In countries where cysticercosis is endemic, the proportion of epilepsy due to cysticercosis is not well documented. To investigate the association between cysticercosis and epilepsy, we used the enzyme-linked immunoelectrotransfer blot (EITB) assay to detect serum antibodies to Taenia solium in 498 consecutive outpatients at a neurology clinic in Lima, Peru. Every patient was classified as epileptic (n = 189) or non-epileptic (n = 309) after neurological, and where possible electroencephalographic, examination. A substantially higher proportion of epileptic than non-epileptic patients was seropositive in the EITB (22 [12%] vs 8 [3%], p < 0.001). 19% of epileptic patients born outside Lima, 20% of those with late-onset epilepsy, and 29% of patients with both these characteristics were seropositive. Thus, in Peru, cysticercosis is an important aetiological factor for epilepsy.

There is concern that feeding full-strength animal milk to infants aged less than 6 months with diarrhoea may have adverse consequences. We assessed the effects on clinical course of two feeding regimens in 159 Guatemalan and Brazilian infants aged 2 weeks to 6 months who had had acute diarrhoea for 120 h or less, showed signs of mild to moderate dehydration, and had no complications. After correction of dehydration, infants were assigned randomly to receive continued full-strength milk feeding or initial feeding with diluted milk with regrading to full-strength milk over 48 h. There were no significant differences between feeding groups in rate of treatment failures (-1%, 95% Cl -14 to 12%) or mean (SD) total stool output (full-strength milk 335 [268] g/kg, diluted milk 338 [354] g/kg) and duration of diarrhoea (92 [50] vs 92 [44] h). A significant association was found between presence of reducing substances in stools and treatment failure (OR 4.3, 95% CI 1.1 to 16.8), but reducing substances in stools were common both in treatment successes (61%) and in failures (87%). Our study supports the conclusion that, for infants under 6 months of age with diarrhoea whose only food is animal milk or formula, the milk or formula normally given should be provided in full strength as soon as dehydration has been corrected.

Our ability to control both the cellular and humoral components of xenograft rejection in laboratory experiments, together with an organ shortage that has placed limits on clinical transplantation services, prompted us to undertake a liver transplantation from a baboon to a 35-year-old man with B virus-associated chronic active hepatitis and human immunodeficiency virus infection. Liver replacement was performed according to conventional surgical techniques. Immunosuppression was with the FK 506-prednisone-prostaglandin regimen used routinely for hepatic allotransplantation, to which a daily non-myelotoxic dose of cyclophosphamide was added. During 70 days of survival, there was little evidence of hepatic rejection by biochemical monitoring or histopathological examination. Products of hepatic synthesis, including clotting factors, became those of the baboon liver with no obvious adverse effects. Death followed a cerebral and subarachnoid haemorrhage that was caused by an angioinvasive aspergillus infection. However, the underlying cause of death was widespread biliary sludge that formed in the biliary tree despite a seemingly satisfactory choledochojejunostomy. During life and in necropsy samples, there was evidence of the chimerism that we believe is integral to the acceptance of both xenografts and allografts. Our experience has shown the feasibility of controlling the rejection of the baboon liver xenograft in a human recipient. The biliary stasis that was the beginning of lethal infectious complications may be correctable by modifications of surgical technique. In further trials, the error of over-immunosuppression should be avoidable.

Although vitamin A deficiency in children seems to increase susceptibility to infection and community trials have shown that vitamin A supplementation can reduce childhood mortality from infectious diseases, the underlying biological mechanisms are largely unknown. We conducted a randomised, double-masked, placebo-controlled clinical trial among children in West Java, Indonesia, to determine whether vitamin A deficiency is associated with abnormalities in T-cell subsets and whether vitamin A supplementation affects T-cell subsets. We studied 55 children aged 3-6 years--30 with xerophthalmia and 25 without. Acutely malnourished children (< 80% of reference weight-for-height) were excluded. CD4/CD8 ratios and the proportions of circulating CD4 naive, CD4 memory, CD8, CD45RA, and CD8, CD45RO T-cell subsets were measured. Children with xerophthalmia had lower CD4/CD8 ratios (p < 0.08), lower proportions of CD4 naive T cells (p < 0.03), and higher proportions of CD8, CD45RO T cells (p < 0.04) than those without xerophthalmia. 26 children were given vitamin A supplementation (60 mg retinol equivalent) and 29 received placebo. 5 weeks later the vitamin A group had higher CD4/CD8 ratios (p < 0.001), higher proportions of CD4 naive T cells (p < 0.01), and lower proportions of CD8, CD45RO T cells (p < 0.05) than the placebo group. Vitamin-A-deficient children have underlying immune abnormalities in T-cell subsets and these abnormalities are reversible with vitamin A supplementation.

We describe three patients with known or suspected small-cell lung cancer (SCLC), paraneoplastic neurological syndromes, and antineuronal antibodies who had unusually benign clinical courses. One patient survived 8 years free of disease and was positive for the anti-Hu antibody. A second patient survived 6 years after spontaneous tumour regression and had an atypical antineuronal antibody. A third patient with both the anti-Hu and atypical antineuronal antibody had spontaneous regression of a lung mass. All three patients had a subacute sensory neuropathy. Since paraneoplastic antineuronal antibodies also bind to tumour cells, these cases suggest that some (paraneoplastic) neurological syndromes without identifiable tumour may result from immune-mediated eradication of tumour cells.

An association between raised renin levels and myocardial infarction has been reported. We studied the effects of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, on the development of myocardial infarction and unstable angina in 6797 patients with ejection fractions < or = 0.35 enrolled into the two Studies of Left Ventricular Dysfunction (SOLVD) trials. Patients were randomly assigned to placebo (n = 3401) or enalapril (n = 3396) at doses of 2.5-20 mg per day in two concurrent double-blind trials with the same protocol. Patients with heart failure entered the treatment trial (n = 2569) and those without heart failure entered the prevention trial (n = 4228). Follow-up averaged 40 months. In each trial there were significant reductions in the number of patients developing myocardial infarction (treatment trial: 158 placebo vs 127 enalapril, p < 0.02; prevention trial: 204 vs 161 p < 0.01) or unstable angina (240 vs 187 p < 0.001; 355 vs 312, p < 0.05). Combined, there were 362 placebo group patients with myocardial infarction compared with 288 in the enalapril group (risk reduction 23%, 95% CI 11-34%; p < 0.001). 595 placebo group patients developed unstable angina compared with 499 in the enalapril group (risk reduction 20%, 95% CI 9-29%, p < 0.001). There was also a reduction in cardiac deaths (711 placebo, 615 enalapril; p < 0.003), so that the reduction in the combined endpoint of deaths, myocardial infarction, and unstable angina was highly significant (20% risk reduction, 95% CI 14-26%; p < 0.0001). Enalapril treatment significantly reduced myocardial infarction, unstable angina, and cardiac mortality in patients with low ejection fractions.

"Endozepines" are endogenous ligands for the benzodiazepine recognition sites on gamma-aminobutyric acid A receptors in the nervous system. Idiopathic recurring stupor (IRS) is a syndrome of spontaneous stupor or coma that is not associated with known metabolic, toxic, or structural abnormalities but can be reversed by flumazenil, a pure benzodiazepine antagonist. We measured endozepine-2 and endozepine-4 by high-performance liquid chromatography and radioreceptor assay in serum and cerebrospinal fluid from three patients with IRS. During episodes of stupor there was a large (up to 300-fold compared with control patients) increase of endozepine-4 content in cerebrospinal fluid and serum, but a return to normal concentrations between attacks. Endozepine-4 may contribute to, or be the cause of, IRS. The reasons for abnormal concentrations of endozepine in blood and brain are unknown.

We have previously reported data from clinical and laboratory animal observations which suggest that organ tolerance after transplantation depends on a state of balanced lymphodendritic cell chimerism between the host and donor graft. We have sought further evidence to support this hypothesis by investigating HLA-mismatched liver allograft recipients. 9 of 9 female recipients of livers from male donors had chimerism in their allografts and extrahepatic tissues, according to in-situ hybridisation and molecular techniques 10 to 19 years posttransplantation. In 8 women with good graft function, evidence of the Y chromosome was found in the blood (6/8), skin (8/8), and lymph nodes (7/8). A ninth patient whose transplant failed after 12 years from recurrent chronic viral hepatitis had chimerism in her lymph nodes, skin, jejunum, and aorta at the time of retransplantation. Although cell migration is thought to take place after all types of transplantation, the large population of migratory cells in, and the extent of their seeding from, hepatic grafts may explain the privileged tolerogenicity of the liver compared with other organs.