Antagonistic and synergistic interactions between aluminum and manganese on growth of Vigna unguiculata at low ionic strength

Concentrations of soluble aluminum (Al) and manganese (Mn) frequently reach phytotoxic levels in acid soils. While dose response relationships for these metals are well documented, the effects of combined exposure have received less attention. We have examined the effect of combinations of Al and Mn on growth and metal accumulation in Vigna unguiculata (L.) Walp. grown in solution culture under conditions of low ionic strength (conductivities typically < 100 µS cm⁻¹). The nature of interaction between these metals varied with the specific physiological response, the part of the plant investigated, and the relative amount of stress imposed. Analysis of growth data provided evidence for amelioration of metal toxicity (antagonistic effects), although this effect was dose dependent. Analysis of metal content data provided evidence for antagonistic and synergistic (exacerbation of toxicity) effects, again depending on dose. Analysis of foliar symptoms also provided evidence for antagonisms and synergisms, with the nature of the response dependent on the specific physiological response and specific plant part investigated. In contrast with previous reports, evidence for antagonistic, synergistic, and multiplicative effects on growth, metal uptake, and expression of foliar symptoms have been obtained under physiologically and environmentally relevant conditions. These results suggest a more detailed analysis of the potential for interactions between metals in the environment is required.     

抑郁症易感基因和抗抑郁药物靶点相关[]神经细胞类型及相互作用网络分析

基于抑郁症的全基因组关联分析研究(GWAS),对于获得的单核苷酸多态性位点(SNP)使用Haploreg软件进行基因注释,得到SNP注释的102个易感基因.。使用MAGMA软件对GWAS的汇总统计数据做基因水平的分析,获得了270个校正之后显著的基因,两者合并共得到320个抑郁症易感基因。通过药物数据库Drugbank获取133个抗抑郁药物靶点基因。使用EWCE包对抑郁症易感基因和抗抑郁药物靶点在三套脑组织单细胞测序数据中,分别进行神经细胞类型富集分析。结果发现大脑皮质的GABA神经元(抑制性神经元)和谷氨酸能神经元(兴奋性神经元)是抑郁症易感基因和抗抑郁药物靶点共同的神经元。这两种类型的神经细胞可能是抗抑郁药物与抑郁症易感基因相互作用的神经细胞,另外少突胶质前体细胞可能是抑郁症特有的易感神经细胞。使用Network Calculator软件构建网络并进行进行网络拓扑学参数分析。结果表明抑郁症易感基因与抗抑郁药物靶点组成了一个具有显著的相互连接的网络。本研究从单细胞层面揭示抑郁症的遗传机制,在网络层面为寻找新的抗抑郁药物靶点提供了一定的启示。     

Factors associated with maternal depressive symptoms among low-income,African American smokers enrolled in a secondhand smoke reduction programme

Introduction Maternal depressive symptoms increase the risk of poor maternal and child health outcomes, and are a primary barrier to health behaviour change. Social cognitive theory can guide our understanding of risk factors that may have an impact on maternal depressive symptoms. The aim of this paper was to understand the correlates of maternal depressive symptoms among low-income African American smokers completing a 16-week intervention trial to reduce young children''s second-hand smoke exposure (SHSe).Methods This study presents a secondary analysis of depression symptoms among 227 maternal smokers completing the SHSe-reduction trial. The end-of-treatment Center of Epidemiologic Studies Depression Scale (CES-D) score was used to assess depressive symptoms (dichotomised as 0 = score of < 16 and 1 = score of ≥ 16). Multivariate logistic regression analysis was used to test the one-way hypothesis that odds of significant depressive symptoms would be associated with greater total number of household smokers, greater number of paediatric sick visits, greater daily exposure of child to cigarette smoke by their mother, greater life-event stress, and lower social support, marital status, employment status and level of educational attainment.Results Number of household smokers (OR = 1.57, P = 0.049), social support (OR = 0.88, P < 0.001) and life-event stress (OR = 1.04, P = 0.001) predicted significant maternal depressive symptoms; all other variables were not significant predictors in the model.Conclusion Number of household smokers is a novel risk factor for understanding significant maternal depressive symptoms in the context of a childhood SHSe-reduction trial. Improving our understanding of the household-level social milieu in the context of SHSe-reduction interventions will assist in reducing the risk of maternal depressive symptoms.     

Redox homeostasis is compromised in vivo by the metabolites accumulating in 3-hydroxy-3-methylglutaryl-CoA lyase deficiency in rat cerebral cortex and liver

Abstract

3-Hydroxy-3-methylglutaryl-CoA lyase (HL) deficiency is a disorder biochemically characterized by the predominant accumulation of 3-hydroxy-3-methylglutarate (HMG), 3-methylglutarate (MGA), 3-methylglutaconate and 3-hydroxyisovalerate in tissues and biological fluids of the affected patients. Neurological symptoms and hepatopathy are commonly found in HL deficiency, especially during metabolic crises. Since the mechanisms of tissue damage in this disorder are not well understood, in the present study we evaluated the ex vivo effects of acute administration of HMG and MGA on important parameters of oxidative stress in cerebral cortex and liver from young rats. In vivo administration of HMG and MGA provoked an increase of carbonyl and carboxy-methyl-lysine formation in cerebral cortex, but not in liver, indicating that these metabolites induce protein oxidative damage in the brain. We also verified that HMG and MGA significantly decreased glutathione concentrations in both cerebral cortex and liver, implying a reduction of antioxidant defenses. Furthermore, HMG and MGA increased 2’,7’-dichlorofluorescin oxidation, but did not alter nitrate and nitrite content in cerebral cortex and liver, indicating that HMG and MGA effects are mainly mediated by reactive oxygen species. HMG and MGA also increased the activities of superoxide dismutase and catalase in cerebral cortex and liver, whereas MGA decreased glutathione peroxidase activity in cerebral cortex. Our present data showing a disruption of redox homeostasis in cerebral cortex and liver caused by in vivo administration of HMG and MGA suggest that this pathomechanism may possibly contribute to the brain and liver abnormalities observed in HL-deficient patients.     

Toxicities of soluble Al, Cu, and La include ruptures to rhizodermal and root cortical cells of cowpea

Elevated levels of many metals are toxic to plant roots, but their modes of action are not well understood. We investigated the toxicities of aluminium (Al), copper (Cu), and lanthanum (La) in solution on the growth and external morphology of 3-d-old cowpea (Vigna unguiculata L.) roots for periods of up to 48 h. Root elongation rate decreased by 50% at ca. 30 μM Al, 0.3 μM Cu, or 2.0 μM La, accompanied by a decrease in the distance from the root tip to the proximal lateral root. Kinks developed in some roots 2.0 ± 0.4 mm from the root apex on exposure to Al or La (but not Cu). Light and scanning electron microscopy showed that soluble Al, Cu, or La caused similar transverse ruptures to develop > 1 mm from the root apex through the breaking and separation of the rhizodermis and outer cortex from inner-layers. The metals differed, however, in the range in concentration at which they had this effect; developing in solutions containing 54 to‑600 μM Al, but only from 0.85 to 1.8 μM Cu or 2.0 to 5.5 μM La. These findings suggest that Al, Cu, and La bind to the walls of cells, causing increased cell wall rigidity and eventual cell rupturing of the rhizodermis and outer cortex in the elongating zone. We propose that this is a major toxic effect of Al, and that Cu and La also have additional toxic effects.     

Valproic acid inhibits substance P-induced activation of protein kinase C epsilon and expression of the substance P receptor

The neuropeptide substance P (SP) has been hypothesized to be involved in the etiopathology of affective disorders. This hypothesis is based on the findings that neurokinin-1-receptor antagonists have antidepressant effects in depressed patients and that SP may worsen mood. In this study, we investigated the effect of the mood-stabilizing agents valproic acid (VPA), carbamazepine, and lithium on SP-induced gene expression. As a model system, we used primary rat astrocytes and human astrocytoma cells, which both express functional SP-receptors and, upon stimulation with SP, synthesize interleukin-6 (IL-6), a cytokine which has been shown to be elevated during the acute depressive state. We found that VPA dose-dependently inhibited SP-induced IL-6 synthesis which was seen with pre-incubation periods of 30 min, 3, 7 and 14 days, whereas carbamazepine and lithium showed no inhibitory effect. The inhibitory effect of VPA was not mediated by inhibition of the stress-regulated kinases p38 and p42/44 (Erk1/2) but by inhibition of protein kinase C epsilon activation. Furthermore, VPA down-regulated the expression of the substance P receptor (neurokinin(NK)-1-receptor) as assessed by real-time PCR. Whether both mechanisms contribute to the mood-stabilizing properties of VPA has to be evaluated in further studies.     

TRAINING LOAD,IMMUNE SYSTEM,UPPER RESPIRATORY SYMPTOMS AND PERFORMANCE IN WELL-TRAINED CYCLISTS THROUGHOUT A COMPETITIVE SEASON

This study aimed to evaluate the leukocyte subset counts, serum immunoglobulin A, performance and upper respiratory symptoms (URS), as well as their interrelationships, of well-trained cyclists for a 29-week training season using monitored loads. The season was divided into three phases: preparatory (nine weeks), first competitive phase (nine weeks) and second competitive phase (11 weeks). The sample consisted of eight well-trained cyclists, aged 18 ± 2 years. Immunological parameters and performance were evaluated during weeks 1 (baseline), 10 (early first competitive phase), 19 (early second competitive phase) and 29 (end of the second competitive phase). The training loads (volume x rating of perceived exertion) were monitored daily while the monitoring of URS was performed every 15 days using the WURSS-44 questionnaire. The data were analyzed using a one-way ANOVA and a Pearson correlation test with the significance level set at p ≤ 0.05. No significant differences were found for training load, leukocyte subset counts or serum immunoglobulin A among the three phases. However, serum immunoglobulin A was 50.9% below the control group values. URS were significantly higher during the preparatory period, and there were significant correlations between URS and training load (strain) in the preparatory period (r = 0.72, p = 0.032) and second competitive phase (r = 0.73, p = 0.036). In conclusion, indicators of training load without a significant change throughout the season did not significantly affect immune parameters measured; however, the increase of strain can cause an increase of upper respiratory symptoms throughout the season, but without loss of performance.     

Diagnosis of light leaf spot (Pyrenopeziza brassicae) on winter oilseed rape (Brassica napus) in the UK

Light leaf spot lesions were generally first observed as light green areas on leaves of UK winter oilseed rape crops in January or February and later became brittle and bleached. Elongated lesions, which were brown with indistinct edges, developed on stems in the spring and summer, when lesions were also observed on flower buds, pedicels and pods. Development of diagnostic white pustules (spore masses of Pyrenopeziza brassicae, which erupt through surfaces of infected tissues) for confirmation of light leaf spot infection on symptomless plants or plants with indistinct or ambiguous symptoms in the autumn, winter or spring was enhanced by incubating plants in polyethylene bags. In experiments with artificially inoculated plants, glasshouse-grown plants exposed in infected crops and plants sampled from crops, white pustules developed at all incubation temperatures from 2^oC to 20^oC on infected leaves of different cultivars. The period of incubation required before the appearance of pustules decreased as the time that had already elapsed since the initial infection increased. The longest periods of incubation were required at the lowest temperatures (2^oC or 5^oC) but leaves senesced and abscised from plants most quickly at the highest temperatures (15^oC or 20^oC), suggesting that the optimal incubation temperature was between 10^oC and 15^oC.     

The severity of psychiatric disorders

The issue of the severity of psychiatric disorders has great clinical importance. For example, severity influences decisions about level of care, and affects decisions to seek government assistance due to psychiatric disability. Controversy exists as to the efficacy of antidepressants across the spectrum of depression severity, and whether patients with severe depression should be preferentially treated with medication rather than psychotherapy. Measures of severity are used to evaluate outcome in treatment studies and may be used as meaningful endpoints in clinical practice. But, what does it mean to say that someone has a severe illness? Does severity refer to the number of symptoms a patient is experiencing? To the intensity of the symptoms? To symptom frequency or persistence? To the impact of symptoms on functioning or on quality of life? To the likelihood of the illness resulting in permanent disability or death? Putting aside the issue of how severity should be operationalized, another consideration is whether severity should be conceptualized similarly for all illnesses or be disorder specific. In this paper, we examine how severity is characterized in research and contemporary psychiatric diagnostic systems, with a special focus on depression and personality disorders. Our review shows that the DSM‐5 has defined the severity of various disorders in different ways, and that researchers have adopted a myriad of ways of defining severity for both depression and personality disorders, although the severity of the former was predominantly defined according to scores on symptom rating scales, whereas the severity of the latter was often linked with impairments in functioning. Because the functional impact of symptom‐defined disorders depends on factors extrinsic to those disorders, such as self‐efficacy, resilience, coping ability, social support, cultural and social expectations, as well as the responsibilities related to one's primary role function and the availability of others to assume those responsibilities, we argue that the severity of such disorders should be defined independently from functional impairment.     

Temperature response,pathogenicity, seed infection and mutant evaluation against Macrophomina phaseolina causing charcoal rot disease of sesame

Charcoal rot caused by Macrophomina phaseolina is a serious disease of sesame in Pakistan. M. phaseolina sesame isolate was subjected to growth rate test at 10, 15, 20, 25, 30, 35 and 40°C. The optimum temperature for fungal growth and microsclerotia production was found to be 30–35°C. Gray to black, radial fungal colonies with intermediate mycelial growth and jet black oval to round microsclerotia were observed at this optimum range. M. phaseolina was found to be pathogenic against all the 18 tested plant species and this pathogenicity proved its necrophytic behavior. Seed infection efficiency of M. phaseolina was 100% with significant reduction in seed index. For two consecutive years 21 mutants/varieties were screened in the field for their reactions to charcoal rot disease. During 2007 three mutants NS11704S1, NS11304S2 and NS26004 were ranked as resistant while others were moderately resistant to highly susceptible. During 2008 all mutants showed a susceptible to highly susceptible reaction with variable disease reactions. All over screening results revealed that four mutants viz, NS13P1, NS163-1, NS270P1 and NS26004 showed about 50% stand with consistent performance during both years under optimum disease conditions and can be used to manage the disease following the disease management strategies, however in the future improvement for high seed yield along with resistance is a prerequisite for sustainable high production.