[Restrictive respiratory distress caused by major subcutaneous emphysema]. / Détresse respiratoire restrictive sur un emphysème sous-cutané majeur.

We describe the case of subcutaneous emphysema that resulted in major respiratory distress. Drainage was performed thanks to the insertion of subcutaneous catheters. This technique has already been described and involves few complications. It represents a potentially easy and lifesaving procedure.

Nous décrivons un cas d'emphysème sous-cutané ayant entraîné une détresse respiratoire majeure. Un drainage décompressif a été réalisé grâce à l'insertion de cathéters sous-cutanés. Cette technique a déjà été décrite et comporte peu de risques et de complications. Elle représente potentiellement un geste simple et salvateur.

Catastrophic antiphospholipid syndrome: case reports and review of the literature.

This paper reports two cases of successfully treated patients suffering from a rare entity, the catastrophic anti-phospholipid syndrome (CAPS). Management of those patients is discussed at the light of existing literature.

[Pharmaceutical traceability integrated with the patient file. Development of a computerized hospital application]. / Traçabilité pharmaceutique intégrée au dossier patient. Développement d'une application informatique hospitalière.

The Clinical Pharmacy Department (CPD) of the Gustave Roussy Institute, has developed a traceability software package that is integrated with the patient file. The Traceability & Medical Devices Functional Unit manages the Blood Derivative Medicinal Product traceability circuits, the circuits of over 400 Sterile Medical Devices and, generally speaking, those for all pharmaceutical goods for which traceability is imperative. The SIMBAD-TRACE software package has been developed in situ and was first open for access in March 1999. It enables pharmaceutical traceability data to be accessed from 500 networked workstations. The references tracked generated about 10,000 movements per year. In terms of performance, the system achieves three complementary objectives: 1) reporting traceability scores which reflect the ability of CPD and the establishment to pertinently respond to a complex regulatory requirement on a daily basis; 2) the contribution of the tool to cost containment with respect to allocating rare goods; the contribution of the software package to the implementation of medical device vigilance inquiries, particularly descending inquiries. Finally, SIMBAD-TRACE is one of the pillars of our Quality Assurance Program (QAP).

Downregulation of corticotropin-releasing factor mRNA, but not vasopressin mRNA, in the paraventricular hypothalamic nucleus of rats following nutritional stress.

Stress can cause disturbance of homeostasis to result in illness. Stress can also induce various gene expression in different neuronal systems. For example, nutritional stress induced by acute food deprivation upregulates corticotropin-releasing factor (CRF) mRNA, whereas osmotic stress increases vasopressin (VP) mRNA. However, it is unknown if nutritional stress induced by chronic food deprivation has synergistic effects on CRF and VP mRNAs. We have used in situ hybridization in conjunction with quantitative autoradiography to demonstrate that nutritional stress induced by a 4-day food deprivation results in a body-weight loss with a significant decrease of CRF mRNAs, but not VP mRNAs in the paraventricular hypothalamic nucleus (PVN) of Sprague-Dawley rats. The present study has thus indicated that a chronic nutritional stress does not have synergistic effects on CRF and VP mRNAs. The decrease of CRF mRNAs is obviously related to the body-weight loss induced by food deprivation. This study thus supports a notion that the CRF, but not VP, neurons in the PVN play an important role in their neuroadaptation associated with body weight loss. Thus, it is conceivable that downregulated CRF neurons in the hypothalamus could be involved in pathogenesis of human eating disorder with severe weight loss, whereas upregulated CRF neurons could be associated with an opposite form of the eating disorder that causes obesity.