[Dynamics of brain CD68+ and stabilin-1+ macrophage infiltration in patients with myocardial infarction].

Te aim of the study was to evaluate the temporal dynamics of brain CD68+ and stabilin-1+ macrophage infltration in patients with fatal myocardial infarction (MI) type 1. MATERIALS AND METHODS: Te study included 31 patients with fatal MI type I. Te control group comprised 10 patients of 18-40 age group who died from injuries incompatible with life. Patients with MI were divided into two groups. Group 1 comprised patients who died during the frst 72 hours of MI, group 2 comprised patients who died on days 4‒28. Macrophage infltration in the brain was assessed by immunohistochemical analysis. We used CD68 as a marker for the cells of the macrophage lineage and stabilin-1 as an M2-like macrophage biomarker. RESULTS: In group 1 the number of brain CD68+ macrophages was signifcantly higher than in the control group. In group 2 the intensity of brain CD68+ cells infltration was lower than in group 1 and higher than in the control group. Tere was a small amount of stabilin-1+ macrophages in the brain of healthy people, as well as of patients who died from MI. Tere were no signifcant differences in the number of stabilin-1+ cells between group 1 and group 2. Correlation analysis revealed the presence of positive correlation between the number of CD68 + macrophages in the infarct, peri-infarct, and non-infarct areas of the myocardium and the number of CD68+ macrophages in the brain in patients with MI. Tere were not correlations between the number of CD68 + and stabilin-1+ cells and the presence of diabetes mellitus, history of stroke, history of MI, and pre-infarction angina. CONCLUSION: Te number of brain CD68+ macrophages signifcantly increased during the frst three days of MI. Te number of brain stabilin-1+ macrophages did not increase and did not differ from the control values. We observed a positive correlation between the number of CD68+ macrophages in the brain and myocardium.

Induction of apoptosis in human leukemia cells by 3-deazaadenosine is mediated by caspase-3-like activity.

3-Deazaadenosine (DZA), one of the potent inhibitors of S-adenosylhomocysteine hydrolase, is known to possess several biological properties including an induction of apoptosis. To evaluate a possibility that DZA may be utilized for the treatment of human leukemia, we studied molecular events of cell death induced by DZA in human leukemia HL-60 and U-937 cells. DZA induced a specific cleavage of poly ADP-ribose polymerase (PARP) and an activation of the cysteine protease caspase-3/CPP32 which is known to cleave PARP. DZA-mediated nuclear DNA-fragmentation was completely blocked in the presence of a universal inhibitor of caspases (z-VAD-fmk) or the specific inhibitor of caspase-3 (z-DEVD-fmk) unlike of cycloheximide (CHX). DNA fragmentation was preceded by the lowering of c-myc mRNA in the DZA treated cells. In addition, DZA-induced apoptosis was blocked by pretreatment with adenosine transporter inhibitors such as nitrobenzylthioinosine (NBTI) and dipyridamole (DPD). Taken together, these results demonstrate that DZA-induced apoptosis initiated through an active transport of DZA into human leukemia cells, is dependent on the caspase-3-like activity without de novo synthesis of proteins and possibly involves c-myc down-regulation.

Activation of caspase-8 in 3-deazaadenosine-induced apoptosis of U-937 cells occurs downstream of caspase-3 and caspase-9 without Fas receptor-ligand interaction.

3-Deazaadenosine (DZA), a cellular methylation blocker was reported to induce the caspase-3-like activities-dependent apoptosis in U-937 cells. In this study, we analyzed the activation pathway of the caspase cascade involved in the DZA-induced apoptosis using specific inhibitors of caspases. In the U-937 cells treated with DZA, cytochrome c release from mitochondria and subsequent activation of caspase-9, -8 and -3 were observed before the induction of apoptosis. zDEVD-Fmk, a specific inhibitor of caspase-3, and zLEHD-Fmk, a specific inhibitor of caspase-9, prevented the activation of caspase-8 but neither caspase-3 nor caspase-9, indicating that caspase-8 is downstream of both caspase-3 and caspase-9, which are activated by independent pathways. zVAD-Fmk, a universal inhibitor of caspases, kept the caspase-3 from being activated but not caspase-9. Moreover, ZB4, an antagonistic Fas-antibody, exerted no effect on the activation of caspase-8 and induction of apoptosis by DZA. In addition, zVAD-Fmk and mitochondrial permeability transition pore (MPTP) inhibitors such as cyclosporin A (CsA) and bongkrekic acid (BA) did not block the release of cytochrome c from mitochondria. Taken together, these results suggest that in the DZA-induced apoptosis, caspase-8 may serve as an executioner caspase and be activated downstream of both caspase-3 and caspase-9, independently of Fas receptor-ligand interaction. And caspase-3 seems to be activated by other caspses including IETDase-like enzyme and caspse-9 seems to be activated by cytochrome c released from mitochondria without the involvement of caspases and CsA- and BA- inhibitory MPTP.

[Methods of suppression of adrenal hyperfunction]. / Sposoby podavleniia giperfunktsii nadpochechnikov.

Evolution of the methods for suppression of adrenal hyperfunction has now made it possible to give up bilateral adrenalectomy in favour of portalization of the adrenal blood flow from the left adrenal by its autotransplantation with maintained blood supply into the transverse mesocolon and cryodestruction of the right adrenal. Analysis of the mortality showed two-stage suppression of adrenal hyperfunction to be advisable.

[A study of the effects of health contracts on the performance level for activities of daily living in the hemiplegic patients].

The purpose of this study was to test the effects of health contract on the performance level for activity of daily living (ADL) in the hemiplegic patients. A quasi-experimental research for health contract, which was approved as an effective method of nursing intervention, was attempted to increase the performance of the hemiplegic patients' ADL. As a purpose sample, 69 hemiplegic patients hospitalized at Oriental medicine hospital of K university were taken and divided into the experimental group and the control group by means of random assignment. After Contracting with the experimental group, they were reinforced everyday for 20 minutes. The experimental group and the control group were observed and interviewed for five times at the interval of 3-4 days by the trained nurses for this research. The data Collected through above mentioned methods were compute analyzed by t-test and ANOVA according to the purpose of this study. The data collected through above mentioned methods were computer analyzed by t-test and ANOVA according to the purpose of this study. Strate increased the performance level for ADL than the Control group" was supported (t = 2.96, df = 52.76, p = .004). Sub Hypothesis 1,2,4,5: "The hypothesis that the experimental group with health contract will demonstrate increased the performance level for eating (t = 2.29, df = 42.70, p = .027), personal hygiene and grooming (t = 4.04, df = 43.10, p = .000), dressing (t = 3.32, df = 67, p = .001) and undressing (t = 3.47, df = 48.44, p = .001) than the control group" was supported. Sub Hypothesis 3.6: "The hypothesis that the experimental group with health contract will demonstrate increased the performance level for toiletting (t = .19, df = 67, p = .849) and mobilization (t = .30, df = 67, p = .765) than the control group" was not supported. The conclusion can be that the positive relationship between the nurse and the patient results in the desired performance level for ADL in the hemiplegic patients.