Neonatal and post-natal growth

Growth velocity is higher in late intra-uterine and early post-natal life than at any time thereafter, and accurate measurements are essential for appropriate monitoring. The accuracy with which such measurements are made and recorded is frequently questionable, however, and short- and medium-term changes in growth may be difficult to interpret in the light of normal variations in the pattern of growth. Infants who are small at birth must be accurately classified because intra-uterine growth retardation and small for gestational age have different implications for both causation and outcome. Prediction of expected growth on the basis of mid-parental height is essential but frequently omitted. Post-natal growth impairment is common in pre-term infants and is often rapid in onset. Poor growth may continue for many months, and catch-up may be incomplete. Early growth failure may have a significant influence on subsequent morbidity and mortality.     

Peptide growth factor interactions in embryonic and fetal growth.

Peptide growth factors are expressed by multiple tissues in the animal and human embryo and fetus. They undergo specific interactions which control the rate of cellular proliferation, tissue differentiation and the induction of specific morphogenic events such as mesoderm formation in the embryo. Biologic control may not only be exerted at the level of growth factor synthesis and receptor expression but by the sequestration and storage of growth factors by extracellular matrix molecules. In the case of insulin-like growth factors (IGFs), storage maybe mediated by attachment to specific IGF-binding proteins which may additionally modulate biological potency. Basic fibroblast growth factor (basic FGF) and transforming growth factor-beta (TGF beta) directly bind to glycosaminoglycan molecules. Release of growth factors from these stores may be by local proteolytic action. A sequential expression of basic FGF, IGF-II and TGF beta occurs in the ovine fetal epiphyseal growth plate as chondrocytes progress from a proliferative to a postmitotic, hypertrophic state. Cellular phenotype may be largely explained by the relative amounts of these autocrine growth factors within the growth plate.     

Variation of hydrophobicity of human urinary epidermal growth factor

Epidermal growth factor is present in human urine in large amounts, but its biological significance is not known. The results of this study indicate that the predominant 6000-dalton form of epidermal growth factor in human urine is divided by hydrophobic interaction chromatography into four fractions; only 3% of the total 6000-dalton epidermal growth factor coeluted with the biosynthetic epidermal growth factor and the rest was separated into three different peaks. These different forms may lack one or two amino or carboxy terminal amino acids from the 53 amino acids present in epidermal growth factor, or they may be products of deamidation or oxidation of amino acid(s). Further knowledge of these micromodifications of epidermal growth factor secreted in urine may reveal the origin and function of epidermal growth factor in humans.     

Tumor necrosis factor mediates autocrine growth inhibition in a chronic leukemia

Autocrine production of growth factors may contribute to the rapid and fatal proliferation of acute hematologic malignancies. We have investigated whether the more controlled growth of less aggressive malignancies such as chronic myeloid leukemia (CML) may be associated with autocrine production of growth inhibitory factors. TNF inhibits the growth of both normal and leukemic hemopoietic progenitor cells. We find that exogenous TNF reduces the viability and DNA synthesis of purified myeloid cells from patients with CML and inhibits myeloid colony formation by patient progenitor cells. However, unlike progenitor cells from normal donors, patient myeloid progenitor cells also constitutively express mRNA for TNF and secrete functional TNF protein in culture. This endogenous TNF impedes the growth of CML cells because anti-TNF mAb shown to neutralize bioactive human TNF increases CML cell DNA synthesis whereas non-neutralizing anti-TNF mAb has no effect. Production of TNF by CML cells is not associated with production of lymphotoxin (TNF-beta), IL-1 or IL-6. TNF-mediated autocrine growth inhibition may contribute to the maintenance of the stable, chronic phase of this disease and similar mechanisms may operate in other malignancies to limit tumor proliferation. Competition between autocrine growth promoting and inhibiting factors may underlie the observed differences in biologic behavior between acute and chronic malignancies.     

Production of an auto-stimulatory growth factor by human hepatoma cells abrogates requirement for a brain-derived factor

Summary Human hepatoma cells grow at high cell density in the absence of exogenous growth factors. At low cell density, two different hepatoma cell lines required a novel growth factor from brain tissue. A factor with similar physico-chemical properties in the concentrated medium from high density cultures completely substituted for the brain extract. The autogenous secretion of a novel liver cell growth factor that is concentrated in brain tissue may underlie in part the unregulated growth of hepatomas. EDITOR'S STATEMENT Collective properties of growth factor activities for hepatoma cells in bovine brain extract and the medium of hepatoma cells suggest a neural tissue-derived liver cell growth factor that may be autogenously produced by liver tumor cells. Purification and characterization of such a factor may lead to selective inhibition of hepatoma, cell proliferation. David W. Barnes     

Puberty in chronically diseased patients

Delayed onset of puberty and a reduced pubertal growth spurt are often reported in patients suffering from chronic diseases. The basis of abnormal puberty in these patients is multifactorial. Nutritional deficiency may contribute to growth disorders and delayed puberty. Insufficient food supply and/or eating disorders and/or malabsorption of nutrients can be observed in these patients. Moreover, increased energy supplies are often needed in patients with chronic lung disease, infection or inflammation. More specific factors due to the disease itself may be involved in growth and puberty disorders. Abnormalities of the growth hormone (GH)-insulin-like growth factor (IGF)1 axis and gonadotrophin secretion have been described in patients with chronic renal failure, cystic fibrosis and Crohn's disease. More recently, it has been shown that cytokines produced during chronic diseases such as juvenile idiopathic arthritis may affect the GH-IGF1 axis. Finally, concomitant medication, namely corticosteroids, which are often given to these patients, may contribute to delayed puberty and poor pubertal growth.     

A meta-analysis of the relation between mating system,growth form and genotypic diversity in clonal plant species

Next to its well-described ecological advantages, clonal growth in plants may incur fitness costs, which are associated with the effects of typically large clonal individuals on the patterns of pollen dispersal. These fitness costs include increased selfing and inbreeding depression in self-compatible species, and reduced mate availability in self-incompatible species. Although fitness costs may affect mating system evolution, there is currently no strong evidence available that either self-compatibility or self-incompatibility is associated with clonality. One reason for this may be the variety in growth forms (from guerrilla to phalanx habits) within clonal species, and the fact that growth form may strongly affect mating patterns. We present the results of a formal meta-analysis of 72 published studies, aiming at reporting genotypic diversities across studies and at relating mating system with clonal growth form and genotypic diversity. We found lower genotypic diversities in clonal self-incompatible species compared to self-compatible species, suggesting that mate availability may indeed be reduced in clonal self- incompatible species. We also cannot confirm that mating system is associated with clonal growth form.     

Growth estimates from otolith increment widths of juvenile chinook salmon (Oncorhynchus tshawytscha) reared in changing environments

For otolith increments to provide useful estimates of fish growth, otolith growth must covary closely with somatic growth. We reared groups of juvenile chinook salmon ( Oncorhynchus tshawytscha Walbaum) for 70 days, changing ration or temperature during a 20-day treatment period. Restricted rations halted somatic growth, however increment widths decreased gradually; somatic growth was overestimated from increment width. Otolith growth followed changes in water temperature more closely than changes in ration, supporting a hypothesized effect of metabolic rate on otolith growth. Increment growth was only loosely coupled to fish growth rate, and may also be affected by past growth histories. For juvenile fish, increment widths may not be sensitive indicators of short-term changes in growing conditions.     

Life History theory hypotheses on child growth: Potential implications for short and long‐term child growth,development and health

Life history theory integrates ecological, physiological, and molecular layers within an evolutionary framework to understand organisms’ strategies to optimize survival and reproduction. Two life history hypotheses and their implications for child growth, development, and health (illustrated in the South African context) are reviewed here. One hypothesis suggests that there is an energy trade‐off between linear growth and brain growth. Undernutrition in infancy and childhood may trigger adaptive physiological mechanisms prioritizing the brain at the expense of body growth. Another hypothesis is that the period from conception to infancy is a critical window of developmental plasticity of linear growth, the duration of which may vary between and within populations. The transition from infancy to childhood may mark the end of a critical window of opportunity for improving child growth. Both hypotheses emphasize the developmental plasticity of linear growth and the potential determinants of growth variability (including the role of parent–offspring conflict in maternal resources allocation). Implications of these hypotheses in populations with high burdens of undernutrition and infections are discussed. In South Africa, HIV/AIDS during pregnancy (associated with adverse birth outcomes, short duration of breastfeeding, and social consequences) may lead to a shortened window of developmental plasticity of growth. Furthermore, undernutrition and infectious diseases in children living in South Africa, a country undergoing a rapid nutrition transition, may have adverse consequences on individuals’ cognitive abilities and risks of cardio‐metabolic diseases. Studies are needed to identify physiological mechanisms underlying energy allocation between biological functions and their potential impacts on health.     

Mathematical models of bacterial growth,inhibition and death under combined stress conditions

Summary In this report we review the history of growth theories. We show how classical growth models may be derived as special cases of a generic growth rate equation. We show how growth models may be modified to represent survival data. We use linear combinations of growth and survival models to represent complex growth/survival curves and give practical examples utilizing nonlinear regression analysis. We show that traditional methods of estimating D values are inappropriate for complex, multiphasic growth/survival data. We show how such data may be modeled mathematically and illustrate methods for estimating true D values from such data.     

Nutrient growth conditions for Oscillatoria spp. and diatoms in two Norwegian lakes

The growth conditions and development of Asterionella formosa Hass., Tabellaria fenestrata (Lyngb.) Kütz., Fragilaria crotonensis Kitt., and Oscillatoria spp. have been studied in Lake Vansjø and Lake Mjøsa for many years. Some batch culture experiments have been performed with dilute phytoplankton populations in filtered water samples to support the field data. The results indicate that the concentrations of phosphate, nitrate, silicate or chelators/Fe were important factors regulating the spatial and temporal distribution of the populations. Based on the assumption that the growth rates were strongly dependent on the external nutrient concentration, S, the growth conditions were divided into three types. The nutrient concentration may be too low to support growth, i.e. the growth rate k ≤ 0, or the population is nutrient growth limited (0 < k < km) or not growth limited, i.e. the population has maximum growth rate (km). The nutrient concentration may be population density dependent, i.e. resource competition may occur, or density independent separately or in combination. The growth strategies of the populations in the two lakes were partly explained by studying the nutrient growth conditions of the populations.     

Protéines nucléaires basiques et croissance chez l'hypocotyle de Lupinus albus L.

Summary Characteristic changes in the basic nuclear proteins/DNA ratio may be observed during the residual growth of lupine seedling hypocotyls.This ratio decreases at the very beginning of hypocotyl growth (growth initiation) but increases during its active growth. A second decline coincides with gemmule development. No further increase in the relative amount of basic proteins can be observed during the diminishing elongation before growth ceases.These results may be related to the known regulating action of the gemmule on hypocotyl growth.     

THE RATE OF OVULATION IN THE DOMESTIC FOWL DURING THE PULLET YEAR

The rate of ovulation of the domestic fowl may be expressed by the equation of an autocatalytic chemical reaction. This is not surprising in view of the fact that the rate of growth may also be expressed by such an equation, and that the rate of ovulation is probably an index of the growth of the eggs. This brings the phenomenon of ovulation in the hen under the general subject of growth, and substantiates the generality and the probability of the hypothesis that growth, or at any rate the limiting factor of growth, is an autocatalytic reaction.     

Growth strategies and optimal body size in temperate pararginii butterflies

In temperate insects the evolution of growth strategies andthe optimal age and size at maturity will depend strongly onseasonal variation in temperature and other resources. However,compared to photoperiod, temperature itself is a relativelypoor predictor of seasonal change and timing decisions in insectsare often most strongly influenced by the photoperiod. HereI review the evolution of seasonal growth strategies in thebutterfly tribe Pararginii (Satyrinae: Nymphalidae) and relateit to life history theory. The results indicate that individuallarvae may adjust their growth trajectories in relation to informationon time horizons obtained from the photoperiod. The growth strategiescan be characterized by a set of state-dependent decision rulesthat specify how an individual should respond to its internalstate and external circumstances. These decision rules may alsoinfluence how individual growth change with a rise in temperature,showing that the standard expectation of increased growth rateswith increasing temperatures may not always be true. With lesstime available individual larvae increase growth rates and therebyachieve shorter development times, most often without any effectson final sizes. One reason for the apparent optimization ofgrowth rate seems to be that growing fast may incur costs thatlarvae developing under lower time limitations chose to avoid.The patterns of growth found in these and many other studiesare difficult to reconcile with common assumptions of what typicallydetermines optimal body size in insects. In particular it seemsas if there should be some costs of a large body size that,so far, have been poorly documented.     

Compensatory growth strategies are affected by the strength of environmental time constraints in anuran larvae

Organisms normally grow at a sub-maximal rate. After experiencing a period of arrested growth, individuals often show compensatory growth responses by modifying their life-history, behaviour and physiology. However, the strength of compensatory responses may vary across broad geographic scales as populations differ in their exposition to varying time constraints. We examined differences in compensatory growth strategies in common frog (Rana temporaria) populations from southern and northern Sweden. Tadpoles from four populations were reared in the laboratory and exposed to low temperature to evaluate the patterns and mechanisms of compensatory growth responses. We determined tadpoles’ growth rate, food intake and growth efficiency during the compensation period. In the absence of arrested growth conditions, tadpoles from all the populations showed similar (size-corrected) growth rates, food intake and growth efficiency. After being exposed to low temperature for 1 week, only larvae from the northern populations increased growth rates by increasing both food intake and growth efficiency. These geographic differences in compensatory growth mechanisms suggest that the strategies for recovering after a period of growth deprivation may depend on the strength of time constraints faced by the populations. Due to the costs of fast growth, only populations exposed to the strong time constraints are prone to develop fast recovering strategies in order to metamorphose before conditions deteriorate. Understanding how organisms balance the cost and benefits of growth strategies may help in forecasting the impact of fluctuating environmental conditions on life-history strategies of populations likely to be exposed to increasing environmental variation in the future.     

Growth regulation by oncogenes--new insights from model organisms

A great deal of work has focused on how oncogenes regulate the cell cycle during normal development and in cancer, yet their roles in regulating cell growth have been largely unexplored. Recent work in several model organisms has demonstrated that homologs of several oncogenes regulate cell growth and has suggested that some of the effects of oncogenes on the cell cycle may be a result of growth promotion. These studies have also suggested how growth and cell-cycle progression may be coupled.     

Juvenile Chinook salmon (<Emphasis Type="Italic">Oncorhynchus tshawytscha</Emphasis>) growth in off-channel and main-channel habitats on the Sacramento River,CA using otolith increment widths

Few studies have quantified juvenile salmon growth among different habitats or evaluated the mechanisms controlling salmon growth and survival. We used otolith microstructure to compare daily relative growth rates among main-channel riverine areas, off-channel ponds, and non-natal seasonal tributaries of the Sacramento River, CA. We compared prey availability, prey preference, and stomach fullness between these sites. We observed larger average otolith growth increments, higher prey densities, and warmer water temperatures in both off-channel ponds and non-natal seasonal tributaries compared to the main-channel areas in both 2001 and 2002. Our findings suggest that warmer temperatures and abundant prey in off-channel habitats during Central Valley Chinook salmon rearing periods may lead to higher growth rates, which in turn may improve juvenile survival. Our results suggest that off-channel habitats may be critical habitats to include in conservation and management plans for juvenile salmon.     

Signalling pathways and the host-parasite relationship: putative targets for control interventions against schistosomiasis: signalling pathways and future anti-schistosome therapies

A better understanding of how schistosomes exploit host nutrients, neuro-endocrine hormones and signalling pathways for growth, development and maturation may provide new insights for improved interventions in the control of schistosomiasis. This paper describes recent advances in the identification and characterisation of schistosome tyrosine kinase and signalling pathways. It discusses the potential intervention value of insulin signalling, which may play an important role in glucose uptake and carbohydrate metabolism in schistosomes, providing the nutrients essential for parasite growth, development and, notably, female fecundity. Significant progress has also been made in the characterisation of other schistosome growth factor receptors, such as transforming growth factor beta receptor and epidermal growth factor receptor, and in our understanding of their roles in the host-parasite molecular dialogue and parasite development. The use of parasite signal transduction components as novel vaccine or drug targets may prove invaluable in prevention, treatment and control strategies to combat schistosomiasis.     

Longitudinal analysis of length growth in the chimpanzee (Pan troglodytes)

The adolescent growth spurt in linear dimension in humans is considered to be unique among mammals, but few comparative studies have been done, even on chimpanzees. Growth of the summed length of crown to rump, thigh, and leg was studied longitudinally in 12 chimpanzees. We took body weight growth and reproductive maturation into consideration. Reproductive maturation was monitored by the swelling of sexual skin and menarche in females, and by testicular development in males. We applied two relationships found in humans between body length growth and the environment to the chimpanzees. The first relationship was the robustness of the growth spurt, meaning that the spurt is absent only in individuals under the most severe environmental pressure. Subjects maturing in a favorable or even mediocre environment are anticipated to show the growth spurt. The second relationship was catch-up growth, where, when the environment is ameliorated, growth may be accelerated to attain the target size. Catch-up growth at the end of the juvenile period may mimic the adolescent growth spurt. Results showed that subjects living under favorable conditions did not exhibit a growth spurt, and that it was only the subjects who had delayed growth in the juvenile period that showed a spurt in adolescence, the period when reproductive maturation occurred. Although we have concluded that chimpanzees do not have an adolescent growth spurt, except in cases of catch-up growth, this does not mean that they have a different growth pattern from that of humans. The absence of a growth spurt may be associated with adaptations to chimpanzee patrilineal society, where adolescent males are incorporated into the adult hierarchy at a low rank.