Atlantic Water Circulation and Properties Northwest of Svalbard During Anomalous Southerly Winds

Atlantic Water (AW), the main source of heat and salt for the Arctic Ocean, undergoes large transformations (cooling and freshening) north of Svalbard as it flows near the surface above the Yermak Plateau (YP). In September 2017, a SeaExplorer ocean glider deployed in the West Spitsbergen Current (WSC) and recovered north of Svalbard documented the circulation and properties of the AW crossing the YP. The glider sampled the different branches of the AW flowing into the Arctic around the YP: the WSC, the Svalbard Branch (SB), the Yermak Pass Branch, and the Yermak Branch. Unusual southerly winds prevailed in summer 2017 impacting AW circulation in the region. Cold and fresh lenses of shelf-origin waters detached from the slope in the WSC to reach their density level below the core of the AW. This resulted in cooling and freshening of the AW inflow from below. The eastward current associated with the SB was found to be weak at its usual location above the 400 m isobath, likely the result of the adjustment of the flow influenced by anomalous southerly wind conditions.publishedVersio

A new model depicting the role of PME during dehydration and germination of pollen grain

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Targeting of proConA to the Plant Vacuole depends on its Nine Amino-acid C-terminal Propeptide

Concanavalin A (ConA) is a well characterized and extensively used lectin accumulated in the protein bodies of jack bean cotyledons. ConA is synthesized as an inactive precursor proConA. The maturation of inactive proConA into biologically active ConA is a complex process including the removal of an internal glycopeptide and a C-terminal propeptide (CTPP), followed by a head-to-tail ligation of the two largest polypeptides. The cDNA encoding proConA was cloned and expressed in tobacco BY-2 cells. ProConA was slowly transported to the vacuole where its maturation into ConA was similar to that in jack bean cotyledons, apart from an incomplete final ligation. To investigate the role of the nine amino acid CTPP, a truncated form lacking the propeptide (proConAΔ9) was expressed in BY-2 cells. In contrast to proConA, proConAΔ9 was rapidly chased out of the endoplasmic reticulum (ER) and secreted into the culture medium. The CTPP was then fused to the C-terminal end of a secreted form of green fluorescent protein (secGFP). When expressed in tobacco BY-2 cells and leaf protoplasts, the chimaeric protein was located in the vacuole whereas secGFP was located in the culture medium and in the vacuole. Altogether, our results show we have isolated a new C-terminal vacuolar sorting determinan

Visualizing antibody affinity maturation in germinal centers

open12siAntibodies somatically mutate to attain high affinity in germinal centers (GCs). There, competition between B cell clones and among somatic mutants of each clone drives an increase in average affinity across the population. The extent to which higher-affinity cells eliminating competitors restricts clonal diversity is unknown. By combining multiphoton microscopy and sequencing, we show that tens to hundreds of distinct B cell clones seed each GC and that GCs lose clonal diversity at widely disparate rates. Furthermore, efficient affinity maturation can occur in the absence of homogenizing selection, ensuring that many clones can mature in parallel within the same GC. Our findings have implications for development of vaccines in which antibodies with nonimmunodominant specificities must be elicited, as is the case for HIV-1 and influenza.openTas J.M.J.; Mesin L.; Pasqual G.; Targ S.; Jacobsen J.T.; Mano Y.M.; Chen C.S.; Weill J.-C.; Reynaud C.-A.; Browne E.P.; Meyer-Hermann M.; Victora G.D.Tas, J. M. J.; Mesin, L.; Pasqual, G.; Targ, S.; Jacobsen, J. T.; Mano, Y. M.; Chen, C. S.; Weill, J. -C.; Reynaud, C. -A.; Browne, E. P.; Meyer-Hermann, M.; Victora, G. D

Loss of independence in Katz's ADL ability in connection with an acute hospitalization: early clinical markers in French older people

Background: The preservation of autonomy and the ability of elderly to carry out the basic activities of daily living, beyond the therapeutic care of any pathologies, appears as one of the main objectives of care during hospitalization. Objectives: To identify early clinical markers associated with the loss of independence in elderly people in short stay hospitals. Methods: Among the 1,306 subjects making up the prospective and multicenter SAFEs cohort study (Sujet Agé Fragile: Évolution et suivi—Frail elderly subjects, evaluation and follow-up), 619 medical inpatients, not disabled at baseline and hospitalized through an emergency department were considered. Data used in a multinomial logistic regression were obtained through a comprehensive geriatric assessment (CGA) conducted in the first week of hospitalization. Dependency levels were assessed at baseline, at inclusion and at 30days using Katz's ADL index. Baseline was defined as the dependence level before occurrence of the event motivating hospitalization. To limit the influence of rehabilitation on the level of dependence, only stays shorter than 30days were considered. Results: About 514 patients were eligible, 15 died and 90 were still hospitalized at end point (n=619). Two-thirds of subjects were women, with a mean age of 83. At day 30 162 patients (31%) were not disabled; 61 (12%) were moderately disabled and 291 severely disabled (57%). No socio-demographic variables seemed to influence the day 30 dependence level. Lack of autonomy (odds ratio (OR)=1.9, 95% confidence interval (CI)=1.2-3.6), walking difficulties (OR=2.7, 95% CI=1.3-5.6), fall risk (OR=2.1, 95% CI=1.3-6.8) and malnutrition risk (OR=2.2, 95% CI=1.5-7.6) were found in multifactorial analysis to be clinical markers for loss of independence. Conclusions: Beyond considerations on the designing of preventive policies targeting the populations at risk that have been identified here, the identification of functional factors (lack of autonomy, walking difficulties, risk of falling) suggests above all that consideration needs to be given to the organization per se of the French geriatric hospital care system, and in particular to the relevance of maintaining sector-type segregation between wards for care of acute care and those involved in rehabilitatio

Recurrent American Cutaneous Leishmaniasis

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Haploinsufficiency of Dmxl2, Encoding a Synaptic Protein, Causes Infertility Associated with a Loss of GnRH Neurons in Mouse

International audienceCharacterization of the genetic defects causing gonadotropic deficiency has made a major contribution to elucidation of the fundamental role of Kisspeptins and Neurokinin B in puberty onset and reproduction. The absence of puberty may also reveal neurodevelopmental disorders caused by molecular defects in various cellular pathways. Investigations of these neurodevelopmental disorders may provide information about the neuronal processes controlling puberty onset and reproductive capacity. We describe here a new syndrome observed in three brothers, which involves gonadotropic axis deficiency, central hypothyroidism, peripheral demyelinating sensorimotor polyneuropathy, mental retardation, and profound hypoglycemia, progressing to nonautoimmune insulin-dependent diabetes mellitus. High-throughput sequencing revealed a homozygous in-frame deletion of 15 nucleotides in DMXL2 in all three affected patients. This homozygous deletion was associated with lower DMXL2 mRNA levels in the blood lymphocytes of the patients. DMXL2 encodes the synaptic protein rabconnectin-3a, which has been identified as a putative scaffold protein for Rab3-GAP and Rab3-GEP, two regulators of the GTPase Rab3a. We found that rabconnectin-3a was expressed in exocytosis vesicles in gonadotropin-releasing hormone (GnRH) axonal extremities in the median eminence of the hypothalamus. It was also specifically expressed in cells expressing luteinizing hormone (LH) and follicle-stimulating hormone (FSH) within the pituitary. The conditional heterozygous deletion of Dmxl2 from mouse neurons delayed puberty and resulted in very low fertility. This reproductive phenotype was associated with a lower number of GnRH neurons in the hypothalamus of adult mice. Finally, Dmxl2 knockdown in an insulin-secreting cell line showed that rabconnectin-3a controlled the constitutive and glucose-induced secretion of insulin. In conclusion, this study shows that low levels of DMXL2 expression cause a complex neurological phenotype, with abnormal glucose metabolism and gonadotropic axis deficiency due to a loss of GnRH neurons. Our findings identify rabconectin-3a as a key controller of neuronal and endocrine homeostatic processes