Susto, Coraje, and Abuse: Depression and Beliefs About Diabetes

Mexican immigrants in the US often incorporate folk beliefs into diabetes etiologies but little is known about the relationship between such beliefs and depression. This study examines the relationship of diabetes beliefs and depression among 404 first- and second-generation Mexican immigrants seeking diabetes care in safety-net clinics in Chicago and San Francisco. We used multivariate linear regression to compare the association of depression with beliefs that susto (fright), coraje (anger), and/or interpersonal abuse cause diabetes, adjusting for gender, age, income, education, diabetes duration, co-morbidities, language preference, and acculturation. We incorporated the belief that abuse causes diabetes based on previous ethnographic research. Individuals reporting belief that abuse contributes to diabetes were significantly more likely to report symptoms of depression before (β?=?1.37; p?相似文献   

How chimpanzees solve collective action problems

We presented small groups of chimpanzees with two collective action situations, in which action was necessary for reward but there was a disincentive for individuals to act owing to the possibility of free-riding on the efforts of others. We found that in simpler scenarios (experiment 1) in which group size was small, there was a positive relationship between rank and action with more dominant individuals volunteering to act more often, particularly when the reward was less dispersed. Social tolerance also seemed to mediate action whereby higher tolerance levels within a group resulted in individuals of lower ranks sometimes acting and appropriating more of the reward. In more complex scenarios, when group size was larger and cooperation was necessary (experiment 2), overcoming the problem was more challenging. There was highly significant variability in the action rates of different individuals as well as between dyads, suggesting success was more greatly influenced by the individual personalities and personal relationships present in the group.     

Does the {Delta}F508-CFTR mutation induce a proinflammatory response in human airway epithelial cells?

In the clinical setting, mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene enhance the inflammatory response in the lung to Pseudomonas aeruginosa (P. aeruginosa) infection. However, studies on human airway epithelial cells in vitro have produced conflicting results regarding the effect of mutations in CFTR on the inflammatory response to P. aeruginosa, and there are no comprehensive studies evaluating the effect of P. aeruginosa on the inflammatory response in airway epithelial cells with the ΔF508/ΔF508 genotype and their matched CF cell line rescued with wild-type (wt)-CFTR. CFBE41o- cells (ΔF508/ΔF508) and CFBE41o- cells complemented with wt-CFTR (CFBE-wt-CFTR) have been used extensively as an experimental model to study CF. Thus the goal of this study was to examine the effect of P. aeruginosa on gene expression and cytokine/chemokine production in this pair of cells. P. aeruginosa elicited a more robust increase in cytokine and chemokine expression (e.g., IL-8, CXCL1, CXCL2 and TNF-α) in CFBE-wt-CFTR cells compared with CFBE-ΔF508-CFTR cells. These results demonstrate that CFBE41o- cells complemented with wt-CFTR mount a more robust inflammatory response to P. aeruginosa than CFBE41o-ΔF508/ΔF508-CFTR cells. Taken together with other published studies, our data demonstrate that there is no compelling evidence to support the view that mutations in CFTR induce a hyperinflammatory response in human airway epithelial cells in vivo. Although the lungs of patients with CF have abundant levels of proinflammatory cytokines and chemokines, because the lung is populated by immune cells and epithelial cells there is no way to know, a priori, whether airway epithelial cells in the CF lung in vivo are hyperinflammatory in response to P. aeruginosa compared with non-CF lung epithelial cells. Thus studies on human airway epithelial cell lines and primary cells in vitro that propose to examine the effect of mutations in CFTR on the inflammatory response to P. aeruginosa have uncertain clinical significance with regard to CF.     

Regulation of phosphatidylcholine homeostasis by Sec14

Phosphatidylcholine is the major phospholipid in eukaryotic cells and serves as both a permeability barrier as well as a modulator of a plethora of cellular and biological functions. This review touches on the importance of proper regulation of phosphatidylcholine metabolism on health, and discusses how yeast genetics has contributed to furthering our understanding of the precise molecular events regulated by alterations in phosphatidylcholine metabolism. Yeast studies have determined that the phosphatidylcholine and (or) phosphatidylinositol binding protein, Sec14, is a major regulator of phosphatidylcholine homeostasis. Sec14 itself regulates vesicular transport from the Golgi, and the interrelationship between phosphatidylcholine metabolism and membrane movement within the cell is described in detail. The recent convergence of the yeast genetic studies with that of mammalian cell biology in how cells maintain phosphatidylcholine homeostasis is highlighted.     

Activity and expression of ecto-5′-nucleotidase/CD73 are increased by thyroid hormones in vascular smooth muscle cells

Extracellular nucleotides ATP, ADP, AMP and adenosine are well known signaling molecules of the cardiovascular system that are involved in several physiological processes: cell proliferation, platelet aggregation, inflammatory processes and vascular tonus. The levels of these molecules are controlled by ecto-NTPDases and ecto-5′-nucleotidase/CD73 (ecto-5′-NT/CD73) actions, which are responsible for the complete ATP degradation to adenosine. The thyroid hormones, thyroxine (T₄) and triiodothyronine (T₃), play important roles in the vascular system promoting vasodilatation. Here we investigated the influence of thyroid hormones on the enzyme cascade that catalyzes the interconversion of purine nucleotides in vascular smooth muscle cells (VSMC). Exposure of VSMCs to 50nM T₃ or T₄ did not change ATP and ADP hydrolysis significantly. However, the same treatment caused an increase of 75% in AMP hydrolysis, which was time-dependent but dose-independent. Moreover, T₃ treatment significantly increased ecto-5′-NT/CD73 mRNA expression, which suggests a genomic effect of this hormone upon ecto-5′-NT/CD73. In addition to the importance of the ecto-5′-NT in cell proliferation and differentiation, its overexpression could result in higher extracellular levels of adenosine, an important local vasodilatator molecule.     

The proteins encoded by the pogo-like Lemi1 element bind the TIRs and subterminal repeated motifs of the Arabidopsis Emigrant MITE: consequences for the transposition mechanism of MITEs

MITEs (miniature inverted-repeated transposable elements) are a particular class of defective DNA transposons usually present within genomes as high copy number populations of highly homogeneous elements. Although an active MITE, the mPing element, has recently been characterized in rice, the transposition mechanism of MITEs remains unknown. It has been proposed that transposases of related transposons could mobilize MITEs in trans. Moreover, it has also been proposed that the presence of conserved terminal inverted-repeated (TIR) sequences could be the only requirement of MITEs for mobilization, allowing divergent or unrelated elements to be mobilized by a particular transposase. We present here evidence for a recent mobility of the Arabidopsis Emigrant MITE and we report on the capacity of the proteins encoded by the related Lemi1 transposon, a pogo-related element, to specifically bind Emigrant elements. This suggests that Lemi1 could mobilize Emigrant elements and makes the Lemi1/Emigrant couple an ideal system to study the transposition mechanism of MITEs. Our results show that Lemi1 proteins bind Emigrant TIRs but also bind cooperatively to subterminal repeated motifs. The requirement of internal sequences for the formation of proper DNA/protein structure could affect the capacity of divergent MITEs to be mobilized by distantly related transposases.     

Does Temporal Variation in Predation Risk Influence the Intensity of Antipredator Responses? A Test of the Risk Allocation Hypothesis

Temporal variation in predation risk may fundamentally influence antipredator responses of prey animals. To maximize lifetime fitness, prey must be able to optimize energy gain and minimize predation risk, and responses to current levels of risk may be influenced by background levels of risk. A ‘risk allocation’ model has recently been proposed to predict the intensity of antipredator responses that should occur as predation risk varies over time. Prey animals from high‐risk environments should respond to predators with relatively low intensities of antipredator behaviour because long periods of antipredator behaviour may result in unacceptable decreases in levels of foraging activity. Moreover, animals that are under frequent risk should devote more energy to foraging during brief pulses of safety compared with animals under infrequent attack. In this study, we experimentally tested the risk allocation hypothesis. We exposed juvenile rainbow trout, Oncorhynchus mykiss, to three levels of risk (high, moderate and low) crossed with two levels of temporal variation (exposed to risk three times a day and once a day). In accordance with the model, we found that trout exposed to risky situations more frequently responded with significantly less intense antipredator behaviour than trout exposed to risk infrequently. The intensity of response of trout exposed to moderate risk three times a day decreased to levels similar to situations of no risk. However, in contrast to the second prediction of the model, animals under frequent risk were not more active during periods of safety compared with animals under infrequent risk. Although behaviour in the face of predation risk was dependent on the broader temporal context in which risk varied, the specific predictions of the risk allocation model were only partly supported.     

Tenacibaculosis infection in marine fish caused by Tenacibaculum maritimum: a review

Tenacibaculum maritimum is the aetiological agent of an ulcerative disease known as tenacibaculosis, which affects a large number of marine fish species in the world and is of considerable economic significance to aquaculture producers. Problems associated with epizootics include high mortality rates, increased susceptibility to other pathogens, high labour costs of treatment and enormous expenditures on chemotherapy. In the present article we review current knowledge on this bacterial pathogen, focusing on important aspects such as the phenotypic, serologic and genetic characterization of the bacterium, its geographical distribution and the host species affected. The epizootiology of the disease, the routes of transmission and the putative reservoirs of T. maritimum are also discussed. We include a summary of molecular diagnostic procedures, the current status of prevention and control strategies, the main virulence mechanisms of the pathogen, and we attempt to highlight fruitful areas for continued research.     

Comprehensive mutational analysis of yeast DEXD/H box RNA helicases involved in large ribosomal subunit biogenesis

DEXD/H box putative RNA helicases are required for pre-rRNA processing in Saccharomyces cerevisiae, although their exact roles and substrates are unknown. To characterize the significance of the conserved motifs for helicase function, a series of five mutations were created in each of the eight essential RNA helicases (Has1, Dbp6, Dbp10, Mak5, Mtr4, Drs1, Spb4, and Dbp9) involved in 60S ribosomal subunit biogenesis. Each mutant helicase was screened for the ability to confer dominant negative growth defects and for functional complementation. Different mutations showed different degrees of growth inhibition among the helicases, suggesting that the conserved regions do not function identically in vivo. Mutations in motif I and motif II (the DEXD/H box) often conferred dominant negative growth defects, indicating that these mutations do not interfere with substrate binding. In addition, mutations in the putative unwinding domains (motif III) demonstrated that conserved amino acids are often not essential for function. Northern analysis of steady-state RNA from strains expressing mutant helicases showed that the dominant negative mutations also altered pre-rRNA processing. Coimmunoprecipitation experiments indicated that some RNA helicases associated with each other. In addition, we found that yeasts disrupted in expression of the two nonessential RNA helicases, Dbp3 and Dbp7, grew worse than when either one alone was disrupted.