慢性持续期哮喘患者自我效能水平及相关因素分析

目的:探讨慢性持续期哮喘患者的自我效能水平及其相关因素。方法:采用一般资料调查表、自我效能量表、社会支持量表(SSRS)、综合性医院焦虑抑郁量表(HADS)等,对我院2009年3月至2011年6月呼吸科门诊随诊的79例慢性持续期哮喘患者进行调查。结果:所有患者的平均自我效能总分为(57.15±9.03)分。患者自我效能水平与病程、经济状况、吸烟情况、发作次数及发作程度呈负相关(P<0.05)。结论:慢性持续期哮喘患者自我效能水平有不同程度的降低,哮喘发作次数、焦虑抑郁情绪以及社会支持水平是影响患者自我效能水平的主要因素。     

长白山露水河林业局森林景观格局动态

基于1987、1995、2003年长白山露水河林业局森林资源二类调查资料,利用ArcGIS和FRAGSTATS等软件,在景观水平和斑块水平上分析了1987-2003年该区景观格局变化及其与森林经营机制之间的关系.结果表明：研究期间,研究区森林景观破碎化程度加剧、景观异质性程度加大;1987-2003年,研究区斑块数增加979块,最大斑块面积比例逐渐下降,由1987年的28.7%降至2003年的12.7%;由于经营方式的转变,该区景观基质由1987年的阔叶混交林转变为1995年后的混合景观基质;景观破碎化程度在1995-2003年的变化趋势较1987-1995年有所减缓;期间,该区阔叶混交林的平均斑块面积下降最多、边界分割程度最高,表明天然次生林受人类干扰最大.     

Metabonomics study of the acute graft rejection in rat renal transplantation using reversed-phase liquid chromatography and hydrophilic interaction chromatography coupled with mass spectrometry

Acute graft rejection is one of the most common and serious post complications in renal transplantation, noninvasive diagnosis of acute graft rejection is essential for reducing risk of surgery and timely treatment. In this study, a non-targeted metabonomics approach based on ultra performance liquid chromatography (UPLC) coupled with quadrupole time-of-flight mass spectrometry (MS) is used to investigate the effect of acute graft rejection in rat renal transplantation on metabolism. To collect more metabolite information both hydrophilic interaction chromatography and reversed-phase liquid chromatography were used. Using the partial least squares-discriminant analysis, we found that the change of metabonome in a sham-operated group and a non-graft rejection group had a similar trend, while that of the acute graft rejection group was clearly different. Several discriminating metabolites of the acute graft rejection were identified, including creatinine, phosphatidyl-cholines, lyso-phosphatidylcholines, carnitine C16:0, free fatty acids and indoxyl sulfate etc. These discriminating metabolites suggested that acute graft rejection in renal transplantation can lead to the accumulation of creatinine in the body, and also the abnormal metabolism of phospholipids. These findings are useful to understand the mechanisms of the rejection, it also means that a UPLC-MS metabonomic approach is a suitable tool to investigate the metabolic abnormality in the acute graft rejection in renal transplantation.     

驱油生物表面活性剂生产菌的筛选与评价

目的:筛选适合油田的生物表面活性剂生产菌。方法:通过发酵培养,研究生物表面活性剂生产菌生长代谢规律;采用正交试验法,优选出其最佳培养条件;通过室内驱油实验评价生物表面活性剂驱油效果。结果:2#菌株最佳培养时间为96小时,最优发酵培养条件为:葡萄糖4.0 g、玉米浆1.6 g、Na2HPO40.1 g、KH2PO40.05 g、MgSO40.05 g、CaCl20.005 g、水100 mL、pH 7.2,培养温度35℃,摇床转速120 r/min,生物表面活性剂驱油提高采收率6.16%。结论:筛选出最优生物表面活性剂产生菌2#,菌株具备产表面活性剂的能力且产物量较高,其生物表面活性剂驱油效果良好。     

Genistein Suppresses LPS-Induced Inflammatory Response through Inhibiting NF-κB following AMP Kinase Activation in RAW 264.7 Macrophages

Genistein, the major isoflavone in soybean, was recently reported to exert beneficial effects in metabolic disorders and inflammatory diseases. In the present study, we investigated the effects and mechanisms of a dietary concentration of genistein on the inflammatory response in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Our results demonstrated that genistein effectively inhibited the LPS-induced overproduction of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6), as well as LPS-induced nuclear factor kappa B (NF-κB) activation. In addition, the data also showed that genistein prevented LPS-induced decrease in adenosine monophosphate-activated protein kinase (AMPK) phosphorylation. These effects were obviously attenuated by an AMPK inhibitor. Taken together, our results suggest that the dietary concentration of genistein is able to attenuate inflammatory responses via inhibition of NF-κB activation following AMPK stimulation. The data provide direct evidence for the potential application of low concentrations of genistein in the prevention and treatment of inflammatory diseases.     

Dynamics of a Cytokine Storm

Six volunteers experienced severe inflammatory response during the Phase I clinical trial of a monoclonal antibody that was designed to stimulate a regulatory T cell response. Soon after the trial began, each volunteer experienced a “cytokine storm”, a dramatic increase in cytokine concentrations. The monoclonal antibody, TGN1412, raised serum concentrations of both pro- and anti-inflammatory cytokines το very hiγh values during the first day, while lymphocyte and monocyte concentrations plummeted. Because the subjects were healthy and had no prior indications of immune deficiency, this event provided an unusual opportunity to study the dynamic interactions of cytokines and other measured parameters. Here, the response histories of nine cytokines have been modeled by a set of linear ordinary differential equations. A general search procedure identifies parameters of the model, whose response fits the data well during the five-day measurement period. The eighteenth-order model reveals plausible cause-and-effect relationships among the cytokines, showing how each cytokine induces or inhibits other cytokines. It suggests that perturbations in IL2, IL8, and IL10 have the most significant inductive effect, while IFN-γ and IL12 have the greatest inhibiting effect on other cytokine concentrations. Although TNF-α is a major pro-inflammatory factor, IFN-γ and three other cytokines have faster initial and median response to TGN1412 infusion. Principal-component analysis of the data reveals three clusters of similar cytokine responses: [TNF-α, IL1, IL10], [IFN-γ, IL2, IL4, IL8, and IL12], and [IL6]. IL1, IL6, IL10, and TNF-α have the highest degree of variability in response to uncertain initial conditions, exogenous effects, and parameter estimates. This study illuminates details of a cytokine storm event, and it demonstrates the value of linear modeling for interpreting complex, coupled biological system dynamics from empirical data.     

水曲柳腋芽离体快繁研究初报

以水曲柳带顶芽、腋芽茎段为外植体进行离体培养,研究其适宜的灭菌方法、基本培养基种类和激素对腋芽萌发、丛芽产生、芽苗增殖的影响。结果表明,水曲柳的腋芽茎段为快繁的适宜外植体,茎段灭菌以用0.05%HgCl₂处理2 min最好。在萌芽培养中,BA和2ip均可促进腋芽萌发,但以8 mg·L^-1 BA处理时萌发效果最好,萌发率达100％;将腋芽萌发后长成的新枝转入添加ZT的培养基中,出现丛芽,在添加1.0 mg·L^-1的ZT的培养基中增殖效果最好,增殖系数达到3.0。无论在萌芽培养还是增殖培养中均发现WPM培养基最适合水曲柳腋芽的离体快繁。     

Biological implications of genetic variations in autism spectrum disorders from genomics studies

Autism spectrum disorder (ASD) is a highly heterogeneous neurodevelopmental condition characterized by atypical social interaction and communication together with repetitive behaviors and restricted interests. The prevalence of ASD has been increased these years. Compelling evidence has shown that genetic factors contribute largely to the development of ASD. However, knowledge about its genetic etiology and pathogenesis is limited. Broad applications of genomics studies have revealed the importance of gene mutations at protein-coding regions as well as the interrupted non-coding regions in the development of ASD. In this review, we summarize the current evidence for the known molecular genetic basis and possible pathological mechanisms as well as the risk genes and loci of ASD. Functional studies for the underlying mechanisms are also implicated. The understanding of the genetics and genomics of ASD is important for the genetic diagnosis and intervention for this condition.     

Endothelial S1pr1 regulates pressure overload‐induced cardiac remodelling through AKT‐eNOS pathway

Cardiac vascular microenvironment is crucial for cardiac remodelling during the process of heart failure. Sphingosine 1‐phosphate (S1P) tightly regulates vascular homeostasis via its receptor, S1pr1. We therefore hypothesize that endothelial S1pr1 might be involved in pathological cardiac remodelling. In this study, heart failure was induced by transverse aortic constriction (TAC) operation. S1pr1 expression is significantly increased in microvascular endothelial cells (ECs) of post‐TAC hearts. Endothelial‐specific deletion of S1pr1 significantly aggravated cardiac dysfunction and deteriorated cardiac hypertrophy and fibrosis in myocardium. In vitro experiments demonstrated that S1P/S1pr1 praxis activated AKT/eNOS signalling pathway, leading to more production of nitric oxide (NO), which is an essential cardiac protective factor. Inhibition of AKT/eNOS pathway reversed the inhibitory effect of EC‐S1pr1‐overexpression on angiotensin II (AngII)‐induced cardiomyocyte (CM) hypertrophy, as well as on TGF‐β‐mediated cardiac fibroblast proliferation and transformation towards myofibroblasts. Finally, pharmacological activation of S1pr1 ameliorated TAC‐induced cardiac hypertrophy and fibrosis, leading to an improvement in cardiac function. Together, our results suggest that EC‐S1pr1 might prevent the development of pressure overload‐induced heart failure via AKT/eNOS pathway, and thus pharmacological activation of S1pr1 or EC‐targeting S1pr1‐AKT‐eNOS pathway could provide a future novel therapy to improve cardiac function during heart failure development.