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Severe acute respiratory syndrome caused by the novel coronavirus (SARS-CoV-2) is frequently associated with gastrointestinal manifestations. Herein we evaluated the interest in measuring the intestinal fatty acid-binding protein (I-FABP), a biomarker of intestinal injury, in COVID-19 patients. Serum I-FABP was analyzed in 28 consecutive patients hospitalized for a PCR-confirmed COVID-19, in 24 hospitalized patients with non-COVID-19 pulmonary diseases, and 79 patients admitted to the emergency room for abdominal pain. I-FABP serum concentrations were significantly lower in patients with COVID-19, as compared to patients with non-COVID-19 pulmonary diseases [70.3 pg/mL (47-167.9) vs. 161.1 pg/mL (88.98-305.2), respectively, p = 0.008]. I-FABP concentrations in these two populations were significantly lower than in patients with abdominal pain without COVID-19 [344.8 pg/mL (268.9-579.6)]. I-FABP was neither associated with severity nor the duration of symptoms. I-FABP was correlated with polymorphonuclear cell counts. In this pilot study, we observed a low I-FABP concentration in COVID-19 patients either with or without gastrointestinal symptoms, of which the pathophysiological mechanisms and clinical impact remain to be established. Further explorations on a larger cohort of patients will be needed to unravel the molecular mechanism of such observation, including the effects of malabsorption and/or abnormal lipid metabolism.

Antithrombin (AT) is a major physiological inhibitor of hemostasis. We report 22 novel antithrombin gene (SERPINC1) mutations associated with antithrombin deficiency in 17 French and five German families. They were all present at the heterozygous state. Nine missense mutations accounted for type I deficiency, defined by equally low antithrombin activity and antigen level. Most of them (7/9) affected highly conserved serpin residues and were associated with venous thrombosis occuring at a young age (before age 32). One splice site, one nonsense mutation, three small deletions and one insertion were also identified as a cause for type I antithrombin deficiency. Seven other missense mutations were identified in type II or unclassified AT deficiency; g.5270C>T (p.T147I, T115I) and g.5281A>T (p.I151F, I119F) change residues in the heparin binding region, g.13267C>G (p.P439A, P407A) and g.13271T>C (p.F440S, F408S) affect amino acids in the pleiotropic region, g.2372G>A (p.G25D, G‐8D) changes a signal peptide amino acid, g.2456G>C (p.C53S, C21S) affects one of the three disulfide bonds of the protein, and g.7585A>T (p.M347K, M315K) changes a nonconserved residue on strand 2C. © 2006 Wiley‐Liss, Inc.

A 24-year-old man was admitted for recent acute abdominal pain, chills, vomiting, and 39 °C fever. His clinical examination revealed no neurological (specifically, no neck stiffness) or cutaneous abnormalities.

Several errors are present in Table 1; most of them originated in translating our initial antithrombin gene numbering system (Olds RJ et al., Biochemistry, 1993, 32, 4216–4224) into the HGVS gene numbering system, where nucleotide +1 corresponds to the A of the ATG initiation codon of the H. sapiens antithrombin gene (SERPINC1; GenBank accession number X68793.1). This does not affect the discussion on the consequences of the mutations. Corrections are as follows, and corrections to mutations #5 and #22 apply to the (line 13) and Results and Discussion sections (lines 19 and 71). © 2006 Wiley‐Liss, Inc.

Gastric cancer (GC) is the third cause of cancer-related mortality worldwide and is often diagnosed at advanced stages of the disease. This makes the development of more comprehensive models and efficient treatments crucial. One option is based on repurposing already marketed drugs as adjuvants to chemotherapy. Accordingly, we have previously developed the combination of docetaxel and the cholesterol-lowering drug, lovastatin, as a powerful trigger of HGT-1 human GC cells’ apoptosis using 2D cultures. Because 3D models, known as spheroids, are getting recognized as possibly better suited than 2Ds in toxicological research, we aimed to investigate the efficacy of this drug combination with such a model. We established monocellular spheroids from two human (GC) cell lines, HGT-1 and AGS, and bicellular spheroids from these cells mixed with cancer-associated fibroblasts. With these, we surveyed drug-induced cytotoxicity with MTT assays. In addition, we used the Incucyte live imaging and analysis system to follow spheroid growth and apoptosis. Taken together, our results showed that the lovastatin + docetaxel combination was an efficient strategy to eliminate GC cells grown in 2D or 3D cultures, lending further support in favor of repurposing lovastatin as an adjuvant to taxane-based anticancer treatment.

Forests provide essential ecosystem services such as wood production and soil carbon storage, which can be influenced by forest management. Fertilisation and understory removal are common practices set up in managed forests to reduce tree mortality and relieve trees from their main limitations, but their effects on belowground functioning and soil carbon storage are still unclear. In this study, we investigated the effects of phosphorus fertilisation, understory removal and their interaction on the carbon stored in the ecosystem and soil enzyme activities in two contrasting moorlands in south-western France (dry and wet moorlands) planted with maritime pines (Pinus pinaster Ait.). In the wet moorland, we found that fertilisation and understory removal had a positive effect on tree biomass, but they did not affect soil carbon stocks nor carbon-related enzyme activities. In the dry moorland, understory removal had a significant positive effect on tree biomass and a strong negative effect on topsoil organic carbon stocks and carbon-related enzyme activities. Overall, understory removal did not affect total carbon stocks at the ecosystem scale due to compensatory effects between carbon pools, i.e. the increase in carbon stored in the aboveground biomass was cancelled by a decrease in carbon stored in the soil. These results highlight the importance of adapting forest practices depending on the environmental context and carbon sequestration objectives.

Brain protection of the newborn remains a challenging priority and represents a totally unmet medical need. Pharmacological inhibition of caspases appears as a promising strategy for neuroprotection. In a translational perspective, we have developed a pentapeptide-based group II caspase inhibitor, TRP601/ORPHA133563, which reaches the brain, and inhibits caspases activation, mitochondrial release of cytochrome c , and apoptosis in vivo . Single administration of TRP601 protects newborn rodent brain against excitotoxicity, hypoxia–ischemia, and perinatal arterial stroke with a 6-h therapeutic time window, and has no adverse effects on physiological parameters. Safety pharmacology investigations, and toxicology studies in rodent and canine neonates, suggest that TRP601 is a lead compound for further drug development to treat ischemic brain damage in human newborns.

Treatment teams use different approaches for correcting the alveolar cleft sector of labio-palatal clefts. Age of patient, whether or not bone grafts are used, and the type of bone grafted are some of the differences. Our team performs a gingivoperioplasty with a graft of iliac cancellous bone on patients 4 to 6 years old. This procedure is carried out within the framework of orthodontic treatment designed to restore transverse dimension pre-operatively with a quad helix and to retain the expansion with 6 months of retention. The gingivoperioplasty is accomplished in a zone free of any scar tissue that might have resulted from a primary cheiloplasty followed by closure of the palatal cleft. In our view all teams must eventually utilize cone beam X-rays for their radiographic evaluations because they are the only tool that provides results of objective analysis that are of high quality and have demanded a very low level of radiation. [PUBLICATION ABSTRACT]

Large flat clathrin plaques are stable features of the plasma membrane associated with sites of strong adhesion suggesting that they could also play a role in force transduction. Here, we analyzed how clathrin plaques interact with the cytoskeleton and how they respond to mechanical cues in skeletal muscle myotubes. We show that branched actin networks surrounding clathrin plaques are directly regulated by dynamin 2, anchor intermediate filaments and sequester YAP at the plasma membrane. Dynamin 2, clathrin and desmin intermediate filaments are all required for basal YAP nucleocytoplasmic distribution and efficient nuclear translocation in response to mechanical stimuli. Dynamin 2 mutations that are responsible for centronuclear myopathy in humans disorganize the desmin network and deregulate YAP signaling both in vitro and in vivo. Thus, clathrin plaques and associated dynamin 2 are defined here as a new sensor conveying mechanical cues and integrate cell signaling with cytoskeletal regulation.