Characterization and chlorine reactivity of particulate matter released by bathers in indoor swimming pools.

Disinfecting swimming pool water is essential for preventing waterborne diseases. An unforeseen consequence of treating water with disinfectants is the formation of disinfection by-products (DPBs) that can cause harmful effects to health through the interactions between the added disinfectant and organic matter in the water. The present work focuses on the chlorine reactivity with particles released by bathers. Such particles are collected in the filter backwash water of swimming pools and this study intends to distinguish DPBs generated from dissolved chemicals from those formed by particulate matter. Therefore, filtered and unfiltered backwash waters were collected from several swimming pools, analysed physicochemically and chemically, and then chlorinated as is (79 mgL-1) and as diluted suspensions (36.2 and 11.9 mgL-1) at varying concentrations of chlorine (1.2 mg and 24 mgCl2L-1). Utilizing a DPD colorimetric technique and GC-ECD, respectively, the kinetics of chlorine consumption and DPBs production have been investigated. Up to 25.7 µgL-1 of chloroform was produced within 96 h at 1.2 mgCl2L-1, followed by haloacetic acids (HAAs) and haloacetonitriles (HANs). Within 96 h, the concentration of trichloroacetic acid reached a maximum of 231.8 µgL-1 at a chlorine concentration of 231.8 µgL-1. The formations of 0.13 µmol THMs, 0.31 µmol HAAs, and 0.04 µmol HANs per mg of dissolved organic carbon (DOC) were finally determined by correlating the organic content of particles with the nature of the DBPs generated. Comparing the quantities of DBPs generated in filtered and unfiltered samples helps us conclude that ∼50% of DBPs formed during the chlorination of swimming pool water are derived from particles brought by bathers.

[Intravitreal bevacizumab pretreatment in vitrectomy for severe diabetic retinopathy: a series of six cases]. / Utilisation du bévacizumab (Avastin(®)) en injection intravitréenne avant vitrectomie pour rétinopathie diabétique sévère, à propos de six cas.

INTRODUCTION: Bevacizumab (Avastin(®), Roche) is a full-length humanized monoclonal antibody applicable to all subtypes of vascular endothelial growth factor (VEGF). The purpose of this study was to report the results of its use as a surgical additive in severe cases of proliferative diabetic retinopathy (PDR). PATIENTS AND METHOD: This retrospective study focused on six eyes of six patients with complicated diabetic retinopathy. A vitrectomy was performed within 13.6 days after an intravitreal bevacizumab injection of 0.1 mL (2.5mg), with dissection of the fibrovascular proliferation using a mono- or bimanual delamination technique. RESULTS: The mean follow-up after intravitreal injection was 13.3 months. The mean surgery time was 64 minutes. The bimanual technique was not necessary. Only one iatrogenic retinal tear was repaired. The intraoperative bleeding was negligible. No adverse events resulting from the drug nor recurrence were observed throughout the follow-up period. CONCLUSION: Intravitreal bevacizumab is useful as a surgical additive in severe cases of PDR, significantly improving surgical conditions. Nevertheless, its use beyond approved indications should be reserved for complex surgical cases.

Requirement for Daxx in mature T-cell proliferation and activation.

The protein Daxx promotes Fas-mediated cell death through activation of apoptosis signal-regulating kinase 1, leading to the activation of the MAPKs JNK and p38. Owing to the in utero lethality of daxx-deficient mice, the in vivo role of Daxx has been so far difficult to analyze. We have generated transgenic mice expressing a dominant-negative form of Daxx (Daxx-DN) in the T-cell lineage. We show that Daxx is recruited to the Fas receptor upon FasL engagement and that Daxx-DN expression protects activated T cells from Fas-induced cell death, by preventing the death-inducing signal complex to be properly formed. Normal lymphocyte development and homeostasis are nevertheless observed. Interestingly, we report that both in vitro and in vivo stimulation of Daxx-DN T-lymphocytes leads to increased proliferative T-cell responses. This increased proliferation is associated with a marked increase in tyrosine phosphorylation of LAT and ZAP70 as Daxx-DN favor their recruitment to the T-cell receptor (TCR) complex. These findings identify Daxx as a critical regulator of T-lymphocyte homeostasis by decreasing TCR-induced cell proliferation and by promoting Fas-mediated cell death.