N-myc modulates expression of p73 in neuroblastoma

The human p73 gene is a homolog of p53, which has been localized to chromosome 1p36 in a region that is frequently deleted in neuroblastoma. Transfection of the p73 gene into neuroblastoma cells that lack detectable p73 protein has been shown to result in growth suppression and to induce neuronal differentiation. In this study, we have identified by means of restriction landmark genome scanning (RLGS) a genomic fragment that was frequently reduced in intensity in neuroblastomas. The cloned fragment contained exon 1 of p73 as well as intronic and promoter sequences. We investigated the genomic and expression status of p73 and N-myc in 34 neuroblastoma tumors and 12 neuroblastoma cell lines. Approximately a third of neuroblastomas in our series exhibited deletion of p73. Most tumors analyzed exhibited reduced expression of p73, as determined by quantitative RT-PCR, in the absence of detectable p73 gene deletion. The reduced expression of p73 correlated with overexpression of N-myc in a statistically significant manner. The N-myc gene was transfected into two neuroblastoma cell lines that lacked N-myc amplification to determine its effect on p73 RNA levels. p73 was detectable at low level by RT-PCR in untransfected SK-N-AS cells and became undetectable following N-myc transfection, whereas in SH-EP1 cells, p73 levels were substantially reduced following transfection but remained detectable. Our data suggest that the N-myc gene modulates expression of p73, allowing neuroblastoma cells to escape the growth suppressing properties of p73.     

雌性大鼠骨矿密度和骨矿含量与体重和月龄的相关性分析

目的 :观察大鼠全身骨矿密度 (BMD)和骨矿含量 (BMC)与体重 (BW )和月龄 (MO)的关系。方法 :利用DEXA人前臂骨密度软件测定 4、8和 2 0月龄雌性SD大鼠全身BMD、BMC和骨投影面积 (AREA )。在SPSSforWindows统计软件上进行BMD、BMC和AREA对BW的一元直线回归 ,和对BW、MO的二元直线回归 ,并作偏相关分析等。结果 :BMD、BMC和AREA与BW及MO的二元直线回归方程 :BMD =0 .179 0 .0 0 0 196BW (克 ) -0 .0 0 0 680MO(月 ) g/cm2 ,复相关系数r =0 .711;BMC =3 .472 0 .0 13 7BW -0 .0 0 912MOg ,r =0 .92 5 ;AREA =2 2 .66 0 .0 3 0 2BW -0 .13 9MOcm2 ,r =0 .92 2。偏相关分析表明BMD与BW中度正相关 (R =0 .63 4) ,与MO弱负相关 (R =-0 .2 5 8) ;BMC与BW高度正相关 (R =0 .82 5 ) ,与MO无明显相关性 (R =0 .0 91) ;AREA与BW高度正相关 (R =0 .73 9) ,与MO弱正相关 (R =0 .42 7)。结论 :大鼠体重对BMD和BMC均有明显影响 ,月龄只对BMD有轻度影响 ,对BMC无明显影响。     

贝那普利与美托洛尔联合治疗慢性心力衰竭疗效观察

目的探讨贝那普利与美托洛尔联合治疗慢性心力衰竭的临床疗效。方法选择Ⅱ～Ⅳ级的慢性心力衰竭患者80例，随机分成治疗组45例和对照组35例，对照组给予利尿剂、强心剂、硝酸酯类等扩血管药物常规治疗，治疗组在常规治疗的基础上加用贝那普利和美托洛尔，半年后比较两组在治疗前后6min内步行距离、左室射血分数及心功能改善情况。结果治疗组心功能改善显效率及总有效率优于对照组，差异有统计学意义（P〈0．05）。结论贝那普利与美托洛尔联合治疗慢性心力衰竭的临床疗效可靠，可改善患者的预后、提高生活质量。     

PDCA循环在ICU护生带教管理中应用的探讨

目的探讨PDCA循环在ICU护生临床护理教学中的应用。方法将PDCA循环引入ICU带教管理工作中，保证教学质量控制的有效性和适宜性。结果提高了带教老师的教学积极性和临床带教的满意度，搞高了护生整体护理能力。结论在ICU护生教学管理中应用PDCA循环，能明显提高护生的整体素质，保证ICU临床教学的质量。     

重症中暑院前地塞米松干预疗效研究

目的分析重症中暑患者院前地塞米松干预的疗效及对预后影响。方法重症中暑患者47例,均给予降温,吸氧,补液,纠正水、电解质、酸碱平衡紊乱和预防感染等治疗。根据有无院前地塞米松干预将47例重症中暑患者分为两组:地塞米松组21例和对照组26例。比较两组的临床症状、体征及实验室检测指标。结果地塞米松组昏迷程度、部分凝血活酶时间(APTT)、死亡与对照组比较,均有统计学差异(p<0.05)。结论重症中暑患者院前地塞米松干预能改善凝血功能、降低死亡率,可能是重症中暑患者重要治疗手段。     

牛磺酸对力竭运动大鼠白肌线粒体的保护作用

目的探讨外源性牛磺酸对力竭运动后大鼠白肌线粒体自由基代谢的影响,从亚细胞水平研究牛磺酸抗运动性疲劳的机制。方法以大鼠力竭性运动为模型,观察了牛磺酸对力竭运动时大鼠白肌线粒体脂质过氧化、抗氧化系统及总Ca2+浓度的影响。结果牛磺酸可降低大鼠力竭运动后白肌线粒体脂质过氧化水平,提高大鼠力竭运动后白肌线粒体超氧化物歧化酶(SOD)的活性,保持大鼠力竭运动后白肌线粒体还原性谷胱甘肽含量及总Ca2+浓度。结论牛磺酸可减少力竭运动后因脂质过氧化而产生的自由基,降低自由基对白肌线粒体的攻击,维持线粒体膜的功能。     

Effect of rs1063843 in the CAMKK2 gene on the dorsolateral prefrontal cortex

Recently, a single nucleotide polymorphism (SNP) in the CAMKK2 gene (rs1063843) was found to be associated with lower expression of the gene in the dorsolateral prefrontal cortex (DLPFC) and with schizophrenia (SCZ) and deficits in working memory and executive function. However, the brain mechanism underlying this association is poorly understood. A functional magnetic resonance imaging (fMRI) study (N = 84 healthy volunteers) involving multiple cognitive tasks, including a Stroop task (to measure attentional executive control), an N‐back task (to measure working memory), and a delay discounting task (to measure decision making) to identify the brain regions affected by rs1063843 was performed. Across all three tasks, it was found that carriers of the risk allele consistently exhibited increased activation of the left DLPFC. In addition, the risk allele carriers also exhibited increased activation of the right DLPFC and the left cerebellum during the Stroop task and of the left caudate nucleus during the N‐back task. These findings helped to elucidate the role of CAMKK2 in cognitive functions and in the etiology of SCZ. Hum Brain Mapp 37:2398–2406, 2016. © 2016 Wiley Periodicals, Inc .     

2005—2007年丽水出入境人员梅毒感染情况和流行病学分析

目的了解丽水出入境人群梅毒感染的流行分布状况与趋势,以确定重点监测对象,为国境卫生检疫监管工作提供科学依据。方法对2005～2007年的18848名丽水出入境人员进行血清学检测,2005～2006年间采用甲苯胺红不加热血清试验（TRUST）进行初筛,初筛阳性后再采用梅毒螺旋体明胶颗粒疑集试验（TPPA）进行确认;2007年起首先使用梅毒螺旋体明胶颗粒疑集试验（TPPA）进行普查,TPPA阳性者再采用甲苯胺红不加热血清实验（TRUST）进一步检测。并对梅毒感染者进行流行病学调查和统计学分析。结果共检出梅毒感染者211人,检出率为1．12％,其中男性检出率为1．17％,女性检出率为1．07％,各年龄组中以60岁以上年龄组检出率最高,为8．87％;以性传播为主要传播途径。结论要加强对丽水出入境人员的行为干预,特别是加强性病防护知识的宣传教育,降低这一人群的梅毒感染率。     

Stimulatory effect of puerarin on bone formation through activation of PI3K/Akt pathway in rat calvaria osteoblasts

Puerarin, a natural isoflavonoid found in Chinese Pueraria lobata (Wild.) Ohwi, has received increasing attention because of its possible role in the prevention of osteoporosis. However, the relationship between puerarin and bone formation remains unknown. In the present study, rat osteoblasts isolated from newborn Wistar rats were used to investigate the effect of puerarin on osteoblasts, and its possible molecular mechanism. Data showed that puerarin caused a significant increase in cell viability, alkaline phosphatase (ALP) activity and mineral nodules formation in osteoblasts, suggesting that puerarin had a stimulatory effect on osteoblastic bone formation. This functional improvement by puerarin was accompanied by activation and nuclear translocation of Akt. Furthermore, puerarin-stimulated osteoblastic growth, Akt activation and redistribution were significantly blocked by the specific PI3K inhibitor, LY294002. These results strongly suggested that puerarin stimulated osteoblastic proliferation and Akt activation in a PI3K-dependent manner. In summary, puerarin derived from Chinese Pueraria lobata (Wild.) Ohwi can promote bone formation in cultured rat osteoblasts, which might be mediated by activation of the PI3K/Akt pathway. DMEM:Dulbecco's modification of Eagel's medium PBS:phosphate buffered saline DMSO:dimethyl sulfoxide EDTA:ethylene diamine tetraacetic acid SDS:sodium dodecyl sulfate SDS-PAGE:sodium dodecylsulfate polyacrylamide gel electrophoresis FITC:fluorescein isothiocyanate HRP:horseradish peroxidase PI3K:phosphatidylinositol 3-kinase.     

Role for nitric oxide in permeability of hippocampal neuronal hemichannels during oxygen glucose deprivation

Increased hemichannel opening induced by oxygen glucose deprivation (OGD) was reported in the hippocampal pyramidal neuron. It was suggested that the pannexin1 hemichannel opening could mediate ionic flux dysregulation, anoxic depolarization, and energy-depleting efflux of glucose and ATP for ischemic neurons. However, the regulatory mechanisms of pannexin1 hemichannel opening have been poorly understood. Here we showed that excessive generation of nitric oxide (NO) during ischemia could induce the calcein leakage from neurons, which was markedly reduced by NO synthase inhibitor. The calcein leakage from neurons during OGD was also attenuated by the application of N-ethylmaleimide (NEM), an SH-alkylating agent, and dithiothreitol (DTT), a reducer of oxidized sulfhydryl groups. However, the soluble guanylyl cyclase (sGC) inhibitor had a minor effect on the calcein leakage during OGD. Furthermore, the elevated intracellular but not extracellular levels of glutathione could also inhibit the calcein leakage during OGD. Similar results were observed in metabolic inhibition (MI), which is another ischemic-like condition. Finally, immunocytochemical and immunoblotting analysis revealed that, after 1 hr of OGD stimulation, the distribution and expression of pannexin1 showed no significant difference compared with control. However, the pannexin1 mRNA expression was elevated after 1 hr of OGD and a sustained increase was maintained during reperfusion. These results implied that the reactive oxygen species (ROS), especially NO, might be involved in the enhanced pannexin1 hemichannel opening and that the S-nitrosylation but not the NO/cGMP pathway played a more important role in this event.