Interaction between sleep mechanisms and orexin neurons

Orexin is a neuropeptide that plays a highly important role in mechanisms that regulate sleep/wake states. Lack of the orexin gene or orexin-producing neurons (orexin neurons) results in narcolepsy in several mammalian species, suggesting that orexin is an important factor for the maintenance of wakefulness. Constitutive, ectopic expression of orexin in transgenic mice resulted in severe fragmentation of non–rapid eye movement sleep, along with abnormal muscle tone regulation during REM sleep, suggesting that activity of orexin neurons should be appropriately decreased during sleep to maintain consolidated sleep states. This review will discuss the mechanisms by which the orexin system is regulated during sleep.

     

Expression of the poly-glutamine-ataxin-3 transgene causes loss of orexin expression: A rat model of narcolepsy

Sleep and Biological Rhythms -     

Ultrastructure of polymorphicMucor as observed by means of freeze-etching

Dormant sporangiospore ofMucor was observed by means of freezeetching. There was considerable inter- and intraspecies variation in spore size. Large spores were clearly multinucleate. The spore wall was covered with two thin layers, each about 10 nm thick, which may correspond to ordinary spore sheath. However, fracture never occurred along the spore surface. The cell membrane did not have invaginations like those of higher fungi. Instead, there were numerous round depressions about 50 nm in diameter. They revealed a small hollow when crossfractured. Occasionally they combined to form a structure resembling a rod-like invagination. This, presumably, is one step towards generation of the rod-like invagination of conidiospore. Mitochondria became much larger than those found in the vegetative forms, and showed wide and deep invaginations of membrane. Cristae became indistinct. Lipid droplets had multilayered shells and were much more highly developed than those found in mycelial cells, yeast or arthrospores of this organism. No endoplasmic reticulum or vacuoles were found.     

The heterogeneity of dermatan sulfate and heparan sulfate in rat liver and a shift in the glycosaminoglycan contents in carbon tetrachloride-damaged liver

The glycosaminoglycan of rat liver can be separated into five distinct fractions; a hyaluronic acid franction, a heparan sulfate fraction with a molar ratio of sulfate to hexosamine (S/HexN) around 0.7, a heparan sulfate fraction with a S/HexN ratio around 1.4, a dermatan sulfate fraction with a S/HexN ratio near unity, and a dermatan sulfate fraction with a S/HexN ratio around 1.3.Enzymatic analysis of the two dermatan sulfate fractions indicates that they differ significantly in that the high sulfated fraction contains relatively more N-acetylgalactosamine 4,6-bissulfate units (about 26% of the total hexosamine). In experimental injury produced by carbon tetrachloride, the low sulfated fraction increases as much as 9-fold on a dry weight basis, bearing no linear relationship to the amount of the high sulfated fraction which increases only 2-fold. A significant shift is also observed in the levels of the two heparan sulfate fractions. In this case, however, the high sulfated fraction shows a much more pronounced increase than does the low sulfated fraction. On the basis of these observations, it is suggested that for each of the dermatan sulfate and heparan sulfate classes are at least two pools, distinguished by sulfation degree and perhaps by turnover rate and physiological function.     

A preliminary study on the function tests of the vibration syndrome in tropical rain forest workers.

Working situations and health hazards directly related to the work of the tropical rain forest workers were studied in Papua New Guinea. The results of the function tests of the vibration syndrome were reported in the preliminary step of this study. Among 61 workers including 16 chain saw operators no clear evidence was found that was related to the health effects of hand-arm vibration, but a possibility existed of an occurrence of subclinical dysfunction of peripheral circulation and peripheral neuropathies. The principal component analysis suggests that the reactiveness of peripheral circulation significantly reflects the duration of the chain saw operation.     

Regulation of Rad17 Protein Turnover Unveils an Impact of Rad17-APC Cascade in Breast Carcinogenesis and Treatment

Aberrant regulation of DNA damage checkpoint function leads to genome instability that in turn can predispose cellular tissues to become cancerous. Previous works from us and others demonstrated the role of Rad17 in either activation or termination of DNA damage checkpoint function. In the current study, we have revealed the unexpected accumulation of Rad17 in various types of breast cancer cell lines as well as human breast cancer tissues. We observed that Rad17 protein turnover rate in breast epithelial cells is much faster than in breast cancer cells, where the turnover of Rad17 is regulated by the Cdh1/APC pathway. We further observed that Rad17-mediated checkpoint function is modulated by proteolysis. Stabilization of Rad17 disrupts cellular response to chemotherapeutic drug-induced DNA damage and enhances cellular transformation. In addition, manipulation of Rad17 by RNA interference or stabilization of Rad17 significantly sensitize breast cancer cell to various chemotherapeutic drugs. Our present results indicate the manipulation of Rad17 proteolysis could be a valuable approach to sensitize breast cancer cell to the chemotherapeutic treatment despite of the critical role in governing DNA damage response and cellular recovery from genotoxic stress.