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Biomedical subjects

D Bernard

Publications and source records attributed to D Bernard.

At least 181 records · Page 10Linked to original sources

Surgical treatment of severe postshunt hepatic encephalopathy.

Hepatic encephalopathy is a major complication of portal-systemic shunts with an incidence ranging up to 52%. A small fraction of these patients are refractory to medical therapy. Shunt ligation and colonic procedures are the main surgical approaches. The goal of the latter is to diminish the colonic absorption of nitrogenous substances which are involved in the pathophysiology of hepatic encephalopathy. Six patients, whose average age was 55.7 +/- 2.6 years, were operated for severe postshunt encephalopathy requiring 4.3 +/- 0.9 admissions for a total duration of 76 +/- 26 days over 1-11 years. One patient had undergone a splenoral shunt and 5 had a portacaval shunt. One ligation of the shunt and 5 colon exclusions were performed. The average postoperative hospital stay was 21.5 +/- 3.9 days. The mean follow-up was 47 +/- 20 months. The patient with the shunt ligation remains free of encephalopathy 94 months after the procedure and has not bled from his esophageal varices. Among the 5 colon exclusion patients, there were 1 death and 3 complications. Three patients were completely relieved of their hepatic encephalopathy. One of those 3 died of a subarachnoid hemorrhage 28 months after the surgery. The fourth still needs medication to control a persistent, although improved, encephalopathy that required 2 further hospitalizations. Colon exclusion is a useful intervention in very selected cases. It has a lower operative mortality than total colectomy and the advantage over shunt ligation of not reestablishing hypertension in the portal system.

Hepatic Encephalopathy↗

Evidence for autoimmune antibodies directed against embryonic neural cell adhesion molecules (N-CAM) in patients with group B meningitis.

Human brain tissue shares alpha 2-8 linked polymers of neuraminic acid with the carbohydrates expressed on the capsule of group B Neisseria meningitidis bacteria (Finne et al. (1983) Lancet ii, 355-357; Finne (1985) Trends Biochem. Sci. 10, 129-132; Rougon et al. (1986) J. Cell. Biol. 103, 2429-2437). We report that sera from patients suffering from group B meningitis exhibited IgM antibodies directed against the embryonic, but not the adult, form of neural cell adhesion molecules (N-CAM). These sera also stained live ATt20 cells as well as neuron membranes in mouse embryonic brain cultures. We have demonstrated that such antibodies, directed against carbohydrate moieties of bacterial capsula, were able to lyse cells expressing embryonic N-CAM in a complement-dependent cytotoxic assay. These data infer (1) that humans are able to develop anti-MenB humoral responses, (2) that such responses could initiate autoimmune disorders or be potentially detrimental by interfering with processes mediated by N-CAM interactions, (3) that the development of a vaccine against group B meningitidis should be considered with caution.

Antibodies, Bacterial↗

Lithostathine and pancreatitis-associated protein are involved in the very early stages of Alzheimer's disease.

According to one of the theories formulated to explain the etiology of Alzheimer's disease (AD), amylosis may reflect a specific inflammatory response. Two inflammatory proteins, lithostathine and PAP, were evidenced by immunohistochemistry in senile plaques and neurofibrillary tangles of patients with AD. In addition, lithostathine and PAP were significantly increased in the cerebrospinal fluid of patients with AD when compared to patients with multiple sclerosis, another inflammatory disease, and to normal control subjects. However, no correlation was observed with age of occurrence. Furthermore, lithostathine and PAP were increased even at the very early stages of AD, and their level remained elevated during the course of the AD unlike TNFalpha whose level, very high at very early stages, regularly decreased. Finally, if part of lithostathine and PAP are synthesized in the brain, a large part comes from serum by passage over the blood-brain barrier. These results indicate (i) the existence of an acute phase response followed by a chronic inflammation in AD, and (ii) that lithostathine and PAP are involved even at the first pre-clinical biochemical events of AD. In addition, because lithostathine undergoes an autolytic cleavage leading to its precipitation and the formation of fibrils, we believe that it may be involved in amyloidosis and tangles by allowing heterogeneous precipitation of other proteins.

Acute-Phase Proteins↗

Electron dose calculation using multiple-scattering theory: thin planar inhomogeneities.

In this article in our series on electron dose calculation using multiple-scattering theory, we apply the Fermi-Eyges theory to the problem of a thin planar inhomogeneity present in an otherwise-layered medium. We derive expressions for the distribution function P and the location distribution L (which multiplied by the restricted mass collision stopping power is the dose directly deposited by the primary electrons) for various types of incident beams: a completely arbitrary distribution, a Gaussian point source, a pencil beam, an isotropic point source, and a broad parallel beam. We show how divergent-beam dose distributions can be determined from parallel-beam calculations, through use of equivalent configurations dependent upon the depth of dose calculation. Also, we indicate how this work can be applied to the design of wedges (or "compensators") for beam shaping to provide desired dose distributions or to match juxtaposed radiation fields. Explicit formulas for thin plates are then worked out, and we examine the appearance of hot and cold spots distal to the edge of a localized inhomogeneity, for thin half-slabs and for narrow strips. Finally, considering the case of a thin straight wedge-shaped inhomogeneity, we theoretically discover the phenomenon of a "focused hot spot" without an accompanying cold spot, and suggest the design of a "multiple-scattering lens".

Electrons↗