Optimal gestational age at delivery for congenital diaphragmatic hernia.

OBJECTIVE: To evaluate the neonatal morbidity and mortality of babies with isolated congenital diaphragmatic hernia (CDH) according to gestational age at delivery. METHODS: We conducted a retrospective study in the University Hospitals of Antoine Béclère-Bicêtre and Leuven between January 1, 2010 and December 31, 2018. Isolated left-sided CDH cases were included. The Kaplan-Meier method was used to calculate cumulative survival at 28 days according to gestational age at delivery. The association between gestational age at delivery, as a continuous variable, and survival at 28 days was modeled using a fractional polynomial. Adjustment for position of the liver, management center, and mode of delivery was performed. The association was studied according to the severity of the CDH, defined by the o/e LHR, categorized in three classes: below 25%, between 25 and 45%, above 45%. RESULTS: We included 213 fetuses with isolated left-sided CDH, with a median gestational age at delivery of 38+2 WG [IQR: 37+0 -39+6 ]. Survival rates at 28 days and 6 months were 66.7% (142/213) and 64.3% (137/213), respectively. Kaplan-Meier curves showed higher survival up to 28 days for babies born between 37+0 and 39+0 WG than for those born after 39+0 WG (log-rank test, p<.001). In the subgroup of moderate forms, the survival rates at 28 days and 6 months were significantly higher for newborns delivered between 37+0 and 39+0 WG, compared to newborns delivered after 39+0 WG: 81.5% vs 61.5% (p=0.03). In this subgroup, 28-day survival significantly increased with advancing gestational age at birth until 38-39 WG (p=0.005) and significantly decreased from 39 WG. CONCLUSIONS: Delivery between 37+0 and 39+0 WG is associated with a higher survival rate at 28 days of life for moderate forms independently of intrathoracic liver, management center, and mode of delivery. This article is protected by copyright. All rights reserved.status: Published onlin

Fusarium oxysporum f. sp. radicis-vanillae is the causal agent of root and stem rot of vanilla

International audienceRoot and stem rot (RSR) is a very detrimental disease of vanilla worldwide. Fusarium oxysporum is frequently associated with the disease but other Fusarium species are also reported. In this international study, 52 vanilla plots were surveyed in three of the most important vanilla producing countries (Madagascar, Reunion Island and French Polynesia) in order to determine the aetiology of RSR disease. Subsets from the 377 single-spored Fusarium isolates recovered from rotten roots and stems in the surveys were characterized by molecular genotyping (EF1α and IGS gene sequences) and pathogenicity assays on Vanilla planifolia and V. ×tahitensis, the two commercially grown vanilla species. Fusarium oxysporum was shown to be the principal species responsible for the disease, representing 79% of the isolates recovered from the RSR tissues, 40% of which induced severe symptoms on inoculated plantlets. Fusarium oxysporum isolates were highly polyphyletic regardless of geographic origin or pathogenicity. Fusarium solani, found in 15% of the samples and inducing only mild symptoms on plantlets, was considered a secondary pathogen of vanilla. Three additional Fusarium species were occasionally isolated in the study (F. proliferatum, F. concentricum and F. mangiferae) but were nonpathogenic. Histopathological preparations observed in wide field and multiphoton microscopy showed that F. oxysporum penetrated the root hair region of roots, then invaded the cortical cells where it induced necrosis in both V. planifolia and V. ×tahitensis. The hyphae never invaded the root vascular system up to 9 days post-inoculation. As a whole, the data demonstrated that RSR of vanilla is present worldwide and that its causal agent should be named F. oxysporum f. sp. radicis-vanillae. (Résumé d'auteur

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Autoimmune Subepidermal Bullous Diseases of the Skin and Mucosae: Clinical Features, Diagnosis, and Management.

Autoimmune subepidermal blistering diseases of the skin and mucosae constitute a large group of sometimes devastating diseases, encompassing bullous pemphigoid, gestational pemphigoid, mucous membrane pemphigoid, epidermolysis bullosa acquisita, and anti-p200 pemphigoid. Their clinical presentation is polymorphic. These autoimmune blistering diseases are associated with autoantibodies that target distinct components of the basement membrane zone of stratified epithelia. These autoantigens represent structural proteins important for maintenance of dermo-epidermal integrity. Bullous pemphigoid (BP) is the most common subepidermal autoimmune blistering disease of the skin and mucosae. Although the disease typically presents with a generalized blistering eruption associated with itch, atypical variants with either localized bullous lesions or "non-bullous" presentations are observed in approximately 20% of patients. A peculiar form of BP typically associated with pregnancy is pemphigoid gestationis. In anti-p200 pemphigoid, patients present with tense blisters on erythematosus or normal skin resembling BP, with a predilection for acral surfaces. These patients have antibodies targeting the 200-kDa basement membrane protein. Epidermolysis bullosa is a rare autoimmune blistering disease associated with autoantibodies against type VII collagen that can have several phenotypes including a classical form mimicking dystrophic epidermolysis bullosa, an inflammatory presentation mimicking BP, or mucous membrane pemphigoid-like lesions. Mucous membrane pemphigoid (MMP) is the term agreed upon by international consensus for an autoimmune blistering disorder, which affects one or more mucous membrane and may involve the skin. The condition involves a number of different autoantigens in the basement membrane zone. It may result in severe complications from scarring, such as blindness and strictures. Diagnosis of these diseases relies on direct immunofluorescence microscopy studies and immunoserological assays. Management of affected patients is often challenging. We will here review the clinical and immunopathological features as well as the pathophysiology of this group of organ-specific autoimmune diseases. Finally, we will discuss the diagnostic approach and the principles of management in clinical practice