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At least 19 recordsLinked to original sources
PubMed1976

Stability of population growth determined by 2 X 2 Leslie matrix with density-dependent elements.

The matrix considered contains four elements, each a function of total number. A special case for which the matrix may be appropriate is when the population may be divided into juveniles and adults, and the survival rates and fecundity are the same for all members of each group. This is true, at least approximatley, for many species of birds. The conditions for stability are determined and are illustrated with a model based on the data collected on the Marley Wood, Oxford, population of the Great tit (Parus major L.). A reformulation of the conditons permits comparison with the conditions for a population with identical survival rates and fecundity for all age groups, i.e., a population without effective age structure. Conditions under which the age structure may be ignored when discussing stability are considered.

Age Factors↗
PubMed1991

Patterns in the effects of infectious diseases on population growth.

An infectious disease may reduce or even stop the exponential growth of a population. We consider two very simple models for microparasitic and macroparasitic diseases, respectively, and study how the effect depends on a contact parameter kappa. The results are presented as bifurcation diagrams involving several threshold values of kappa. The precise form of the bifurcation diagram depends critically on a second parameter xi, measuring the influence of the disease on the fertility of the hosts. A striking outcome of the analysis is that for certain ranges of parameter values bistable behaviour occurs: either the population grows exponentially or it oscillates periodically with large amplitude.

Birth Rate↗
PubMed1988

Effects of antimycotic azoles on growth and sterol biosynthesis of Leishmania promastigotes.

Promastigotes of 36 World Health Organization reference (and other) strains of 6 species and 10 subspecies of Leishmania were cultured in the presence of 3 antimycotic azole drugs (ketoconazole, itraconazole, fluconazole) and their population growth determined. A representative of each subspecies was also analyzed for its sterol composition. For all strains the order of azole drug activity with respect to both growth and sterol biosynthesis inhibition was itraconazole greater than or equal to ketoconazole greater than fluconazole. The inhibitory actions of the three azole drugs were greater on L. donovani and L. braziliensis subspecies and on L. mexicana amazonensis than on L. aethiopica, L. major, L. tropica and L. mexicana mexicana. The nature of the changes in sterol composition caused by the drugs was the same for all strains. The normal, major endogenous sterols of the promastigotes (5-dehydroepisterol and ergosterol) were reduced in amount to 1-2% of the total free sterols and were replaced by endogenous 14 alpha-methyl sterols and exogenous cholesterol. The changes occurred rapidly, were drug concentration dependent and coincided with growth inhibition. Six strains of those Leishmania species less sensitive to the azole drugs could be subcultured indefinitely at reduced growth rates in the presence of a ketoconazole concentration causing the same extraordinary alterations in sterol composition. This suggested that the bulk membrane functions of sterols in leishmanias can be served by 14 alpha-methyl sterols and cholesterol, albeit imperfectly, while traces of 14 alpha-desmethyl sterols are needed for uncharacterized metabolic functions.

Animals↗
PubMed1993

Demic expansions and human evolution.

Geographic expansions are caused by successful innovations, biological or cultural, that favor local growth and movement. They have had a powerful effect in determining the present patterns of human genetic geography. Modern human populations expanded rapidly across the Earth in the last 100,000 years. At the end of the Paleolithic (10,000 years ago) only a few islands and other areas were unoccupied. The number of inhabitants was then about one thousand times smaller than it is now. Population densities were low throughout the Paleolithic, and random genetic drift was therefore especially effective. Major genetic differences between living human groups must have evolved at that time. Population growths that began afterward, especially with the spread of agriculture, progressively reduced the drift in population and the resulting genetic differentiation. Genetic traces of the expansions that these growths determined are still recognizable.

Animals↗
PubMed1995

Susceptible-infected-removed epidemic models with dynamic partnerships.

The author extends the classical, stochastic, Susceptible-Infected-Removed (SIR) epidemic model to allow for disease transmission through a dynamic network of partnerships. A new method of analysis allows for a fairly complete understanding of the dynamics of the system for small and large time. The key insight is to analyze the model by tracking the configurations of all possible dyads, rather than individuals. For large populations, the initial dynamics are approximated by a branching process whose threshold for growth determines the epidemic threshold, R0, and whose growth rate, lambda, determines the rate at which the number of cases increases. The fraction of the population that is ever infected, omega, is shown to bear the same relationship to R0 as in models without partnerships. Explicit formulas for these three fundamental quantities are obtained for the simplest version of the model, in which the population is treated as homogeneous, and all transitions are Markov. The formulas allow a modeler to determine the error introduced by the usual assumption of instantaneous contacts for any particular set of biological and sociological parameters. The model and the formulas are then generalized to allow for non-Markov partnership dynamics, non-uniform contact rates within partnerships, and variable infectivity. The model and the method of analysis could also be further generalized to allow for demographic effects, recurrent susceptibility and heterogeneous populations, using the same strategies that have been developed for models without partnerships.

Communicable Diseases↗
PubMedDate not supplied

A path analysis of some determinants of infant growth in Khartoum.

The interrelationships between some socioeconomic and behavioural characteristics of mothers and the growth and illness experience of their infants in poor Khartoum townships have been examined by path analysis. For both infant body weight and supine length it is shown that weaning age and illness experience are important determinants of growth. It is also shown that greater maternal income has disadvantageous effects through encouraging early weaning. Most importantly the infants of housewives have later weaning, less illness and greater weight and length at 1 year of age than the infants of mothers with jobs, showing the value of time for caring in the prevailing environmental circumstances.

Adolescent↗
PubMed1992

The mediating effect of maternal nutrition knowledge on the association between maternal schooling and child nutritional status in Lesotho.

The present study tested whether maternal nutrition knowledge was a mediating factor in the association between maternal schooling and child nutritional status, and whether the mechanism involved differed according to socioeconomic status. The data were collected in Lesotho on 921 mother-child pairs and included scores from a nutrition knowledge test, socioeconomic and demographic information, and the child's anthropometric data. A wealth factor derived from a factor analysis was used to stratify the sample into two socioeconomic groups. Two-stage least-squares estimation was used to test the mediating role of nutrition knowledge between maternal schooling and child weight-for-age. Results showed that both the importance of maternal schooling and the mechanism by which it affects the child's weight-for-age are contingent upon the family's socioeconomic status. While maternal schooling was positively associated with weight-for-age for both wealthier and poorer households, the size of the effect was much larger for the latter group. The effect of maternal schooling on weight-for-age was mediated by the mother's nutrition knowledge only among wealthier households. These results imply that, in Lesotho, nutrition education for mothers could contribute to improving children's growth, but only in households that have access to a minimum level of resources. For poorer households, nutrition education would not be sufficient.

Adult↗
PubMed1994

Is complete catch-up possible for stunted malnourished children?

Although malnourished children are stunted, their bone maturity is usually retarded to a comparable degree. This is seen in impoverished societies as well as in diseases such as coeliac disease, inflammatory bowel disease and hormonal deficiency. When these children are followed to adulthood they normally have some degree of spontaneous catch-up. With a change in environment, through adoption, emigration or with treatment of the disease there is usually definite catch-up growth, although it is often not to the NCHS standards. If puberty is delayed and/or growth continues into the early or mid twenties, then an acceptable final adult height is achieved. However, there may be a limitation imposed on an individual's maximum height by genetic imprinting in very early development. This may be the case where full catch-up appears to have taken place but is followed by an advanced puberty and early cessation of growth (Proos, Hofvander & Tuvemo, 1991a). The data from US slaves and cases of hormonal replacement, where treatment was initiated after age 18, each show that, if the circumstances of children in the Third World change, almost complete reversal of stunting is possible. The children can reach their own height potentials. Total reversal to affluent societal norms would probably require cross-generational catch-up. The most obvious reason why catch-up is not seen regularly is that an appropriate diet is not available over a sufficient period of time. We do not know the optimum ingredients for such a diet. Sulphur has been neglected as an essential nutrient; its economy should be examined in relation to skeletal growth in stunted populations.

Adolescent↗
PubMed1993

Growth dynamics during the first two years of life: a prospective study in the Philippines.

This study examines determinants of growth from birth to 24 months in a sample of approximately 3000 urban and rural Filipino children. Individual, household, and community data were collected bimonthly during the Cebu Longitudinal Health and Nutrition Survey. Separate longitudinal, multivariate models were used to identify determinants of weight in children from birth to 6 months and 6-24 months of age. Previous weight, male gender, mother's height, and season of the year showed significant positive associations with weight in all models. Full and mixed breast-feeding significantly increased weight, but the effects of breast-feeding declined as children got older. Breast-feeding had a direct growth-enhancing effect in addition to its indirect effect through the prevention of diarrheal morbidity. Detrimental effects of recent diarrheal morbidity were particularly important in the older age group, but these effects were mitigated by breast-feeding. Since infant feeding variables are included in the models, the results strongly suggest an effect of diarrheal morbidity on growth independent of its known effects on infant feeding and dietary intake. Febrile respiratory infections had important detrimental effects on weight in both age groups.

Body Height↗
PubMed1983

Maternal nutritional status and adolescent pregnancy outcome.

To investigate the determinants of low birth weight of infants born to adolescent mothers, we studied the obstetric population attended at the Maternity Hospital of Lima, Peru. From this population we selected for study a sample of 1256 adolescent mothers ranging in age from 12 to 25 yr. The study included anthropometric and biochemical measurements used to evaluate nutritional status and physiological maturity of the mother and newborn. Findings from the present research indicate that the low birth weight of infants born to adolescent mothers is not due to premature delivery (short gestation) or low gynecological maturity. Furthermore, young adolescent mothers had smaller and thinner newborns than those born to older women who were adjusted for nutritional status during pregnancy and at delivery. That is, despite the similar nutritional status among the young adolescent mothers, the availability of nutrients for the accumulation of calories in the fetus (measured by skinfold thickness) was less than that of older women. Furthermore, the pregnancy weight gain associated with an optimal or average newborn weight is greater for young teenagers than for older women. These findings support the hypothesis that among rapidly growing teenagers the nutritional requirements of pregnancy may be greater than those of older women, and that this increased requirement competes with the growth needs of the fetus.

Adolescent↗
PubMed1994

Nutritional influences on linear growth: a general review.

The first section of this paper reviews what is known about the roles of specific nutrients in the general linear growth faltering that occurs in developing countries. Those reviewed are energy, protein, zinc, iron, copper, iodine and vitamin A. For none of these nutrients was there clear, consistent evidence that supplementation with the nutrient benefited linear growth. Rather, interventions with each specific nutrient had a positive effect on length gain in some studies, while in others these affected only weight gain or had no effect. Reasons for these conflicting results are suggested, including the strong probability that growth is limited by multiple, simultaneous deficiencies in many populations. This point is illustrated with data from the Nutrition Collaborative Research Support Program (CRSP) and other reports. Most interventions with single nutrients have been tested on children older than the age when linear growth faltering is most rapid, that is, within a few months of birth. Possible reasons why growth stunting begins so early in life are presented, but these are mostly hypothetical because of the paucity of information on this topic.

Body Height↗
PubMed1994

Onset and evolution of stunting in infants and children. Examples from the Human Nutrition Collaborative Research Support Program. Kenya and Egypt studies.

The etiology of the early onset of stunting is diverse among populations of varying biological, environmental and cultural circumstances. This is exemplified within the Nutrition CRSP project, which took place in three different populations and ecological conditions. Within each study area a different mix and varying proportions of causative factors were identified. At least in Kenya, and probably in Mexico, the problem has its antecedents in prepregnancy and pregnancy. Powerful determinants of the infants' size at birth and during the first 6 months of life are maternal size upon entry into pregnancy, and weight and fat gain during pregnancy and lactation. In all three countries a low pregnancy weight gain was observed. Notably in Kenya, where the energy intake of the mother decreases progressively throughout pregnancy, not only do mothers gain only half as much as European or North American women, but they even lose weight and fat in the last month of pregnancy, and some mothers gain no weight or lose weight during the whole of pregnancy. Mothers in Kenya start lactation with relatively poor fat stores. Although their energy intake increases somewhat during lactation, preliminary estimates suggest that these increases may be insufficient to maintain their bodily integrity, to carry out their normal tasks of daily living, and to produce a sufficient amount of milk for optimal infant growth. In addition to an energy deficit, diet quality is a problem, particularly in Kenya and Mexico and less so in Egypt. Intakes of animal products and animal protein are very low. Zinc and iron intakes are not only low, but the bioavailability of these nutrients is poor because of the high phytate, fiber and tea content of the diet. Also vitamin B12 intake is extremely low, and at least mild-to-moderate iodine deficiency (IDD) is present in Kenya. The above micronutrients have been demonstrated to affect the linear growth of the Kenyan children, even after confounding factors have been controlled. The early use of supplemental feeding in Kenya is a double-edged sword. On the one hand, there is a slight increase in febrile illness and possible displacement of breast milk intake in the supplemented infants, although mothers do not decrease breast feeding frequency and duration. On the other hand, even the modest amounts of available zinc and B12 in supplemental foods appear to have a positive effect on linear growth.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1994

Weaning in southern Brazil: is there a "weanling's dilemma"?

In Pelotas, Brazil, 400 newborns from low income families were followed-up until 26 wk of life to study the relationship between their feeding patterns and growth as modified by access to water and by diarrhea. Effects of access to water were the strongest among non-breastfed infants. In houses without indoor water taps, the weight gain of non-breastfed infants during the first 3 mo was approximately half that of partially or predominantly breastfed infants (P < 0.001). In houses with indoor water taps, non-breastfed infants' growth was similar to or exceeded that of predominantly breastfed infants from 2 mo. Predominantly breastfed infants' growth was similar in houses with and without water taps. Breastfed infants had less weight loss per day of diarrhea than non-breastfed infants during the first 4 mo and less diarrhea through 6 mo of life, particularly in houses without taps, in which diarrhea was most prevalent. The existence of a "weanling's dilemma" was approached by comparing the duration of the detrimental effects of not breastfeeding (i.e., 0-3 mo in this study) with the age at which breast milk alone becomes less than optimal for growth (i.e., at 5 mo). Because these two points did not coincide, we conclude that there is no "weaning's dilemma" in this population.

Brazil↗
PubMed1985

Kinetics of DNA replication in C3H 10T1/2 cells synchronized by aphidicolin.

Aphidicolin is an inhibitor of DNA polymerase alpha and blocks nuclear DNA replication without interfering with mitochondrial DNA synthesis. The efficacy of this mycotoxin as a tool in cell synchronization was evaluated in C3H 10T1/2 clone 8 cells. At concentrations of 1-2 micrograms/mL, aphidicolin quickly reduced the [3H]thymidine uptake to less than 5% of control levels in the first 5 min of incubation. This inhibition was easily reversed by washing and refeeding cells with fresh medium. The synchronization protocol consisted of first blocking cells by confluence arrest, replating them at lower density, and then treating the cells with aphidicolin for 24 h. Once the inhibitor was removed, DNA replication started without any delay. The cell population traversed the S phase in about 8 h and synchronously doubled in cell number. Autoradiography studies revealed a labeling index of 89-93% during the S phase. However, it was also observed that 10T1/2 cells were able to enter S phase in the presence of aphidicolin. The extent of the ensuing replication in the nucleus was dependent on the time that cells remained arrested in early S phase. Analyses of the newly replicated DNA in alkaline sucrose gradients revealed a fairly homogeneous distribution of sizes of nascent DNA in synchronized cells pulse-labeled at the beginning of the S phase. Upon chase in nonradioactive medium, the average molecular weight of the nascent DNA increased linearly with time of DNA synthesis for 2 h. The apparent rate of DNA chain growth determined from pulse and chase experiments was 1.2 micron/min. This rate was strongly inhibited (93%) by aphidicolin at a concentration of 2 micrograms/mL.

Animals↗
PubMed1991

Interactions of dimethyl sulfoxide and granulocyte-macrophage colony-stimulating factor on the cell cycle kinetics and phosphoproteins of G1-enriched HL-60 cells: evidence of early effects on lamin B phosphorylation.

We have found that GM-CSF and DMSO have antagonistic effects on the proliferation but not maturation of asynchronously growing HL-60 cells such that growth in the presence of both more closely resembles normal hematopoiesis (Brennan et al., J. Cell Physiol. 132:246, 1987). Studies were undertaken to determine whether or not the agents affected the same mitogenic pathway and locus in the cell cycle. HL-60 populations containing at least 90% G1 cells were obtained by centrifugal elutriation, exposed to 100 u/ml recombinant human GM-CSF and/or 0-1.25% DMSO, and phosphoprotein changes quantified on autoradiograms of [32P]-orthophosphate-labeled cell proteins separated by giant 2-D gel electrophoresis. Results were correlated with 1) intracellular pH, determined by measurement of BCECF fluorescence; 2) [32P]-orthophosphate uptake; 3) cell cycle progression, determined by flow quantitation of DNA content in mithramycin or propidium iodide-stained cells; and 4) growth, determined by cell volume and concentration. GM-CSF stimulated and DMSO inhibited the GM-CSF-stimulated phosphorylation of 1 protein (approximately 65 kDa, p.i. 5.6) within 2 min of exposure. These effects were sustained through G1, not associated with changes in intracellular pH, and preceded similar antagonistic effects on phosphate uptake (15-30 minutes), cell volume change (16-24 hr), and cell concentration increase (28-32 hr). GM-CSF accelerated and DMSO inhibited G1 to S transit with the most marked antagonism observed in the second cycle following synchronization (28 to 40 hrs). Cell maturation (morphology, NBT reduction) was dominated by DMSO and not antagonized by GM-CSF. We have identified p65 as the nuclear intermediate filament protein, lamin B, on the basis of its locus on gels and its binding of a monoclonal antibody to intermediate filaments and antiserum to human lamin B on immunoblots. These studies suggest that at least part of the GM-CSF-DMSO antagonism is exerted through the same mitogenic pathway, that a major locus of cytokinetic effect is on G1 to S transit, and that nuclear envelope protein phosphorylation is an important early event.

Cell Cycle↗
PubMed1995

Determinants of term intrauterine growth retardation: the Saudi experience.

In a clinical study from an unselected Saudi obstetric population, the incidence of and risk factors for intrauterine growth retardation among live births were investigated. From a total study group of 4578 consecutive live births, 76 (1.7%) infants were found to be growth retarded. These infants were then compared with a randomly selected control group of 76 term newborns with appropriate birthweight for their gestational ages. Delivery at term of a growth-retarded infant was significantly associated with maternal age under 20 years, maternal body mass index less than 23, first degree consanguinity, poor housing, primiparity, and inadequate prenatal care in univariate analysis. When considered jointly in multivariate logistic regression analysis, the significant determinants were reduced to primiparity, first degree consanguinity, and poor housing. These risk factors correctly predicted 63% and 71% of the intrauterine growth-retarded infants or normal birthweight infants, respectively.

Adult↗