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Summary Behavioural analyses have been made of effects brought about by both single and combined injections of dopamine, haloperidol, carbachol and atropine into the caput nuclei caudati of rhesus monkeys. High doses of dopamine produced the subsequent development of three types of behavioural changes: an increase in the number of skilled manipulation movements (the dynamic phase); the appearance of a dystonic torticollis (the dystonic phase); and, finally, the appearance of an oro-lingual-facial dyskinesia and a number of dyskinetic activities in the extremities (the dyskinetic phase). Low doses of dopamine solely produced the dynamic phase. Haloperidol only inhibited the dopamine-induced dynamic and dystonic phase: it did not suppress the dyskinetic phase. High doses of carbachol produced the subsequent development of four phases: a dynamic, dystonic, dyskinetic and epileptoid phase. The last one was marked by the appearance of secondary generalized epileptic seizures. Low doses of carbachol solely produced the dynamic phase. Atropine inhibited the carbachol-induced dynamic, dystonic and epileptoid phase; it did not suppress the dyskinetic phase. High doses of dopamine strongly modified the carbachol-induced phases: dopamine intensified the dystonic phase on the one hand, but it abolished the generalized epileptic seizures on the other hand.

Sixteen kidney transplant recipients received the IgG2a anti-CD3 monoclonal antibody OKT3 and azathioprine as rejection prophylaxis during the first two postoperative weeks. Concomitant immunosuppression consisted of low dose steroids while cyclosporine A therapy was instituted on day 12. Side effects included fever, bronchospasm, hypotension and diarrhoea. OKT3 caused T cell modulation resulting in CD3 dim +, CD4+ or CD8+, CD5+, WT31− and 11F2−cells. Anti-OKT3 antibodies were found in approximately 50% of the patients. The protocol induced a 100% patient and graft survival and a 81% actuarial freedom of rejection at 18 months. It prevented CsA associated nephrotoxicity in the direct postoperative phase.

A retrospective study was initiated to investigate the influence of recipients' Lewis subtype and HLA-matching on cadaveric kidney graft outcome. A total of 1111 patients receiving a first cadaveric kidney graft were analyzed. No difference in one-year graft survival was found between Lewis-negative (73, n=133) and Lewis-positive (73, n=978) recipients. Further subdivision of the study group into HLA-A,-B well-matched (0 or 1 mismatches [MM]) and poorly matched (2, 3, or 4 MM) revealed a strong deleterious effect of HLA-A,-B mismatching in the Lewis-negative group only. One year graft survival in Lewis-negative HLA-A,-B poorly matched (2, 3, or 4 A,B MM) patients was 60 (n=67) versus 86 (n=66) in the Lewis-negative HLA-A.-B well-matched (0 or 1 A,B MM) group (P=0.004). For the Lewis-positive group the one-year graft survival rates were 72 (2, 3, or 4 A,B MM; n=498) and 74 (0 or 1 A,B MM; n=480), respectively (P=n.s.).

Four different immunoassays were used to measure cyclosporine A (CsA) plasma (20°C) levels in heart and kidney transplant recipients. Two radioimmunoassays (RIAs) (Sandimmune and Cyclotrac) and the fluorescence polarization immunoassay (FPIA) were based on polyclonal antibodies, whereas the fourth (Cyclotrac-SP) used a CsA-specific mouse monoclonal antibody. We found considerable differences in measured CsA concentrations, which were dependent on the method used and the clinical situation of the patient. Correlation coefficients between the nonspecific assays ranged from 0.899 to 0.901 with plasma values increasing in the order Sandimmune < Cyclotrac < FPIA. In the CsA-specific RIA, values were lower, and the correlation with the nonspecific assays ranged from 0.761 to 0.795. In the first 21 days posttransplantation, the heart transplant group showed a higher ratio of nonspecific/specific CsA (mean 4.0) compared with the subsequent period (mean 2.3) or with renal transplant recipients (mean 2.4). The TDX method showed the best assay characteristics. In heart transplant patients with specific and nonspecific 125I-RIA methods, mean CsA levels were 25 lower during rejection periods compared with periods without signs of rejection.

A population-based case-control study of the association between head trauma and Alzheimer's disease was conducted in the Netherlands from 1980 to 1987. The study comprised 198 patients with clinically diagnosed early onset Alzheimer's disease and 198 age- and sex-matched population controls. Adjusted for sex, age, family history of dementia, and education, the odds ratio of a history of head trauma with loss of consciousness was 1.6 (95% confidence interval (CI) 0.8-3.4). The odds ratio for men was 2.5 (95% CI 0.9-7.0), and that for women was 0.9 (95% CI 0.3-2.8). The increase in odds ratio was limited to head trauma that occurred within the period of 10 years prior to the onset of dementia (odds ratio = 10.0; 95% CI 1.0-96.8). There was no evidence of effect modification by family history of dementia as measured on a multiplicative scale. However, the power to show interaction may have been low in this study. The authors' findings are compatible with the view that head trauma may be implicated in Alzheimer's disease, with a short lag time between the head trauma and the first symptoms of disease. The association needs to be confirmed in a prospective follow-up study to fully exclude the possibility of recall bias.