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Many Mechanisms (many + mechanism)
Selected AbstractsWhat Is the mechanism of SIDS?DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2009Clues from epidemiology Abstract The cause of sudden infant death syndrome (SIDS) is unknown. Many mechanisms have been postulated, although thermal stress, rebreathing of expired gases and infection/inflammation seem the most viable hypotheses for the causation of SIDS. Deaths from SIDS have reduced dramatically following the recommendation not to place infants to sleep prone. Epidemiological data have shown that prone sleeping position is more risky in winter, colder latitudes, higher altitudes, if the infant is unwell or has excessive bedding or clothing. This suggests prone sleeping position involves either directly or indirectly a thermal mechanism. SIDS caused by an infective/inflammatory mechanism might be associated with deaths occurring during the night. Rebreathing of expired gases, airway obstruction, long QT syndrome and other genetic conditions may explain a small number of sudden unexpected deaths in infancy. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 215,222, 2009 [source] Predictions and tests of climate-based hypotheses of broad-scale variation in taxonomic richnessECOLOGY LETTERS, Issue 12 2004David J. Currie Abstract Broad-scale variation in taxonomic richness is strongly correlated with climate. Many mechanisms have been hypothesized to explain these patterns; however, testable predictions that would distinguish among them have rarely been derived. Here, we examine several prominent hypotheses for climate,richness relationships, deriving and testing predictions based on their hypothesized mechanisms. The ,energy,richness hypothesis' (also called the ,more individuals hypothesis') postulates that more productive areas have more individuals and therefore more species. More productive areas do often have more species, but extant data are not consistent with the expected causal relationship from energy to numbers of individuals to numbers of species. We reject the energy,richness hypothesis in its standard form and consider some proposed modifications. The ,physiological tolerance hypothesis' postulates that richness varies according to the tolerances of individual species for different sets of climatic conditions. This hypothesis predicts that more combinations of physiological parameters can survive under warm and wet than cold or dry conditions. Data are qualitatively consistent with this prediction, but are inconsistent with the prediction that species should fill climatically suitable areas. Finally, the ,speciation rate hypothesis' postulates that speciation rates should vary with climate, due either to faster evolutionary rates or stronger biotic interactions increasing the opportunity for evolutionary diversification in some regions. The biotic interactions mechanism also has the potential to amplify shallower, underlying gradients in richness. Tests of speciation rate hypotheses are few (to date), and their results are mixed. [source] Understanding cisplatin resistance using cellular modelsIUBMB LIFE, Issue 11 2007Britta Stordal Abstract Many mechanisms of cisplatin resistance have been proposed from studies of cellular models of resistance including changes in cellular drug accumulation, detoxification of the drug, inhibition of apoptosis and repair of the DNA adducts. A series of resistant models were developed from CCRF-CEM leukaemia cells with increasing doses of cisplatin from 100 ng/ml. This produced increasing resistance up to 7-fold with a treatment dose of 1.6 ,g/ml. Cisplatin resistance in these cells correlated with increases in the antioxidant glutathione, yet treatment with buthionine sulphoximine, an inhibitor of glutathione synthesis, had no effect on resistance, suggesting that the increase in glutathione was not directly involved in cisplatin resistance. Two models were developed from H69 SCLC cells, H69-CP and H69CIS200 using 100 ng/ml or 200 ng/ml cisplatin respectively. Both cell models were 2-4 fold resistant to cisplatin, and have decreased expression of p21 which may increase the cell's ability to progress through the cell cycle in the presence of DNA damage. Both the H69-CP and H69CIS200 cells showed no decrease in cellular cisplatin accumulation. However, the H69-CP cells have increased levels of cellular glutathione and are cross resistant to radiation whereas the H69CIS200 cells have neither of these changes. This suggests that increases in glutathione may contribute to cross-resistance to other drugs and radiation, but not directly to cisplatin resistance. There are multiple resistance mechanisms induced by cisplatin treatment, even in the same cell type. How then should cisplatin-resistant cancers be treated? Cisplatin-resistant cell lines are often more sensitive to another chemotherapeutic drug paclitaxel (H69CIS200), or are able to be sensitized to cisplatin with paclitaxel pre-treatment (H69-CP). The understanding of this sensitization by paclitaxel using cell models of cisplatin resistance will lead to improvements in the clinical treatment of cisplatin resistant tumours. IUBMB Life, 59: 696-699, 2007 [source] REVIEW ARTICLE: Hyperglycemia: a prothrombotic factor?JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2010B. A. LEMKES Summary., Diabetes mellitus is characterized by a high risk of atherothrombotic events. What is more, venous thrombosis has also been found to occur more frequently in this patient group. This prothrombotic condition in diabetes is underpinned by laboratory findings of elevated coagulation factors and impaired fibrinolysis. Hyperglycemia plays an important role in the development of these hemostatic abnormalities, as is illustrated by the association with glycemic control and the improvement upon treatment of hyperglycemia. Interestingly, stress induced hyperglycemia, which is often transient, has also been associated with poor outcome in thrombotic disease. Similar laboratory findings suggest a common effect of acute vs. chronic hyperglycemia on the coagulation system. Many mechanisms have been proposed to explain this prothrombotic shift in hyperglycemia, such as a direct effect on gene transcription of coagulation factors caused by hyperglycemia-induced oxidative stress, loss of the endothelial glycocalyx layer, which harbours coagulation factors, and direct glycation of coagulation factors, altering their activity. In addition, both chronic and acute hyperglycemia are often accompanied by hyperinsulinemia, which has been shown to have prothrombotic effects as well. In conclusion, the laboratory evidence of the effects of both chronic and acute hyperglycemia suggests a prothrombotic shift. Additionally, hyperglycemia is associated with poor clinical outcome of thrombotic events. Whether intensive treatment of hyperglycemia can prevent hypercoagulability and improve clinical outcome remains to be investigated. [source] Regulation of bacterial gene expression by the NTP substrates of transcription initiationMOLECULAR MICROBIOLOGY, Issue 1 2008Charles L. Turnbough Summary Many mechanisms of gene regulation in bacteria do not employ repressor or activator proteins. One class of these mechanisms includes those in which the key regulatory element is the control of transcription initiation by the availability of NTP substrates. In this commentary, several distinct examples of initiating NTP-mediated gene regulation are discussed, including a mechanism reported by Krásnýet al. in this issue of Molecular Microbiology. These researchers show that during the stringent response induced by amino acid starvation of Bacillus subtilis, increases in the intracellular level of ATP permit upregulation of promoters with +1A start sites, while concurrent decreases in the intracellular level of GTP cause downregulation of promoters with +1G start sites. This regulation is restricted to stringently controlled promoters. [source] Obesity, serious mental illness and antipsychotic drugsDIABETES OBESITY & METABOLISM, Issue 7 2009Richard I. G. Holt The prevalence of overweight and obesity is higher in people with mental illness than in the general population. Body weight is tightly regulated by a complex system involving the cortex and limbic system, the hypothalamus and the gastrointestinal tract. While there are justifiable concerns about the weight gain associated with antipsychotic medication, it is too simplistic to ascribe all obesity in people with serious mental illness (SMI) to their drug treatment. The development of obesity in SMI results from the complex interaction of the genotype and environment of the person with mental illness, the mental illness itself and antipsychotic medication. There are dysfunctional reward mechanisms in SMI that may contribute to poor food choices and overeating. While it is clear that antipsychotics have profound effects to stimulate appetite, no one receptor interaction provides an adequate explanation for this effect, and many mechanisms are likely to be involved. The complexity of the system regulating body weight allows us to start to understand why some individuals appear much more prone to weight gain and obesity than others. [source] How many mechanisms do regulatory T cells need?EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 4 2008Dario Vignali Dr. Abstract A plethora of new regulatory T cell (Treg) mechanisms have recently emerged. This raises two important questions. First, how many molecules or mechanisms are required for Treg to work? Second, how should we evaluate the contribution of any given Treg molecule/mechanism and how is this likely to relate (or not) to the phenotype seen in Scurfy/Foxp3-deficient mice? In this discussion piece, I will briefly outline our current understanding of the Treg arsenal and address these important questions. See accompanying commentary: http://dx.doi.org/10.1002/eji.200838143 [source] Co-option of endocytic functions of cellular caveolae by pathogensIMMUNOLOGY, Issue 1 2001J.-S. Shin Summary It is increasingly becoming clear that various immune cells are infected by the very pathogens that they are supposed to attack. Although many mechanisms for microbial entry exist, it appears that a common route of entry shared by certain bacteria, viruses and parasites involves cellular lipid-rich microdomains sometimes called caveolae. These cellular entities, which are characterized by their preferential accumulation of glycosylphosphatidylinositol (GPI)-anchored molecules, cholesterol and various glycolipids, and a distinct protein (caveolin), are present in many effector cells of the immune system including neutrophils, macrophages, mast cells and dendritic cells. These structures have an innate capacity to endocytoze various ligands and traffic them to different intracellular sites and sometimes, back to the extracellular cell surface. Because caveolae do not typically fuse with lysosomes, the ligands borne by caveolar vesicles are essentially intact, which is in marked contrast to ligands endocytozed via the classical endosome,lysosome pathway. A number of microbes or their exotoxins co-opt the unique features of caveolae to enter and traffic, without any apparent loss of viability and function, to different sites within immune and other host cells. In spite of their wide disparity in size and other structural attributes, we predict that a common feature among caveolae-utilizing pathogens and toxins is that their cognate receptor(s) are localized within plasmalemmal caveolae of the host cell. [source] Mechanisms in macroecology: AWOL or purloined letter?OIKOS, Issue 4 2010Towards a pragmatic view of mechanism Ecologists often believe the discovery of mechanism to be the central goal of scientific research. While many macroecologists have inherited this view, to date they have been much more efficient at producing patterns than identifying their underlying processes. We discuss several possible attitudes for macroecologists to adopt in this context while also arguing that in fact macroecology already has many mechanisms that are ignored. We briefly describe six of these: central limit theorem, fractals, random sampling and placement, neutral theory (and descendents), concordance of forces, and maximum entropy. We explore why these mechanisms are overlooked and discuss whether they should be. We conclude that macroecology needs to take a more pragmatic, less ideological approach to mechanism. We apply this viewpoint to the recent controversy over maximum entropy and suggest that maximum entropy needs to be viewed more pragmatically and less ideologically. [source] Spatial distributions of tree species in a subtropical forest of ChinaOIKOS, Issue 4 2009Lin Li The spatial dispersion of individuals in a species is an important pattern that is controlled by many mechanisms. In this study we analyzed spatial distributions of tree species in a large-scale (20 ha) stem-mapping plot in a species-rich subtropical forest of China. O-ring statistic was used to measure spatial patterns of species with abundance >10. ,0,10, the mean conspecific density within 10 m of a tree, was used as a measure of the intensity of aggregation of a species. Our results showed: (1) aggregated distribution was the dominant pattern in the plot. The percentage of aggregated species decreased with increased spatial scale. (2) The percentages of significantly aggregated species decreased from abundant to intermediate and to rare species. Rare species was more strongly aggregated than common species. Aggregation was weaker in larger diameter classes. (3) Seed traits determined the spatial patterns of trees. Seed dispersal mode can influence spatial patterns of species, with species dispersed by both modes being less clumped than species dispersed by animal or wind, respectively. Considering these results, we concluded that seed dispersal limitation, self-thinning and habitat heterogeneity primarily contributed to spatial patterns and species coexistence in the forest. [source] Laryngeal sensitivity in the neonatal period: From bench to bedsidePEDIATRIC PULMONOLOGY, Issue 8 2007Philippe Reix MD Abstract Laryngeal sensitivity in the newborn has been a subject of great interest for both researchers and clinicians for a number of years. From a clinical standpoint, laryngeal sensitivity is essential for both preventing foreign substances from entering into the lower airway and for finely tuning upper airway resistance. However, heightened reflexes originating from the laryngeal receptors in newborns and infants, due to neural immaturity, can lead to potentially dangerous cardiorespiratory events. The latter have been linked to apneas of prematurity, apparent life-threatening events, and sudden infant death syndrome (SIDS). From a physiological standpoint, many mechanisms pertaining to reflexes originating from laryngeal receptors are yet to be fully understood. This short review is an attempt to summarize current knowledge on laryngeal sensitivity and its potential consequences upon control of breathing abnormalities encountered within the first weeks of life. Pediatr Pulmonol. 2007; 42:674,682. © 2007 Wiley-Liss, Inc. [source] Immigration, employment relations, and health: Developing a research agendaAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 4 2010Joan Benach Abstract Background International migration has emerged as a global issue that has transformed the lives of hundreds of millions of persons. Migrant workers contribute to the economic growth of high-income countries often serving as the labour force performing dangerous, dirty and degrading work that nationals are reluctant to perform. Methods Critical examination of the scientific and "grey" literatures on immigration, employment relations and health. Results Both lay and scientific literatures indicate that public health researchers should be concerned about the health consequences of migration processes. Migrant workers are more represented in dangerous industries and in hazardous jobs, occupations and tasks. They are often hired as labourers in precarious jobs with poverty wages and experience more serious abuse and exploitation at the workplace. Also, analyses document migrant workers' problems of social exclusion, lack of health and safety training, fear of reprisals for demanding better working conditions, linguistic and cultural barriers that minimize the effectiveness of training, incomplete OHS surveillance of foreign workers and difficulty accessing care and compensation when injured. Therefore migrant status can be an important source of occupational health inequalities. Conclusions Available evidence shows that the employment conditions and associated work organization of most migrant workers are dangerous to their health. The overall impact of immigration on population health, however, still is poorly understood and many mechanisms, pathways and overall health impact are poorly documented. Current limitations highlight the need to engage in explicit analytical, intervention and policy research. Am. J. Ind. Med. 53:338,343, 2010. © 2009 Wiley-Liss, Inc. [source] Dermatitis caused by physical irritantsBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2002R. Morris-Jones SummaryBackground Although physical irritant contact dermatitis (PICD) is a common occupational dermatosis, it is one of the least well understood because of its multiple types, lack of diagnostic test, and the many mechanisms involved in its production. Objectives To characterize the materials and mechanisms of physical irritation of the skin. Methods We did a retrospective analysis over the past 20 years of all patients with a diagnosis of PICD at St John's Institute of Dermatology Contact Dermatitis Clinic. Results Of the 29 000 patients who attended the clinic over the study period, 392 patients were diagnosed with PICD and of these, 335 files were analysed. Conclusions Our findings show that PICD accounted for 1·15% of all patients attending the contact clinic over the study period. Diverse occupations and materials were implicated. The most common cause of PICD was low humidity due to air-conditioning, which caused dermatitis of the face and neck in office workers due to drying out of the skin. [source] Can we face the challenge of expanding use of intravenous immunoglobulin in neurology?ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2010I. Elovaara Elovaara I, Hietaharju A. Can we face the challenge of expanding use of intravenous immunoglobulin in neurology? Acta Neurol Scand: 2010: 122: 309,315. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. The use of high-dose polyclonal intravenous immunoglobulin (IVIG) in the treatment of autoimmune neurological diseases has expanded over the last decade. Based on controlled clinical trials IVIG can be considered currently as the first-line treatment in Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy and multifocal motor neuropathy, and it may be used as a rescue therapy in worsening myasthenia gravis. IVIG is a second-line therapy in dermatomyositis, stiff-person syndrome and pregnancy-associated or postpartum relapses of multiple sclerosis. Although the biological efficacy of IVIG is due to multiple effects on the immune system, many mechanisms are still unknown. The awareness of risks and complications of IVIG therapy has increased, but severe side effects are still considered rare. Due to increasing costs of this treatment, careful selection of patients who will benefit from IVIG is extremely important. [source] | |||||||||||||