Antibody to intercellular adhesion molecule 1 protects the kidney against ischemic injury.

The pathophysiology of ischemic acute renal failure is complex, and the role of leukocyte adhesion in this process is not well defined. A monoclonal antibody (mAb) against intracellular adhesion molecule 1 (anti-ICAM-1), administered at the time of bilateral renal ischemia in the rat, prevented both functional impairment and histologic changes of acute renal failure. Plasma creatinine measured (mg/dl) 24 hr after 30 min of ischemia was 0.61 +/- 0.05 in the anti-ICAM-1-treated animals compared with 2.4 +/- 0.14 (P < 0.0001) in the vehicle-treated ischemic group. Forty-eight hours after ischemia, creatinine values were 0.46 +/- 0.05 and 2.03 +/- 0.22 (P < 0.0001) in anti-ICAM-1 and vehicle-treated groups, respectively. A low dose of anti-ICAM-1 that was itself nonprotective, when given with partially protective doses of a mAb against lymphocyte function-associated antigen-1 (anti-LFA-1), acted synergistically to prevent renal failure. Anti-ICAM-1 mAb also protected the kidney when administered 0.5 or 2 hr but not 8 hr after restoration of blood flow and when the ischemic period was extended to 40 min. Ischemia-induced increases in tissue myeloperoxidase, a marker of neutrophil infiltration, were mitigated with anti-ICAM-1 treatment. Thus, anti-ICAM-1 mAb protected the kidney against ischemic renal failure, even when the antibody was administered after the ischemic period. These results suggest a critical role for leukocytes and adhesion molecules in the pathophysiology of ischemic injury and may have important therapeutic implications.     

The human homologous pairing protein HPP-1 is specifically stimulated by the cognate single-stranded binding protein hRP-A.

Homologous pairing and strand exchange of DNA are catalyzed by the human homologous pairing protein HPP-1 in a magnesium-dependent, ATP-independent reaction that requires homologous DNA substrates and stoichiometric quantities of HPP-1. Here we show that the addition of the purified human single-strand binding (SSB) protein hRP-A to the reaction mixture stimulates the rate of homologous pairing 70-fold and reduces the amount of HPP-1 required for the reaction at least 10-fold. The identification of hRP-A as a stimulatory factor of HPP-1-catalyzed reaction was facilitated by its recognition as a member of a high molecular weight complex of recombination components. Neither the Escherichia coli SSB protein, bacteriophage T4 gene 32 protein, nor the highly conserved Saccharomyces cerevisiae yRP-A SSB protein could substitute for hRP-A in this stimulation. Because only the cognate SSB was capable of stimulating HPP-1, these results suggest that eukaryotes depend on unique and specific interactions between DNA recombination components.     

Caring and cancer nursing: framing the reality using selected social science theory

Caring and cancer nursing: framing the reality using selected social science theory Despite the recent interest in caring for both academic and clinical nursing, the theoretical basis of this concept may appear somewhat elusive as the research and debate vary widely in their focus. As a result, the available literature may fail to consider the specific contextual issues which characterize caring as it is understood across different health care settings. Consideration of theory from disciplines close to nursing, it is suggested, may be useful in understanding the nature of such 'real world' caring. In this discussion the concept of caring within cancer nursing is explored by drawing on a number of social science and nursing sources. It is known that cancer provokes unique caring demands for nurses practising in this area. By examining the context of cancer, it is argued that effective caring deserves to be recognized as an important clinical variable which can influence a diverse range of issues such as patient satisfaction or therapeutic outcome. It is suggested that other nursing specialisms should also explore the psychosocial dimensions of caring in relation to their own role.     

Closed neural tube defects: neurologic, orthopedic, and gait outcomes.

PURPOSE: The purpose of our study was to obtain a clear understanding of the various diagnoses within the closed neural tube defect (NTD) groups included in the large database of clients in our Spina Bifida Clinic and a clear picture of the outcomes for the various NTD groups. METHODS: One hundred and four clients with closed NTD were categorized using a classification system devised by Tortori-Donati et al. Various clinical markers were investigated, including ambulation and the need for orthoses and wheelchairs. RESULTS: Most clients are ambulatory, requiring an orthoses, but not a wheelchair, despite the high incidence of ankle/foot abnormalities. CONCLUSIONS: This classification system has enhanced our knowledge of this group of clients, provided a greater understanding of the varied outcomes of these children and clinical management required.     

Influence of handedness on calcaneal ultrasound: Implications for assessment of osteoporosis and study design

Calcaneal ultrasound has been increasingly studied for its potential in the assessment of osteoporotic fracture risk. The accuracy of such an assessment is, in part, dependent on the reproducibility of the measurement. This study examines the impact of handedness on ultrasound measurements [broadband ultrasound attenuation (BUA) and velocity of sound (VOS)] in the calcaneus. Two hundred and sixty-four subjects (57 men and 297 women) aged 51.1+13.6 years (mean ± SD) were studied. For each subject, calcaneal ultrasound measurements were performed on both heels with a McCue CUBA ultrasound densitometer. Right-handed dominance (94.7%) was determined by structured interview. In men, BUA measurements were significantly higher on the dominant side: mean difference 4.1±1.5 dB/MHz (mean ± SD;p=0.009), equivalent to 4.2+1.5% and more than 4 times the average rate of annual change in BUA. The difference between sides was greater in young (<50 years) than old men (>50 years). Among the women, the difference was not statistically significant (0.7±0.9 dB/MHz;p=0.4); however, it was significant in younger women (20–30 years) (99±4 vs 90±4 dB/MHz,p=0.01). By contrast VOS did not differ between sides in either men or women irrespective of age. Within-subject standard deviation of BUA was 9.8 dB/MHz for men and 8.6 dB/ MHz for women and the component due to right and left difference was 8.4 dB/MHz for men and 6.9 dB/MHz for women. This variability of BUA between right and left heels could increase the false-positive rate by up to 28% for a cut-off of 2 SD below the mean. These data indicate that variation between left and right heel measurements of BUA is higher than that of random error measurements, particularly in men and younger, presumably more physically active subjects. Although VOS measurements were not side dependent, in the smaller number of studies examining VOS and fracture risk, VOS appears to have a weaker predictive power than BUA. Clinical and epidemiological studies involving calcaneal BUA measurements should standardize the side measured to either the dominant or non-dominant heel, to reduce within-subject variation and increase their power.     

Effects of the 5-HT1A partial agonists gepirone,ipsapirone and buspirone on local cerebral glucose utilization in the conscious rat

The azospirones gepirone (10 mg/kg), ipsapirone (10 mg/kg) and buspirone (10 mg/kg) were examined for their effect on regional cerebral glucose utilization in conscious rats using quantitative 2-deoxyglucose autoradiography. All three 5-HT_1A partial agonists reduced glucose utilization in the hippocampus and dentate gyrus by 20–25% and increased glucose utilization by 38–65% in the lateral habenular nucleus; an important relay between striatal/limbic areas and the mid-brain raphe nuclei. The findings emphasize the potential importance of the hippocampus as a site of action for 5-HT_1A receptor active drugs in vivo and also suggest that functional activity in the striatal/limbichabenular-raphe pathway may be influenced by gepirone, ipsapirone and buspirone.