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Biomedical subjects

B Wilson

Publications and source records attributed to B Wilson.

At least 37 records · Page 2Linked to original sources

Ultrasound assessment and conservative management of inversion injuries of the ankle in children: plaster of Paris versus Tubigrip.

We studied 45 children who presented with an inversion injury of the ankle. The clinical signs suggested injury to the distal growth plate of the fibula, but the plain radiographs appeared normal. Ultrasound examination of the joint in 40 patients showed a subperiosteal haematoma consistent with a growth-plate injury in 23 (57.5%). Children who had been treated with a tubular bandage and crutches by random selection had a mean time to return of normal activity of 14.22 days compared with 21.60 days for those treated with a plaster-of-Paris cast (t=3.60, p=0.0032; d=7.38, 95% CI 3.0 to 11.8). We conclude that children with inversion ankle injuries who have clinical signs of injury to the distal fibular growth plate but a normal radiological appearance, should be treated with a tubular bandage and crutches.

Activities of Daily Living

Selective killing of cholinergic neurons by microglial activation in basal forebrain mixed neuronal/glial cultures.

Microglia activation by lipopolysaccharides (LPS) significantly decreased choline acetyltransferase-immunopositive (ChAT+) neuron number and ChAT activity in rat primary basal forebrain mixed neuronal/glial cultures. The number of non-cholinergic (ChAT(-)) neurons was unaffected. LPS induced nitric oxide synthase (NOS) in microglia, increased the media level of the NO metabolite nitrite, and the NOS inhibitor Ng-nitro-L-arginine methylester (NAME) protected the ChAT+ neurons from LPS. The combination of beta-amyloid peptide (1-42) and interferon-gamma (INF-gamma) also increased the media nitrite level and decreased ChAT+ neuron number. Cholinergic neurons are lost early in the course of Alzheimer's disease, and the enhanced sensitivity of these neurons to microglial activation in mixed neuronal/glial culture may be useful for modeling Alzheimer's disease and developing therapeutic strategies to combat this disease.

Amyloid beta-Peptides

In vivo murine studies on the biochemical mechanism of acetaminophen cataractogenicity.

C57BL/6 and DBA/2 mice are, respectively, susceptible and resistant both to the induction of aryl hydrocarbon hydroxylase (cytochrome P450 1A1, or CYP1A1) and to the cataractogenicity of acetaminophen, which may involve its bioactivation to a toxic reactive intermediate, catalysed by P450 and (or) prostaglandin H synthase (PHS). Following induction of P450 using beta-naphthoflavone, the cataractogenicity of acetaminophen (400 mg/kg ip) in C57BL/6 mice was reduced by pretreatment with the P450 inhibitors SKF 525A and metyrapone, the glutathione precursor N-acetylcysteine, the antioxidant vitamin E, and the free radical spin trapping agent alpha-phenyl-N-t-butylnitrone (p < 0.05). Acetaminophen (200 mg/kg) cataractogenicity was enhanced by pretreatment with the glutathione depletor diethyl maleate (DEM) and the gamma-glutamylcysteine synthetase inhibitor buthionine sulfoximine (BSO) (p < 0.05). No significant effect on acetaminophen cataractogenicity was observed using the PHS cyclooxygenase inhibitors aspirin or naproxen, or the glutathione reductase inhibitor 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). Accordingly, acetaminophen cataractogenicity in C57BL/6 mice does not appear to be dependent upon bioactivation by PHS. In DBA/2 mice treated with beta-naphthoflavone, a high dose of acetaminophen (750 mg/kg ip) was not cataractogenic, even after pretreatment with DEM, BSO, or BCNU. The resistance of DBA/2 mice to acetaminophen cataractogenesis, despite concomitant pretreatments with an inducer of P450 and several agents that interfere with glutathione-dependent detoxifying pathways, suggests differences in this strain involving cytoprotective pathways subsequent to acetaminophen bioactivation and detoxification of the cataractogenic reactive intermediate. These results indicate that acetaminophen cataractogenicity in C57BL/6 mice results from P450-catalysed bioactivation of acetaminophen to a reactive intermediate, possibly a benzoquinone imine and (or) a free radical, the toxicity of which is reduced by glutathione-dependent reactions.

Acetaminophen

Biomechanical responses of elite swimmers to staleness and recovery.

Tethered swimming forces (TSF), average distance achieved per stroke (D/S) during a submaximal effort swim, and time and D/S for a maximal effort swim were measured to determine changes occurring with staleness and recovery. Fourteen nationally ranked male and female swimmers were studied five times (i.e. early-, mid-, and late-season, during tapering, and after competition). ANOVA and Newman-Keuls post-hoc tests were used to assess changes during the season. Three swimmers were classified as stale and showed a deterioration (0.7%) in maximal performance time from early- to late-season which was significantly different (P < 0.05) from the improvement (3.1%) demonstrated by the non-stale swimmers. Daily self-ratings of fatigue, kept by the swimmers in log books during the season, were significantly higher (P < 0.001) for the stale compared with the non-stale swimmers. No significant differences were established between the stale and non-stale swimmers in TSF or D/S during the season or in the response to tapering. A significant improvement (P < 0.05) in TSF was observed from before to after tapering. It was concluded that TSF and D/S may not change significantly with staleness and that the recovery period of tapering prior to competition allows swimmers to generate greater forces in the water.

Adaptation, Physiological

Magnesium deficiency in the eosinophilia-myalgia syndrome. Report of clinical and biochemical improvement with repletion.

We describe a patient with the eosinophilia-myalgia syndrome (EMS) with persistent myalgias, cramping, and weakness that were not responsive to treatment. Despite a normal serum magnesium level, a loading study was performed, and the results suggested low tissue levels of magnesium. He was given parenteral magnesium and had dramatic improvement in symptoms as well as in muscle intracellular levels of this cation. After cessation of magnesium therapy the symptoms recurred, and magnesium repletion again led to an improvement in symptoms and ATP levels. Low tissue levels of magnesium, even in the setting of normal serum levels, may lead to the neuromuscular symptoms in EMS and related disorders.

Adenosine Triphosphate

Space shuttle flight (STS-45) of L8 myoblast cells results in the isolation of a nonfusing cell line variant.

Myoblast cell cultures have been widely employed in conventional (1g) studies of biological processes because characteristics of intact muscle can be readily observed in these cultured cells. We decided to investigate the effects of spaceflight on muscle by utilizing a well characterized myoblast cell line (L8 rat myoblasts) as cultured in the recently designed Space Tissue Loss Flight Module "A" (STL-A). The STL-A is a "state of the art," compact, fully contained, automated cell culture apparatus which replaces a single mid-deck locker on the Space Shuttle. The L8 cells were successfully flown in the STL-A on the Space Shuttle STS-45 mission. Upon return to earth, reculturing of these spaceflown L8 cells (L8SF) resulted in their unexpected failure to fuse and differentiate into myotubes. This inability of the L8SF cells to fuse was found to be a permanent phenotypic alteration. Scanning electron microscopic examination of L8SF cells growing at 1g on fibronectin-coated polypropylene fibers exhibited a strikingly different morphology as compared to control cells. In addition to their failure to fuse into myotubes, L8SF cells also piled up on top of each other. When assayed in fusion-promoting soft agar, L8SF cells gave rise to substantially more and larger colonies than did either preflight (L8AT) or ground control (L8GC) cells. All data to this point indicate that flying L8 rat myoblasts on the Space Shuttle for a duration of 7-10 d at subconfluent densities results in several permanent phenotypic alterations in these cells.

Animals

Dependence of laser photocoagulation on interstitial delivery parameters.

Photocoagulation was performed ex vivo between tissue slabs by delivering continuous-wave laser energy from an optical fiber either directly, or by depositing the energy into a 2.4 mm diameter steel sphere at the fiber tip. The dependence of photocoagulation lesions on the following variables was assessed: (1) energy source: Nd:YAG-532 nm, 1,064 nm +/- steel sphere, (2) tissue type: porcine muscle (light), bovine muscle (dark), (3) delivered power: P = 1.5-3.0 W (porcine), 1.0-2.5 W (bovine), (4) exposure duration: T = 300-1500 s. The resulting cross-sectional photocoagulation lesions are summarized as follows: 532 nm: elongated; central charring in all cases; 1,064 nm: circular; central charring only in bovine for P > or = 2.0 W, T > or = 500 s; sphere: circular; central charring in bovine for P > or = 1.5 W and porcine for P > or = 2.0 W. These experiments suggest photocoagulation lesion size decreases as optical penetration increases. The results indicate that interstitial laser photocoagulation lesions > 10 mm diameter can be made without charring in both lightly and heavily pigmented tissues ex vivo by delivering 1,064 nm laser energy at sufficiently low power for at least 1,000 s from well-polished optical fibers.

Animals

Herpes simplex encephalitis: long term magnetic resonance imaging and neuropsychological profile.

The first comprehensive in vivo documentation of the long term profile of pathological and spared tissue is described in a group of 10 patients with a diagnosis of herpes simplex encephalitis, who were left with memory difficulties as a major residual sequel of their condition. With a dedicated MRI protocol, which included high resolution images of temporal lobe and limbic system areas, data are provided on structures that have recently gained importance as anatomical substrates for amnesia. The major features of the lesion profile were: (1) unilateral or bilateral hippocampal damage never occurred in isolation, and was often accompanied by damage to the parahippocampus, the amygdala, specific temporal lobe gyri, and the temporal poles; (2) the insula was always abnormal; (3) neocortical temporal lobe damage was usually unilateral or asymmetric. It never occurred in isolation, and was invariably associated with more medial pathological changes; (4) anterior and inferior temporal lobe gyri were damaged more often and more severely than posterior and superior temporal lobe gyri; (5) pronounced abnormality was often present in the substantia innominata (region of the basal forebrain/anterior perforated substance); (6) there was evidence of significant abnormality in the fornix; (7) there was evidence of damage to the mammillary bodies; (8) thalamic nuclei were affected in around 50% of cases, with damage usually unilateral; (9) frontal lobe damage was present in a few patients, and affected medial areas more than dorsolateral areas; (10) there was some involvement of the striatum, although this was usually unilateral and mild; (11) there was usually limited involvement of the cingulate gyrus and of the parietal and occipital lobes; (12) the cerebellum and brain stem were never damaged. Lesion covariance analysis indicated a close relation between the presence of abnormalities in temporal lobe and limbic-diencephalic regions. Unlike severe head injury, lesions in the temporal pole were not associated with the presence of lesions in the orbitofrontal cortex. Long term neuropsychological impairments were characterised by a dense amnesia in 60% of cases, and a less serve but noticeable anterograde memory impairment in the others. Naming and problem solving deficits were found in a small number of cases. Only two patients were able to return to open employment. Severity of amnesia showed a significant relation with severity of damage to medical limbic system structures such as the hippocampus, with bilateral damage being particularly important. By contrast, there was a minimal relation between memory loss and severity of damage to the thalamus, to lateral temporal lobe areas, or to the frontal lobes.

Adult

Monitoring Peach Harvest Workers Exposed to Azinphosmethyl Residues in Sutter County, California, 1991

Peach harvest workers were evaluated for exposure to azinphosmethyl residues by measuring foliar residues, urinary alkylphosphate metabolites, butyrylcholinesterase (BChE), acetylcholinesterase (AChE), and dermal residues using clothing and skin washes. Workers entered orchards 51 days after application and worked in treated fields for 10 of the next 17 days. Dislodgeable foliar residues ranged from 0.82 to 1.72 microg/cm2 and did not change significantly over the study period. Combined mean dermal exposure for the 3 consecutive monitoring days was 32 mg and ranged from 17.9 to 60.5 mg. Overall mean excretion levels for the 5 monitoring days were 1.7 mg dimethylphosphate and 1.9 mg dimethlythiophosphate. There was no significant difference in BChE between the exposed harvesters and minimally exposed sorters. The exposed group had significantly lower AChE values than the sorters for 2 post-exposure blood draws by three testing methods, while no significant difference was found for the pre-exposure blood draw. The AChE values for the post-exposure blood samples for the exposed workers decreased significantly about 10-20% over the 3-week exposure period but increased or remained constant for the sorters. Urinary metabolite excretion increased with continuous exposure and was inversely correlated with both AChE and BChE but was not correlated with dermal exposure measurements. High correlations were generally observed between AChE measurements taken in the field using a new spectrophotometric kit and laboratory AChE measurements.

Journal Article

General pharmacology of gemcitabine hydrochloride in animals.

Gemcitabine (2',2'-difluorodeoxycytidine monohydrochloride, LY188011 hydrochloride, CAS 122111-03-9) is a nucleoside analog with a broad spectrum of antitumor activity in murine models and is currently undergoing clinical evaluation. The profile of the pharmacological effects of this agent was assessed in studies evaluating the cardiovascular and respiratory systems, renal function, the gastrointestinal system, the central nervous system, and the autonomic nervous system. In vivo doses ranged from 0.15 to 300 mg/kg given by the intravenous route, while in vitro concentrations up to 1 x 10-3 mol/l were used. Gemcitabine was inactive in the autonomic nervous system, gastrointestinal function, and central nervous system studies. Only minimal changes were seen in the cardiovascular and respiratory study, with a slight decrease in pulmonary arterial pressure at the mid dose and a stroke volume increase at the high dose. In the renal function studies, a slight decrease in the urine pH at the high dose and decreased serum creatinine at the mid dose levels were observed. In summary, gemcitabine had minimal effect in these pharmacodynamic studies. These results indicate that gemcitabine has a low potential to produce adverse pharmacologic effects.

Animals

Staff nurse perception of job empowerment and organizational commitment. A test of Kanter's theory of structural power in organizations.

In this study, Rosabeth Kanter's structural theory of organizational behavior was tested in a nursing population by examining the relationship between 161 staff nurses' perceived job empowerment and their commitment to the organization. Data were collected using the Organizational Description Opinionnaire, the Organizational Commitment Questionnaire, a modified version of the Conditions for Work Effectiveness Questionnaire, and a demographic questionnaire. Consistent with Kanter's theory, a strong positive relationship was found between nurses' perceptions of power and opportunity and their commitment to the organization. In addition, overall empowerment was correlated positively with nurses' perceptions of their immediate managers' power. The results suggest that nurse administrators can empower their staff and improve organizational commitment by manipulating the structures in the work environment to allow greater access to the power and opportunity structures that Kanter maintains are important to overall work effectiveness.

Adult

Uniparental disomy occurs infrequently in Wilms tumor patients.

Wilms tumors commonly exhibit loss of heterozygosity for polymorphic DNA markers located on the short arm of chromosome 11 at band p15. In some instances, the deleted region does not include 11p13, the location of the WT1 gene, suggesting the existence of a second Wilms tumor gene on 11p. Both the exclusive loss of the maternally derived allele in Wilms tumors and the recent description of constitutional paternal isodisomy for this region in patients with either the Beckwith-Wiedemann syndrome (BWS) or isolated hemihypertrophy have suggested that this second locus is subject to sex-specific genomic imprinting. Given that one of these isodisomic patients had minimal congenital anomalies (hemihypertrophy), we hypothesized that a proportion of Wilms tumors which had not lost heterozygosity for 11p markers (about 60% of all cases) might have arisen consequent to 11p paternal heterodisomy and that patients constitutionally homozygous at 11p15 might harbor paternal isodisomy. We have analyzed 40 Wilms tumor cases to determine the parental origin of the child's 11p15 alleles. Paternal heterodisomy could be excluded in all 28 unilateral and 8/9 bilateral potential candidates. It is intriguing that somatic mosaicism for 11p paternal isodisomy was detected in one child with bilateral Wilms tumor and macroglossia. Isodisomy could only be excluded in one of the three possible cases. Thus, 11p paternal hetero- and isodisomy appear to be uncommon causes of non-anomaly-associated Wilms tumors but may be more frequent in Wilms tumor patients with BWS-associated anomalies.

Aneuploidy