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Biomedical subjects

K Leslie

Publications and source records attributed to K Leslie.

88 records · Page 5Linked to original sources
PubMed1993

Helicobacter pylori infection in adolescents with eating disorders and dyspeptic symptoms.

The potential role of Helicobacter pylori infection of the antrum as a cause of symptoms of dyspepsia in patients with eating disorders was evaluated with an assay to detect H. pylori-specific IgG in serum. H. pylori-specific optical-density readings were comparable for adolescents with eating disorders (0.133 +/- 0.063, mean +/- SD) and for two comparison groups, and were lower than readings for children with documented H. pylori infection. Symptoms referable to the gastrointestinal tract did not correlate with H. pylori status in the teenagers with eating disorders.

Adolescent↗
PubMed1993

The effect of elective total hip replacement on health-related quality of life.

The effect of total hip replacement on the health-related quality of life of patients who have osteoarthrosis was examined as part of a randomized, controlled trial comparing femoral head prostheses that were inserted with or without cement. One hundred and eighty-eight patients were followed for three months: 179 of them, for six months; 156, for one year; and ninety, for two years. The health-related quality of life was assessed with use of the Harris hip score, the Merle d'Aubigné hip score, the Sickness Impact Profile, the Western Ontario and McMaster University (WOMAC) Osteoarthritis Index, the McMaster--Toronto Arthritis (MACTAR) Patient Preference Disability Questionnaire, and the time trade-off technique as a measure of utility. Patients also took the six-minute-walk test. The mean age of the patients in the study was sixty-four years (range, forty to seventy-five years); ninety-seven patients (53 per cent) were men and ninety-four (50 per cent) had a prosthesis inserted with cement. Only three of 188 patients refused to return for quality-of-life assessments. There was significant improvement in all health-related quality-of-life measures and in the six-minute-walk test after the operation (p < 0.01 for all items, except for the work dimension of the Sickness Impact Profile at three months [p = 0.07]). Most of the improvement had occurred by three months postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effect of intravenous clonidine on the dose of thiopental required to induce anesthesia.

A randomized, double-blind, controlled trial was conducted to investigate the influence of intravenous clonidine on thiopental dose requirements when used for induction of anesthesia and associated hemodynamic effects. Sixty ASA physical status I or II patients were randomly allocated to one of three treatment groups: normal saline solution (control, n = 20); clonidine (2.5 micrograms/kg, n = 20); or clonidine (5 micrograms/kg, n = 20). The test drug was administered 15 min before induction of anesthesia with intravenous thiopental. The dose of thiopental to produce loss of lash reflex was recorded as well as mean arterial blood pressure and heart rate at 3-min intervals up to induction of anesthesia and then at 1-min intervals for 5 min. Significant decreases in thiopental dose were observed in both groups receiving clonidine compared with the control group, but there was no significant difference between clonidine groups. With dosage calculated according to total body mass, the control group required 5.50 +/- 1.15 mg/kg (mean +/- SD) of thiopental, whereas those who received 2.5 micrograms/kg of clonidine required 4.15 +/- 1.46 mg/kg of thiopental (a reduction of 25%), and those who received 5.0 micrograms/kg of clonidine required 3.48 +/- 1.06 mg/kg of thiopental (a reduction of 37%). When thiopental dose was adjusted for lean body mass, similar reductions were obtained. Clonidine, in both doses, produced more sedation than control, and the 2.5-mg/kg dose produced less sedation than the larger dose. Mean arterial blood pressure was lower in the groups receiving clonidine. There were no significant differences in heart rate among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Evaluation of the effects of low molecular weight heparin on inflammation and collagen deposition in chronic coxsackievirus B3-induced myocarditis in A/J mice.

Coxsackievirus, Group B, type 3 (CVB3) infection of A/J male mice induces chronic myocarditis with increased interstitial fibrosis and collagen deposition. Heparin, a naturally occurring sulfated glycosaminoglycan, has both anti-inflammatory and antifibrotic activities besides its well-known anticoagulant activity. This study determined whether heparin treatment could decrease either cardiac inflammation or fibrosis in chronic CVB3-induced myocarditis. Control mice were either untreated or treated with heparin (4 micrograms/g body weight, subcutaneously 5 times weekly) beginning 2 days before infection of other groups. Additional groups received either virus only (1 x 10(4) plaque-forming units [PFU]), virus followed by heparin beginning 14 days after CVB3 inoculation, or virus and heparin beginning 2 days before CVB3 inoculation. Animals were sacrificed 14, 28, and 58 days after infection. Heparin treatment begun either before or after virus inoculation reduced animal mortality by approximately 20%. Heparin did not alter virus infection or replication in the heart. Histologically, only animals treated with heparin before virus inoculation showed reduced myocardial inflammation, and only at day 58. However, heparin treatment begun either before or after virus infection significantly decreased collagen deposition in the heart (fibrosis).

Animals↗
PubMed1991

Lean tissue mass is a useful predictor of induction dose requirements for propofol.

The effect of age and sex on ED50 values for propofol was studied in 92 patients aged between 16 and 85 years. All doses were based on lean tissue mass (LTM). The end-point for loss of consciousness was loss of the ability to hold a light object. The mean of the ED50 values for males was 1.31 mg.kg LTM-1 and for females 1.28 mg.kg LTM-1. For males the ED50 values ranged from 0.94 to 1.69 mg.kg LTM-1. For females, the range was 1.06-1.57 mg.kg LTM-1. On statistical analysis, these differences were not significant. These data contrast with other studies in which dosage was based on total body mass where a decrease in dose requirement with age was demonstrated. We propose that by using lean tissue mass to calculate dosage, considerable normalisation of patient response can be achieved. There is considerable inter-individual variation in response to propofol. Age is less important than this variation in determining the correct dose for each patient, provided doses are based on LTM.

Adolescent↗
PubMed1990

Potency of propofol for loss of consciousness after a single dose.

A dose-response curve for loss of consciousness after administration of propofol was obtained using 56 unselected, premedicated patients presenting for surgery. Propofol was given in doses according to the calculated lean tissue mass (LTM) of the patient. The end-point for loss of consciousness was loss of ability to grasp a light object. Using probit analysis, the ED50 for propofol was found to be 1.34 mg/kg of LTM and the ED95 was found to be 2.56 mg/kg of LTM. Comparison with previously published data for thiopentone showed propofol to be approximately twice as potent as thiopentone at ED50 and the slope of its dose-response curve to be shallower than that of thiopentone.

Adolescent↗
PubMed1989

Clinical and experimental aspects of viral myocarditis.

Picornaviruses are frequently implicated as the etiological agents of acute myocarditis. This association is based historically on serological evidence of rising antibody titers to specific pathogens and more recently on identification of viral genomic material in endocardial biopsy specimens through in situ hybridization. Only rarely is infectious virus isolated from either the patient or the heart during periods of maximum myocardial inflammation and injury. Thus, despite a probable viral etiology, much interest centers on the role of the immune system in cardiac damage and the likelihood that the infection triggers an autoimmune response to heart-specific antigens. Heart-reactive antibodies and T cells are found in most myocarditis patients, and immunosuppressive therapy has proven beneficial in many, though not all, cases. Furthermore, murine models of coxsackievirus group B type 3-induced myocarditis also demonstrate that virus infection initiates autoimmunity and that these autoimmune effectors are predominately responsible for tissue injury. How virus-host interactions overcome presumed self-tolerance to heart antigens is discussed, and evidence supporting various theories of virus-initiated autoimmunity and disease pathogenesis are delineated.

Animals↗
PubMed1989

Alpha-smooth muscle actin in parenchymal cells of bleomycin-injured rat lung.

Bleomycin causes focally diffuse interstitial fibrosis characterized by increases in the number and volume of contractile filament-laden parenchymal cells, as well as increased parenchymal contractility. However, the origin of these cells and their relationship to altered contractility, remain unknown. We now have used immunohistochemical methods to ask if cells containing smooth muscle actin and myosin are present in involved regions of parenchyma. Staining of the parenchyma of control lungs with a monoclonal antibody against alpha-smooth muscle actin is sparse, consisting of reactivity with the alveolar entrance ring (septal tip) cells as well as occasional reactivity of alveolar wall cells that may represent pericytes or contractile interstitial cells. Increased alpha-smooth muscle actin staining was observed in areas of parenchymal damage in lungs from animals sacrificed between 1 and 4 weeks postbleomycin instillation. This reactivity included altered staining of the airway and vessel smooth muscle coat as well as thickened septal tips. In addition, newly reactive cells were observed in interstitial and intraalveolar regions and in bands of thickened submesothelial tissue. Staining was most intense in the focal fibrotic lesions which are characteristic of this injury. By contrast, parenchymal reactivity with a polyclonal antibody against smooth muscle myosin at the later time points shows only a mild increase in punctate staining in the damaged foci. We hypothesize that the substantial increase in alpha-smooth muscle actin containing cells in fibrotic regions of involved parenchyma after bleomycin injury is responsible for the altered morphologic, biochemical, and mechanical properties that we have observed.

Actins↗
PubMed1989

Coxsackievirus-induced disease. CD4+ cells initiate both myocarditis and pancreatitis in DBA/2 mice.

DBA/2 male mice inoculated intraperitoneally with 1.8 X 10(5) plaque-forming units (PFU) coxsackievirus B-3 (CVB3) showed extensive inflammatory cell infiltration of the myocardium and acinar tissue of the pancreas in 7 days. Selective depletion of T lymphocyte subpopulations indicated that CD4 cells were either completely or partially responsible for cell damage in both organs. Other organs such as the liver were infected and contained virus titers equivalent to those seen in the heart and pancreas but showed no apparent tissue injury. The role of the CD4 cell was confirmed by positive selection of either T cell subpopulation from CVB3-immune lymphocytes in vitro and adoptive transfer of these cells into T cell-deficient (thymectomized, irradiated, bone marrow reconstituted, TXBM) DBA/2 recipients. Lymphocytes from CVB3-infected donor mice were adsorbed to myocyte, skin fibroblast, or liver vascular endothelial cell (VEC) monolayers. The adherent population was retrieved and adoptively transferred into uninfected syngeneic recipients. When killed 7 days later, the animals receiving unfractionated immune lymphocytes or cells eluted from heart monolayers developed both myocarditis and pancreatitis. Anti-Thy 1.2 and C' treatment of the unfractionated cells completely abrogated transfer of disease. Cells eluted from either fibroblast or liver VEC monolayers showed no pathogenicity. Adsorption of immune cells to heart monolayers in the presence of anti-IAd (class II major histocompatibility complex antigen, MHC) inhibited attachment of the pathogenic T cell, whereas anti KdDd (a class I MHC antigen) had no effect.

Animals↗
PubMed1989

A technology assessment study design.

Randomized controlled trials of drug therapies are now required before the licensing and use of almost all medications. Other health care technologies should be similarly evaluated. The area of competing technologies requires more research, and cemented and noncemented hip prostheses have recently been identified as an important example of such a technology. Although trials such as ours require considerable care in their planning and execution, they can be conducted on a busy clinical teaching ward without adversely affecting the quality and quantity of clinical care.

Bone Cements↗
PubMedDate not supplied

Diet-induced hyperlipidemia and auditory dysfunction.

Chinchillas rendered hyperlipidemic by a 1% cholesterol diet or maintained on a normal diet were either exposed to a 2-octave bandpass noise (700-2,800 Hz for 220 min at 105 or 114 dB) or else not exposed to noise. The animals were assessed with tone-burst (2-16 kHz) elicited compound action potentials (CAP). Compared with normal diet animals, the hyperlipidemic animals: not exposed to noise exhibited elevated thresholds at 8 kHz and higher frequencies; exposed to 105-dB noise exhibited elevated thresholds at 16 kHz; and exposed to 114-dB noise exhibited elevated thresholds at 2-16 kH. Surface preparations were made of the left cochleae of all noise-exposed animals. There was essentially no difference in hair cell counts between hyperlipidemic animals exposed to the 105-dB noise and normal animals similarly exposed. The hyperlipidemic animals exposed to the 114-dB noise exhibited a greater hair cell loss in the first turn of the cochlea than did similarly exposed normal animals. We conclude that maintenance on a high-cholesterol diet can cause a high-frequency hearing loss, probably due to vascular pathology resulting from a hyperlipidemic state. Furthermore, maintenance on a high-cholesterol diet can increase susceptibility to noise-induced hearing losses.

Animals↗