Lithium suppresses excitotoxicity-induced striatal lesions in a rat model of Huntington's disease

Huntington's disease is a progressive, inherited neurodegenerative disorder characterized by the loss of subsets of neurons primarily in the striatum. In this study, we assessed the neuroprotective effect of lithium against striatal lesion formation in a rat model of Huntington's disease in which quinolinic acid was unilaterally infused into the striatum. For this purpose, we used a dopamine receptor autoradiography and glutamic acid decarboxylase mRNA in situ hybridization analysis, methods previously shown to be adequate for quantitative analysis of the excitotoxin-induced striatal lesion size.Here we demonstrated that subcutaneous injections of LiCl for 16 days prior to quinolinic acid infusion considerably reduced the size of quinolinic acid-induced striatal lesion. Furthermore, these lithium pre-treatments also decreased the number of striatal neurons labeled with the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. Immunohistochemistry and western blotting demonstrated that lithium-elicited neuroprotection was associated with an increase in Bcl-2 protein levels.Our results raise the possibility that lithium may be considered as a neuroprotective agent in treatment of neurodegenerative diseases such as Huntington's disease.     

Aerobic-hemodynamic support of physical exertion in virtually healthy persons with different levels of cholesterol in the blood and in patients with stenocardia of effort

Oxygen transport and central hemodynamics were studied in 66 healthy males with different blood cholesterol levels and 24 patients with angina of effort under standard exercise test. Increased blood cholesterol was found to influence exercise energy maintenance in healthy people. Subnormal efficacy of oxygen transport system provokes intensification of cardiac activity. Oxygen-hemodynamic maintenance of exercise in healthy subjects with hypercholesterolemia is similar to that in patients with ischemic heart disease. This indicates the same pathophysiological processes in the above individuals.     

One-Year Follow-up of Duodenal Ulcers after 1-Wk Triple Therapy for Helicobacter pylori

Objective : to study the ulcer recurrence rate of Helicobacter pylori-positive duodenal ulcers at 1 yr after eradication of the bacteria by triple therapy. Method : Patients with H. pylori-positive duodenal ulcers were randomized to receive either triple therapy for 1 wk plus omeprazole for 4 wk (THple+OMP) (n = 78), or omeprazole alone (OMP) for 4 wk (N = 77). Patients were followed up every 3 months for symptom enquiry. At 1 yr, all asymptomatic patients were invited to attend for gastroscopy. Results : At 8 wk, 16 patients in the OMP group and four in the Triple+OMP group had an ulcer. During the 1-yr period, 12 patients in the OMP group and no patient in the Triple+OMP group developed symptomatic ulcers. At follow-up endoscopy at 1 yr, another 10 ulcers were detected in the OMP group and two in the Triple+OMP group. Fifteen patients in the OMP group and 13 in the Triple+OMP group were lost to follow-up. In total, ulcers were de-tected in 39 of 61 (64%) assessahle patients in the OMP group, and in six of 65 (97o) assessahle patients in the Triple+OMP group after I yr (χ² test: p < 0.001). Of the patients whose H, pytori were successfully eradicated hy Triple+OMP at 8 wk, 90% remained H. pylori negative at 1 yr. Conclusion : Triple therapy for 1 wk eradicates H, pylori infection and significantly reduces duodenal ulcer relapses.