26 research outputs found
Methylene Diphenyl Diisocyanate
The report provides the comprehensive risk assessment of the substance Methylenediphenyl diisocyanate (MDI). It has been prepared by Belgium in the frame of Council Regulation (EEC) No. 793/93 on the evaluation and control of the risks of existing substances, following the principles for assessment of the risks to humans and the environment, laid down in Commission Regulation (EC) No. 1488/94.
Part I - Environment
This part of the evaluation considers the emissions and the resulting exposure to the environment in all life cycle steps. Following the exposure assessment, the environmental risk characterisation for each protection goal in the aquatic, terrestrial and atmospheric compartment has been determined. The environmental risk assessment concludes that there is no concern.
Part II ¿ Human Health
This part of the evaluation considers the emissions and the resulting exposure to human populations in all life cycle steps. The scenarios for occupational exposure, consumer exposure and humans exposed via the environment have been examined and the possible risks have been identified. The human health risk assessment concludes that there is concern for workers and consumers with regard to irritation of skin, eye and respiratory tract, skin sensitisation and lung effects induced by repeated inhalation exposure. There is a need for further information and for testing (on hold) on the toxicity for fertility for workers and consumers. For humans exposed via the environment and for human health (physico-chemical properties) there is no concern. The conclusions of this report will lead to risk reduction measures to be proposed by the Commission¿s committee on risk reduction strategies set up in support of Council Regulation (EEC) N. 793/93.JRC.DDG.I.2-Chemical assessment and testin
Protocolized Brain Oxygen Optimization in Subarachnoid Hemorrhage.
Brain tissue hypoxia (P <sub>bt</sub> O <sub>2</sub> < 20 mmHg) is common after subarachnoid hemorrhage (SAH) and associated with poor outcome. Recent data suggest that brain oxygen optimization is feasible and reduces the time spent with P <sub>bt</sub> O <sub>2</sub> < 20 mmHg from 45 to 16% in patients with severe traumatic brain injury. Here, we intended to quantify the brain tissue hypoxia burden despite implementation of a protocolized treatment approach in poor-grade SAH patients and to identify the simultaneous occurrence of pathologic values potentially amenable to treatment.
We present a bi-centric observational cohort study including 100 poor-grade SAH patients admitted to two tertiary care centers who underwent multimodal brain monitoring and were managed with a P <sub>bt</sub> O <sub>2</sub> -targeted protocolized approach. P <sub>bt</sub> O <sub>2</sub> optimization (≥ 20 mmHg) included a stepwise neuro-intensive care approach, aiming to prevent low cerebral perfusion pressure (CPP), and blood hemoglobin, and to keep normocapnia, normoxemia, and normothermia. Based on routine blood gas analysis, hemoglobin, PaCO <sub>2,</sub> and PaO <sub>2</sub> data were matched to 2-h averaged data of continuous CPP, P <sub>bt</sub> O <sub>2</sub> , core temperature, and to hourly cerebral microdialysis (CMD) samples over the first 11 days.
Patients had a Glasgow Coma Scale of 3 (IQR 3-4) and were 58 years old (IQR 48-66). Overall incidence of brain tissue hypoxia was 25%, which was not different between both sites despite differences in the treatment approach. During brain tissue hypoxia, episodes of CPP < 70 mmHg (27%), PaCO <sub>2</sub> < 35 mmHg (19%), PaO <sub>2</sub> < 80 mmHg (14%), Hb < 9 g/dL (11%), metabolic crisis (CMD-lactate/pyruvate ratio > 40, and CMD-glucose < 0.7 mmol/L; 7%), and temperature > 38.3 °C (4%) were common.
Our results demonstrate that brain tissue hypoxia remains common despite implementation of a P <sub>bt</sub> O <sub>2</sub> -targeted therapy in poor-grade SAH patients, suggesting room for further optimization
Enfer et paradis: la toxicité de l'oxygène chez les organismes abyssaux = Heaven and Hell: Oxygen toxicity in abyssal organisms
Oxygen, although an essential molecule for animal life, may become toxic when converted into reactive species, notably during mitochondrial respiration. These compounds react with most cellular components and may result in cell death or carcinogenesis. Whereas resistance of terrestrial organisms to oxygen toxicity is fairly well studied and understood, notably in the framework of pathological studies, it is largely unexplored in deep-sea organisms. There, contrasted situations occur. It may be Heaven for pelagic animals with a lowered body temperature and a lesser environmental oxygen concentration, sheltered from photochemical reactions that generate singulet oxygen and hydrogen peroxide in surface seawater. Moreover, respiratory metabolism decreases exponentially with depth. Consequently these animals face a much reduced oxidative stress. Bioluminescence, fairly common in deep sea animals, may be derived from antioxidant defence systems which have become less necessary with the colonization of deep sea. However, these animals could be threatened by pollution, some pollutants such as organochloride compounds generating oxidative stress. But it may be Hell for deep-sea hydrothermal vent animals where high temperatures and elevated concentration of metals and radioactive elements prevail, and where sulfur compounds may counter antioxidative mechanisms. Their enzymatic defences are specific with some enzymes being directed towards oxygen reactive species originating from respiratory metabolism while others could be directed towards exogenous threats
Epizootologie de la pasteurellose bovine en République du Tchad : importance de l'immunité naturelle acquise
En République du Tchad, les foyers de Pasteurellose bovine sont rares et la maladie peu connue, sauf peut-être pour la région du Mayo-Kebbi. Une enquête sérologique effectuée sur 411 zébus adultes, par le moyen de deux tests: hémagglutination passive et séroprotection de la souris, montre qu'un grand nombre d'entre eux possèdent des anticorps spécifiques (82 sont protecteurs). L'immunité naturelle acquise est fréquente et due vraisemblablement à des contaminations naturelles; l'enzootie y serait donc très étendue. Les résultats sérologiques sont analysés statistiquemen