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Biomedical subjects

J Seale

Publications and source records attributed to J Seale.

16 recordsLinked to original sources
PubMed1995

Validity of urine-blood hydrational measures to assess total body water changes during mountaineering in the sub-Arctic.

Mountaineering involves high altitude and cold exposure which are each associated with significant levels of dehydration (via altitude-cold diuresis, high energy expenditures, and poor access to water). The purpose of this study was to identify and validate urine and blood indices of dehydration as compared to changes in total body water (which served as the reference standard). Male subjects (n = 10) were studied during a 14 day mountaineering expedition in the sub-Arctic during which they climbed to an altitude of 5245 +/- 229 m (mean +/- SE). Daily activity consisted of approximately 10-15 hours skiing, hiking, and performing mountaineering tasks with heavy loads (> 30 kg). Various measurements were made immediately before ascending (Pre) and after descending (Post) the mountain: body weight (Bw) and composition (%Fat), urine specific gravity (USG), urine protein (UP), plasma electrolytes (K+, Cl-, Na+), plasma proteins (PP), plasma and urinary osmolality (UOsm), hematocrit (Hct), hemoglobin (Hb), blood urea nitrogen (BUN), plasma aldosterone, and total body water (TBW determined via deuterium oxide). Post the expedition significant (p < 0.05) decreases were observed in Bw, and %Fat, while significant increases were found in Na+, K+, USG, UOsm and UP. TBW was slightly reduced, however, changes were non-significant (Pre = 52.9 +/- 1.2 L vs. Post = 52.6 +/- 1.3 L). USG is often used to monitor hydration status in field settings; however, no significant correlations were found between changes in TBW and USG, nor between changes in TBW and other typical urinary indicators of dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of high altitude and cold exposure on resting thyroid hormone concentrations.

This study examined the effect of high altitude and cold exposure on thyroid hormone status during a mountaineering expedition. There were 15 males participating in an expedition to climb Mt. McKinley, AK. Resting blood samples were collected and analyzed for thyroid-stimulating hormone (TSH), total (T)-free (f) thyroxine (T4), triiodothyronine (T3), reverse T3 (rT3), and cortisol. Measurements were made on three occasions: baseline in the continental U.S. one week pre-expedition (PRE-I), baseline in Alaska immediately pre-expedition (PRE-II), and immediately upon descent post-expedition (POST). Statistical analysis indicated that no significant trial PRE-I vs. PRE-II (p > 0.05) differences occurred. Significant (p < 0.05) reduction, however, occurred from PRE-II to POST expedition in TSH, TT3, and fT3. Also rT3 and cortisol increased significantly PRE-II to POST while TT4 and fT4 were unchanged. The increase (delta = POST minus PRE-II) in cortisol was negatively correlated with the decrease (delta) in TSH (r = -0.52, p = 0.05) and TT3 (r = -0.49, p < 0.06). Moreover, the reduction in TT3 was inversely correlated with the rT3 increase (delta comparison, r = -0.66, p < 0.01). The findings demonstrate that the resting concentrations of thyroid hormones are disrupted by a mountaineering expedition, specifically an environmental stress-related "low T3 condition" seems to develop. These changes would seem to be related to an impaired peripheral conversion of T4 to T3, possibly brought about by elevations in the circulating cortisol levels.

Adult↗
PubMed1992

Failure of salmeterol to inhibit circulating white cell responses and bronchoconstriction induced by platelet activating factor.

BACKGROUND: Platelet activating factor (PAF) is a potent mediator of inflammation. Inhalation of PAF causes acute bronchoconstriction and a transient fall in white blood cell count in humans. Salmeterol inhibits pulmonary inflammation induced by PAF in guinea pigs. METHODS: The effect of salmeterol on effects induced by PAF was investigated in eight normal subjects who inhaled salmeterol (50 micrograms) twice daily or a matched placebo for one week before challenge with PAF. Blood samples were taken from a forearm catheter for total white cell and neutrophil counts before and for 30 minutes after administration of PAF (48 micrograms) through a Mefar dosimeter. Blood films were stained for unsegmented neutrophils before and after treatment with PAF on a placebo day. RESULTS: Mean baseline total white cell counts and neutrophil counts did not differ on the two days. Mean baseline sGaw was significantly higher after inhaled salmeterol (1.84 (95% C1 1.45-2.23) s-1kPa-1) than after placebo (1.53 (1.24-1.82)). After placebo mean total white cell counts, neutrophil counts, and sGaw were reduced to 60 (43-78)%, 39 (14-64)%, and 82 (71-93)% of baseline respectively five minutes after inhaled PAF. After salmeterol treatment mean reductions five minutes after inhaled PAF were 59 (45-73)%, 40 (19-61)%, and 82 (71-93)% of baseline respectively. At 30 minutes after treatment with PAF the neutrophil count rebounded to 143 (82-204)% of baseline after placebo and to 127 (93-161)% after inhaled salmeterol. There was no significant difference in the percentage of immature neutrophils before and after treatment with PAF (2.0 (0.5-2.6)% compared with 3.9 (2.2-5.6)%. CONCLUSIONS: Treatment with salmeterol did not inhibit reduction in total white cell count or neutrophil count, rebound neutrophilia, acute bronchoconstriction, or transient flushing after inhalation of PAF. These results conflict with the inhibitory effect of salmeterol on lung inflammation in guinea pigs but are consistent with the lack of effect of salbutamol in humans. Salmeterol does not have an anti-PAF effect in vivo in humans.

Adrenergic beta-Agonists↗
PubMed1991

Energy requirements of a postobese man reporting a low energy intake at weight maintenance.

Three experiments were performed to test the validity of the low reported energy intake of weight maintenance in a postobese man. In the first experiment the subject reported a mean energy intake of 8008 kJ/d during 16 d and he maintained a stable body weight. This finding was not reproduced in the second experiment, which consisted of a 6-d inpatient study during which the subject was confined to a whole-body calorimeter for 5 d. Indeed, he lost weight when fed a controlled energy intake of 7950 kJ/d. Moreover, this experiment showed that direct and indirect calorimetry provided comparable energy-expenditure measurements during this period. Finally, when the subject was refed a controlled energy intake of 7950 kJ/d for 21 d, body weight and fat losses were observed. Therefore, these observations do not support the validity of the low energy intake that may be reported by people predisposed to obesity.

Body Weight↗
PubMed1989

Sensitivity of methods for calculating energy expenditure by use of doubly labeled water.

Attempts to estimate human energy expenditure by use of doubly labeled water have produced three methods currently used for calculating carbon dioxide production from isotope disappearance data: 1) the two-point method, 2) the regression method, and 3) the integration method. An ideal data set was used to determine the error produced in the calculated energy expenditure for each method when specific variables were perturbed. The analysis indicates that some of the calculation methods are more susceptible to perturbations in certain variables than others. Results from an experiment on one adult human subject are used to illustrate the potential for error in actual data. Samples of second void urine, 24-h urine, and breath collected every other day for 21 days are used to calculate the average daily energy expenditure by three calculation methods. The difference between calculated energy expenditure and metabolizable energy on a weight-maintenance diet is used to estimate the error associated with the doubly labeled water method.

Adult↗
PubMed1988

"Artificial" HIV?

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Biological Evolution↗
PubMed1984

[Epidemiology of AIDS].

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Acquired Immunodeficiency Syndrome↗
PubMed1981

Lymphatic clearance during compressive loading.

Lymphatic clearance of radioactive sulfur colloid is measured as a function of externally applied pressure on the hind limb of mongrel dogs. A dead weight device is placed over the site of subcutaneous injection. A solid state Si (Li) is placed into a slot at the bottom of the device to continuously record activity of the tracer. An exponential decrease in activity is modeled as a dual decay resulting from both tracer half life decay and lymphatic clearance of the tagged sulfur colloid. External pressure is seen to enhance lymph clearance until a critical closing pressure is reached, whereupon the vessel collapses and lymph flow is drastically reduced. A closing pressure of 60 mmHg is observed for several experiments. Lymph flow per tissue volume is seen to rise from a mean of 0.324 ml/hr/ml for uncompressed tissue to 0.96 ml/hr/ml for fully enhanced flow in other experiments at 60 mmHg. Results at a pressure of 75 mmHg show almost no lymph clearance suggesting complete vessel closure.

Animals↗
PubMed1980

Lymphatic clearance of radioactive sulfur colloid.

Lymphatic clearance of radioactive sulfur colloid is measured in the hind limb of five mongrel dogs. A solid state Si(Li) detector is placed onto the skin to continuously record activity over the site of subcutaneous injection. Decrease in activity follows an exponential decay which is modeled as a dual decay occurring from both the radioactive decay of the tracer and the lymph clearance of the tagged sulfur colloid. The calculated decay constants for lymph clearance flow per tissue volume result in a mean value of 0.233 +/- 0.077 ml/hr/ml which is consistent with results of other investigators. Adjacent lymph nodes are monitored with a scintillation detector to show that the colloid is absorbed by the lymph vessels. The carotid artery and liver are similarly monitored to show that there is little or no capillary absorption of the tagged colloid.

Animals↗
PubMedDate not supplied

Infectious AIDS.

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Acquired Immunodeficiency Syndrome↗