非缺陷性网状内皮组织增生病毒的血清学区别

26株来自各种禽的网状内皮组织增生病毒(REV),用多克隆的抗REV鸡血清做交叉中和试验,用REV、T株,Coo1株所制备的单克隆抗体做免疫荧光试验,比较这些毒株之间的抗原关系,从交叉中和试验结果看,它们之间的抗原关系十分接近,可以认为同属于单一血清型;但也确实存在微小差异,因此又可以将它们分为三个血清亚型,这一结果巳被单克隆抗体检验所证实。     

Lifestyle Interventions Limit Gestational Weight Gain in Women with Overweight or Obesity: LIFE‐Moms Prospective Meta‐Analysis

Objective

This study aimed to evaluate the effects of varied lifestyle intervention programs designed to ameliorate excess gestational weight gain (GWG) in pregnant women with overweight or obesity compared with standard care, including effects on pregnancy outcomes.

Methods

Seven clinical centers conducted separate randomized clinical trials to test different lifestyle intervention strategies to modify GWG in diverse populations. Eligibility criteria, specific outcome measures, and assessment procedures were standardized across trials. The results of the separate trials were combined using an individual‐participant data meta‐analysis.

Results

For the 1,150 women randomized, the percent with excess GWG per week was significantly lower in the intervention group compared with the standard care group (61.8% vs. 75.0%; odds ratio [95% CI]: 0.52 [0.40 to 0.67]). Total GWG from enrollment to 36 weeks' gestation was also lower in the intervention group (8.1 ± 5.2 vs. 9.7 ± 5.4 kg; mean difference: ?1.59 kg [95% CI:?2.18 to ?0.99 kg]). The results from the individual trials were similar. The intervention and standard care groups did not differ in preeclampsia, gestational diabetes, cesarean delivery, or birth weight.

Conclusions

Behavioral lifestyle interventions focusing primarily on diet and physical activity among women with overweight and obesity resulted in a significantly lower proportion of women with excess GWG. This modest beneficial effect was consistent across diverse intervention modalities in a large, racially and socioeconomically diverse US population of pregnant women.

     

黑龙江省上白垩统青山口组松花江粗强壳叶肢介的扫描电镜特征

通过对松花江粗强壳叶肢介 (Cratostracussonghuajiangensis)的正模标本进行扫描电镜研究 ,发现原来没有描述的生长线下缘锯齿状构造 。     

机械刺激诱导的烟草悬浮细胞一氧化氮产生途径及其与C矿和钙调素的关系

通过提高摇床转速对烟草细胞施加机械刺激（Ms）可诱导其胞内一氧化氮（No）的快速产生和一氧化氮合酶（Nos）活性的提高,这种MS诱导的NO产生可被N0清除剂cPTIO和NOS抑制剂L-NMMA显著抑制。此外,Ca2＋螯合剂EGTA、质膜Ca＋通道阻断剂La3＋、胞内Ca2＋通道拮抗剂钌红,以及钙调素抑制剂CPZ和TFP预处理均不同程度地抑制了机械刺激诱导的烟草细胞NO的产生,而机械刺激过程中钙调素活性显著上升并与NOS活性和NO含量的变化相一致。这些结果暗示着（类）Nos酶催化的精氨酸依赖途径可能是机械刺激诱发烟草细胞NO产生的主要途径,Ca2＋／CAM可能通过调节（类）NOS活性来调控No的产生。     

柳杉凋落物在中国亚热带和热带的分解

柳杉(Cryptomeria fortunei)为我国特有种,具有很高的经济价值,而且在吸收二氧化碳和净化空气方面具有重要作用。为探究全球气候变暖对森林凋落物分解速率的影响,分别在中亚热带的千岛湖、南亚热带的鼎湖山和热带的尖峰岭,用分解袋法对柳杉凋落物进行分解实验,3个实验样地的主要差异为温度。结果表明:凋落物在3个样地的分解速率顺序为尖峰岭、鼎湖山、千岛湖,且不同样地之间的分解速率具有显著差异(P0.01)。在千岛湖样地分解速率常数k值与初始C/N呈显著相关(P0.05);在鼎湖山样地分解速率常数k值与初始碳含量呈极显著相关(P0.01);在尖峰岭样地,凋落物的分解速率常数k值与凋落物各初始化学元素含量相关性均不显著,推测可能是气候起主要作用。     

齿孔酸对高尿酸血症黄嘌呤氧化酶活性的影响

采用紫外分光光度法检测齿孔酸在体外对黄嘌呤氧化酶的作用,并进行动力学研究探讨其作用机制;采用酵母联合氧嗪酸钾诱导高尿酸血症小鼠模型,观察齿孔酸对高尿酸血症小鼠血清尿酸水平、血清黄嘌呤氧化酶活性、肝脏黄嘌呤氧化酶活性及血糖血脂的影响。研究发现,齿孔酸体在外能抑制黄嘌呤氧化酶活性,降低高尿酸血症小鼠血清尿酸水平、血清黄嘌呤氧化酶活性、肝脏黄嘌呤氧化酶活性,同时明显降低空腹血糖、总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平,升高高密度脂蛋白胆固醇水平,提高口服糖耐受量。结果表明,齿孔酸是黄嘌呤氧化酶竞争性抑制剂,还能缓解高尿酸血症小鼠糖脂代谢紊乱,对高尿酸血症及痛风的防治具有潜在意义。     

桉树人工林冠层、凋落物及土壤水文生态效应

水文功能是森林生态功能的重要方面,为了解桉树人工林的水文生态效应,采用定位研究并结合室内测定的实验方法,研究了广东肇庆桉树人工林冠层降雨再分配、凋落物持水能力、土壤水分物理及蓄水能力。结果表明,研究期间(2006-05-2007-05)的大气降雨量为2016.7mm,通过林冠层后降雨被重新分配,穿透降雨量、树干茎流量和林冠截留量分别占总降雨量的85.70%、3.62%和10.68%。产生树干茎流的临界降雨量为3.93mm,穿透雨量、树干茎流量与林外降雨量均呈极显著正相关(P0.01);林冠截留率与降雨量呈显著的负相关(P0.05),降雨量超过20mm后,林冠截留率基本保持稳定。本研究桉树人工林的凋落物最大持水量为4.27mm,凋落物中树叶的最大持水量最大,为2.54mm。0-100cm土层的最大蓄水量为470.06mm,其中非毛管蓄水量为98.22mm,土壤总孔隙度和非毛管孔隙度随土壤深度增加呈递减趋势;0-10cm土壤层的初渗速率和稳渗速率分别为25.03mm.min-1和8.83mm.min-1,且随土壤深度增加而逐渐减小。     

Study of Cytotoxic Chemotherapy as an Adjuvant to Surgery in Carcinoma of the Bronchus

This report gives the findings after two years of a study of long-term oral cytotoxic chemotherapy with busulphan or cyclophoshamide in carcinoma of the bronchus compared with two placebos, identical in appearance to the drug-containing tablets. A total of 753 patients who had had a total resection of the tumour, who had no detectable extrathoracic metastasis, and who were able to attend chest clinics monthly were admitted to the study from January 1965 to January 1968. Twenty-seven patients were excluded from all the analyses.The 217 patients admitted up to December 1965 form the “early” intake, the remaining 509 the “late” intake. There were no significant differences between the series in either intake period in a number of pretreatment factors studied. At 24 months 46% of the busulphan, 44% of the cyclophosphamide, and 49% of the placebo series were alive in the early intake, as were 49%, 50%, and 50% respectively in the late intake. There were no important differences between the series in survival related to pretreatment condition, cause of death, time of detection of metastases, and condition of the survivors at 24 months. Maintenance chemotherapy was interrupted to a greater extent in the busulphan than in the cyclophosphamide series and least in the placebo series.In both intakes clinical toxicity was more frequent in the cyclophosphamide series and similar in frequency in the busulphan and placebo series. Haematological toxicity was particularly frequent and severe in the busulphan series, especially in the early intake, platelet depression being the predominant manifestation.It is concluded that there is no evidence that either of the two cytotoxic drugs in the dosage prescribed improved survival for the two-year period of observation, though a final evaluation of the adjuvant chemotherapy as studied in this investigation will have to await the results at five years.     

BDNF VAL66MET polymorphism and memory decline across the spectrum of Alzheimer's disease

The brain-derived neurotrophic factor (BDNF) Val66Met (rs6265) polymorphism has been shown to moderate the extent to which memory decline manifests in preclinical Alzheimer's disease (AD). To date, no study has examined the relationship between BDNF and memory in individuals across biologically confirmed AD clinical stages (i.e., Aβ+). We aimed to understand the effect of BDNF on episodic memory decline and clinical disease progression over 126 months in individuals with preclinical, prodromal and clinical AD. Participants enrolled in the Australian Imaging, Biomarkers and Lifestyle (AIBL) study who were Aβ + (according to positron emission tomography), and cognitively normal (CN; n = 238), classified as having mild cognitive impairment (MCI; n = 80), or AD (n = 66) were included in this study. Cognition was evaluated at 18 month intervals using an established episodic memory composite score over 126 months. We observed that in Aβ + CNs, Met66 was associated with greater memory decline with increasing age and were 1.5 times more likely to progress to MCI/AD over 126 months. In Aβ + MCIs, there was no effect of Met66 on memory decline or on disease progression to AD over 126 months. In Aβ + AD, Val66 homozygotes showed greater memory decline, while Met66 carriers performed at a constant and very impaired level. Our current results illustrate the importance of time and disease severity to clinicopathological models of the role of BDNF Val66Met in memory decline and AD clinical progression. Specifically, the effect of BDNF on memory decline is greatest in preclinical AD and reduces as AD clinical disease severity increases.