Time dependent changes in CRF and its mRNA in the neurons of the inferior olive following surgical transection of the olivocerebellar tract in the rat.

Changes in corticotropin-releasing factor (CRF) immunostaining and CRF mRNA in neurons of the inferior olive were compared following unilateral surgical transections of the olivocerebellar tract. Alterations in CRF immunoreactivity could not be observed earlier than 24 h after surgery. The difference--an accumulation in the contralateral side--was most pronounced at 3 days, and disappeared by the 7th postoperative day. On the other hand, changes in mRNA could be observed as early as 5-30 min after the transection. The most significant accumulation was present at 3 h after the cut and no difference could be observed from the 3rd day following surgery. The results suggest that changes in mRNA levels by axotomy may occur at an earlier time point than previously thought.     

Geriatric competencies for RNs in hospitals.

Nurses in staff development are responsible for assuring nurses' competence in the delivery of care. Older patients are the predominant population in hospitals, yet there are no instruments that specifically assess the competency of nurses to deliver care to older patients. This article reports on the development and testing of an instrument, Geriatric Competencies for RNs in Hospitals, and makes recommendations as to how staff development educators can use the geriatric competency instrument with staff nurses.     

A novel 37-Kd adhesive membrane protein from cloned murine bone marrow stromal cells and cloned murine hematopoietic progenitor cells

The adhesion of hematopoietic progenitor cells to bone marrow stromal cells is critical to hematopoiesis and involves multiple effector molecules. Stromal cell molecules that participate in this interaction were sought by analyzing the detergent-soluble membrane proteins of GBI/6 stromal cells that could be adsorbed by intact FDCP-1 progenitor cells. A single-chain protein from GBI/6 cells having an apparent molecular weight of 37 Kd was selectively adsorbed by FDCP-1 cells. This protein, designated p37, could be surface-radiolabeled and thus appeared to be exposed on the cell membrane. An apparently identical 37- Kd protein was expressed by three stromal cell lines, by Swiss 3T3 fibroblastic cells, and by FDCP-1 and FDCP-2 progenitor cells. p37 was selectively adsorbed from membrane lysates by a variety of murine hematopoietic cells, including erythrocytes, but not by human erythrocytes. Binding of p37 to cells was calcium-dependent, and was not affected by inhibitors of the hematopoietic homing receptor or the cell-binding or heparin-binding functions of fibronectin. It is proposed that p37 may be a novel adhesive molecule expressed on the surface of a variety of hematopoietic cells that could participate in both homotypic and heterotypic interactions of stromal and progenitor cells.     

Pyridoxine Deficiency and Ethanol-induced Liver Injury

It has been suggested that pyridoxine deficiency may potentiate ethanol-induced liver injury. Our purpose was to clarify the effect of pyridoxine deficiency on ethanol-associated liver injury by comparing liver histology, serum liver enzymes, and the viability of cultured hepatocytes from pyridoxine-deficient and pyridoxine-sufficient rats that had been chronically fed ethanol-enriched diets. Our data fail to substantiate that pyridoxine-deficient animals are more susceptible to the hepatotoxic effects of ethanol than pair-fed pyridoxine-sufficient controls. Furthermore, the addition of pyridoxine to hepatocyte cultures fails to prevent in vitro cytotoxicity of added ethanol. Pyridoxine deficiency may augment ethanol-induced enhancement of hepatic urea synthesis. These data suggest that pyridoxine deficiency may contribute to the abnormal plasma amino acid profiles and nitrogen balance of chronic alcoholics, but that it does not potentiate ethanol-induced liver injury.