Physical exercise and the quantitative characteristics of moisture- excreting function of the lungs

Physical loading has been used as a test to study the regulation of moisture excretion in the act of breathing in 101 healthy students, 62 men with external risk factors, and in 73 patients with respiratory diseases (chronic bronchitis, acute pneumonia, bronchial asthma). The correlation of moisture excretion with the parameters of ventilation, age, sex, body weight of examinees proved that physical loading in the age-groups above 50 with excess body weight and with hyperventilation resulted in blocking effect on the volume of moisture loss during breathing. Thus, these endogenic factors determine the individual reaction in dynamics of moisture loss during physical loading and could be considered as risk factors in deteriorations of moisture excreting function of lungs.     

Soil microbial responses to warming and increased precipitation and their implications for ecosystem C cycling

A better understanding of soil microbial ecology is critical to gaining an understanding of terrestrial carbon (C) cycle–climate change feedbacks. However, current knowledge limits our ability to predict microbial community dynamics in the face of multiple global change drivers and their implications for respiratory loss of soil carbon. Whether microorganisms will acclimate to climate warming and ameliorate predicted respiratory C losses is still debated. It also remains unclear how precipitation, another important climate change driver, will interact with warming to affect microorganisms and their regulation of respiratory C loss. We explore the dynamics of microorganisms and their contributions to respiratory C loss using a 4-year (2006–2009) field experiment in a semi-arid grassland with increased temperature and precipitation in a full factorial design. We found no response of mass-specific (per unit microbial biomass C) heterotrophic respiration to warming, suggesting that respiratory C loss is directly from microbial growth rather than total physiological respiratory responses to warming. Increased precipitation did stimulate both microbial biomass and mass-specific respiration, both of which make large contributions to respiratory loss of soil carbon. Taken together, these results suggest that, in semi-arid grasslands, soil moisture and related substrate availability may inhibit physiological respiratory responses to warming (where soil moisture was significantly lower), while they are not inhibited under elevated precipitation. Although we found no total physiological response to warming, warming increased bacterial C utilization (measured by BIOLOG EcoPlates) and increased bacterial oxidation of carbohydrates and phenols. Non-metric multidimensional scaling analysis as well as ANOVA testing showed that warming or increased precipitation did not change microbial community structure, which could suggest that microbial communities in semi-arid grasslands are already adapted to fluctuating climatic conditions. In summary, our results support the idea that microbial responses to climate change are multifaceted and, even with no large shifts in community structure, microbial mediation of soil carbon loss could still occur under future climate scenarios.     

蛋白质精氨酸甲基化修饰在糖代谢调节中的作用

蛋白质精氨酸甲基化是重要的细胞翻译后修饰方式,参与众多生命过程. 精氨酸的甲基化修饰与糖代谢相关疾病如糖尿病、糖耐量异常密切相关. 蛋白质精氨酸甲基化转移酶(protein arginine methyltransferases, PRMTs)活性下降及表达异常是糖代谢疾病的重要发病基础. 目前研究表明,PRMT1、PRMT4、PRMT5在糖代谢调节中均扮演重要角色,与糖代谢关键酶如磷酸烯醇式丙酮酸羧基激酶、葡萄糖6磷酸酶,胰岛素受体 胰岛素受体配体1 磷脂酰肌醇3激酶通道及其它通路密切相关. 给予甲基化抑制剂MTA及siRNA干扰甲基化则可引发糖代谢紊乱,进而诱发糖代谢疾病. 糖尿病药物罗格列酮、氨基胍与蛋白质精氨酸甲基化也有一定联系. 深入研究蛋白质精氨酸甲基化与糖代谢调节之间的联系及机制,可为防治糖代谢疾病及相关并发症提供更多的理论依据.     

Contribution of apoptotic cell death to renal injury

Cell number abnormalities are frequent in renal diseases, and range from the hypercellularity of postinfectious glomerulonephritis to the cell depletion of chronic renal atrophy. Recent research has shown that apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The role of apoptosis ranges from induction to repair and progression of renal injury. Death ligands and receptors, such as TNF and FasL, proapoptotic and antiapoptotic Bcl-2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal injury. These proteins represent potential therapeutic targets, which should be further explored.     

Nitrate regulation of anaerobic respiratory gene expression in narX deletion mutants of Escherichia coli K-12.

Previous studies have shown that narL+ is required for nitrate regulation of anaerobic respiratory enzyme synthesis, including formate dehydrogenase-N, nitrate reductase, and fumarate reductase. Insertions in the closely linked narX gene decrease, but do not abolish, nitrate regulation of anaerobic enzyme synthesis. Analysis of sequence similarities suggests that NarX and NarL comprise a two-component regulatory pair. We constructed lacZ operon and gene fusions to investigate the operon structure of narXL. We found evidence for a complex operon with at least two promoters; PXL-narX-PL-narL. We also investigated the role of NarX in nitrate regulation of anaerobic respiratory enzyme synthesis by constructing nonpolar loss of function narX alleles. These deletions were studied on narL+ lambda specialized transducing bacteriophage. The narX deletions had no effect on nitrate regulation in delta (narXL) strains. This finding suggest that the subtle effects of previously studied narX insertions are due to decreased expression of narL and that narX+ is not essential for normal nitrate regulation. The role of NarX in nitrate regulation remains to be determined.     

The role of PGC-1 coactivators in aging skeletal muscle and heart

Aging is the progressive decline in cellular, tissue, and organ function. This complex process often manifests as loss of muscular strength, cardiovascular function, and cognitive ability. Mitochondrial dysfunction and decreased mitochondrial biogenesis are believed to participate in metabolic abnormalities and loss of organ function, which will eventually contribute to aging and decreased lifespan. In this review, we discuss what is currently known about mitochondrial dysfunction in the aging skeletal muscle and heart. We focused our discussion on the role of PGC-1 coactivators in the regulation of mitochondrial biogenesis and function and possible therapeutic benefits of increased mitochondrial biogenesis in compensating for mitochondrial dysfunction and circumventing aging and aging-related diseases.     

MicroRNA与心脏疾病

微RNA（microRNA,miRNA)是小分子非编码调控RNA,含有大约22个核苷酸,可和靶基因mRNA的3′非编码区相互配对结合,在转录后水平负调控靶基因的表达.微RNA调控细胞的生长、代谢、分化和凋亡, 进而参与生物体的生长发育. 研究表明,微RNA参与人类多种生理和病理过程的调控．最近几年,对微RNA表达调控机制及其调控相关疾病的研究取得了诸多显著性的进展, 心脏疾病相关微RNA更加成为研究的热点.此外,一系列基于微RNA治疗心脏疾病的策略方法,例如用反义寡核苷酸抑制微RNA和微RNA补偿的方法,也取得了突破的成果. 总之,微RNA的研究及应用将为心脏疾病的诊断和治疗提供新的途径.     

硒蛋白S基因多态性研究进展

硒蛋白S（selenoprotein S,SELS）是一种在内质网和细胞膜潴留的硒蛋白,是一种新发现的炎症负调控因子,可以保护细胞免受氧化损伤,参与炎症和免疫反应。SELS基因多态性与肿瘤、心血管疾病、缺血性中风和先兆子痫等疾病的发生风险相关。简要介绍SELS的生物学功能,并对近年来SELS基因多态性与疾病易感性的研究进行回顾。     

The Class Ⅲ Histone Deacetylase Sirtuin 1 in Immune Suppression and Its Therapeutic Potential in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic debilitating disease of the joints. Both the innate and adaptive immune responses participate in the development and progression of RA. While several therapeutic reagents, such as TNF-α agonists, have been successfully developed for the clinical use in the treatment of RA, more than half of the patients do not respond to anti-TNF therapy. Therefore, new therapeutic reagents are needed. Recent studies have shown that sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, is a critical negative regulator of both the innate and adaptive immune response in mice, and its altered functions are likely to be involved in autoimmune diseases. Small molecules that modulate Sirt1 functions are potential therapeutic reagents for autoimmune inflammatory diseases. This review highlights the role of Sirt1 in immune regulation and RA.     

Age related mitochondrial degenerative disorders in humans

Disorders caused by mitochondrial respiratory chain deficiency due to mutations in mitochondrial DNA have varied phenotypes but many involve neurological features often associated with cell loss within specific brain regions. These disorders, along with the increasing evidence of decline in mitochondrial function with ageing, have raised speculation that primary changes in mitochondria could have an important role in age-related neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD). Evidence supporting a role for mitochondria in common neurodegenerative diseases comes from studies with the toxin MPP+ and familial PD, which has been shown to involve proteins such as DJ-1 and Pink1 (both of which are predicted to have a role in mitochondrial function and oxidative stress). Mutations within the mitochondrial genome have been shown to accumulate with age and in common neurodegenerative diseases. Mitochondrial DNA haplogroups have also been shown to be associated with certain neurodegenerative conditions. This review covers the primary mitochondrial diseases but also discuss the potential role of mitochondria and mitochondrial DNA mutations in mitochondrial and neurodegenerative diseases, in particular in PD and in AD.     

Insect eggs exert rapid control over an oxygen-water tradeoff

In terrestrial environments, the exchange of respiratory gases exacts a water cost: obtaining oxygen or carbon dioxide requires losing water. Insect eggs should be especially sensitive to this tradeoff-because they are unable to forage for water, have high surface area-to-volume ratios, and experience large temperature-driven changes in oxygen demand. Previous work from our laboratory, on eggs of a common hawk-moth, Manduca sexta, has shown that, during development, metabolic rate and water loss rates rise in parallel. These correlative data suggest that eggshell conductance increases to accommodate increasing metabolic demand. Here, we test this idea experimentally by subjecting eggs of M. sexta to 15, 21 (normoxia) and 35% oxygen for 24h, while measuring rates of metabolism (as carbon dioxide emission) and water loss. Hypoxia depressed egg metabolic rates, but led to pronounced, rapid increases in water loss. By contrast, hyperoxia had no significant effect on metabolism or water loss. These data demonstrate that insect eggs actively participate in balancing oxygen gain and water loss, and that they use tissue oxygen status, or some correlate of it, as a cue for increasing eggshell conductance. Rapid control over conductance may allow eggs to conserve water during an initial period of low metabolic demand, thereby deferring water costs of respiratory gas exchange until late in development.     

The influence of gas permeability of the culture lid on calcium uptake and stomatal function in Dianthus microplants

The establishment of microplants has been shown to be related to the moisture vapour transmission rate of the culture vessel lid. Lids allowing high moisture vapour loss from the container give increased microplant establishment rates. Further, it has been shown that calcium accumulation in the leaves of microplants is correlated with the moisture vapour transmission rate of the vessel lid and this is related to stomatal function in vitro and ex vitrum and to decreased desiccation in the microplants. It is hypothesized that the increased moisture vapour transmission rate of the lid results in increased transpiration in vitro, which in turn causes increased calcium uptake into the leaves of the microplants with consequential increased stomatal function and reduced losses due to desiccation ex vitrum.Abbreviations MVTR moisture vapour transmission rate     

Nitric oxide paradox in asthma

Asthma results from allergen-driven intrapulmonary Th2 response, and is characterized by intermittent airway obstruction, airway hyperreactivity (AHR), and airway inflammation. Accumulating evidence indicates that inflammatory diseases of the respiratory tract are commonly associated with elevated production of nitric oxide (NO). It has been shown that exhaled NO may be derived from constitutive NO synthase (NOS) such as endothelial (NOS 3) and neural (NOS 1) in normal airways, while increased levels of NO in asthma appear to be derived from inducible NOS2 expressed in the inflamed airways. Nevertheless, the functional role of NO and NOS isoforms in the regulation of AHR and airway inflammation in human or experimental models of asthma is still highly controversial. In the present commentary we will discuss the role of lipopolysaccharides contamination of allergens as key element in the controversy related to the regulation of NOS2 activity in experimental asthma.     

辅酶Ⅰ体内代谢调控研究进展

辅酶Ⅰ——烟酰胺腺嘌呤二核苷酸（nicotinamide adenine dinucleotide,NAD⁺）是一种在糖酵解、糖异生、三羧酸循环及呼吸链中发挥重要作用的辅酶,广泛参与DNA修复、组蛋白去乙酰化等生命过程。近年来研究表明NAD⁺合成的前体和中间化合物（具有维生素B3活性的烟酸、烟酰胺、烟酰胺核苷和烟酰胺单核苷酸）在预防糙皮病、延缓衰老,治疗神经和心血管多种疾病、调节胰岛素分泌、调控mRNA的表达等方面具有重要疗效。着重介绍了辅酶Ⅰ体内的合成代谢以及参与的调节衰老进程,以期为利用合成生物学技术在大肠杆菌中富集NAD⁺中间化合物提供理论依据和技术支撑。