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Biomedical subjects

M Kearney

Publications and source records attributed to M Kearney.

104 records · Page 6Linked to original sources
PubMed1985

Urinary gamma-glutamyl transpeptidase activity in dogs with gentamicin-induced nephrotoxicity.

Serum creatinine concentrations, 24-hour endogenous creatinine clearance, and 24-hour urinary gamma-glutamyl transpeptidase (UGGT) activity were measured daily in 6 dogs given nephrotoxic dosages of gentamicin (10 mg/kg of body weight) every 8 hours for 10 days. Mean UGGT activity was significantly increased by day 5 (P less than 0.05) and preceded significant increases in serum creatinine values (greater than 2.0 mg/dl) observed on day 9. Endogenous creatinine clearance remained within normal limits (2.98 +/- 0.96 ml/min/kg) until day 8. Urinalyses performed 8 days after initiation of gentamicin treatment indicated renal tubular damage (granular casts) in 1 of the 6 dogs, and glucosuria in 3 of the 6 dogs. Measurement of UGGT activity was a more sensitive and reliable method of assessing acute renal tubular damage induced by gentamicin than were serum creatinine concentrations or 24-hour endogenous creatinine clearance.

Animals↗
PubMedDate not supplied

Making evidence-based practice a reality in your institution.

There are many barriers to ensuring that nursing practice is based on research evidence. This article provides several resources to help the practicing nurse identify what evidence is available upon which to make practice changes. Additionally, strategies for supporting change are discussed and a case study of one particular evidenced-based change--1:1 support by nurses for women in labor--is examined.

Databases as Topic↗
PubMedDate not supplied

Restoration of E2F expression rescues vascular endothelial cells from tumor necrosis factor-alpha-induced apoptosis.

BACKGROUND: Normally, quiescent endothelial cells (EC) line the inner surface of arteries and protect against thrombosis and neointimal growth. A variety of noxious stimuli, including balloon angioplasty, may compromise EC integrity, thereby initiating proliferation and triggering the local release of cytokines, including tumor necrosis factor-alpha (TNF-alpha). METHODS AND RESULTS: In vivo blockade of TNF-alpha using a soluble receptor molecule results in accelerated reendothelialization at sites of balloon angioplasty, suggesting an important physiological role of TNF-alpha in attenuating regrowth of endothelium after balloon angioplasty. Our studies reveal that TNF-alpha, an apoptosis-inducing cytokine, induces G1 cell-cycle arrest in proliferating EC. Quiescent EC are relatively immune to TNF-induced apoptosis versus proliferating EC, which display repression of the E2F transcription factor coincident with TNF-induced apoptosis and cell-cycle arrest. We also show that in this setting, E2F overexpression exerts a survival effect in proliferating EC and restores cell-cycle progression, in direct contrast to results of prior reports, which revealed that deregulated expression of E2F in normally cycling cells induces apoptosis. CONCLUSIONS: These data demonstrate that TNF-induced apoptosis is highly dependent on cell-cycle activity and that E2F can function as survival factor under certain conditions.

Angioplasty, Balloon↗
PubMedDate not supplied

Age-dependent impairment of angiogenesis.

BACKGROUND: The effect of aging on angiogenesis in ischemic vascular disease has not been studied. Accordingly, we investigated the hypothesis that angiogenesis is impaired as a function of age. METHODS AND RESULTS: Forty days after the resection of 1 femoral artery, collateral vessel development was significantly impaired in old (aged 4 to 5 years; n=7) versus young (aged 6 to 8 months; n=6) New Zealand White (NZW) rabbits on the basis of reduced hindlimb perfusion (ischemic: normal blood pressure ratio=0.58+/-0.05 versus 0.77+/-0.06; P<0.005), reduced number of angiographically visible vessels (angiographic score=0.48+/-0.05 versus 0.70+/-0.05; P<0.01), and lower capillary density in the ischemic limb (130.3+/-5.8/mm2 versus 171.4+/-9.5/mm2; P<0.001). Angiogenesis was also impaired in old (aged 2 years) versus young (aged 12 weeks) mice as shown by reduced hindlimb perfusion (measured by laser Doppler imaging) and lower capillary density (353.0+/-14.3/mm2 versus 713.3+/-63.4/mm2; P<0.01). Impaired angiogenesis in old animals was the result of impaired endothelial function (lower basal NO release and decreased vasodilation in response to acetylcholine) and a lower expression of vascular endothelial growth factor (VEGF) in ischemic tissues (by Northern blot, Western blot, and immunohistochemistry). When recombinant VEGF protein was administered to young and old rabbits, both groups exhibited a significant and similar increase in blood pressure ratio, angiographic score, and capillary density. CONCLUSIONS: Angiogenesis responsible for collateral development in limb ischemia is impaired with aging; responsible mechanisms include age-related endothelial dysfunction and reduced VEGF expression. Advanced age, however, does not preclude augmentation of collateral vessel development in response to exogenous angiogenic cytokines.

Aging↗
PubMedDate not supplied

Patient, wound, and treatment characteristics associated with healing in pressure ulcers.

OBJECTIVE: To examine the associations among selected patient, wound, and treatment factors and healing in pressure ulcers. DESIGN: Nonexperimental, retrospective study using data extracted from charts of patients having a Stage II, III, or IV pressure ulcer between July 1994 and November 1996. SETTING: A long-term-care facility associated with a major metropolitan medical center. RESULTS: Evidence of healing was significantly associated with patient weight (P < .05) and negatively associated with body temperature (P < .05), time on a pressure-relieving bed (P < .05), amount of exudate (P < .001), and stage of pressure ulcer (P < .001). In a regression analysis, pressure ulcer stage, patient weight, and mean body temperature explained 25% of the variability in healing; specifically, lower pressure ulcer stage, higher patient weight, and lower mean body temperature predicted improved healing. Healing was not predicted by chronologic age, pressure ulcer location, number of illnesses, use of tube feedings, use of pressure-relieving beds, mean arterial pressure, or Braden Scale score. In a regression analysis of patient factors alone, lower body temperature and higher weight together predicted 9% of the variance in healing. When wound variables were analyzed, 19% of the variability in healing was explained by the stage of the pressure ulcer. Of the treatment variables, only shorter time on a pressure-relieving bed predicted healing, explaining 6% of the variance. CONCLUSIONS: Strategies for healing pressure ulcers in nursing home patients should include programs for early recognition of pressure injury and prevention of pressure ulcer progression to higher stages; attention to weight gain and/or weight maintenance in at-risk patients; and early recognition and treatment of infections and febrile episodes.

Aged↗