Objective To confirm the role of human parvovirus B 19 ( B19) infection in childhood immune thrombocytopenia ( ITP) patients.Methods A total of 416 cases of newly diagnosed childhood ITP patients from Jan .2011 to Dec.2013 had been summarized to be cases group , Then a total of 130 childhood patients with common respiratory tract infection were selected randomly as the control group . All patients had been divided in grouped by age as <1 years group(n=187), 1-3 years group(n=127), 3-7 years group(n=71), and 7-14 years group(n=31).The incidence rate of B19 infection in all age groups, the prognosis conditions in B19 infection positive and negative groups after the same therapy protocol were obserred .Results The B19 infection rate had no statistical significance in re-search groups and control groups .And no significant difference in the same age groups compared with control groups (all P>0.05) was found.All the ITP patients had not been given anti -B19 treatment.The PLT remission rate,respectively, after treated with the same pro-tocol including glucocorticoid and/or immunoglobulin had a declining trend as the ages increasing .The B19 infection groups of all ages al-so had no significant difference PLT remission rate had been confirmed in non -B19 infection patients in each age groups (all P>0.05). Conclusions B19 infection may not be a major cause in childhood newly ITP , and treatment protocol with no anti -B19 treatment had no influence on the clinical curative efficacy .

ObjectiveTo investigate the association between nucleotide polymorphisms (SNP) of rs2282430 and rs2031234 inSLC26A9 gene and clinical characteristics of asthma in Han children in central China.MethodsA case-control study was performed. Two hundreds and three children with asthma were recruited in this study and 221 normal children were selected as controls. The genotypes of two SNPs inSLC26A9 gene were examined using PCR-RFLP.ResultsBetween children with asthma and controls, the distribution of three genotypes (AA, AG and GG) in rs2282430 locus had signiifcant difference (P=0.042). The percentage of AA genotype was higher in children with asthma than that in controls. In implicit mode (AAvs. AG+GG), the two groups was statistically signiifcant difference (P=0.028). The frequency of A allele was higher in children with asthma than that in controls (P=0.011). Between children with asthma and controls, the distribution of three genotypes (TT, GT, and GG) in rs12031234 locus had no signiifcant difference (P=0.479). The frequency of alleles in rs12031234 locus also had no signiifcant difference (P=0.215). Among asthmatic children with different genotype of rs2282430, the lymphocytecounts (LYM), C-reaction protein (CRP), IgE, neutrophils (NEU%), and eosinophils (EOS%) were not signiifcantly different (P>0.05). Conclu-sionsThe rs2282430 polymorphism inSLC26A9 gene is associated with childhood asthma in the central China and the A allele is the risk factor. The rs2282430 polymorphism is not associated with LYM counts, CRP level, IgE level, NEU%, and EOS%.

This study chiefly aimed at investigating the effects of Dan Zhi Jiang Tang Capsule (DJC) on myocardial Toll-like receptor 4 (TLR4),tumor necrosis factor α (TNFα) and interleukin-8 (IL-8) and the cardiopathologic changes in diabetic rats.Fifty male rats,excluding 8 rats in the control group,had been administered with high fat forage for 4 weeks,which established the diabetic rat model combined with the intraperitoneal injection of streptozotocin (STZ) at 35 mg· kg-1.The established model rats were randomly divided into the model group,the DJC high-dose group,the DJC low-dose group and the pioglitazone group.The rats in the model group and the control group were intragastrically administered with DJC at 1.08 and 0.54 g· kg-1 each day,while those of the pioglitazone group were treated with pioglitazone at 10 mg· kg-1 each day,and those of the model group and control group with saline of the same volume.The administrations lasted 8 weeks with the continues high-fat diet.The levels of TLR4,TNFα and IL-8 protein in myocardium of the rats were determined,and so were the blood glucose,HbA1c and blood lipids.Compared with the control group,the expressions of myocardial TLR4,TNFα and IL-8 in the model group were significantly increased (P＜ 0.01).The expressions of TLR4,TNFα and IL-8 in the DJC high-dose and low-dose groups were significantly decreased (P＜0.05 or P＜0.01).The cardiopathological report showed severe myocardial lesion in the model group.However,myocardial lesion in the DJC high-dose group was significantly mitigated,which presented better therapeutic effects than the DJC low-dose group and the pioglitazone group.The levels of blood glucose,HbA1c,TG,TC,LDL-C in the model group were significantly higher than those in the control group (P＜0.05 or P＜0.01).The levels of blood glucose,HbA1c,TG,TC and LDL-C were significantly decreased in the DJC high-dose and low-dose groups in comparison with the model group (P＜ 0.05 or P＜ 0.01).In conclusion,DJC down-regulated the expressions of TLR4,TNFα and IL-8 and improved the degree of myocardial lesion in the diabetic rats,showing favorable hypoglycemic and lipid-lowering effects.

Objective To explore the clinical and genetic features of Rubinstein-Taybi syndrome (RSTS). Methods The clinical data of 2 children with RSTS were reviewed and analyzed. Results Two male children (3 years old and 4 months old) were admitted to hospital because of growth retardation. Both of them were characterized by short stature, language and motor retardation, excessive hairiness and cryptorchidism. Case 1 had slightly broad thumbs and toes, and case 2 had distinctive facial features of high arched palate, broad nasal bridge, ptosis, and obviously broad thumbs and toes. Cardiac dysplasia was found in both of them by echocardiography. The c.152T>G (L51X) heterozygous mutation was found in case 1 by high throughput sequencing and genomic chip technology, and this mutation has not been reported. Deletion of 2.5 Mb in chromosome 16p13.3 region was found in case 2. Conclusions The main clinical manifestations of RSTS are excess hair, deformity of thumbs and toes, deformity of the heart development, and growth retardation. Molecular detection can help the clinical diagnosis.

OBJECTIVE: To investigate the protective effect of protein kinase C (PKC) inhibitor rottlerin on rat renal vascular endothelial injury induced by lipopolysaccharide (LPS). METHODS: Rat renal microvascular endothelial cells cultured for 3-6 generations were divided into three groups according to random number table: blank control group in which cells were not challenged, LPS group in which cells were only stimulated by LPS 10 mg/L for 24 hours, and PKC inhibitor group in which cells were treated with PKC inhibitor rottlerin 2 μmol/L 30 minutes before LPS stimulation. The levels of tumor necrosis factor-α (TNF-α) and interleukins (IL-1β, IL-8) were determined by enzyme-linked immunosorbent assay (ELISA). Monolayer permeability was determined by Transwell assay. The expressions of PKC, RhoA and vascular endothelial-cadherin (VE-cadherin) were detected by Western Blot. The morphological characteristic and distribution of F-actin was measured by laser confocal fluorescence microscope. RESULTS: Compared with blank control group, the levels of inflammatory cytokines at 24 hours after 10 mg/L LPS stimulation were significantly increased in LPS group [TNF-α (ng/L): 397.3±25.4 vs. 46.8±8.9, IL-1β (ng/L): 76.7±11.2 vs. 12.6±3.2, IL-8 (ng/L): 574.5±31.4 vs. 73.2±9.6, all P < 0.05], the permeability of endothelial cells was significantly increased (A value: 1.32±0.03 vs. 0.36±0.02, P < 0.05), while the expressions of PKC and RhoA were significantly up-regulated (PKC/β-actin: 0.88±0.02 vs. 0.61±0.03, RhoA/β-actin: 0.96±0.01 vs. 0.49±0.03, both P < 0.05), VE-cadherin expression was significantly down-regulated (VE-cadherin/β-actin: 0.51±0.01 vs. 0.72±0.04, P < 0.05), and the F-actin distribution disorder had obvious stress fiber formation. Compared with LPS group, the levels of inflammatory cytokines were significantly lowered in PKC inhibitor group [TNF-α (ng/L): 127.4±14.6 vs. 397.3±25.4, IL-1β(ng/L): 43.2±7.8 vs. 76.7±11.2, IL-8 (ng/L): 212.7±18.2 vs. 574.5±31.4, all P < 0.05], the permeability of endothelial cells was significantly decreased (A value: 0.81±0.02 vs. 1.32±0.03, P < 0.05), the expressions of PKC and RhoA were significantly down-regulated (PKC/β-actin: 0.44±0.03 vs. 0.88±0.02, RhoA/β-actin: 0.63±0.05 vs. 0.96±0.01, both P < 0.05), the VE-cadherin expression was significantly up-regulated (VE-cadherin/β-actin: 0.69±0.03 vs. 0.51±0.01, P < 0.05), and the F-actin remodeling and stress fiber formation were significantly reduced. CONCLUSIONS PKC inhibitor could significantly attenuate the damage of vascular endothelial barrier induced by LPS, and plays an important role in endothelial cell barrier.
Acute Kidney Injury/prevention & control* ; Animals ; Endothelium, Vascular/drug effects* ; Interleukin-1beta ; Lipopolysaccharides/toxicity* ; Protein Kinase C/antagonists & inhibitors* ; Protein Kinase Inhibitors/pharmacology* ; Random Allocation ; Rats