[Quality proceedings in point-of-care testing: tetanus test example]. / Démarche qualité en biologie délocalisée: exemple du test tétanos.

In front of the increase of frequentation of emergency departments for pathological situations associated with tetanic risk, and the difficulty to know if the patients are immunized or not, the consequence is an unsuitable consumption of vaccination and/or antitetanic immunoglobulins. At the emergency department of Armentieres's hospital, in a perspective of an accreditation and following a medical request, we wanted to improve patient's care with tetanic risk wound by using a quick test for the detection of specific antitetanic antibodies (tetanos Fumouze test), under laboratory's authority. This test would allow a quickly and reliable immunity evaluation of patients with tetanic risk wound. The use of this point-of-care test was made possible with a good cooperation between clinicians, biologists and nurses. After six months, we wanted to evaluate monitoring and respect for qualities procedures established by laboratory and the medical and cost impact of this test.

High serum thymus and activation-regulated chemokine levels in the lymphocytic variant of the hypereosinophilic syndrome.

The idiopathic hypereosinophilic syndrome is associated with expansion of an IL-5-producing T-cell subset in a subgroup of patients. Identification of such patients is critical to adequate management because there is some evidence that they present an increased risk for development of T-cell lymphoma. Although the T(H)2-like cells often bear an aberrant surface phenotype and can readily be detected with flow cytometry, we now show that lymphocyte phenotyping might be normal in some cases. In contrast, serum thymus and activation-regulated chemokine levels are consistently increased in such patients compared with others with persistent idiopathic hyper-eosinophilia and could therefore represent a useful diagnostic tool.

A suppressive effect of the adenovirus 5 protein E1B 55K on apoptosis induced by IL-3 deprivation and gamma-irradiation.

The murine IL-3-dependent myeloid cell line 32D undergoes a rapid death when deprived of interleukin-3 (IL-3), a process that is suppressed or delayed by the constitutive expression of Bcl-2 or the Bcl-2-related Bcl-xL survival protein. The adenovirus type 5 E1B region encodes an E1B 55K protein, that has been reported to bind and inactivate the p53 protein that plays an important role in the induction of apoptosis. In order to explore the potential effect of the E1B 55K protein on IL-3 deprival-induced cell death, we have established 32D cell lines overexpressing the adenovirus E1B 55K protein and compared its ability to modulate the cell death with that of the human Bcl-2 protein. We observed that E1B 55K, as Bcl-2, delays the cell death caused by either IL-3-deprivation or DNA damage induced by gamma-irradiation. Cell-cycle analysis after IL-3 deprivation indicated that surviving Bcl-2 transfectants accumulate predominantly in the G0/G1 phase of the cell cycle, while E1B 55K transfectants survive in both G0/G1 and the S and G2/M phases of the cell cycle. zVAD-fmk, a broad caspase inhibitor, prevented chromatin condensation and fragmentation, but not cell death, suggesting that IL-3 deprivation induces a cell death program in which the caspases are dispensable. In contrast, both E1B 55K and Bcl-2 allowed cell survival and prevented the typical features of programmed cell death, such as phosphatidyl-serine exposure, loss of mitochondrial membrane potential, and chromatin condensation and fragmentation. Our findings indicate that the adenovirus 5 E1B 55K protein has the capability to act as a survival factor, and suggest that E1B 55K exerts its effect upstream of the activation of effector caspases, by preventing the loss of mitochondrial membrane potential induced by IL-3 deprivation.