Survival Strategies for Nurse-Midwifery Students

Nurse-midwifery students face multiple stressors in their educational experience. Strategies to resolve stress and promote adaptation to the new role are examined and measures used to promote students' adaptation to the educational experience are described.     

A Psychosociocultural Perspective, Part 2

Building on the foundation of understanding and comprehensive assessment of battered women, this article addresses service planning and intervention. Strategies are approached within the framework of a Crisis Paradigm developed from field research with battered women and their families. They include mechanisms such as support groups which link crisis service to the long-term needs of battered women, and systematic approaches to removing the obstacles which keep women victimized. An Assessment and Service Planning Guide (ASPG) is proposed for inclusion in routine health care of abused women. The article concludes with strategies for preventing violence at interpersonal and societal levels.     

Cystic renal melanoma: CT/ultrasound correlation

A new computed tomographic and sonographic appearance of renal metastatic melanoma is described. Bilateral cystic masses with thick walls, many with mural nodules, were noted. Sonography also demonstrated complex echopenic masses with irregularly thickened walls and mural nodules.     

The effect of design of residential homes in creating dependency among confused elderly residents: A study of elderly demented residents and their ability to find their way around homes for the elderly

A study of 13 homes for elderly people examining the effect of the environment on demented residents looked into the complexity of the design from the residents' point of view. Two principal tools were used in this investigation: ‘route diagrams’, which describe a resident's use of the home, and a measure devised to indicate each resident's ability to find her way around the home. These are described and the relationship between them explored. From this the following tentative conclusions are drawn:

• (i) The variables that influence a resident's ability to find her way around differ between group and communally designed homes.
• (ii) It would appear that group homes provide a more favourable design, especially in the case of physically frail demented elderly people.
• (iii) In group homes, the level of lighting is an important aid to a demented person in finding her way around.
• (iv) In communal homes, residents seem most able to find their way around homes that have been adapted from older premises.
• (v) In both types of home, ‘meaningful decision points’ can be seen as aids to a resident finding her way around.

     

Epidermal growth factor and trefoil factor family 2 synergistically trigger chemotaxis on BEAS-2B cells via different signaling cascades

Injured areas of the respiratory epithelium are subject to rapid repair by the migration of adjacent epithelial cells, a process termed "restitution". Rapid re-epithelialization is promoted by interactions between migrating cells and the extracellular matrix proteins. Furthermore, epidermal growth factor (EGF) as well as trefoil factor family (TFF) peptides are well known regulators of epithelial restitution due to their motogenic effects. Migration of the human bronchial epithelial cell line BEAS-2B in modified Boyden chambers was used as a model system for airway restitution. EGF or recombinant human TFF2 or TFF3 showed mainly chemotactic activity. The motogenic response was strictly dependent upon a haptotactic substrate, but to different degrees. EGF induced phosphorylation of extracellular signal-regulated kinases (ERK) 1/2, c-Jun-N-terminal kinase, p38, Akt, and p70S6K in BEAS-2B cells. Using specific inhibitors, the signaling cascades responsible for the motogenic response were shown to differ drastically when EGF was compared with TFF2. The motogenic effect of TFF2 was previously demonstrated to depend on ERK1/2 and protein kinase C activation; whereas the EGF-triggered motogenic response was completely independent of ERK1/2 activation but sensitive to the inhibition of phosphoinositide 3-kinase, p38, protein kinase C, or nuclear factor kappaB. However, the motogenic effects of EGF and TFF2 are additive. These data suggest that luminal EGF and TFF peptides can act synergistically in the human respiratory epithelium to enhance rapid repair processes in the course of diseases such as asthma.     

Upregulation of the Golgi protein GP73 by adenovirus infection requires the E1A CtBP interaction domain

GP73 is a novel type II Golgi transmembrane protein that is expressed at high levels in the hepatocytes of patients with viral hepatitis (R. D. Kladney, G. A. Bulla, L. Guo, A. L. Mason, A. E. Tollefson, D. J. Simon, Z. Koutoubi, and C. J. Fimmel, 2000, Gene 249, 53-65) and is induced in cultured cells by infection with viruses including adenoviruses. Its biological function and the mechanisms by which its expression may be regulated by viral infection are unknown. Here we report that GP73 is induced at the RNA and protein level in human Hep3B hepatoma cells infected by human Ad5 and Ad2. Hep3B cells were infected with wild-type or mutant adenoviruses. GP73 expression was measured by RNase protection assay, immunoblotting, or immunofluorescence microscopy. GP73 RNA and protein levels were strikingly induced following infection. The rise in GP73 expression coincided with the appearance of the adenovirus E1A and DBP proteins and preceded the expression of the fiber protein, a marker of the late phase of infection. Infection did not affect the expression of giantin, GPP130, or golgin-84, three integral Golgi membrane proteins with structural similarities to GP73. Mapping studies using a panel of mutant adenoviruses demonstrated that the E1A C-terminus, specifically its CtBP interaction domain (CID), is required for GP73 expression. Subsequently, Hep3B cells were transiently transfected with plasmids expressing wild-type or mutant E1A proteins. These studies confirmed that E1A induced GP73 expression via the CID. Our studies establish GP73 as a novel adenovirus-induced cellular protein whose expression is regulated through the CID of the E1A protein.