Objective:To investigate the impact of social determinants of health on the inequality of child health and health care utilization.Methods:Information of 1 118 children aged 0 to 16 is extracted from the Chinese Family Panel Studies(CFPS)year 2008 cross sectional survey data for the analysis.Age standardized concentration curves and concentration indices are employed to assess the inequalities for incidence of low birth weight,self reported good health,adequate timing of breast feeding,health insurance coverage and incidence of catastrophic health expenditures for these children.Concentration indices are decomposed to four levels of social determinants of health(community,family,mother and individual level)to understand their contributions to health inequality respectively.Results:There are health inequalities existing in the investigated children,among which social factors at mother and family level have the largest contribution.Conclusion:To respond to the call by the WHO to achieve health equity through action on the social determinants of health in a generation,the inequalities of health and health care utilization amongst Chinese children should be put on the policy agenda,and social policies should intervene from multiple social dimensions,especially from family and mother levels.

Aerenchyrna formation has been described in depth in a number of species at a histological level. But large gaps remain in our understanding of its regulation as a developmental process. It is attempted to analyse essential mineral elements like K, Mg, Cu, Zn, Ca and P in the cell wall of aerenchyma cells in petioles ofS. trifolia at five different developmental stages by CSEM-EDX technique. At early stage, K and Cl concentrations in cell wall were high up to 36% and 4.3% of dry weight, respectively. It supported the hypotheses that aerenchyma spaces are filled with liquid at early developmental stages of aerenchyma in S. trifolia petiole. Mg concentration was high at stage 2, up to 0.86% of dry weight. Zinc and Cu were detected only at rapid expansion stages, during which the concentrations were up to 1.5% and 2.5%, respectively. Calcium was detected in the cell wall only at mature stages, the concentration was high up to 1.3% of dry weight at stages 4 and 5. These results confirmed that the element concentration of aerenehyma cell wall undergoes dynamic changes during different developmental stages, and a low Ca with high Zn and Cu concentration are needed for cell expansion. Copper and Zn deposition in the cell wall showed a significant positive linear correlation, suggesting that these two elements share same or similar uptake and transport mechanism in plants.

OBJECTIVETo observe the expressions of Calbindin(CB) and Parvalbumin (PV), the two calcium-binding protein, in auditory pathway in mice of wild type C57BL/6J and kit⁺/kitW⁻ ²Bao, a kit gene mutant.

METHODSSix mutated kit gene kit⁺/kitW⁻ ²Bao mice and 6 wild type C57BL/6J (B6) mice were anaesthetized i. p. with chloral hydrate. After the mice were fixed by heart perfusion, the brains were removed and coronal sections were cut with a freezing microtome.

RESULTSWe found that wild type mice had significant expressions of PV on ventral cochlear nucleus, anterior part (AVCN), ventral cochlear nucleus, posterior part (PVCN), inferior colliculus (IC) and auditory cortex (AC). CB was expressed in wild type mice on PVCN and nucleus of the trapezoid body (Tz). The mutant of kit gene induced the less expression of PV on PVCN, IC and AC (P < 0.01), but increased the expression of Tz (P < 0.01). CB could not be observed on PVCN in mutant mice, and the expression of AC was increased( P < 0.01).

CONCLUSIONCB and PV has differential expression level in auditory pathway. Since mutated kit gene can affect expression of PV on PVCN, IC, Tz and AC, as well as CB on PVCN and AC, it suggests that the mutation of kit gene can affect the advanced function of central nervous system in auditory pathway.

Animals ; Auditory Cortex ; metabolism ; Auditory Pathways ; metabolism ; Calbindins ; metabolism ; Inferior Colliculi ; metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Parvalbumins ; metabolism ; Pons ; metabolism ; Proto-Oncogene Proteins c-kit ; genetics

Objective To study the effect of angiotensinⅡ(AngⅡ) on apoptosis in endothelial cells(EC). Methods Human umbilical endothelial cells were cultured in vitro and treated with AngⅡ in various concentrations alone and in combination with fumonisin B1(FB1, an inhibitor of ceramidase). TUNEL was employed to determine the apoptosis of the cultured EC. The bax mRNA and protein levels of EC were detected by RT-PCR and Western-blot techniques. Results The results showed that the number of apoptotic cells was significantly higher in AngⅡ-treated endothelium than in the control group(P0.05). Conclusion AngⅡ may induce apoptosis of endothelial cells via ceramide and up-regulating the bax mRNA and protein expression. Ceramide is the upper stream of bax and induces apoptosis by bax pathway.

Objective To establish the platelet antigen panel for identifying the specificity of platelet antibodies which cause platelet transfusion refractoriness and neonatal alloimmune thrombocytopenia and provide evidence for clinical therapy and platelet genotyping research.Methods Based on the frequency distribution of human platelet alloantigen (HPA)-1 to HPA-16 gene in China, the frequencies of HPA-1 to HPA-6,HPA-15 alleles in blood group O donors were genotyped by the polymerase chain reaction with sequence-specific primers (PCR-SSP) method, and suitable donors were chosen to establish platelet-specific antigen panel.Using the established platelet-specific antigen panel, the specificity of platelet antibodies caused by alloimmune reaction was identified by using simplified sensitized erythrocyte platelet serology assay (SEPSA).Results Eleven ptatelet donors with blood group O were chosen to establish platelet-specific antigen panel which can identify specificity of HPA-1 to HPA-6, HPA-15 antibodies.One case of HPA-4b (Penb) and two cases of HPA-15a (Govb) platelet specific antibodies were detected in 1 120 samples.Conclusion Identifying the specific platelet antibodies using platelet specific antigen panel has profound significance on increasing the safety and effectiveness of clinical platelet transfusion and prevention of neonatal alloimmune thrombocytopenia.

OBJECTIVETo discuss the clinical effects and superiority of applying external fixation and bone transport to treat osteomyelitis and bone defect of femoral bone.

METHODSFrom August 2008 to December 2013,16 patients with osteomyelitis and bone defect of femoral bone were treated including 11 males and 5 females with an average age of 42 years old ranging from 13 to 62 years old. The average course of disease was 18 months ranging from 2 months to 4.5 years, and the average length of bone defect was 7.8 cm ranging from 4.5 to 15 cm. The bone defect of all cases were treated by external fixation and bone transport, the bone transport began at 1 week after operation, 1 mm per day and 4 times per day.

RESULTSAll patients were followed up for 10 to 36 months (means 22.5 months). One patient did not cooperate with treatment leads to the failure, then took the amputation. The remaining 15 cases of osteomyelitis were under control, including 12 cases of bone transport achieved one stage bone union, 3 cases achieved bone union via bone graft from iliac bone. The bone union time was 5 to 13 months(means 7.9 months). Thirteen patients almost obtained the same length of two lower extremities,2 patients had shortening of 1.5 to 2 cm. The time of moving the external fixation was from 6 to 16 months (means 9.3 months).

CONCLUSIONApplication of external fixation and bone transport is an effective method in treating the osteomyelitis and bone defect that can control the infection, eradicate wounds, and be the equalization of limb length.

Adolescent ; Adult ; Bone Transplantation ; External Fixators ; Female ; Femur ; surgery ; Humans ; Male ; Middle Aged ; Osteomyelitis ; surgery

Background Congenital heart disease (CHD) is a diverse group of diseases determined by genetic and environmental factors.Considerable research has been done on genes associated with the development of the heart.Recently,focus is on the role of transcription factor NFATc1 in the development of proper valve and septa.As part of a larger study,high density single nucleotide polymorphism (SNP) scanning was used to explore the relationship between NFATc1 gene polymorphism and susceptibility to ventricular septal defect (VSD) in the Chinese Han population.Methods One hundred and ninety-two pediatric patients with congenital VSD and 192 matching healthy control subjects were studied.The haplotype reconstructions were calculated by PHASE2.0 software.Haploview software was used to perform linkage disequilibrium assessment and define haplotype blocks.The algorithm used for defining the blocks was the confidence interval method.Results The NFATc1 gene region can be divided into 11 haplotype blocks.Strong linkage disequilibrium existed within blocks 6,8,9,and 11.Three SNPs (rs7240256,rs11665469,and rs754505) within the NFATc1 gene had significant correlation with VSD by single marker association analysis.In addition,two haplotypes correlated with VSD.Conclusions NFATc1 is associated with the occurrence of VSD and it may be a predisposing gene to CHD in Han Chinese.This finding has set a direction for further genetic and functional studies.

Aim To explore whether edaravone (EDA), a novel free radical scavenger, protects H9c2 cardiac cells against doxorubicin ( DOX )-induced car-diotoxicity. Methods H9c2 cells were treated with 5μmol·L-1 DOX to establish a model of DOX cardio-toxicity. Cell viability was examined by cell counter kit ( CCK-8 ) . Changes in morphology and amount of ap-optotic cells were detected by Hoechst 33258 staining;intracellular level of reactive oxygen species ( ROS ) was measured by DCFH-DA staining and photofluorog-raphy;mitochondrial membrane potential ( MMP) was observed by rhodamine 123 ( RH123 ) staining and photoflurograph; the expression level of caspase-3 was determined by Western blot assay. Results Pretreat-ment of H9 c2 cells with 20 , 40 and 80 μmol · L-1 EDA for 60 min markedly inhibited cytotoxicity in-duced by 5 μmol · L-1 DOX, respectively, as evi-denced by an increase in cell viability. The protective effect induced by 40 μmol · L-1 EDA was maximal. Pretreatment of H9 c2 cells with 40 μmol · L-1 EDA for 30 , 60 , 90 and 120 min significantly attenuated DOX-induced cytotoxicity, respectively, having a max-imal protection at 60 min. Furthermore, pretreatment of H9 c2 cells with 40 μmol · L-1 EDA for 60 min be-fore exposure to 5 μmol · L-1 DOX for 24 h obviously reduced cardiac injuries, as evidenced by decreases in the DOX-induced intracellular ROS generation, num-ber of apoptotic cells, and expression of cleaved caspase-3, as well as loss of MMP. Conclusions EDA can protect H9 c2 cardiac cells against DOX-in-duced cardiotoxicity, this protection may be associated with inhibition of ROS production and preservation of MMP.

Objective To establish a stable cell line secreting human IgE Cε2-4 protein, and in-vestigate the binding capacity of receptor FcεR Ⅰ Methods The E24 gene was derived from SKO-O07 cell line, and was then cloned into pcDNA3.1 (+) (signal peptides were synthesized and fused at the 5'-end of E24 gene) or pCMV-L vector. After transient transfection into 293T cell, the secreted F24 protein was ana-lyzed by sandwich ELISA. The best vector was chosen to be transfected into CHO cells with LipofectAMI-NETM 2000 reagent. After being selected by G418 and subcloned three times by limited-dilution method, two stable cell lines were established. E24 gene was amplified by RT-PCR, and the E24 protein in the superna-tant was identified by ELISA. Besides, the binding capacity of FceR ⅠⅡ was analyzed by flow cytometry method. Results Three mammalian expression vector SP-E24-F3. 1, SP lI-E24-P3.1 and E24-PL were constructed and transient transfected to 293T cells. The output of E24 protein in the supernatant were 19.1, 19.4 and 8.7 μg/ml, respectively. Then the vector SP IX-E24-P3.1 was transfected into CHO cells. Final-ly, two single clones secreting E24 protein were stably obtained. The output of E24 were all at least 25 μg/ml. RT-PCR could detect the E24 gene from one of the two clones. Furthermore, flow cytometry results showed that E24 could bind the receptor in a dose-dependent manner. Conclusion Two stable cell line se- creting E24 protein were obtained, while E24 could specifically bind FcεR Ⅰ.

Objective To design and express a novel peptide based on ricin toxin antibody in E. coli, and to evaluate its biological activity. Methods Based on the crystal structure of ricin toxin A chain (RTA) and the RTA-rRNA interact in the complex model, the steric conformation of RTA was theoretical modeled and its functional domain was preliminarily determined. The humanized single-domain RTA antibody was designed rationally by computer-guidod molecular design method. Its coding sequence was ob- tained by overlapping extension PCR, and cloned into the pET-32a vector. The fusion protein was then ex-pressed in E. coli BL21 (DE3), identified by Western blot, and purified with Ni-NTA agarose. The binding and neutralizing activity of this novel peptide for riein was evaluated by competitive ELlSA assay and MTT assay. Results A recombinant human single-domain antibody expressing a polypeptide against RTA in the CDR3 loop was designed. The fusion protein was successfully expressed in E. coll. The purified protein can bind to ricin, and neutralize its activity in SP2/0 viability assay. Conclusion The success of the novel pep-tide based on riein toxin antibody provides a novel method to develop new generation of ricin antagonists.