青年军人与大学生睡眠质量及影响因素比较

目的:比较青年军人和大学生的睡眠质量及影响因素。方法:整群抽取556名青年军人和571名大学生,采用匹兹堡睡眠质量指数、人际关系综合诊断量表、心理弹性量表、社会支持量表进行调查。结果:青年军人和大学生的睡眠问题检出率分别为27.9%和10.2%;睡眠质量、人际困扰的类别和资历(年级)的交互作用显著,心理弹性和社会支持的类别和资历(年级)的主效应显著。人际困扰对青年军人睡眠质量变异解释率最高,心理弹性对大学生睡眠质量变异解释率最高。结论:青年军人的睡眠问题较青年大学生严重;随着资历(年级)的增加,青年军人的睡眠质量呈下降趋势,而大学生的睡眠质量保持稳定。需要采取不同措施改善青年军人和大学生的睡眠状况。     

Periostin expression contributes to cortical bone loss during unloading

Periostin (a product of Postn gene) is a matricellular protein which is increased in periosteal osteoblasts and osteocytes upon mechanical stimulation. We previously reported that periostin-deficient mice (Postn^−/−) have low bone mass and a diminished response to physical activity due to a lack of sclerostin (a product of Sost gene) inhibition by mechanical loading. Here we hypothesized that periostin could play a central role in the control of bone loss during unloading induced by hindlimb suspension (HU).In Postn^+/+ mice (wildtype littermate), HU significantly decreased femur BMD, as well as trabecular BV/TV and thickness (Tb.Th). Cortical bone volume and thickness at the femoral midshaft, also significantly decreased. These changes were explained by an inhibition of endocortical and periosteal bone formation activity and correlated with a decrease of Postn expression and a consecutive increase in Sost early after HU. Whereas trabecular bone loss in Postn^−/− mice was comparable to Postn^+/+ mice, HU did not significantly alter cortical bone microstructure and strength in Postn^−/− mice. Bone formation remained unchanged in these mice, as Sost did not increase in the absence of periostin. In contrast, changes in Dkk1, Rankl and Opg expression in response to HU were similar to Postn^+/+ mice, indicating that changes in periostin expression were quite specifically related to changes in Sost. In conclusion, HU inhibits periostin expression, which in turn plays an important role in cortical bone loss through an increase in Sost. These results further indicate that periostin is an essential mediator of cortical bone response to mechanical forces (loading and unloading).     

How you look versus how you feel: Associations between BMI z-score,body dissatisfaction,peer victimization,and self-worth for African American and white adolescents

Being overweight and having negative self-perceptions (body dissatisfaction) can have problematic consequences for adolescents physically, socially, and psychologically. Understanding associations between weight, self-perceptions, and peer experiences across ethnicities is particularly important given recent increases in obesity among ethnic minorities. The current study aimed to address these issues by examining Body Mass Index (BMI) z-scores and body dissatisfaction predicting change in general self-worth over time via peer victimization experiences in a diverse sample of 236 youth (ages 10–16 years). Body dissatisfaction predicted decreases in self-worth over time even after controlling for BMI z-score. BMI z-scores predicted decreases in self-worth over time only for white adolescents, whereas body dissatisfaction directly predicted decreases in self-worth for African American youth and indirectly via peer victimization for white youth. Associations were also considered by gender. Implications for intervention efforts for both white and African American adolescents are discussed.     

新医改中县级医院竞争力状况报告（二）

为探究医改下沉的一年中我国县级医院的竞争力状况，本文从运营规模、医疗技术、经济资源三大竞争力维度及其12个二级指标入手，对2011年中国百强县级医院竞争力进行描述性统计分析和独立样本t检验，并与2010年数据进行比较，得到如下主要结果：这两年对百强县级医院来说，①区域间运营规模影响最大的二级指标是年门诊量，院均年手术量减少，其它三个指标都增加；②区域间医疗技术影响院均高/中级职称人数高于院均员工总数，院均中高级职称比例下降，地区间的差距拉大；③组间对比发现，五十强医院在上述两年中三维度的各个二级指标比较稳定。为县级医院如何增强竞争力指出解决方向，同时也借此达到进一步完善县级医院竞争力的量化测评体系的目的。     

Induction of apoptosis in human liver carcinoma HepG2 cell line by 5-allyl-7-gen-difluoromethylenechrysin

AIM： To investigate the effect of 5-allyl-7-gen-difluoromethylenechrysin （ADFMChR） on apoptosis of human liver carcinoma HepG2 cell line and the molecular mechanisms involved.METHODS： HepG2 cells and L-02 cells were cultured in vitro and the inhibitory effect of ADFMChR on their proliferation was measured by MTT assay. The apoptosis of HepG2 cells was determined by flow cytometry （FCM） using propidium iodide （PI） fluorescence staining. DNA ladder bands were observed by DNA agarose gel electrophoresis. The influence of ADFMChR on the proxisome proliferator-activated receptor γ （PPARγ）, NF-κB, Bcl-2 and Bax protein expression of HepG2 cells were analyzed by Western blotting.RESULTS： MTT assay showed that ADFMChR significantly inhibited proliferation of HepG2 cells in a dose- dependent manner, with little effect on growth of L-02 cells, and when ICs0 was measured as 8.45 μmol/L and 191.55 μmol/L respectively, the potency of ADFMChR to HepG2 cells, was found to be similar to 5-fluorouracil （5-FU, ICso was 9.27 μmol/L）. The selective index of ADFMChR cytotoxicity to HepG2 cells was 22.67 （191.55/8.45）, higher than 5-FU （SI was 7.05 （65.37/9.27）. FCM with PI staining demonstrated that the apoptosis rates of HepG2 cells treated with 3.0, 10.0 and 30.0 μmol/L ADFMChR for 48 h were 5.79%, 9.29% and 37.8%, respectively, and were significantly higher when treated with 30.0 μmol/L ADFMChR than when treated with 30.0 μmol/L ChR （16.0%） （P 〈 0.05） and were similar to those obtained with 30.0 μmol/L 5-FU（41.0%）. DNA agarose gel electrophoresis showed that treatment of HepG2 cells with 10.0 μmol/L ADFMChR for 48 h and 72 h resulted in typical DNA ladders which could be reversed by 10.00 pmol/1 GW9662, a blocker of PPARy. Western blotting analysis revealed that aEer 24 h of treatment with 3.0, 10.0, 30.0 μmol/L ADFMChR, PPARy and Bax protein expression in HepG2 cells increased but Bcl-2 and NF-κB expression decreased; however, pre-incubation with 10.0 μmol/L GW9662 could efficiently antagonize and weaken the regulatory effect of 3.0, 30.0 μmol/L ADFMChR on PPARy and NF-KB protein expression in HepG2 cells.CONCLUSION： ADFMChR induces apoptosis of HepG2 cell lines by activating PPARγ, inhibiting protein expression of Bcl-2 and NF-κB, and increasing Bax expression.     

Identification of newly polymorphic intron 40 markers of the von Willebrand factor gene in a Japanese population

We investigated a region of repetitive DNA located in intron 40 of the von Willebrand factor (vWF) gene (nucleotides [nt] 1639–2404; i.e., F8VWF). We identified 13 alleles and 33 genotypes in 49 unrelated Japanese individuals. The heterozygosity of the region was 0.897. Direct sequence analyses revealed five single-base substitutions, one tetranucleotide (TTAT) insertion, and seven short tandem repeats (STRs) in the intron; four of the STRs and one single-base substitution had been reported previously. The four new base substitutions we identified were 1849T>A, 2122C>T, 2180C>T, and 2192C>T. The novel TTAT tetranucleotide was inserted between nt 2057 and 2058. The three newly identified STRs were 1978(TATC)_1–2, 2193(ATCT)_5–13, and 2234(TGTA)_5–7. The five single-base substitutions and the TTAT insertion were identified only with 3′ downstream of vWA allele 14.