The HHQK domain of beta-amyloid provides a structural basis for the immunopathology of Alzheimer's disease.

The beta-amyloid peptide 1-42 (Abeta1-42), a major component of neuritic and core plaques found in Alzheimer's disease, activates microglia to kill neurons. Selective modifications of amino acids near the N terminus of Abeta showed that residues 13-16, the HHQK domain, bind to microglial cells. This same cluster of basic amino acids is also known as a domain with high binding affinity for heparan sulfate. Both Abeta binding to microglia and Abeta induction of microglial killing of neurons were sensitive to heparitinase cleavage and to competition with heparan sulfate, suggesting membrane-associated heparan sulfate mediated plaque-microglia interactions through the HHQK domain. Importantly, small peptides containing HHQK inhibited Abeta1-42 cell binding as well as plaque induction of neurotoxicity in human microglia. In vivo experiments confirmed that the HHQK peptide reduces rat brain inflammation elicited after infusion of Abeta peptides or implantation of native plaque fragments. Strategies which exploit HHQK-like agents may offer a specific therapy to block plaque-induced microgliosis and, in this way, slow the neuronal loss and dementia of Alzheimer's disease.

[Features of the epidemiologic characteristics of ischemic heart disease among scientific research workers]. / Osobennosti épidemiologicheskoi kharakteristiki ishemicheskoi bolezni serdtsa u nauchnykh rabotnikov.

The peculiarities of prevalence of coronary heart disease (CHD), its main risk factors and their interrelationships were studied on the basis of the results of epidemiological surveys of an organized population of men aged 20 to 59 engaged in research, and an unorganized male population in one of Moscow districts. A similar CHD frequency was revealed in both populations (10.5 and 9.5%), however the prevalence of possible CHD was significantly higher among the research workers. In this group more unfavorable epidemiological conditions were noted with relation to such CHD risk factors as hypercholesterolemia, disturbed glucose tolerance, a low physical activity, with practically the same prevalence of excess body mass and lower frequency of arterial hypertension and smoking. The results obtained formed the basis for a design of measures on primary and secondary CHD prevention among research workers.

[Comparative study of drug and dietary correction of dyslipoproteinemias among the population]. / Sravnitel'noe izuchenie medikamentoznoi i dieticheskoi korrektsii dislipoproteidemii v populiatsii.

A comparative study of diet and drug correction of dyslipoproteinemias in individuals with stable hypercholesterolemia showed that following a month of diet treatment of groups selected for the therapy with probucol and ascorbic acid there was a clear-cut decrease in the level of plasma cholesterol. The administration of probucol in combination with the diet therapy decreased cholesterol by 33.6%, triglycerides by 32.8% and high density lipoprotein cholesterol (HDLC) by 19.7% as compared with the baseline values. Ascorbic acid showed virtually no effect on the lipid spectrum of the blood. Throughout the entire period of treatment, the patients in these groups showed a reduction in the body weight and blood pressure. In the group receiving only drug therapy, probucol use was associated with a statistically significant decrease in both total cholesterol and HDLC, with the HDLC/cholesterol ratio remaining almost unaltered while in the group receiving diet and probucol, the proportion of HDLC with regard to total cholesterol was elevated as against the initial values. The body weight in this group of patients remained actually unaltered.