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T A Moore

Publications and source records attributed to T A Moore.

81 records · Page 5Linked to original sources

The Joint Commission survey can be a "SNAP" (Standards for Nursing Awareness Program).

Healthcare facilities' integration of the standards and changes in current Joint Commission survey process means that staff members at all levels must participate and interact with surveyors more than ever before. It no longer is sufficient just to meet the standards; staff members must under stand and invest in the standards' intent. One way to accomplish this is to increase staff members' awareness of the various survey processes. It is not necessary to ¿teach¿ the standards, but rather to relate them to what already is known and understood. Empowering the nursing staff by relating their practices to the Joint Commission standards, from their perspective and within a familiar context, can contribute significantly to a successful survey.

Accreditation↗

Intact cell and cell-free phosphorylation and concomitant activation of a low Km, cAMP phosphodiesterase found in human platelets.

A monoclonal antibody (CGI-5) directed against the cGMP-inhibited phosphodiesterase isolated from bovine heart was used to examine the phosphorylation of this isozyme in human platelets. PGE1 promoted the phosphorylation of this isozyme, identified as a 110 kDa peptide following SDS-gel electrophoresis. Phosphorylation resulted in approximately a 40% increase in the cGMP-inhibited phosphodiesterase activity. Cell-free experiments demonstrated that cAMP-dependent protein kinase phosphorylated the cGMP-inhibited phosphodiesterase, and that this could be blocked by the heat stable inhibitor peptide (PKI). Phosphorylation of the cGMP-inhibited phosphodiesterase increases the Vmax for cAMP hydrolysis approximately 50%, but does not affect the Km for cAMP (0.12 microM).

3',5'-Cyclic-AMP Phosphodiesterases↗

The role of cytokines in bacterial pneumonia: an inflammatory balancing act.

Bacterial pneumonia is a leading cause of morbidity and mortality in both developed and developing countries. While tremendous advances have been made in the treatment of pneumonia using broad-spectrum antibiotic regimens, these approaches have resulted in the recent emergence of multidrug resistant bacteria. To understand better the role of the host immune response to pulmonary bacterial infections, several in vivo animal models have been developed using different bacterial agents: two acute infection models using Klebsiella pneumoniae and Streptococcus pneumoniae and one model of chronic infection using Pseudomonas aeruginosa. To summarize, the resolution of pulmonary bacterial infections involves a finely orchestrated balancing act of proinflammatory and antiinflammatory cytokines. On initial encounter with deposited bacteria, resident alveolar macrophages become activated and secrete proinflammatory cytokines and chemokines, resulting in the eventual generation of a proinflammatory amplification loop between resident or recruited macrophages or polymorphonuclear neutrophils and lymphocytes. As the infection is cleared, a second wave of antiinflammatory cytokines is produced to localize the inflammatory response to within the lung microenvironment and eventually to downmodulate this response. Experimental perturbation of the host inflammatory "cycle" can have either beneficial or detrimental effects on bacterial clearance. With this in mind, a cautionary approach needs to be used in proposing immunoadjuvant therapies for pneumonia treatment.

Animals↗