On the intricate relationship between sexual motivation and arousal

Sexual motivation and sexual arousal are widely used concepts. While there seem to be considerable agreement as to the meaning of sexual motivation, there is certain confusion about the exact meaning of sexual arousal. Some use it as a synonym to sexual motivation and others make it equivalent to erection or vaginal lubrication. An unresolved question is the relationship between sexual arousal and general arousal as well as that between arousal and motivation. I present arguments for the view that arousal refers to the general state of alertness of the organism. Consequently, there is no such thing as a specific sexual arousal. I suggest that this term should be abandoned, or if that is not feasible, to make it a synonym to enhanced genital blood flow. The notion of a subjective sexual arousal, some kind of vaguely described mental state, seems to lack all explanatory value. I then show that general arousal is an important determinant of sexual motivation, and that the execution of copulatory acts leads to increased general arousal. This increase leads to enhanced sexual motivation, making the activation of sexual reflexes requiring high levels of motivation possible. Examples of such reflexes may be ejaculation in males of many species, and perhaps the psychic state of orgasm in women.     

Yeast programmed cell death: an intricate puzzle

Yeasts as eukaryotic microorganisms with simple, well known and tractable genetics, have long been powerful model systems for studying complex biological phenomena such as the cell cycle or vesicle fusion. Until recently, yeast has been assumed as a cellular 'clean room' to study the interactions and the mechanisms of action of mammalian apoptotic regulators. However, the finding of an endogenous programmed cell death (PCD) process in yeast with an apoptotic phenotype has turned yeast into an 'unclean' but even more powerful model for apoptosis research. Yeast cells appear to possess an endogenous apoptotic machinery including its own regulators and pathway(s). Such machinery may not exactly recapitulate that of mammalian systems but it represents a simple and valuable model which will assist in the future understanding of the complex connections between apoptotic and non-apoptotic mammalian PCD pathways. Following this line of thought and in order to validate and make the most of this promising cell death model, researchers must undoubtedly address the following issues: what are the crucial yeast PCD regulators? How do they play together? What are the cell death pathways shared by yeast and mammalian PCD? Solving these questions is currently the most pressing challenge for yeast cell death researchers.     

Neonatal-maternal weight relationship in macaques: an example of intrageneric scaling.

In the genus Macaca, represented by seven species, neonatal weight scales at a power of maternal weight of a = 0.49. This value is lower than those for subordinal and ordinal scaling of neonatal weight in primates (a = 0.63-0.78), but it is higher than the value for intrageneric scaling of brain weight in Macaca (a = 0.18). A causal interpretation is attempted for differing values of a at different taxonomic levels and between different organ systems.     

Oncogene-induced senescence pathways weave an intricate tapestry

The induction of cellular senescence by activated oncogenes acts as a barrier to cell transformation. Now, identify a key component of a senescence pathway that prevents tumorigenesis in a mouse model of skin cancer. They show that the p38-regulated/activated protein kinase (PRAK) induces senescence downstream of oncogenic Ras by directly phosphorylating and activating the tumor-suppressor protein p53.     

Methane emissions from wetlands and their relationship with vascular plants: an Arctic example

This paper investigates the relationship between vascular plant production and CH₄ emissions from an arctic wet tundra ecosystem in north‐east Greenland. Light intensity was manipulated by shading during three consecutive growing seasons (1998–2000). The shading treatment resulted in lower carbon cycling in the ecosystem as mean seasonal net ecosystem exchange (NEE) decreased from ?336 to ?196 mg CO₂ m^?2 h^?1 and from ?476 to ?212 mg CO₂ m^?2 h^?1 in 1999 and 2000, respectively, and total ecosystem respiration decreased from 125 to 94 mg CO₂ m^?2 h^?1 in 1999 and from 409 to 306 mg CO₂ m^?2 h^?1 in 2000. Seasonal mean CH₄ emissions in controls and shaded plots were, respectively, 6.5 and 4.5 mg CH₄ m^?2 h^?1 in 1999 and 8.3 and 6.2 mg CH₄ m^?2 h^?1 in 2000. We found that CH₄ emission was sensitive to NEE and carbon turnover, and it is reasonable to assume that the correlation was due to a combined effect of vegetative CH₄ transport and substrate quality coupled to vascular plant production. Total above‐ground biomass was correlated to mean seasonal CH₄ emission, but separation into species showed that plant‐mediated CH₄ transport was highly species dependent. Potential CH₄ production peaked at the same depth as maximum root density (5–15 cm) and treatment differences further suggest that substrate quality was negatively affected by decreased NEE in the shaded plots. The concentration of dissolved CH₄ decreased in the control plots as the growing season progressed while it was relatively stable in the shaded plots. This suggests that a progressively better developed root system in the controls increased the capacity to transport CH₄ from the soil to the atmosphere. In conclusion, vascular plant photosynthetic rate and subsequent allocation of recently fixed carbon to below‐ground structures seemed to influence both vegetative CH₄ transport and substrate quality.     

肠道细菌微生态与人类疾病关系研究进展

寄居在人类肠道的数以亿计的肠道细菌,已被证实与人类多种疾病有关。就肠道细菌与内分泌系统疾病、消化系统疾病、心血管系统疾病、神经系统疾病、获得性免疫缺陷综合征以及特应性疾病等的关系研究进展进行综述。     

The relationship between biodiversity and population centres: the high Andes region as an example

Several coarse-scale studies have demonstrated a positive correlation between biodiversity and human population density. In this paper this relationship is studied for part of the Andean highland, on a finer spatial scale than in earlier studies, and comparing bird distribution data with pre-Columbian as well as contemporary population centres. A particularly close correspondence was found between ancient population centres and high numbers of species with small distributions. This suggests that the growth of resident human cultures was related, in some way, to local factors which—over a much longer time-scale—stimulated the process of evolution of new species. This correspondence may be a consequence of climate moderation in the mountain areas leading to local persistence, of wild species as well as human communities. However, the result also suggests that we need to study to what extent high biodiversity as such, under certain conditions, yields environmental services which were important for people. It also suggests that traditional efforts to preserve biodiversity in wilderness areas with few people should be supplemented with efforts to promote a more sustainable development in the populated areas, allowing cloud forest and other biologically rich habitats to persist in suitable places near population centres.     

Tissue processing of nitrite in hypoxia: an intricate interplay of nitric oxide-generating and -scavenging systems

Although nitrite (NO(2)(-)) and nitrate (NO(3)(-)) have been considered traditionally inert byproducts of nitric oxide (NO) metabolism, recent studies indicate that NO(2)(-) represents an important source of NO for processes ranging from angiogenesis through hypoxic vasodilation to ischemic organ protection. Despite intense investigation, the mechanisms through which NO(2)(-) exerts its physiological/pharmacological effects remain incompletely understood. We sought to systematically investigate the fate of NO(2)(-) in hypoxia from cellular uptake in vitro to tissue utilization in vivo using the Wistar rat as a mammalian model. We find that most tissues (except erythrocytes) produce free NO at rates that are maximal under hypoxia and that correlate robustly with each tissue's capacity for mitochondrial oxygen consumption. By comparing the kinetics of NO release before and after ferricyanide addition in tissue homogenates to mathematical models of NO(2)(-) reduction/NO scavenging, we show that the amount of nitrosylated products formed greatly exceeds what can be accounted for by NO trapping. This difference suggests that such products are formed directly from NO(2)(-), without passing through the intermediacy of free NO. Inhibitor and subcellular fractionation studies indicate that NO(2)(-) reductase activity involves multiple redundant enzymatic systems (i.e. heme, iron-sulfur cluster, and molybdenum-based reductases) distributed throughout different cellular compartments and acting in concert to elicit NO signaling. These observations hint at conserved roles for the NO(2)(-)-NO pool in cellular processes such as oxygen-sensing and oxygen-dependent modulation of intermediary metabolism.     

Regulation of testicular function in the stallion: an intricate network of endocrine, paracrine and autocrine systems

It is well established in many mammalian species, including the horse that normal testicular function is dependent upon a functional hypothalamic-pituitary-testicular (HPT) axis, which involves classic feedback mechanisms. The major HPT hormones involved in the stallion are gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone (T), estrogens (Es) and inhibin (INH). Although prolactin (PRL) fluctuates with season in the stallion and both PRL and thyroid hormone (TH) affect reproduction in other male species, their effects on stallion reproduction have not been elucidated. Growth hormone (GH) in the stallion may be involved in sperm motility, production and secretion of insulin-like growth factor-1 (IGF-1) and LH-induced testosterone release. The action of these hormones and the products involved for normal spermatogenesis require cell to cell communication within the testis. The somatic cell types, Leydig, Sertoli and peritubular myoid cells, all support germ cell development, maturation and release into the seminiferous tubule lumen. The cell to cell crosstalk involves an intricate network of paracrine-autocrine systems that support the endocrine input to modulate cell function. In other male species, researchers have demonstrated the reproductive effects of such paracrine-autocrine factors as IGF-1, transferrin, androgens, estrogens, inhibin, insulin like peptide 3 (INSL3), beta-endorphin and oxytocin. The specific nature and relative contribution of these various factors on testicular function in fertile and subfertile stallions are under investigation. This review summarizes current information regarding the nature of the multiple endocrine-paracrine-autocrine systems that may be necessary for normal testicular function in the stallion.     

Cellular stress response pathways and ageing: intricate molecular relationships

Ageing is driven by the inexorable and stochastic accumulation of damage in biomolecules vital for proper cellular function. Although this process is fundamentally haphazard and uncontrollable, senescent decline and ageing is broadly influenced by genetic and extrinsic factors. Numerous gene mutations and treatments have been shown to extend the lifespan of diverse organisms ranging from the unicellular Saccharomyces cerevisiae to primates. It is becoming increasingly apparent that most such interventions ultimately interface with cellular stress response mechanisms, suggesting that longevity is intimately related to the ability of the organism to effectively cope with both intrinsic and extrinsic stress. Here, we survey the molecular mechanisms that link ageing to main stress response pathways, and mediate age-related changes in the effectiveness of the response to stress. We also discuss how each pathway contributes to modulate the ageing process. A better understanding of the dynamics and reciprocal interplay between stress responses and ageing is critical for the development of novel therapeutic strategies that exploit endogenous stress combat pathways against age-associated pathologies.     

肠道菌群代谢作用与人体健康关系的研究进展

人体肠道内寄居的大量共生微生物可以通过多方面作用影响人体健康,特别是肠道内菌群的代谢作用,及与人体自身代谢的交互作用在人类的健康促进与疾病的发生、发展中起着重要作用。本文从正反两面讨论了肠道菌群代谢作用对人体健康的影响,并进一步探讨了肠道菌群代谢在健康监测、疾病的预防与治疗,以及个体化医疗方面的运用。     

The regulation of mitochondrial morphology: intricate mechanisms and dynamic machinery

Mitochondria typically form a reticular network radiating from the nucleus, creating an interconnected system that supplies the cell with essential energy and metabolites. These mitochondrial networks are regulated through the complex coordination of fission, fusion and distribution events. While a number of key mitochondrial morphology proteins have been identified, the precise mechanisms which govern their activity remain elusive. Moreover, post translational modifications including ubiquitination, phosphorylation and sumoylation of the core machinery are thought to regulate both fusion and division of the network. These proteins can undergo several different modifications depending on cellular signals, environment and energetic demands of the cell. Proteins involved in mitochondrial morphology may also have dual roles in both dynamics and apoptosis, with regulation of these proteins under tight control of the cell to ensure correct function. The absolute reliance of the cell on a functional mitochondrial network is highlighted in neurons, which are particularly vulnerable to any changes in organelle dynamics due to their unique biochemical requirements. Recent evidence suggests that defects in the shape or distribution of mitochondria correlate with the progression of neurodegenerative diseases such as Alzheimer's, Huntington's and Parkinson's disease. This review focuses on our current understanding of the mitochondrial morphology machinery in cell homeostasis, apoptosis and neurodegeneration, and the post translational modifications that regulate these processes.