DEFICITS DE SOUTIENS ET DIFFICULTES D’ADAPTATION PSYCHOSOCIALE CHEZ LES ELEVES-MERES A ABIDJAN

This study has for objective to estimate the effects of the deficits of supports on the difficulties of psychosocial adaptation of pupil-mother. The site of the investigation is Abidjan (Ivory Coast). 195 people were questioned among which 180 pupils-mothers on the basis of a not probability sample, exactly a sample of snowball. The observation and the semi-direct interview were used. The meditative data were handled (treated) statistically under the descriptive and inferential angle and qualitatively with an accent on the phenomenology. The results of the study show that pupils-mothers show difficulties of psychosocial adaptation: change of humor, depression, aggressiveness, anxiety, instability, led panics. These difficulties are strongly bound to the deficits of family and institutional supports (disappointment, rejection and powerlessness, low institutional coverage. These results validate the ecological theories and the social link. For a better personal and social adjustment, pupils-mothers, a strengthening of the supports within the framework of the solidarities turns out to be necessary

A role for pancreatic beta-cell secretory hyperresponsiveness in catch-up growth hyperinsulinemia: Relevance to thrifty catch-up fat phenotype and risks for type 2 diabetes

Current notions about mechanisms by which catch-up growth predisposes to later type 2 diabetes center upon those that link hyperinsulinemia with an accelerated rate of fat deposition (catch-up fat). Using a rat model of semistarvation-refeeding in which catch-up fat is driven solely by elevated metabolic efficiency associated with hyperinsulinemia, we previously reported that insulin-stimulated glucose utilization is diminished in skeletal muscle but increased in white adipose tissue. Here, we investigated the possibility that hyperinsulinemia during catch-up fat can be contributed by changes in the secretory response of pancreatic beta-cells to glucose. Using the rat model of semistarvation-refeeding showing catch-up fat and hyperinsulinemia, we compared isocalorically refed and control groups for potential differences in pancreatic morphology and in glucose-stimulated insulin secretion during in situ pancreas perfusions as well as ex vivo isolated islet perifusions. Between refed and control animals, no differences were found in islet morphology, insulin content, and the secretory responses of perifused isolated islets upon glucose stimulation. By contrast, the rates of insulin secretion from in situ perfused pancreas showed that raising glucose from 2.8 to 16.7 mmol/l produced a much more pronounced increase in insulin release in refed than in control groups (p < 0.01). These results indicate a role for islet secretory hyperresponsiveness to glucose in the thrifty mechanisms that drive catch-up fat through glucose redistribution between skeletal muscle and adipose tissue. Such beta-cell hyperresponsiveness to glucose may be a key event in the link between catch-up growth, hyperinsulinemia and risks for later type 2 diabetes

Epidemiologically most successful SARS-CoV-2 variant: concurrent mutations in RNA-dependent RNA polymerase and spike protein

The D614G mutation of the Spike protein is thought to be relevant for SARS-CoV-2 infection. Here we report biological and epidemiological aspects of this mutation. Using pseudotyped lentivectors, we were able to confirm that the G614 variant of the Spike protein is markedly more infectious than the ancestral D614 variant. We demonstrate by molecular modelling that the replacement of aspartate by glycine in position 614 facilitates the transition towards an open state of the Spike protein. To understand whether the increased infectivity of the D614 variant explains its epidemiological success, we analysed the evolution of 27,086 high-quality SARS-CoV-2 genome sequences from GISAID. We observed striking coevolution of D614G with the P323L mutation in the viral polymerase. Importantly, exclusive presence of G614 or L323 did not become epidemiologically relevant. In contrast, the combination of the two mutations gave rise to a viral G/L variant that has all but replaced the initial D/P variant. There was no significant correlation between reported COVID mortality in different countries and the prevalence of the Wuhan versus G/L variant. However, when comparing the speed of emergence and the ultimate predominance in individual countries, the G/L variant displays major epidemiological supremacy. Our results suggest that the P323L mutation, located in the interface domain of the RNA-dependent RNA polymerase (RdRp), is a necessary alteration that led to the epidemiological success of the present variant of SARS-CoV-2

TRY plant trait database – enhanced coverage and open access

Plant traits - the morphological, anatomical, physiological, biochemical and phenological characteristics of plants - determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits - almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Mechanisms and functions of glutamate transport in betacell mitochondria for the control of insulin secretion

The mitochondrial glutamate carrier 1 (GC1) was previously cloned from human brain cDNA and showed high levels of expression in the whole pancreas. According to the role that glutamate might play in ß cells as an additive factor in glucose stimulated insulin secretion, it was of interest to determine if GC1 was expressed in insulin secreting cell lines as well as primary cells and to assess whether GC1 suppression would affect glucose stimulated insulin secretion. In the course of this study, we have demonstrated GC1 expression in pancreatic ß cells. The downregulation of GC1 had little impact on mitochondrial proton gradient although it promoted a decrease in glucose evoked insulin secretion at stimulatory glucose concentration. This defect in the secretory response was restored upon provision of cell permeant methyl-glutamate. In conclusion, we have shown that GC1 is necessary for the full development of glucose induced insulin secretion, although the exact site for glutamate action is currently unknown. Further investigation should delineate the specific role of GC1 in insulin release

Resveratrol long-term treatment differentiates INS-1E beta-cell towards improved glucose response and insulin secretion

The clonal INS-1E beta-cell line has proven to be instrumental for numerous studies investigating the mechanisms of glucose-stimulated insulin secretion. The composition of its culture medium has not changed over the years, although some compounds have been recently highlighted for their effects on tissue differentiation. The present study investigated the effects of long-term treatment of INS-1E cells with 1 μM resveratrol on glucose-stimulated insulin secretion, testing an extended glucose dose response. The data demonstrate that chronic exposure to low-dose resveratrol expands the range of the glucose dose response of INS-1E cells beyond 15 mM glucose. We also assessed whether such beneficial effects could be retained after resveratrol withdrawal from the culture medium. This was not the case as INS-1E cells deprived of resveratrol returned to the phenotype of naïve cells, i.e., exhibiting a plateau phase at 15 mM glucose. Of note, although resveratrol has antioxidant properties, it cannot substitute for β-mercaptoethanol normally present in the medium of INS-1E cells as a reducing agent. In conclusion, the addition of resveratrol as a standard component of the culture medium of INS-1E cells improves glucose-stimulated insulin secretion

Tissue specificity of mitochondrial glutamate pathways and the control of metabolic homeostasis

Glutamate is implicated in numerous metabolic and signalling functions that vary according to specific tissues. Glutamate metabolism is tightly controlled by activities of mitochondrial enzymes and transmembrane carriers, in particular glutamate dehydrogenase and mitochondrial glutamate carriers that have been identified in recent years. It is remarkable that, although glutamate-specific enzymes and transporters share similar properties in most tissues, their regulation varies greatly according to particular organs in order to achieve tissue specific functions. This is illustrated in this review when comparing glutamate handling in liver, brain, and pancreatic beta-cells. We describe the main cellular glutamate pathways and their specific functions in different tissues, ultimately contributing to the control of metabolic homeostasis at the organism level

Silencing of the mitochondrial NADH shuttle component aspartate-glutamate carrier AGC1/Aralar1 in INS-1E cells and rat islets

Transfer of reducing equivalents between cytosolic compartments and the mitochondrial matrix is mediated by NADH shuttles. Among these, the malate-aspartate shuttle has been proposed to play a major role in beta-cells for the control of glucose-stimulated insulin secretion. AGC1 or Aralar1 (aspartate-glutamate carrier 1) is a key component of the malate-aspartate shuttle. Overexpression of AGC1 increases the capacity of the malate-aspartate shuttle, resulting in enhanced metabolism-secretion coupling, both in INS-1E cells and rat islets. In the present study, knockdown of AGC1 was achieved in the same beta-cell models, using adenovirus-mediated delivery of shRNA (small-hairpin RNA). Compared with control INS-1E cells, down-regulation of AGC1 blunted NADH formation (-57%; P<0.05), increased lactate production (+16%; P<0.001) and inhibited glucose oxidation (-22%; P<0.01). This correlated with a reduced secretory response at 15 mM glucose (-25%; P<0.05), while insulin release was unchanged at intermediate 7.5 mM and basal 2.5 mM glucose. In isolated rat islets, efficient AGC1 knockdown did not alter insulin exocytosis evoked by 16.7 mM glucose. However, 4 mM amino-oxyacetate, commonly used to block transaminases of the malate-aspartate shuttle, inhibited glucose-stimulated insulin secretion to similar extents in INS-1E cells (-66%; P<0.01) and rat islets (-56%; P<0.01). These results show that down-regulation of the key component of the malate-aspartate shuttle AGC1 reduced glucose-induced oxidative metabolism and insulin secretion in INS-1E cells, whereas similar AGC1 knockdown in rat islets did not affect their secretory response