All four types of responses involve the genetic machineries that

All four types of responses involve the genetic machineries that underlie a number of complex human diseases such as cancer and neurodegenerative diseases, including Alzheimer’s and Parkinson’s. We highlight the types of stress response experiments required to detect the genes and pathways underlying human disease and suggest that studying stress biology in worms can be translated to understanding human disease and provide potential targets for drug discovery.”
“Background: In endothelial dysfunction, vascular cell adhesion molecule-1 (VCAM-1), E-selectin and intercellular adhesion molecule-1 (ICAM-1) expression (collectively termed cell adhesion

molecules; CAMs) EPZ-6438 chemical structure increase at sites of atherosclerosis and are stimulated by proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha). Methods: We evaluated the effect of alpha-tocopherol (AT; 10-150 mu M) and BAY 11-7082 (BAY; 0.1 or 1 mu m) on CAMs mRNA expression as well as their protein in soluble release form (sCAMs) in human aortic

endothelial cells (HAECs) activated by TNF-alpha (1 or 10 ng/ml). Also, we determined the extent of lymphocyte adhesion to activated HAECs. Results: BAY reduced VCAM-1, E-selectin and ICAM-1 mRNA expression by 30, 30 and AMN-107 clinical trial 10%, respectively. Furthermore, protein reduction of sVCAM-1 by 70%, sE-selectin by 51% and sICAM-1 by 25% compared to HAECs stimulated by TNF-alpha was observed (p < 0.05). AT (50, 75 and 150 mu M) decreased VCAM-1 mRNA expression by 30% and sVCAM-1 protein by 33% compared to HAECs stimulated by TNF-alpha (p < 0.05). TNF-alpha-activated HAEC adhesion to human Jurkat T lymphocytes was higher compared

to nonactivated HAECs (p < 0.05). BAY (2 and 5 mu m) reduced this lymphocyte adhesion (p < 0.05). Conclusion: BAY reduces all the CAMs studied as well as cell adhesion, while AT selectively inhibits VCAM-1; both induce endothelial dysfunction improvement. Copyright (C) 2012 S. Karger AG, Basel”
“BACKGROUND: The evidence of or against the presence of a “”July phenomenon”" in resident teaching hospitals has been inconsistent. Moreover, there are limited data on the “”July phenomenon”" in the field of neurosurgery.

OBJECTIVE: To determine whether a “”July phenomenon”" exists for neurosurgical mortality or complications.

METHODS: A search of the National Inpatient Sample database from 1998 to 2008 was performed for all admissions for International Classification of Diseases, 9th Revision codes corresponding to nontraumatic hemorrhage, central nervous system (CNS) trauma, CNS tumor, and hydrocephalus. Generalized linear mixed-model analysis was performed, adjusted for patient demographics and hospital characteristics, for the outcomes of mortality and complications for the month of July compared with all other months in teaching hospitals.

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