Mise à jour thérapeutique et pronostique de la rupture utérine dans une maternité à Bangui, CAR.

BACKGROUND: Maternal mortality rates remain high (882/100,000 births) in the Central African Republic (CAR), primarily due to frequent obstetric complications. Médecins Sans Frontières supports a referral maternity ward in the capital, Bangui. OBJECTIVES: To describe the prevalence, associated factors and fatality of one of the most severe complications, uterine rupture, as well as the effect of a history of uterine surgery. METHODS: This is a cross-sectional study based on retrospectively collected data between January 2018 and December 2021 for women who delivered new-borns weighing over 1,000 g. RESULTS: Of 38,782 deliveries, 229 (0.6%) cases of uterine rupture were recorded. Factors associated with uterine rupture were parity ⩾5 (adjusted odds ratio [aOR] 7.5, 95% confidence interval [CI] 4.6-12.2), non-occipital foetal presentation (aOR 2.8, 95% CI 2.1-3.7) and macrosomia (OR 4, 95% CI 2.6-6.4). The fatality rate was 4.4%, and the stillbirth rate was 64%. Uterine rupture occurred in non-scarred uterus in 150 (66.1%) women. Adverse outcomes were more common in cases of uterine rupture on non-scarred uterus compared to scarred uterus, with higher maternal mortality (6% vs. 0%, P = 0.023) and lower Apgar scores (<2) for new-borns (69.1% vs. 45.8%, P < 0.001). CONCLUSION: Uterine rupture remains a major issue for maternal and perinatal health in the CAR, and efforts are needed to early detect risk factors and increase coverage of the comprehensive emergency obstetric and neonatal care.

Influence of BMI and smoking on IUI outcome with partner and donor sperm.

There is limited literature on the influence of smoking and BMI on success rates after intrauterine insemination (IUI). As a result of a prospective cohort study we could investigate data from 1401 IUI cycles with partner semen and 1264 IUI cycles with donor semen, primary outcome being clinical pregnancy rate (CPR). Univariate statistical analysis showed significant influence of female BMI on clinical pregnancy in the partner insemination group (CPR of 6,5%, 8%, 16,3% and 9,4% for a female BMI < 20, 20-24.9, 25-29.9 and 3 30, p=0.032), while in the donor group this in uence was not signi cant (CPR respectively 11.1% (BMI< 20), 18.5% (20-24.9), 18.0% (25-29.9) and 14.7% for BMI 3 30). Multivariate analysis through generalized estimating equations (GEE) could not confirm this significant influence of female BMI on fecundity in the partner semen group. For smoking, univariate statistical analysis revealed male smoking to be a negative influence for the clinical pregnancy rate in the partner insemination group (10.9% CPR in couples with male non-smokers versus 5.9% with male partners smoking 1-14 cig/day, p=0.017). After multivariate GEE analysis this result remained significant (p< 0,01). In the donor semen group female non-smoking or smoking less than 15 cigarettes a day turned out to be significantly associated with a higher CPR compared to women smoking more than 15 cigarettes daily (16.8% and 24.5% versus 5.6%, p=0,01). These results were also significant after multivariate GEE analysis (p= 0,047 and p= 0,02).

The prognostic value of perifollicular blood flow in the outcome after assisted reproduction: a systematic review.

BACKGROUND: The overall final outcome of assisted reproductive technologies (ART) is still more often a failure than a success. Assessing perifollicular blood flow (PFBF) is one technique to predict and possibly improve this outcome. The aim was to provide a structured review of studies concerning PFBF and its prognostic value in patients undergoing ART, including IUI (intrauterine insemination). METHODS: PUBMED, EMBASE and Cochrane Database of Systematic Reviews were searched for relevant studies published until December 2016. As key words 'Perifollicular blood flow', 'IUI', 'IVF' and 'ICSI' were used. RESULTS: A total of 14 articles were included in the current review. The results are very heterogeneous, though there is evidence that measuring PFBF could be a good prognostic marker for oocyte and embryo quality, but even more for pregnancy rate after IVF/ICSI. This finding is not observed in studies concerning IUI. CONCLUSIONS: Our results highlight an urgent need to investigate the role for PFBF assessment by Power Doppler in ART in randomised controlled trials.

The Microscopic Structure of the Omentum in Healthy Dogs: The Mystery Unravelled.

The canine omentum has many valuable properties but is still an underestimated organ. It contributes in many ways to the protection of the peritoneal cavity through its versatility on immunological level, but also through its role during angiogenesis, absorption, adhesion and fat storage. Despite a wide range of applications, the basic structure of the omentum is not well documented. This study provides an insight in the microscopic structure of the canine omentum through both light microscopic and electron microscopic investigations. Two regions could be distinguished in the canine omentum: translucent and adipose-rich regions. The translucent regions were composed of two different layers: a continuous flattened mesothelium on top of a submesothelial connective tissue matrix. The adipose-rich regions consisted of a substantial layer of adipocytes on which a flattened continuous mesothelium was present. Between those two layers, a few strands of collagen fibres could be detected. Large aggregates of immune cells, the so-called milky spots, were not observed in the omentum of healthy dogs. Only a limited number of leucocytes, macrophages and neutrophils were found, scattered throughout the connective tissue in the translucent regions. At the level of the adipose-rich regions, the immunological population was virtually non-existent.

Prepubertal gonadectomy in cats: different surgical techniques and comparison with gonadectomy at traditional age.

Feasibility, surgical time and complications of different surgical techniques for prepubertal gonadectomy (PPG; 8-12 weeks of age) in cats were studied and compared to gonadectomy at traditional age (TAG; 6-8 months of age). Kittens were randomly assigned to PPG or TAG. Ovarian pedicle haemostasis for PPG was achieved by ligatures (n=47), vascular clips (n=50), bipolar electrocoagulation (n=50), or pedicle tie (n=50); for TAG (n=34) ligatures were used. In male cats, PPG consisted of closed castration by spermatic cord knot (n=92) or ligature (n=91) while TAG (n=34) was an open castration by spermatic cord knot. A linear (surgical time) and a logistic regression (complications) model were designed. Significance was set at 0.05. For female PPG, clips and coagulation were the fastest procedures; placement of ligatures was most time-consuming. In male PPG, knot placement was significantly faster than ligation. In both sexes, very few intraoperative or wound complications were observed, irrespective of the surgical technique used. Surgical times in females (ligatures) as well as in males (knot) were significantly shorter for PPG than for TAG. PPG was as safe as TAG, yet took less time to perform and did not result in a greater rate of postoperative complications.

The neuronal migration defect in mice with Zellweger syndrome (Pex5 knockout) is not caused by the inactivity of peroxisomal beta-oxidation.

The purpose of this study was to investigate whether deficient peroxisomal beta-oxidation is causally involved in the neuronal migration defect observed in Pex5 knockout mice. These mice are models for Zellweger syndrome, a peroxisome biogenesis disorder. Neocortical development was evaluated in mice carrying a partial or complete defect of peroxisomal beta-oxidation at the level of the second enzyme of the pathway, namely, the hydratase-dehydrogenase multifunctional/bifunctional enzymes MFP1/L-PBE and MFP2/D-PBE. In contrast to patients with multifunctional protein 2 deficiency who present with neocortical dysgenesis, impairment of neuronal migration was not observed in the single MFP2 or in the double MFP1/MFP2 knockout mice. At birth, the double knockout pups displayed variable growth retardation and about one half of them were severely hypotonic, whereas the single MFP2 knockout animals were all normal in the perinatal period. These results indicate that in the mouse, defective peroxisomal beta-oxidation does not cause neuronal migration defects by itself. This does not exclude that the inactivity of this metabolic pathway contributes to the brain pathology in mice and patients with complete absence of functional peroxisomes.

Prenatal and postnatal development of peroxisomal lipid-metabolizing pathways in the mouse.

The ontogeny of the following peroxisomal metabolic pathways was evaluated in mouse liver and brain: alpha-oxidation, beta-oxidation and ether phospholipid synthesis. In mouse embryos lacking functional peroxisomes (PEX5(-/-) knock-out), a deficiency of plasmalogens and an accumulation of the very-long-chain fatty acid C(26:0) was observed in comparison with control littermates, indicating that ether phospholipid synthesis and beta-oxidation are already active at mid-gestation in the mouse. Northern analysis revealed that the enzymes required for the beta-oxidation of straight-chain substrates are present in liver and brain during embryonic development but that those responsible for the degradation of branched-chain substrates are present only in liver from late gestation onwards. The expression pattern of transcripts encoding enzymes of the alpha-oxidation pathway suggested that alpha-oxidation is initiated in the liver around birth and is not active in brain throughout development. Remarkably, a strong induction of the mRNA levels of enzymes involved in alpha-oxidation and beta-oxidation was observed around birth in the liver. In contrast, enzyme transcripts that were expressed in brain were present at rather constant levels throughout prenatal and postnatal development. These results suggest that the defective ether phospholipid synthesis and/or peroxisomal beta-oxidation of straight-chain fatty acids might be involved in the pathogenesis of the prenatal organ defects in peroxisome-deficient mice and men.

Inactivation of the peroxisomal multifunctional protein-2 in mice impedes the degradation of not only 2-methyl-branched fatty acids and bile acid intermediates but also of very long chain fatty acids.

According to current views, peroxisomal beta-oxidation is organized as two parallel pathways: the classical pathway that is responsible for the degradation of straight chain fatty acids and a more recently identified pathway that degrades branched chain fatty acids and bile acid intermediates. Multifunctional protein-2 (MFP-2), also called d-bifunctional protein, catalyzes the second (hydration) and third (dehydrogenation) reactions of the latter pathway. In order to further clarify the physiological role of this enzyme in the degradation of fatty carboxylates, MFP-2 knockout mice were generated. MFP-2 deficiency caused a severe growth retardation during the first weeks of life, resulting in the premature death of one-third of the MFP-2(-/-) mice. Furthermore, MFP-2-deficient mice accumulated VLCFA in brain and liver phospholipids, immature C(27) bile acids in bile, and, after supplementation with phytol, pristanic and phytanic acid in liver triacylglycerols. These changes correlated with a severe impairment of peroxisomal beta-oxidation of very long straight chain fatty acids (C(24)), 2-methyl-branched chain fatty acids, and the bile acid intermediate trihydroxycoprostanic acid in fibroblast cultures or liver homogenates derived from the MFP-2 knockout mice. In contrast, peroxisomal beta-oxidation of long straight chain fatty acids (C(16)) was enhanced in liver tissue from MFP-2(-/-) mice, due to the up-regulation of the enzymes of the classical peroxisomal beta-oxidation pathway. The present data indicate that MFP-2 is not only essential for the degradation of 2-methyl-branched fatty acids and the bile acid intermediates di- and trihydroxycoprostanic acid but also for the breakdown of very long chain fatty acids.

ATP-induced Ca2+ signals in bronchial epithelial cells.

Ca2+-dependent Cl- secretion in the respiratory tract occurs physiologically or under pathophysiological conditions when inflammatory mediators are released. The mechanism of intracellular Ca2+ release was investigated in the immortalized bronchial epithelial cell line 16HBE14o-. Experiments on both intact and permeabilized cells revealed that only inositol 1,4,5-trisphosphate (InsP3) receptors and not ryanodine receptors are involved in intracellular Ca2+ release. The expression pattern of the three InsP3 receptor isoforms was assessed both at the mRNA and at the protein level. The level of expression at the mRNA level was type 3 (92.5%) >> type 2 (5.4%) > type 1 (2.1%) and this rank order was also observed at the protein level. The ATP-induced Ca2+ signals in the intact cell, consisting of abortive Ca2+ spikes or fully developed [Ca2+] rises and intracellular Ca2+ waves, were indicative of positive feedback of Ca2+ on the InsP3 receptors. Low Ca2+ concentrations stimulated and high Ca2+ concentrations inhibited InsP3-induced Ca2+ release in permeabilized 16HBE14o- cells. We localized a cytosolic Ca2+-binding site between amino acid residues 2077 and 2101 in the type-2 InsP3 receptor and between amino acids 2030 and 2050 in the type-3 InsP3 receptor by expressing the respective parts of these receptors as glutathione S-transferase fusion proteins in bacteria. We conclude that the InsP3 receptor isoforms expressed in 16HBE14o- cells (mainly type-3 and type-2) are stimulated by Ca2+ and that this phenomenon contributes to the ATP-induced Ca2+ signals in intact 16HBE14o- cells.