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Biomedical subjects

R Holmes

Publications and source records attributed to R Holmes.

At least 109 records · Page 6Linked to original sources
PubMed1987

Respiration in heat stressed camels.

Respiration and heat exchange in relation to brain temperature (Th) and body temperature (Tb) were investigated in four heat stressed camels subjected daily to high temperature (47 degrees C) in a climate chamber while resting when hydrated and dehydrated by approximately 10%, 15% and 20% of initial weight. Diurnally Tb followed patterns described previously. Th was usually 0.2-0.5 degrees C greater than Tb: occasional reversals with brain cooling were observed. Minute ventilation increased with Tb: above 37.5 degrees C it was approximately half as much in dehydrated as in hydrated animals. Respiratory frequency increased with Tb up to 60/min. Tidal volume fell with increasing frequency; above 25 breaths/min, tidal volume approximated dead space volume. Exhaled air was almost always unsaturated with no systematic effect of dehydration. Metabolic rate fell on dehydration reducing ventilatory demand. Th and Tb were measured in two of the animals walking outdoors: then Th fell below Tb if exercise exceeded 30 min. The data indicate that heat stressed camels pant, but turbinate vasoconstriction in a hot environment prevents cooling of the brain by carotid rete heat exchange.

Animals↗
PubMed1987

Lethal skin cancers in hairy cell leukemia (two case reports).

2 patients with hairy cell leukemia (HCL) complicated by multiple cutaneous and other malignancies are described. The second malignancies behaved in a much more aggressive fashion than would be expected in an immunocompetent population, and were lethal in both patients. The literature regarding second malignancies in immune compromised patients, and in HCL in particular, is reviewed.

Aged↗
PubMed1987

The kinetics of monosaccharide absorption by human jejunal biopsies: evidence for active and passive processes.

The kinetics of initial rates of uptake of glucose, galactose, arabinose and mannitol have been measured in jejunal biopsies from normal subjects in order to investigate the existence of multiple uptake systems. Glucose kinetics fitted best a model of a saturable uptake system (app Kt = 2.06 +/- 0.33 mM, app Jmax = 93.85 +/- 1.19 nmol/10 min/mg dry weight), together with a linear uptake indistinguishable from the passive uptake of arabinose and mannitol (app Kd = 0.80 +/- 0.05 nmol/10 min/mg dry weight/mM for glucose, 0.75 +/- 0.03 for arabinose, and 0.83 +/- 0.03 for mannitol). The saturable uptake, but not the linear uptake, was inhibited by phlorizin and by the absence of sodium. Cytochalasin B and phloretin had no effect on overall uptake. Galactose kinetics in the absence of inhibitors fitted best a model of a single saturable uptake system (app Kt = 11.05 +/- 0.12, app Jmax = 201.9 +/- 1.13) with no evidence of linear uptake. In the presence of phlorizin, or in the absence of sodium, uptake was predominantly linear with app Kds of 0.84 +/- 0.03 and 0.79 +/- 0.01, not significantly different from the linear component of glucose uptake. We conclude that hexose uptake in human jejunum in vitro occurs by both active and passive routes, and that the active uptake of galactose appears to be inhibited at high galactose concentration.

Adolescent↗
PubMed1987

Central nervous system complications of a newly recognized subtype of leukemia: AMML with a pericentric inversion of chromosome 16.

Ten patients with acute myelomonocytic leukemia (AMML) and inversion of chromosome 16 who had CNS involvement were identified at M.D. Anderson Hospital between January 1972 and December 1984. The nervous system signs and symptoms were evaluated in detail. CT scans, CSF cytologies, and treatment modalities were reviewed. Two patients underwent biopsies of lesions that proved to be granulocytic sarcomas. AMML with inversion 16 carries a much higher (33%) incidence of CNS involvement in the form of leptomeningeal metastasis and/or granulocytic sarcoma than all other acute nonlymphocytic leukemias (5%). The reason for this appears to be related to the chromosomal aberration and not to prolonged survival.

Adult↗
PubMed1986

Splanchnic bed vascular malformations and the development of portal hypertension.

The vascular lesions, angiomas, and arteriovenous malformations are known to be associated with a number of complications. These lesions, when present in the liver, may precipitate heart failure in infants. Recent reports suggest that although the prognosis is good for the majority of infants who survive the neonatal period, the lesions are capable of causing portal hypertension later in life. We have encountered three patients whose vascular lesions were in continuity with the portal circulation who subsequently went on to develop portal hypertension. One patient had angiomas of the liver, one splenic and colonic angiomas, and the third had diffuse arteriovenous malformations of the intestine. Data are presented and literature is reviewed, which suggest that any vascular lesion that is capable of substantially increasing portal blood flow may lead to the development of portal hypertension. The treatment of such lesions should be aggressive. If surgical management is not possible, alternative treatments such as embolization should be attempted early in order to increase the chance for successful therapy.

Arteriovenous Malformations↗
PubMed1986

Energy expenditure in chronic alcoholics with and without liver disease.

Chronic alcoholism activates metabolic pathways, resulting in wasteful expenditure of energy (Pirola and Lieber, J Nutr 1975;105:1544-8). To study this hypothesis, we measured oxygen consumption (VO2), carbon dioxide production (VCO2), and resting energy expenditure (MREE) utilizing indirect calorimetry in 8 chronic alcoholics with (group I) and 11 chronic alcoholics without (group II) clinical or biochemical evidence of alcoholic liver disease. Seven healthy volunteers served as controls. A statistically increased MREE was observed in group II subjects (p less than 0.05, MREE 999.7 +/- 111.4 kcal X day X m2) as compared to normals (MREE 842.3 +/- 42.1 kcal X day X m2) and group I subjects (MREE 813.4 +/- 101.4 kcal X day X m2). VO2 and VCO2 were also significantly higher (p less than 0.05) in group II than in group I and normals. The predicted resting energy expenditure as calculated by the Harris-Benedict equation was similar in both groups and normals. Theories to explain the increased MREE in group II subjects are presented.

Adult↗
PubMed1986

Clinical zinc deficiency during long-term total enteral nutrition.

Zinc deficiency during long-term total parenteral nutrition has been well reported in the literature. However, there is limited information available on zinc deficiency occurring during total enteral nutrition. Two cases of clinical zinc deficiency in patients on long-term enteral feedings are presented. Nutritional assessment of these two patients on admission revealed hypoalbuminemic malnutrition. Nutritional support in the form of nasogastric tube feedings were initiated in both patients due to altered mental status. The formula used was Ensure (Ross Labs, Columbus, OH), which provided greater than 150% of the RDA for zinc. However, four months and seven months after initiation of adequate nutritional support, both patients developed skin rashes around the groin and under the breasts and axilla. Serum zinc levels were depressed in both patients, to 42 and 54 mg/dL, respectively (normal for the authors' laboratory, 66 to 120 mg/dL). Supplementation with zinc sulfate 220 mg per day via nasogastric tube resulted in disappearance of the rash with return of serum zinc to normal levels. The authors suggest close observation of patients on long-term enteral nutrition for clinical manifestation of zinc deficiency, especially an unexplained skin rash. Further studies are needed to establish minimum daily zinc requirements in patients on long-term enteral feedings.

Aged↗
PubMed1986

Lactose digestion by human jejunal biopsies: the relationship between hydrolysis and absorption.

The relationship between lactose hydrolysis and absorption of released glucose was investigated by determining the kinetics of lactose digestion by jejunal biopsies incubated in vitro. Lactase activity in intact biopsies correlated with conventional assay of tissue homogenates (r = 0.85, p less than 0.001), and glucose uptake from 28 mM lactose was directly proportional to lactase activity (r = 0.95, p less than 0.001) in 21 subjects with normal lactase levels, six with hypolactasia (primary or secondary to coeliac disease) and two with lactose intolerance but normal lactase activity. Kinetic analysis at 0.56-56 mM lactose in five normal subjects showed saturable kinetics for hydrolysis (app Km = 33.9 +/- 2.2 mM; app Vmax = 26.5 +/- 1.1 nmol/min/mg dry weight) but glucose uptake could be fitted to a model either of saturable uptake (app Kt = 47.2 +/- 0.3 mM; app Jmax = 14.1 +/- 0.2 nmol/min/mg) or saturable uptake plus a linear component (app Kt = 21.3 +/- 1.15; app Jmax = 4.59 +/- 0.12; app Kd = 0.093 +/- 0.010 nmol/min/mg/mM). The proportion of glucose taken into the tissue did not significantly exceed 50% of the total released at any lactose concentration suggesting the lack of an efficient capture mechanism for the released glucose. The results suggest that lactose hydrolysis is the rate limiting step in the overall absorption of glucose from lactose in vitro, and that the relationship between hydrolysis and absorption is the same in normal subjects and in hypolactasic subjects.

Adolescent↗
PubMed1985

Adrenergic control of insulin release from isolated islet tissue in the rainbow trout, Salmo gairdneri R.

Immunoreactive insulin levels (IRI) were measured by a homologous fish insulin radioimmunoassay. An in vitro pancreatic islet superfusion technique was employed to monitor the changes in IRI in the presence and absence of specific adrenergic agonists and antagonists. Exogenous adrenaline at low concentrations (10(-10) M) inhibited IRI release but evoked an IRI stimulation at high concentrations (10(-6) M). The stimulation of IRI by adrenaline is thought to involve beta-adrenoceptors located postsynaptically on the beta-cell membrane as the effect of adrenaline was mimicked by the beta-agonist, isoproterenol, and abolished by the beta-antagonist, propranolol. Phentolamine (an alpha-antagonist) potentiated the adrenergic stimulation of IRI, whereas yohimbine (an alpha 2-antagonist) was without effect. Phenylephrine (alpha 1-adrenoceptor agonist) inhibited IRI release suggesting the presence of alpha 1-inhibitory adrenoceptors which exert a modulatory influence on adrenaline-stimulated insulin release.

Animals↗
PubMed1985

The development of a homologous teleost insulin radioimmunoassay and its use in the study of adrenaline on insulin secretion from isolated pancreatic islet tissue of the rainbow trout, Salmo gairdinerii (R.).

A homologous teleost insulin radioimmunoassay (RIA) employing bonito insulin RIA components is described. The RIA sensitivity and specificity was sufficient to measure endogenous immunoreactive insulin (IRI) levels in trout serum, pancreatic islet tissue extract and in vitro culture medium. Adrenaline at 10(-6)M evoked a marked stimulation of basal insulin release from isolated islets; whereas adrenaline at 10(-10)M evoked an inhibition of basal insulin release.

Animals↗