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Biomedical subjects

C J Henry

Publications and source records attributed to C J Henry.

At least 73 records · Page 4Linked to original sources
PubMed1989

The constancy of basal metabolic rate in free-living male subjects.

The object of this work was to investigate the constancy of basal metabolic rate (BMR) over time. The BMR was measured in a group of healthy free-living adult men on three separate occasions over some 2 years. Analysis of variance showed that the coefficient of variation within subjects was 4 per cent and between subjects 8 per cent. The results are compared with those of earlier workers, from Zuntz onwards, who made serial measurements of BMR on the same subjects.

Adult↗
PubMed1988

Protein and energy metabolism in starvation reconsidered.

Current concepts of the metabolic changes during starvation have been heavily influenced by recent studies on grossly obese subjects undergoing therapeutic fasting. It has been suggested that during prolonged starvation the central nervous system develops the ability to utilize ketone bodies, and that the consequent reduction in gluconeogenesis leads to an adaptive sparing of protein catabolism. However, our analysis of classical studies on starvation shows that during prolonged starvation in normal subjects the fraction of total energy expenditure derived from protein (the P ratio) remained unchanged. Although urinary nitrogen was reduced during the progress of the fast, we conclude that this is secondary to the general reduction in metabolic rate, rather than to a specific sparing of protein.

Energy Metabolism↗
PubMed1987

Measures of nutritional status. Survey of young children in north-east Brazil.

In 738 children aged under 5 from three communities in north-east Brazil, nutritional status was assessed by four means-weight for age, height for age, weight for height, and middle upper arm circumference (MUAC). As judged by weight for age, 43% of children were adequately nourished and only 2% were severely malnourished. Stunting (less than 85% height for age) was seen in 8% and wasting (less than 70% weight for height) in 1%. There was poor agreement between MUAC (a measure of wasting) and weight for height when the conventional cut-off points for MUAC were applied. Although agreement improved with new MUAC cut-off points the probability of correct diagnosis of wasting (sensitivity) remained low. Although height for age and weight for height were the most useful measures of nutritional status, MUAC may be the best available in famine victims and refugees.

Age Factors↗
PubMed1987

Basal metabolic rate and diet-induced thermogenesis in Asians living in Britain.

The basal metabolic rate (BMR) and diet-induced thermogenesis (DIT) in 11 Asians (4 men, 7 women) who had lived in Britain for longer than 2 years were compared with a matched group of Europeans. The mean basal oxygen consumption was 226 ml O2/min in the Asians and 218 ml O2/min in the Europeans, values not significantly different. When BMR was expressed in absolute terms, per unit body weight, per unit body surface area or lean body mass, still no significant difference was observed. DIT was measured in the two groups fed a mixed meal containing 2800 kJ. The main increase in the metabolic rate over 20-120 min was 19 per cent in the Asians and 20 per cent in the Europeans. These results indicate that, in contrast to Asians living in the tropics, Asians living in Britain show no difference in BMR or DIT. It is concluded that Asians living in the temperature regions behave metabolically differently from those living in the tropics.

Adult↗
PubMed1986

Chronic inhalation studies in mice. II. Effects of long-term exposure to 2R1 cigarette smoke on (C57BL/Cum x C3H/AnfCum)F1 mice.

Standardized exposure conditions with Kentucky reference 2R1 cigarettes were used to expose 2,053 (C57BL/Cum x C3H/AnfCum)F1 female mice (nose only) to fresh, whole cigarette smoke. In addition, 1,014 mice were sham-exposed, and 449 mice were held as shelf controls. The protocol entailed exposing mice to smoke (or sham-exposure) on a daily basis, 5 days/week, for 110 weeks and observing remaining mice until death. A large number of animals was used so that the smoke generation and animal-holding systems could be tested and evaluated and yet provide significant numbers of animals for exposure to cigarette smoke for a major portion of their lifetime. Deposition of smoke particulates was estimated to be about 125-200 micrograms total particulate matter/lung/day. The only lung cancers observed were diagnosed as alveolar adenocarcinomas (AAC). A total of 19 of 978 smoke-exposed mice and 7 of 651 sham-exposed mice were observed with AAC. The difference between the smoke-and sham-exposed groups was not statistically significant at P less than or equal to .05, but the data suggested that the tumors occurred with a shorter latency in the smoke-exposed group (P = .10). The data were analyzed by various methods, including analysis of subsets of the population of animals. A significant increase in the incidence of lung cancer was observed in one subset; however, this difference was not found in the population as a whole or as a result of any other analyses. Under these exposure conditions, 2R1 cigarette smoke would seem to have weak carcinogenic activity in mouse lung tissue. Other changes associated with smoke exposure were increased incidence of pigmented alveolar macrophage accumulation, otitis media, and head and neck fibrosarcomas. However, the incidence of nephritis, hematopoietic cancers (e.g., leukemias, lymphosarcomas, and reticulum cell sarcomas), and pulmonary congestion was significantly higher in the sham-exposed animals.

Adenocarcinoma↗
PubMed1986

Effect of spiced food on metabolic rate.

Since the time of Lavoisier it has been known that the ingestion of food in animals and man produces an increase in oxygen consumption. This increase in metabolic rate was originally called 'specific dynamic action' (SDA) and is now widely referred to as the thermic effect (TE) of food or diet-induced thermogenesis (DIT) (Rothwell & Stock, 1981). Much of the early work on the thermic effect was confined to the type and amount of food, notably the macronutrients--proteins, fats and carbohydrates. Later, it was shown that certain minor constituents of the diet such as caffeine and associated methylxanthines (Zahorska-Markrewicz, 1980; Jung et al., 1981) in tea and coffee could also have a profound effect on metabolic rate. The consumption of alcohol was also shown to increase metabolic rate (Rosenberg & Durnin, 1978). The work described in this paper reports the effect of another minor constituent of food, spices, on metabolic rate. Although the use of spices in our food has steadily increased with time little information exists on their effect on the metabolic rate. It has been estimated that approximately 40 different spices are used in our diet today. This communication reports the effect of chilli (red pepper, capsicum annuum) and mustard (Brassica juncea).

Adult↗
PubMed1985

Dose-responsive increase in sister-chromatid exchanges in bone-marrow cells of mice exposed nose-only to whole cigarette smoke.

The effect of whole cigarette smoke exposure on bone-marrow sister-chromatid exchanges (SCEs) was studied in B6C3F1 mice. Animals were exposed nose-only to 10% (v/v) cigarette smoke 5 days/week for 2 weeks. Four dose levels of cigarette smoke (1, 4, 9 and 18 exposures/day) were studied using 2 cigarette types, Kentucky reference 3A1 (3A1) and American Blend (AB). A single exposure represented approximately 1 cigarette. A dose-dependent increase in SCEs was observed for both the 3A1 and AB cigarettes at dose levels which had no effect on bone-marrow cell-replication kinetics. These findings represent the first demonstration of a dose-responsive increase in cigarette smoke-induced SCEs in a rodent model system.

Animals↗
PubMed1984

Increased sister-chromatid exchange in bone-marrow cells of mice exposed to whole cigarette smoke.

Using defined cigarette smoke exposure conditions, BC3F1/Cum mice were exposed nose-only to two different types of whole cigarette smoke on a daily basis for 1 week and up to 46 weeks. The number of sister-chromatid exchanges (SCEs) per metaphase was determined in bone-marrow cells. Studies were scheduled so that all cytogenetic observations were made 2-3 days after the last smoke exposure. Exposure to either type of smoke on a daily basis for 1 week or up to 46 weeks resulted in a 2-fold increase in SCEs over sham-exposed control mice. In animals exposed either chronically or for 1 week to either type of smoke, the increase in SCEs persisted for at least 1 week after cessation of smoke exposure. This is the first demonstration of the induction of SCEs in laboratory animals that have been exposed to cigarette smoke in vivo.

Animals↗
PubMed1981

DNA replication and unscheduled DNA synthesis in lungs of mice exposed to cigarette smoke.

Mice of the hybrid strain BC3F1/Cum (C57BL/Cum X C3H/AnfCum) were chronically exposed to measured amounts of machine-generated whole Kentucky reference 2A1 cigarette smoke. DNA replication and unscheduled DNA synthesis (UDS) were measured in lung tissue in vitro using a short-term organ culture method. Within one week of beginning smoke exposure, DNA replicative activity, as indicated by incorporation of [3H]-thymidine into total lung DNA, was increased more than two-fold over sham-exposed controls and remained elevated as long as smoke exposure was continued. Treatment of lung tissues in vitro with either the lung carcinogen 4-nitroquinoline-1-oxide or methylmethane sulfonate stimulated UDS, measured as incorporation of [3H]thymidine into lung DNA in the presence of hydroxyurea, presumably as the result of DNA repair activity. Until the 10th to 12th week of smoke exposure, at which time the accumulated deposition of total particulate material in the lung was approximately 40 mg, the level of UDS stimulated by the alkylating chemicals declined to approximately 50% of that seen in lung tissue from sham-exposed control mice. If the mice were removed from smoke exposure, DNA replicative activity returned to normal levels within one week, but the UDS response to DNA damage remained depressed up to five months after ending smoke exposure. The results show that both transient and apparently permanent changes are produced in mouse lung as the result of exposure to cigarette smoke. The role of these changes in lung neoplasia is under investigation.

4-Nitroquinoline-1-oxide↗
PubMed1981

Lung cancer model system using 3-methylcholanthrene in inbred strains of mice.

A model system has been established for studying lung carcinogenesis using intratracheal instillation of 3-methylcholanthrene in C3H/AnfCum and C57BL/Cum X C3H/AnfCum F1 (hereafter called BC3F1/Cum) mice. The animals in these studies were screened for adventitious agents and were free throughout their lifetime of two important lung viruses, Sendai virus and pneumonia virus of mice. Under these conditions, the occurrence of spontaneous and chemically indiced lung cancers was determined over the lifetime of the animals. Data were analyzed by the actuarial method for lung tumor probability. Probability was found to be dose and time dependent. Over 95% of the 3-methylcholanthrene-treated BC3F1/Cum and over 88% of the C3H/AnfCum mice were found at death to have pulmonary carcinomas. Tumors observed in animals which died up to 40 weeks on test were almost always squamous cell carcinomas (approximately 85%), while tumors which were observed in animals which died after 50 weeks were mainly alveolar adenocarcinomas (approximately 80%). Both tumors types metastasized widely. Spontaneous lung cancers (only alveolar adenocarcinomas were observed) occurred in these two strains at low frequency and were expressed late in life. Thus, the system described affords a suitable model to study the induction, expression, and progression of lung tumors under conditions where a vast majority of animals develop neoplasia.

Animals↗
PubMed1980

Correlation of inducibility of aryl hydrocarbon hydroxylase with susceptibility to 3-methylcholanthrene-induced lung cancers.

C57BL/6Cum, DBA/2Cum, first filia (F1), and backcross progeny from these 2 parental strains of mice were evaluated for their susceptibility to 3-methylcholanthrene-induced lung cancers. In the crosses among these mice, aryl hydrocarbon hydroxylase (AHH) responsiveness segregated as a single autosomal dominant gene (the Ah locus). AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment. Intratracheal administration of 500 microgram MCA for a total of 4 times at weekly intervals yielded a variety of pulmonary cancers, including squamous cell carcinomas, alveolar adenocarcinomas, and adeno-squamous cell carcinomas among mice that survived 1 year after the carcinogen treatment. The AHH responsive C57BL/6Cum, F1, and C57BL/6Cum X F1 animals were much more susceptible to MCA-induced lung cancers than the AHH non-responsive DBA/2Cum mice. The lung cancers were also not randomly distributed in DBA/2Cum X F1 backcross progeny since significantly more lung cancers were found in AHH-responsive progeny than in AHH non-responsive mice. Data support genetic linkage between susceptibility to MCA-induced lung carcinomas and the Ahb allele.

Animals↗
PubMed1979

Biological activity of tobacco smoke and tobacco smoke-related chemicals.

Exposure to whole cigarette smoke from reference cigarettes results in the prompt (peak activity is 6 hrs), but fairly weak (similar to 2 fold), induction of murine pulmonary microsomal monooxygenase activity. This activity can be detected by using as substrates either benzo(a)pyrene or ethoxyresorufin, and can be inhibited by treatment with cycloheximide or actinomycin D. Unlike the induction of pulmonary monooxygenases following intratracheal administration of 3-methylcholanthrene, these cigarette smoke-induced increases were not unequivocally linked to the Ah locus. Whole smoke condensate and fractions derived from these condensates can; a) induce pulmonary monooxygenase activity, b) inhibit benzo(a)pyrene metabolism in vitro, c) be metabolized to forms mutagenic to Salmonella typhimurium tester strains TA153, or TA98, d) transform C3H 10T1/2 cells in vitro, and e) enhance the carcinogenicity of benzo(a)pyrene in murine pulmonary tissue. A potentially important observation is that whereas hepatic tissue is capable of activating whole cigarette smoke condensate to mutagenic forms in vitro, murine pulmonary tissue does not seem capable of such activation. Although these pulmonary-derived tissue homogenates have significant AHH activity and can metabolize Aflatoxin B1, 2-aminofluorene and 7, 8-dihydro-7,8-dihydroxybenzo(a)pyrene to mutagenic forms, these homogenates fail to activate both cigarette smoke condensate and the pro-mutagen, 6-aminochrysene. These results are discussed with reference to the concept that whole cigarette smoke may be both a potential "initiator" and "promotor" of lung cancer in mice, and that this latter property may be the most important in determining cancer risk.

Animals↗
PubMed1976

Analysis of lipophilic carcinogen-membrane interactions using a model human erythrocyte membrane system.

Human erythrocytes have been used as a model for evaluating the chemical carcinogen-plasma membrane interaction. The carcinogenic aromatic amines 2-acetylaminofluorene, dimethylaminoazobenzene, and 3'-methyldimethylaminoazobene stabilize erythrocytes against lysis in hypotonic solution. In general, the stabilization potential of these compounds reflects their oil:water partition coefficients and may be related to both their extracellular distribution and ultimate capacity for penetration of target cells. The polycyclic aromatic hydrocarbons, 3-methylcholanthrene and benz[a]anthracene, confer little protection against hemolysis and simultaneous incubation of nonprotective 3-methylcholanthrene and protective 3'-methyldimethylaminoazobenzene slightly alters the stabilization afforded by the latter. 7,12-dimethylbenz[a]anthracene exhibits greater protective capacity than does benz[a]anthracene. Polycyclic aromatic hydrocarbons manifested considerably higher degrees of absolute binding to erythrocytes in isotonic solution than did aromatic amines. The difference in erythrocyte binding and stabilization exhibited by the 2 classes of carcinogens suggest distinct mechanisms of membrane association that may relate to their metabolic disposition.

2-Acetylaminofluorene↗
PubMed1975

Induction of hepatitis in adult Syrian hamster by H-1 virus.

The induction of hepatitis in adult hamster by H-1 virus was documented by demonstrating an increase in serum SGOT and SGPT at 3-9 wk postinoculation. The electrophoresis pattern of LDH isoenzymes showed a marked increase in the liver fraction (fraction 5) indicating liver damage in infected hamsters. The pathology displayed in diseased livers revealed a focal degeneration of hepatic cells although infiltration of white cells was not observed. H-1 virus is apparently capable of producing hepatitis (without symptoms) in adult hamsters as well as cause hepatitis and severe cerebral disease in newborn hamsters.

Alanine Transaminase↗