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Biomedical subjects

W Bell

Publications and source records attributed to W Bell.

At least 37 records · Page 2Linked to original sources
PubMed1997

Relationship between cardiopulmonary response to exercise and adiposity in survivors of childhood malignancy.

Many long term sequelae result from previous treatment for malignancy in childhood. However, little information exists on cardiopulmonary response and energy expenditure during exercise and their possible associations with excess body fat. Measurements of body composition and exercise capacity both at low intensity and maximal aerobic capacity were made on 56 long term survivors of childhood malignancy (35 survivors of acute lymphoblastic leukaemia (ALL) and 21 survivors of other malignancies) and 32 siblings acting as controls. Female survivors of ALL had significantly greater mean (SD) body fat than survivors of other malignancies and siblings (32.5 (6.4)% v 24.3 (4.4)% and 26.3 (8.5)% respectively, p < 0.005). Energy expenditure at low intensity exercise was reduced in survivors of ALL, and negatively correlated with body fat after controlling for weight (partial r range -0.21 to -0.47, p < 0.05). Stroke volume, measured indirectly, was reduced and heart rate raised in ALL survivors at sub-maximal exercise levels. Peak oxygen consumption was significantly reduced in girls and boys treated for ALL compared with siblings (30.5 v 41.3 ml/kg/min for girls, p < 0.05 and 39.9 v 47.6 ml/kg/min for boys, p < 0.05 respectively). Reduced exercise capacity may account in part for the excess adiposity observed in long term survivors of ALL.

Adolescent↗
PubMed1997

Teaching and assessing clinical skills using virtual reality.

The need to improve the teaching and assessing of students' procedural skills has been well 0 encounters, often with little or no supervision. Assessment of these skills has depended on rudimentary physical models, or standardized patients. The limitations of these methods also are well known. A new technology known as "Virtual Reality" has tremendous potential to assist medical educators in teaching and assessing clinical skills of students, residents and physicians in practice. Virtual Reality consists of a computer-generated three-dimensional simulation in which the user both views and manipulates the contents of the environment. Various degrees of immersion may be experienced that may include elements such as vision, touch or sound. It can provide an environment that so closely represents an actual clinical situation that skills learned will transfer to patients. Many variations in anatomy or other complications can be presented, and trainees can practice hundreds of times until their skills are perfected. This paper describes current activities in this area in the Dalhousie Faculty of Medicine and elsewhere. Various forms of Virtual Reality are described and their application to particular clinical areas are described.

Computer-Assisted Instruction↗
PubMed1996

Body temperature and nesting behavior following influenza challenge in mice: effects of age.

We studied the interaction of age and influenza on core body temperature (Tc) of mice. Following influenza challenge, 2-mo-old female BALB/c mice demonstrated a significant fall in Tc. Female BALB/c mice 24 mo of age had lower baseline Tc than young mice and a larger fall in Tc post influenza challenge. We noted there were marked differences in nesting behavior between the young and aged mice. A nesting score was devised, and we found that at baseline, aged mice had a much lower score than young mice (15.6 +/- 7.4 vs. 24.7 +/- 0.3, P < 0.0001). Following influenza challenge, nesting behavior of young mice dropped considerably, while no significant change occurred in the behavior of aged mice. When mice were housed without bedding, there were significant decreases in Tc of young, but not aged mice. There was a further fall in Tc with influenza challenge in young mice. These data imply that nesting is an important mechanism for maintaining Tc in young mice, but alternative mechanisms are used by aged mice. The lower body temperatures in the aged mice are similar to studies in aging humans.

Aging↗
PubMed1996

Evidence for trehalose-6-phosphate-dependent and -independent mechanisms in the control of sugar influx into yeast glycolysis.

In the yeast Saccharomyces cerevisiae, trehalose-6-phosphate (tre-6-P) synthase encoded by GGS1/TPS1, is not only involved in the production of trehalose but also in restriction of sugar influx into glycolysis in an unknown fashion; it is therefore essential for growth on glucose or fructose. In this work, we have deleted the TPS2 gene encoding tre-6-P phosphatase in a strain which displays very low levels of Ggs1/TPS1, as a result of the presence of the byp 1-3 allele of GGS1/TPS1. The byp 1-3 tps2 delta double mutant showed elevated tre-6-P levels along with improved growth and ethanol production, although the estimated concentrations of glycolytic metabolites indicated excessive sugar influx. In the wild-type strain, the addition of glucose caused a rapid transient increase of tre-6-P. In tps 2 delta mutant cells, which showed a high tre-6-P level before glucose addition, sugar influx into glycolysis appeared to be diminished. Furthermore, we have confirmed that tre-6-P inhibits the hexokinases in vitro. These data are consistent with restriction of sugar influx into glycolysis through inhibition of the hexokinases by tre-6-P during the switch to fermentative metabolism. During logarithmic growth on glucose the tre-6-P level in wild-type cells was lower than that of the byp 1-3 tps2 delta mutant. However, the latter strain arrested growth and ethanol production on glucose after about four generations. Hence, other mechanisms, which also depend on Ggs1/Tps1, appear to control sugar influx during growth on glucose. In addition, we provide evidence that the requirement for Ggs1/Tps1 for sporulation may be unrelated to its involvement in trehalose metabolism or in the system controlling glycolysis.

Ethanol↗
PubMed1996

Body composition derived from whole body counting of potassium in growth hormone-deficient adults: a possible low intracellular potassium concentration.

The validity of total body potassium (TBK) measurement in estimating fat mass and fat-free mass (FFM) in GHD adults was assessed by comparison with the reference technique of dual energy x-ray absorptiometry (DEXA). The TBK and FFM values determined by DEXA were used to calculate the potassium concentration per kg FFM in GH-deficient (GHD) adults and compared with standard values for normal subjects of 59.6 mmol for females and 66.4 mmol for males. There were considerable differences between predicted and measured TBK values for both males (3972 vs. 3577 mmol; P < 0.001) and females (2526 vs. 2277 mmol; P < 0.001). Similarly, the estimation of FFM and fat mass by TBK measurement was significantly inaccurate for both sexes compared to values determined by DEXA. These discrepancies may be accounted for by the lower calculated potassium concentrations compared with standard values for both males (56.2 vs. 66.4 mmol; P < 0.001) and females (53.1 vs. 59.6 mmol; P < 0.001). These observations suggest that caution should be exercised in the interpretation of TBK in GHD adults, and the reduced potassium concentrations would alleviate inaccuracies in the estimation of body composition. Secondly, the decreased intracellular potassium concentration of GHD adults may account for the decreased muscle strength and ease of fatigueability seen in GHD adults.

Absorptiometry, Photon↗
PubMed1995

Control of glucose influx into glycolysis and pleiotropic effects studied in different isogenic sets of Saccharomyces cerevisiae mutants in trehalose biosynthesis.

The GGS1/TPS1 gene of the yeast Saccharomyces cerevisiae encodes the trehalose-6-phosphate synthase subunit of the trehalose synthase complex. Mutants defective in GGS1/TPS1 have been isolated repeatedly and they showed variable pleiotropic phenotypes, in particular with respect to trehalose content, ability to grow on fermentable sugars, glucose-induced signaling and sporulation capacity. We have introduced the fdp1, cif1, byp1 and glc6 alleles and the ggs1/tps1 deletion into three different wild-type strains, M5, SP1 and W303-1A. This set of strains will aid further studies on the molecular basis of the complex pleiotropic phenotypes of ggs1/tps1 mutants. The phenotypes conferred by specific alleles were clearly dependent on the genetic background and also differed for some of the alleles. Our results show that the lethality caused by single gene deletion in one genetic background can become undetectable in another background. The sporulation defect of ggs1/tps1 diploids was neither due to a deficiency in G1 arrest, nor to the inability to accumulate trehalose. Ggs1/tps1 delta mutants were very sensitive to glucose and fructose, even in the presence of a 100-fold higher galactose concentration. Fifty-percent inhibition occurred at concentrations similar to the Km values of glucose and fructose transport. The inhibitory effect of glucose in the presence of a large excess of galactose argues against an overactive glycolytic flux as the cause of the growth defect. Deletion of genes of the glucose carrier family shifted the 50% growth inhibition to higher sugar concentrations. This finding allows for a novel approach to estimate the relevance of the many putative glucose carrier genes in S. cerevisiae. We also show that the GGS1/TPS1 gene product is not only required for the transition from respirative to fermentative metabolism but continuously during logarithmic growth on glucose, in spite of the absence of trehalose under such conditions.

Cell Division↗
PubMed1995

The estimation of body density in rugby union football players.

The general regression equation of Durnin and Womersley for estimating body density from skinfold thicknesses in young men, was examined by comparing the estimated density from this equation, with the measured density of a group of 45 rugby union players of similar age. Body density was measured by hydrostatic weighing with simultaneous measurement of residual volume. Additional measurements included stature, body mass and skinfold thicknesses at the biceps, triceps, subscapular and suprailiac sites. The estimated density was significantly different from the measured density (P < 0.001), equivalent to a mean overestimation of relative fat of approximately 4%. A new set of prediction equations for estimating density was formulated from linear regression using the logarithm of single and sums of skinfold thicknesses. Equations were derived from a validation sample (n = 22) and tested on a crossvalidation sample (n = 23). The standard error of the estimate (s.e.e.) of the equations ranged from 0.0058 to 0.0062 g ml-1. The derived equations were successfully crossvalidated. Differences between measured and estimated densities were not significant (P > 0.05), total errors ranging from 0.0067 to 0.0092 g ml-1. An exploratory assessment was also made of the effect of fatness and aerobic fitness on the prediction equations. The equations should be applied to players of similar age and playing ability, and for the purpose of identifying group characteristics. Application of the equations to individuals may give rise to errors of between -3.9% to +2.5% total body fat in two-thirds of cases.

Adult↗
PubMed1995

The validity of estimating total body fat and fat-free mass from skinfold thickness in adults with growth hormone deficiency.

The regression equations of Durnin and Womersley for estimating total body fat (TBF) and fat-free mass (FFM) from skinfold thickness were validated for adult GH-deficient (GHD) patients by comparing the values of TBF and FFM from the prediction equations with the directly measured values from dual energy x-ray absorptiometry. Twenty-seven male and 24 female patients (aged 21-61 yr) were studied. GHD was isolated in 5 cases and was part of a spectrum of hypopituitarism due to a variety of causes in 46 cases. The mean period of GHD was 6.9 +/- 4.6 yr. All patients were receiving stable replacement therapy. The validation statistics showed no significant differences (P > 0.05) between measured and predicted values of TBF and FFM in either males (24.5 vs. 24.9 and 65.5 vs. 65.8 kg) or females (24.6 vs. 26.3 and 44.7 vs. 43.9 kg). Mean differences were smaller in males (0.4 and 0.2 kg) than females (1.7 and -0.8 kg); they were less than 1% in males and less than 2% in females. Therefore, the Durnin and Womersley equations are suitable for general use with GHD patients. Using TBF (kilograms) from dual energy x-ray absorptiometry as the dependent variable and the log of the sum of skinfold thickness as the independent variable, linear regression equations were formulated to predict TBF in GHD patients. The lowest SE of estimate was 3.8 kg in males and 4.6 kg in females. To determine their general applicability, these equations will need to be cross-validated.

Absorptiometry, Photon↗
PubMed1994

Effects of influenza virus-specific cytotoxic T-lymphocyte responses induced by a synthetic nucleoprotein peptide on the survival of mice challenged with a lethal dose of virus.

Even though virus-induced cytotoxic T lymphocytes (CTLs) recognize antigens as peptides presented on infected cells, short synthetic peptides without any modifications are generally considered unsuitable for inducing antigen-specific CTLs in vivo. Our results demonstrate rapid induction of influenza virus-specific CTLs in Balb/c mice by an unmodified core protein peptide known to be a dominant H-2d-restricted CTL epitope. Additionally, the immunization procedure we employed in these studies produced significant influenza virus-specific CTLs in lymph nodes, spleen and lungs. When challenged with a lethal dose of influenza virus, a statistically significant delay in the day of death was observed in peptide-immunized mice. However, viral clearance was only slightly different from that in control mice. While these results are encouraging, they suggest a requirement for multiple CTL-inducing peptides, helper T cell-inducing peptides and/or virus-specific IgA responses in order to achieve protection from influenza infection.

Amino Acid Sequence↗
PubMed1994

Physiological changes arising from a training programme in under-21 international netball players.

Physiological and anthropometric measurements were taken on 21 members of an under-21 international squad of mean age 18.9 years. The aims of the investigation were (i) to examine the physiological status of players according to playing unit; and (ii) to quantify the changes arising from a four-month training programme. Maximal/peak oxygen uptake was assessed using an incremental test to exhaustion during treadmill running. Anaerobic performance was measured using the 30s Wingate test. Significant differences occurred between playing units in height (p < 0.001), body mass and FVC (p < 0.05), but not in skinfolds or any of the expressions of aerobic or anaerobic performance (p > 0.05). As a consequence of the training programme significant differences were evident in height (169.7 v 170.1 cm, p < 0.01), body mass (62 v 64 kg, p < 0.05), FVC (4.3 v 4.51, p < 0.01), and anaerobic performance (p < 0.01). Increases in VO2 max (3.3 v 3.51.min-1) were not significant (p > 0.05). Standard deviation scores illustrated that aerobic and anaerobic performances were of roughly the same magnitude before training (-0.35 v -0.29, p > 0.05), but that after training the dominant performance was anaerobic (+0.11 v +1.48, p < 0.01).

Adolescent↗
PubMed1994

Hemostatic effects of stress hormone infusion.

BACKGROUND: Surgery causes changes in hemostasis, leading to a hypercoagulable state. This postoperative increase in hemostatic function is attenuated in patients receiving regional anesthesia compared with those receiving general anesthesia. Regional anesthesia also decreases the neuroendocrine response to surgery compared with general anesthesia, and this effect is hypothesized to be responsible for the differences in hemostatis. To test the hypothesis that neuroendocrine hormones cause changes in hemostasis, we infused stress hormones into normal volunteers and measured hemostatic function. METHODS: After drug screening, 12 normal volunteers were studied. On two admissions, volunteers randomly received either stress hormone (epinephrine, cortisol, or glucagon) or placebo infusion for 24 h. During infusion, patients remained at bed rest and received controlled meals. Blood was obtained from indwelling venous catheters before infusion and 2, 8, and 24 h after the start of infusion. Blood was analyzed for neuroendocrine hormone concentrations, glucose, complete blood count, coagulation proteins, platelet reactivity, and activity of the fibrinolytic system. RESULTS: In the stress hormone group, concentrations of epinephrine, norepinephrine, cortisol, glucagon, and insulin were increased during the infusion period compared with those in the placebo group. Glucose concentrations and white blood cell counts were increased in the stress hormone group compared with those in the placebo group. Circulating fibrinogen concentrations increased 30% and ex vivo collagen-induced platelet reactivity increased 123% (aggregation) and 103% (dense granule release) in the stress hormone infusion group, whereas there was no change in the placebo group. Fibrinolytic proteins were similar in both groups, demonstrating a decrease in plasminogen activator inhibitor-1 activity at 8 and 24 h (196% in the hormone group vs. 199% in the placebo group). CONCLUSIONS: Infusion of stress hormones to concentrations found during surgery is safely tolerated and causes metabolic changes observed with surgery. Stress hormone infusion increases ex vivo platelet reactivity and fibrinogen concentrations that resemble changes seen postoperatively but does not recreate the postoperative decrease in fibrinolytic activity. Differences in neuroendocrine response between types of anesthesia may explain some postoperative changes in platelet function and acute phase reactivity, but additional uncharacterized factors are responsible for the differences in fibrinolysis.

Adolescent↗
PubMed1994

Idiopathic intracranial hypertension in children: the Iowa experience.

Idiopathic intracranial hypertension is an uncommon condition in children and is seen only about once a year in a large referral hospital. Sex incidence is equal, and obesity is a feature in about one third of patients. This article reviews the 30-year experience in an institution where idiopathic intracranial hypertension in adults has been extensively studied. Symptomatic causes of intracranial hypertension and both medical and surgical therapeutic options are reviewed.

Adolescent↗
PubMed1994

The effects of bedrest on circadian changes in hemostasis.

Venous stasis occurs when people are at bedrest, because of altered venous flow characteristics. This is commonly believed to be one etiology behind the development of deep venous thrombosis (DVT). The hemostatic effects of bedrest and their possible role in DVT development have not been fully examined. We hypothesized that bedrest would lead to increases in hemostatic function and that these increases could be important in the development of DVT. Twelve non-smoking volunteers were studied during supine positioning for 36 hours. Platelet reactivity and plasma concentrations of fibrinogen, alpha 2-antiplasmin, plasminogen, thromboxane beta 2, plasminogen activator inhibitor-1, tissue plasminogen activator and neuroendocrine hormones (cortisol, epinephrine and norepinephrine) were measured at 8:00 a.m., 10:00 a.m., 4:00 p.m. and 8:00 a.m. Cortisol demonstrated an early morning increase while catecholamines were unchanged throughout. Fibrinogen, alpha 2-antiplasmin, plasminogen and platelet reactivity were no different at any time point. Fibrinolytic proteins changed over time, manifested by decreased PAI-1 antigen and activity levels at 24 h. Based upon the parameters measured, bedrest causes no increase in hemostatic function. In fact, bedrest causes the potential for enhanced fibrinolysis, that differs from that previously reported for normal activity over 24 h. This may represent a protective mechanism to counter the effects of stasis from bedrest.

Adolescent↗
PubMed1993

Disruption of TPS2, the gene encoding the 100-kDa subunit of the trehalose-6-phosphate synthase/phosphatase complex in Saccharomyces cerevisiae, causes accumulation of trehalose-6-phosphate and loss of trehalose-6-phosphate phosphatase activity.

Preparations of the trehalose-6-phosphate synthase/phosphatase complex from Saccharomyces cerevisiae contain three polypeptides with molecular masses 56, 100 and 130 kDa, respectively. Recently, we have cloned the gene for the 56-kDa subunit of this complex (TPS1) and found it to be identical with CIF1, a gene essential for growth on glucose and for the activity of trehalose-6-phosphate synthase. Peptide sequencing of the 100-kDa subunit of the trehalose-6-phosphate synthase/phosphatase complex (TPS2) revealed one sequence to be 100% identical with the deduced amino acid sequence of the upstream region of PPH3 on the right arm of chromosome IV. This sequence was used to clone an upstream region of PPH3 containing an open reading frame of 2685 nucleotides, predicted to encode a polypeptide of 102.8 kDa. The N-terminal sequence, as well as three internal amino acid sequences, obtained from peptide sequencing of the 100-kDa subunit, were identical with specific regions of the deduced amino acid sequence. Thus, the sequence cloned represents TPS2, the gene encoding the 100-kDa subunit of the trehalose-6-phosphate synthase/phosphatase complex. Interestingly, a stretch of about 500 amino acids from the first part of TPS2 was 33% identical with the entire TPS1 sequence. Disruption of TPS2 had no effect on trehalose-6-phosphate synthase activity but caused complete loss of trehalose-6-phosphate phosphatase activity, measured in vitro, and accumulation of excessive amounts of trehalose-6-phosphate instead of trehalose upon heat shock or entrance into stationary phase in vivo. These results suggest that TPS2 codes for the structural gene of the trehalose-6-phosphate phosphatase. Heat shock induced an increase in trehalose-6-phosphate phosphatase activity and this was preceded by an accumulation in TPS2 mRNA, suggesting that the trehalose-6-phosphate phosphatase is subjected to transcriptional control under heat-shock conditions.

Amino Acid Sequence↗
PubMed1993

Body size and shape: a longitudinal investigation of active and sedentary boys during adolescence.

The aims of the present study were to contrast the distance and velocity curves for height, body mass and somatotype between active (n = 33) and sedentary (n = 15) boys studied annually between 12 and 15 years. Raw measurements were rescaled and aligned according to peak velocity in height (PHV). The sedentary boys were taller up to and including PHV, active boys being taller after PHV (P > 0.05). The sedentary group had a PHV of 8.5 +/- 1.2 cm year-1 and the active group one of 9.5 +/- 1.5 cm year-1 (P < 0.05). Their ages at PHV were 14.1 +/- 0.8 and 14.2 +/- 0.9 years, respectively (P > 0.05). The active boys were lighter before PHV but heavier afterwards. Peak body mass velocities (PBMV) were larger for the active children (9.1 +/- 2.7 kg year-1) compared to the sedentary children (8.0 +/- 2.6 kg year-1) (P > 0.05). At PBMV, the active boys were aged 14.3 +/- 0.8 years and the sedentary boys 14.5 +/- 0.7 years (P > 0.05). The representative somatotype for the sedentary group was a mesomorphic ectomorph. For the active group, ectomorphic mesomorphs and mesomorphic ectomorphs were the most prominent. The sedentary children (overall mean 2.4-3.4-4.7) showed an increase in endomorphy and a decrease in mesomorphy and ectomorphy. In contrast, the active children (overall mean 2.3-3.9-4.0) demonstrated reduced endomorphy with mesomorphy and ectomorphy remaining fairly uniform. Velocities showed mesomorphy to be the most stable component in both groups (-3.0 to +0.1 units year-1). Endomorphy and ectomorphy fluctuated to a greater extent but never quite reached a velocity of one-half unit a year. Whole somatotype analyses identified significant differences between groups at PHV (P < 0.05), individual component analyses at PHV and +1 year PHV (P < 0.05).

Adolescent↗
PubMed1993

Perioperative platelet reactivity and the effects of clonidine.

BACKGROUND: Increased postoperative platelet reactivity may contribute to arterial thrombotic complications following surgery. alpha 2 Agonists, which are being used increasingly to blunt the stress response of surgery, increase platelet aggregation in vitro. We compared perioperative changes in platelet reactivity in 21 patients receiving either clonidine or placebo. METHODS: Patients undergoing major abdominal surgery were randomized to receive oral and transdermal clonidine (n = 11) or placebo (n = 10). All patients received similar perioperative management, including preoperative sedation, general anesthesia without neuraxial opioids, or local anesthetics and postoperative patient-controlled intravenous morphine. Blood was obtained for measurement of clonidine level, fibrinogen concentration, platelet count, and platelet reactivity (impedance aggregometry and dense granule release) before induction and 24, 48, and 72 h postoperatively. RESULTS: Thirteen of the 21 patients had biopsy-proven cancer at surgery, 5 of 11 received clonidine and 8 of 10 received placebo (NS). Clonidine levels were therapeutic (1-2 ng/ml) throughout the study period. Clonidine administration had no effect on platelet count or platelet reactivity. Therefore, the groups were combined for further analysis. In this group (n = 21), compared to preoperative values, fibrinogen levels rose maximally (36%) at 72 h postoperatively and platelet counts decreased 22% at 48 h. Platelet reactivity (aggregation and degranulation) to collagen, adenosine diphosphate, arachidonic acid, and ristocetin, increased at 24, 48, and 72 h postoperatively. Thrombin-induced (supramaximal stimulus) dense granule release did not change from preoperative values. CONCLUSIONS: These data indicate that major abdominal surgery causes increased platelet reactivity postoperatively but does not effect maximal degranulation. This increased platelet reactivity occurs within 48 h of surgery, coinciding with the peak incidence of postoperative arterial thrombotic complications. Clonidine administration has no effect on surgically induced changes in platelet reactivity. In this surgical patient population, the use of clonidine should not increase the risk of platelet-induced perioperative arterial thrombosis.

Abdomen↗