[Occupational toxic neuropathies: morphology in peripheral nerve biopsies].

Many peripheral neuropathies are caused by the (acute or chronic) toxic action of metals, solvents, pesticides, and other occupational and environmental contaminants. These agents often reproduce the anatomoclinical pictures of hereditary (e.g.

Clinico-pathological findings in a patient with progressive cerebellar ataxia, autoimmune polyendocrine syndrome, hepatocellular carcinoma and anti-GAD autoantibodies.

Objective: To report clinical and pathological findings of a patient with late onset insulin-dependent diabetes mellitus (IDDM), progressive cerebellar ataxia (PCA) and hepatocellular carcinoma (HCC).

Patient: A 64-year-old woman, with a long lasting IDDM, progressively developed a severe cerebellar syndrome and died 2 years after the onset of the symptoms for a systemic infection. Autoantibodies to antigastric parietal cell and anti-pancreatic islet cell resulted positive.

Influence of type 2 diabetes on functional and structural properties of coronary artery bypass conduits.

Recent studies have reported a high incidence of postoperative unfavorable cardiac-related events in patients with diabetes who underwent coronary artery bypass grafting (CABG). Structural and functional characteristics of CABG conduits, which have been shown to play an important role in patient outcome after myocardial revascularization, have not been fully investigated in diabetic subjects. Therefore, we sought to determine the influence of adult-onset diabetes on vasoreactivity and morphological profile of venous and arterial grafts.

In diffuse atrophic gastritis, routine histology underestimates Helicobacter pylori infection.

Background: histologic detection of shows high diagnostic accuracy in chronic nonatrophic gastritis. However, when atrophy occurs, the sensitivity of bacterial detection varies. This study assessed the routine histologic sensitivity for current infection in patients with atrophic gastritis, with and without intestinal metaplasia.

Ischemia-induced glutamate release in rat frontoparietal cortex after chronic alcohol and withdrawal.

High doses of ethanol increase stroke risk: in this context, a role for excitatory amino acids has been proposed. The present results show that, in frontoparietal cerebral cortex, chronic ethanol treatment (10% v/v in drinking water for 28 days) was able to slightly reduce glutamate release (evaluated through transdialysis coupled with high-pressure liquid chromatography) following focal ischemia as regards non-treated ischemic rats. This reduction was, however, not associated with decreased cerebral damage.