Replicative senescence is a fundamental feature of most, if not all, somatic higher eukaryotic cells. The phenomenon has been studied for more than three decades, during which time the genetics and cell biology of senescent cells were characterized. In recent years, progress has been made on understanding the molecular basis for replicative senescence. At present, we now have a good, albeit still incomplete, understanding of some of the immediate causes for the growth arrest of senescent cells. The challenges for the future will be to understand the molecular bases for the prime causes of senescent phenotype, including the growth arrest and the altered differentiation.

Animals↗

PubMedDate not supplied

Alcohol stimulates the release of dopamine and serotonin in the nucleus accumbens.

The effects of acute IP administration (0.5, 1.0 or 2.0 g/kg) and local perfusion (25, 50 or 100 mM) of ethanol on the extracellular concentrations of dopamine (DA), serotonin (5-HT) and their metabolites in the nucleus accumbens (ACC) of the rat were studied with in vivo microdialysis coupled with a small-bore HPLC electrochemical detection procedure. The IP administration of 1.0 and 2.0 g/kg ethanol significantly (p less than 0.05) increased the extracellular levels of DA and 5-HT in the ACC whereas the 0.5 g/kg dose caused no change. In general, the extracellular levels of the 3 monoamine metabolites were not altered by IP ethanol except for a slight increase in the levels of homovanillic acid following the 2.0 g/kg dose. Local perfusion of 50 and 100 mM ethanol (but not 25 mM) through the microdialysis probe markedly increased (170-200% of control) the extracellular levels of DA in the ACC. Only the 100 mM concentration of ethanol altered the extracellular levels of 5-HT (2-fold increase), 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid. Addition of 100 microM ICS 205-930 (a 5-HT3 antagonist) to the perfusate markedly reduced the 100 mM ethanol-stimulated release of DA and 5-HT. Overall, the data suggest that ethanol can stimulate the release of both DA and 5-HT in the ACC and that the action of ethanol within the ACC may be mediated in part by 5-HT3 receptors.

3,4-Dihydroxyphenylacetic Acid↗

PubMedDate not supplied

Epidemiologic studies of lung disease due to mycobacteria other than Mycobacterium tuberculosis in Japan.

The incidence of lung disease due to mycobacteria other than Mycobacterium tuberculosis (atypical mycobacteria) in Japan was estimated to be 0.9--1.9 per 10(5) population per year in 1971--1979. Although the incidence of lung tuberculosis is steadily decreasing, the incidence of lung disease due to atypical mycobacteria has remained at almost the same level. The number of patients newly infected per year in recent years was calculated to be approximately 2,000. The ratio of the number of patients with lung disease due to atypical mycobacteria to the number of patients with lung disease due to atypical mycobacteria to the number of patients with lung disease due to all species of mycobacteria was highest in hospitals on the southwest coast of the Pacific. The atypical mycobacteria that caused disease most frequently belonged to the Mycobacterium avium-intracellulare complex. Of the 537 cases of disease due to atypical mycobacteria, 491 (89.6%) were due to these organisms; 43 (8.0%), to Mycobacterium kansasii; and 7 (1.3%), to Mycobacterium fortuitum. The disease due to M. kansasii appeared most frequently in hospitals in the Tokyo and Kanagawa prefectures. Patients with lung tuberculosis had a high risk of lung infection due to M. avium-intracellulare. The incidence of such disease in tuberculous patients was estimated to be 18.7 per 10(5) population per year, a rate that is approximately 10 times that found in the general population.

Humans↗

PubMedDate not supplied

Loss of heterozygosity on chromosomes 1 and 11 in sporadic pheochromocytomas.

Molecular genetic analysis was performed with 20 oncogene probes and 32 polymorphic DNA probes on tumor DNA samples from seven pheochromocytomas; namely, one multiple endocrine neoplasia type 2B, and two familial and four sporadic pheochromocytomas. No amplification or rearrangement of the oncogenes was detected in any of the tumors. However, loss of heterozygosity on chromosome 1p, 11p or 11q was detected in these cases. In addition, a locus related to ETS1 was deleted in two of the sporadic tumors. These results suggest that pheochromocytomas may be genetically heterogeneous, and that inactivation of unknown genes on chromosome 1p, 11p or 11q may contribute to their development.

Adrenal Gland Neoplasms↗