This study examined the relationship between caregiver burden and self-care deficit in former rehabilitation patients. We hypothesized that as self-care deficit increases, so does the level of caregiver burden. We employed Spearman correlational analysis and stepwise multiple regression analyses; the mean caregiver burden score was 25.9 (SD = 17.1), indicating mild to moderate burden. Caregiver burden was significantly correlated with social cognition deficit (r = 0.438, p = .001), communication deficit (r = 0.430, p = .001), and self-care deficit (r = .426, p = .002). Significant predictors of burden were social cognition deficit (beta = .408, p = .0018), self-care deficit (beta = .322, p = .0100), and caregiver age (beta = .369, p = .0312).

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Three genes with different functions in transformation are regulated by c-Myb in myeloid cells.

The proto-oncogene c-myb is constitutively expressed in murine leukemia virus-induced myeloid leukemia (MML) due to the integration of virus at this locus. Our recent focus has been the determination of genes regulated by this transcription factor that may be involved in transformation. Data presented here, using conditional expression of Myb in myeloid cells, show that c-Myb directly transactivates the endogenous c-myc and Bcl-2 genes, which explains at least in part how c-Myb regulates proliferation and survival. In addition, c-Myb prevents expression at the RNA level of the tumor suppressor INK4b gene. This gene encodes a cyclin-dependent kinase inhibitor, p15INK4b, that is normally upregulated at the mRNA level during myeloid differentiation and promotes growth arrest. The MMLs are generally characterized as differentiated monocytic tumors and possess the phenotype that is normally associated with p15INK4b expression. c-Myb inhibits expression of this gene, however, and therefore acts to promote a pathway which is abnormal in mature cells. This activity of c-Myb collaborates with its maintenance of c-myc expression to promote growth.

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Anti-inflammatory drugs in experimental atherosclerosis. Part 5. Influence of cortisone acetate on short-term and long-term cholesterol fluxes in atherosclerotic aorta.

Previous studies in this series have shown that cortisone and other anti-inflammatory drugs inhibit atherosclerotic plaque development in cholesterol-fed rabbits. The present study was designed to investigate the influence of cortisone on the processes of cholesterol influx and efflux in the aorta wall. Forty-seven New Zealand white rabbits were fed a 1% cholesterol diet for periods up to 12 weeks. In addition 23 of the animals were fed 5 mg cortisone acetate daily. At 0, 5 and 12 weeks, groups were fed a tracer dose of [3H]cholesterol. Plasma cholesterol specific radioactivity was measured at intervals during the next 10 days. Total aorta cholesterol and its specific activity were measured by killing groups of animals at 2 days and 10 days. Atherosclerotic plaque intensity at 12 weeks, measured planimetrically, averaged 68 +/- 12% in controls vs. only 6 +/- 3% in cortisone-treated animals. During the period between 5 and 12 weeks, net cholesterol accumulation by chemical analysis averaged only 11 micrograms/g aorta/day in cortisone-treated animals vs. 117 micrograms/g in controls. [3H]cholesterol influx (measured during a brief 2-day exposure) at 5 weeks averaged 206 and 199 micrograms/g tissue/day and at 12 weeks 586 micrograms and 281 micrograms/day in control and cortisone-treated animals, respectively. Measured over a longer 10-day period, however, the apparent influx of [3H]cholesterol was much less in cortisone-treated animals, averaging only 53 micrograms/day compared to 269 micrograms/day in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

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Alterations of hepatic drug metabolism in mice following infection with the murine retrovirus LP-BM5.

Infection of mice with the murine retrovirus mixture LP-BM5 caused a retroviral infection with many similarities to human HIV infection. We have reported alterations in hepatic drug metabolism which progressed during the course of this infection. Hexobarbital-induced sleep time increased 1.5-2.2-fold above uninfected controls after 10 to 19 weeks post infection. Inhibition of spectral cytochrome P-450 levels by 25 to 30% was observed between 15 and 17 weeks post-infection, and there were changes in specific microsomal enzyme activities. The microsomal cocaine demethylase activity was reduced by 40%, whereas cytosolic enzyme activities were increased by 1.5-2.0-fold. These alterations may contribute to the altered metabolism of drugs of abuse reported in MAIDS mice. The mechanism for these alterations is not known, although the effects correspond temporally to reported infiltration of the liver with immunoblasts and plasma cells. This suggests a role for the immune system or for mediators released by cells of the immune system which could account for these observations. An understanding of the effects of infection on drug metabolism is important because of their impact on the efficacy and safety of drugs for use in AIDS patients).

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