatocytes were isolated from the mouse liver by the 2 step collagenase perfusion method .The cells were incubated in low glucose ( 5 mmol/L ) , low glucose plus mannitol ( 30 mmol/L ) , or high glucose ( 35 mmol/L ) DMEM medium for 12 h.The cell viability , apoptosis , mitochondrial membrane potential , and caspase enzymatic activities were measured.Furthermore, proteins related to the stress-sensitive signaling pathway of regulating high glucose-induced apoptosis in primary hepatocytes were determined by Western blotting .RESULTS:Incubation with 35 mmol/L glucose re-sulted in a significant decrease in cell viability and an increase in apoptosis , whereas mannitol had no significant effect on the cell viability or apoptosis .A progressive depolarization of the mitochondria , an increase in cytosol cytochrome C and a dramatic decrease in mitochondrial cytochrome C in high-glucose stressed hepatocytes were observed .The enzymatic activi-ties of caspase-9 and caspase-3, but not caspase-8, were significantly increased in high glucose-stressed hepatocytes ( P<0.05).High glucose treatment suppressed the expression of Bcl-2 and Bcl-xL, while it increased the expression of the pro-apoptotic factor Bax .CONCLUSION:High glucose stress reduces mitochondrial membrane potential , initiates mitochon-dria-mediated apoptotic pathways and promotes apoptosis of hepatocytes with steatosis .This may be an important pathologi-cal mechanism of hyperglycemia-induced progression of nonalcoholic fatty liver disease .

Objective To investigate the immunological reaction,serum and liver ?-L-iduronidase(IDUA) activity after human fetal liver cells(FLCs) transplantation therapy on mucopolysaccharidosis(MPS) which attribute to IDUA defect.Methods FLCs were transplanted into IDUA deficiency mice.T cell subsets(CD3,CD4 and CD8) was detected by flow cytometry,while IL-2,TNF-? and IFN-? by ELISA,and serum and liver IDUA activity by fluorospectrophotometer at different stage(before transplantation and 5,10,15 days after transplantation).Results Human FLCs survived in IDUA deficiency mice,bringing elevated serum and liver enzyme activity to receptor.T cell subsets,IL-2,TNF-? and IFN-? was significantly higher 5,10 and 15 days after transplantation than those before transplantation(P

italic>γ-Aminobutyric acid (GABA) is a crucial inhibitory neurotransmitter found in various cells in the human body. While the GABAergic system is typically associated with the nervous system, recent research has revealed that immune cells and tumor cells also express components of this system. In the tumor microenvironment (TME), GABA is secreted to act extracellularly on other cells. GABA is metabolized via the GABA shunt and is involved in the tricarboxylic acid (TCA) cycle by generating succinate, which can provide energy for tumor cells. Activation of GABA receptors (GABARs) is a major pathway through which GABA participates in the regulation of antitumor immune responses. The activation of GABA type A receptors (GABA_ARs) can inhibit the activation and proliferation of T cells, elicit anti-inflammatory macrophages, and promote tumor cell growth and migration, while activation of GABA type B receptors (GABA_BRs) is generally considered to inhibit cancer cell migration and induce cancer cell apoptosis. In general, receptor activation inhibits immune cells, but the effect on tumor cells varies. Additionally, the downregulation of the expression levels of GABA transporters (GATs) is involved in tumor progression. Although antagonists of GABA metabolism and drugs that act on GABA receptors are considered therapeutic drugs for tumors, there have been few clinical studies conducted on them.