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Growth is defined as an increase in tissue mass. Mass increases by hyperplasia early in life and hypertrophy later in life, although hyperplasia of adipose tissue continues throughout life. The growth curve, being mass or cumulative weight plotted against age, is sigmoid, consisting of a prepubertal accelerating phase plus a postpubertal decelerating phase. Mathematically, this curve can be described as a function of mature mass, fractional growth rate, and age. At a specific fraction of mature mass, body composition seems to be constant, but the degree to which nutrition can alter mature mass is not certain. If mature mass is altered, body composition at any given mass will be altered. Mature mass can be decreased by starvation or protein deficiency early in life. Alternatively, retarding the deposition of fat or the administration of estrogenic compounds may increase mature protein mass. Many of the advances in rate and efficiency of growth and in reduced fat of meat cuts can be explained by increased mature protein mass of ruminants. Animals with higher mature weight require more energy for maintenance and reach puberty later in life, so a larger mature mass is not desirable for the breeding herd. Indeed, smaller replacement heifers would prove economical if reproduction were not decreased. A period of restricted growth and fat deposition (as on pasture) can increase the slaughter weight of small cattle into a more desirable range, presumably through increasing mature protein mass. However, calves with retarded growth often make less efficient feedlot gains than do calves finished immediately after being weaned. For growing large-framed heifers, pasture alone often provides an inadequate energy supply for early puberty, but excessive amounts of supplemental feed can enhance fat deposition in the udder, which subsequently decreases milk production. By manipulating the supply of specific nutrients and hormones, it may prove feasible in the future to reduce fat deposition in specific tissues and to alter mature body protein mass.
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The growth, development and population characteristics of Chlorella cells flown for 13 days in space were investigated during their postflight cultivation. The growth rate of flown algae did not differ from that of ground-based controls in terms of increases in the cell number and biomass. All basic parameters of the specimens (generation time, number of developing autospores, time ratio of developmental phases) were ontogentically normal. Exposure of the algae to space flight as a component of the algobacterial cenosis--fish autotrophic-heterotrophic system produced no significant effect of the population or individual specimens during their postflight cultivation.
Differentiation of the metanephrogenic mesenchyme is triggered by an inductive tissue interaction between an inducer tissue and the mesenchyme. It is generally believed that the epithelial ureter bud acts as an inducer during in vivo development. In response to the inductive stimulus most of the mesenchymal cells convert into epithelial cells, while a small fraction differentiates into stromal cells. In vitro, differentiation of isolated mesenchyme to epithelium can be induced by a variety of embryonic tissues, but nothing is known about the molecular nature of the inducing stimulus. In recent years, large numbers of polypeptide growth factors have been described, which in addition to proliferative effects were shown to exert effects on a variety of biological phenomena such as chemotaxis, inflammation, tissue repair, or induction of embryonic development. We therefore analyzed whether growth factors in the absence of inducer tissue can induce isolated kidney mesenchyme to differentiate into epithelium or interstitium. As expected, both growth and differentiation into epithelium were stimulated by an inducer tissue, the spinal cord. We found that none of the various growth factors tested (including epidermal growth factor, transforming growth factors alpha and beta, insulin-like growth factors I and II, fibroblast growth factor, platelet-derived growth factor, and retinoic acid) could mimick the effect of an inducer tissue, although we tested the factors over a wide concentration range. One of the tested factors, epidermal growth factor (EGF) stimulated the mesenchymal cells to become stromal cells, although it could not stimulate development into epithelium. EGF could stimulate stromal development both when the mesenchyme was cultured in isolation and when the mesenchyme was stimulated by an inducer tissue to become epithelium. The expansion of the stromal compartment in response to EGF treatment occurred at the expense of the epithelial cells, but EGF could not completely suppress the formation of epithelium. These data suggest the presence of EGF receptors in the developing kidney, but since application of soluble EGF leads to abnormal development, soluble EGF cannot be the natural ligand. We suggest that locally produced mitogens with an EGF-like structure may regulate the relative amounts of stroma (interstitium) and epithelium in the developing kidney.
Glycosaminoglycans (GAGs) such as heparan sulfate and chondroitin sulfate are polysaccharide chains that are attached to core proteins to form proteoglycans. The biosynthesis of GAGs is a multistep process that includes the attachment of sulfate groups to specific positions of the polysaccharide chains by sulfotransferases. Heparan-sulfate and heparan sulfate-sulfotransferases play important roles in growth factor signaling and animal development. However, the biological importance of chondroitin sulfation during mammalian development and growth factor signaling is poorly understood. We show that a gene trap mutation in the BMP-induced chondroitin-4-sulfotransferase 1 (C4st1) gene (also called carbohydrate sulfotransferase 11 - Chst11), which encodes an enzyme specific for the transfer of sulfate groups to the 4-O-position in chondroitin, causes severe chondrodysplasia characterized by a disorganized cartilage growth plate as well as specific alterations in the orientation of chondrocyte columns. This phenotype is associated with a chondroitin sulfation imbalance, mislocalization of chondroitin sulfate in the growth plate and an imbalance of apoptotic signals. Analysis of several growth factor signaling pathways that are important in cartilage growth plate development showed that the C4st1(gt/gt) mutation led to strong upregulation of TGFbeta signaling with concomitant downregulation of BMP signaling, while Indian hedgehog (Ihh) signaling was unaffected. These results show that chondroitin 4-O-sulfation by C4st1 is required for proper chondroitin sulfate localization, modulation of distinct signaling pathways and cartilage growth plate morphogenesis. Our study demonstrates an important biological role of differential chondroitin sulfation in mammalian development.
UNLABELLED: This study was designed to determine the development and growth-promoting effects of relaxin with or without estrogen on the uterine cervix of prepubertal gilts. Twenty littermate gilts of similar body weight (33 +/- 3 kg; mean +/- SE) at 80 days of age were randomly assigned to four treatments: Vehicle (CONTROL, 1 ml PBS and 1 ml vegetable oil, n = 5); Relaxin (Relaxin, in PBS, 1 ml, 167 micrograms ml-1, n = 5); Estradiol Benzoate (EB, in vegetable oil, 1 ml, 2 mg ml-1, n = 5); and Relaxin plus EB (Relaxin + EB, at the same doses, n = 5), total six intramuscular injections for all treatments. Twenty four hours after the last injection, hysterectomy was performed, and the uterine tissues were immediately frozen at -80 degrees C. Samples were taken from the middle portions of the cervix and the uterine horns and dried to a constant weight to determine the dry weight and water concentration. Homogenates of uterine horns and cervices were analyzed for concentrations and contents of protein, hydroxyproline (collagen index) and DNA. Relaxin alone had no significant effect on any parameters (i.e., wet weight, Relaxin vs. CONTROL: 36 +/- 5 vs. 28 +/- 3 g uterus-1, dry weight 5.6 +/- 0.6 vs. 4.4 +/- 0.4 g uterus-1). EB alone increased significantly (P < 0.05) wet weight of the uterus (EB vs. CONTROL: 85 +/- 23 vs. 28 +/- 3 g uterus-1), dry weight (EB vs. CONTROL: 14.5 +/- 3 vs. 4.4 +/- 0.4 g uterus-1), and hydroxyproline content (EB vs. CONTROL: 47.2 +/- 13 vs. 12.6 +/- 4 mg cervix-1). In the presence of EB, relaxin treatment increased all measurements compared with CONTROL (i.e., wet weight, Relaxin + EB vs. EB: 136 +/- 34 vs. 28 +/- 3 g uterus-1). Compared with EB, Relaxin + EB significantly (P < 0.05) increased the uterine wet weight (Relaxin + EB vs. EB: 136 +/- 34 vs. 85 +/- 23 g uterus-1), the hydroxyproline content (Relaxin + EB vs. EB: 91 +/- 29 vs. 47 +/- 13 mg cervix-1), and DNA content (Relaxin + EB vs. EB: 8.1 +/- 2 vs. 5.4 +/- 1 mg cervix-1). These results indicate that the growth-promoting effects of relaxin on the uterus and cervix may be, at least partly, estrogen-dependent and that the growth and development of the uterus and cervix can be accelerated by a combination of relaxin and estrogen treatment.
Growth rate and heat production of breast carcinomas have been investigated during the natural evolution of 21 untreated cancers, all with small tumour size (greater than or equal to 3 cm) and most of them were treated by surgery (excision of growth, mastectomy). Three original facts have thus been discovered : a) the specific heat power 1 (i.e. the heat quantity generated by the tumour per untis of volume and time, computed from from intramammary temperature and thermal conductivity measurements made using of fluvographic needle probes), is typical of each cancer and re7ains remarkably constant during the growth in spite of themorphological and of the morphological and circulatory changes; b) the tumour doubling time tau2v (calculated from measurements of the tumour size effected at various stages of the evolution by assuming an exponential growth), is univocally related to 1 by a hyperbolic law so that the faster the tumour is growing themore heat generates; c) q is significanty higher and tau2v shorter in all cases where the histological examination has revealed signs of lymphatic dissemination (carcinomatous lymphangitis, lymph node metastases,...). Practically q represents a quantitative criteria useful for setting with objectivity the pre-therapeutical prognosis of cancers clinically classified T1 or T2 and of circumscribed no palpable cancers. Similar but less accurate prognostic information may also be obtained by cutaneous thermography (infrared, liquid crystals) considering the intensity, extent and topography of the skin hyperthermia frequently elicited by the cancer. Thid aid to prognosis of the thermal methods is all the more valuable as the tumour doubling time cannot be evaluated under the customary clinical conditions.
Growth hormone (GH) is known to play a key role in postnatal growth and differentiation. The role of GH and its receptor (GHR) in prenatal development, however, is still controversial. Using reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization (ISH) and immunohistochemistry we demonstrated the presence of GHR mRNA and protein in bovine mammary glands during fetal development. RT-PCR revealed GHR transcripts in fetal mammary glands from the third to the ninth month of pregnancy. By non-radioactive ISH, GHR mRNA was localized in the glandular epithelium, the surrounding mesenchymal cells, endothelial cells of vessels and in the stratum basale of the epidermis of fetal mammary glands. From the sixth month of fetal life onwards, GHR transcripts were also found in the cytoplasm of adipocytes. Immunohistochemical studies using the monoclonal antibody mAb 263 revealed the same distribution pattern as the mRNA. Our results imply that the growth hormone receptor is distinctly expressed in the immature mammary gland, suggesting that GH is involved in growth and differentiation of the fetal mammary gland.
In budding yeast, the Rho-type GTPase Cdc42p is essential for cell division and regulates pseudohyphal development and invasive growth. Here, we isolated novel Cdc42p mutant proteins with single-amino-acid substitutions that are sufficient to uncouple functions of Cdc42p essential for cell division from regulatory functions required for pseudohyphal development and invasive growth. In haploid cells, Cdc42p is able to regulate invasive growth dependent on and independent of FLO11 gene expression. In diploid cells, Cdc42p regulates pseudohyphal development by controlling pseudohyphal cell (PH cell) morphogenesis and invasive growth. Several of the Cdc42p mutants isolated here block PH cell morphogenesis in response to nitrogen starvation without affecting morphology or polarity of yeast form cells in nutrient-rich conditions, indicating that these proteins are impaired for certain signaling functions. Interaction studies between development-specific Cdc42p mutants and known effector proteins indicate that in addition to the p21-activated (PAK)-like protein kinase Ste20p, the Cdc42p/Rac-interactive-binding domain containing Gic1p and Gic2p proteins and the PAK-like protein kinase Skm1p might be further effectors of Cdc42p that regulate pseudohyphal and invasive growth.
This review concerns the importance of zinc in growth, development, and cognitive function in children and the deleterious consequences of its deficiency on children's health. Possible strategies to overcome zinc deficiency and the results of some supplementation trials are discussed.
The distribution of two distinct populations of basement membrane proteoglycans has been monitored through hair growth development in the rat embryo and subsequent hair growth cycle. An antiserum against a small heparan sulfate proteoglycan uniformly stained the dermal-epidermal junction of embryonic rats throughout the period of hair follicle formation. On the other hand, monoclonal antibodies recognizing a basement membrane-specific chondroitin sulfate proteoglycan only weakly stained 16-d embryo dermal-epidermal junction, but strong staining was associated with hair follicle buds as they developed. Through the hair growth cycle, it was found that the heparan sulfate proteoglycan persisted around the follicles, while the chondroitin sulfate proteoglycan decreased in amount through catagen until it was undetectable at the base and dermal papilla of the telogen follicle. As anagen commenced, expression of the chondroitin sulfate proteoglycan was again demonstrated. It therefore appears that a basement membrane-specific proteoglycan shows variation in its distribution in rat skin, expression correlating with morphogenetic activity in hair follicles. It is possible that this newly described basement membrane component is involved in the complex processes of dermal-epidermal interaction that lead to skin appendage formation and growth.
Growth hormone-releasing hormone (GHRH) and its receptor (GHRHR) have long been regarded as the critical molecules for the stimulation of growth hormone (GH) synthesis and release, as well as the regulation of pituitary somatotroph expansion in vertebrates. However, little is known about their expression in the embryonic pituitaries of birds. In this study, the full-length cDNA for chicken GHRHR was cloned from the chicken pituitary. It encodes 419 amino acids and shares high homology with that of the human, rat, and mouse. As in those in mammals, chicken GHRHR is predominantly expressed in the pituitary and weakly expressed in several extra-pituitary tissues including brain, pancreas, testis, and kidney, among 12 tissues examined. Using semiquantitative reverse transcription-PCR, we further examined the expression of GH, GHRH, and GHRHR during embryonic pituitary development. The expression of GHRHR on embryonic d 8 was much lower, but abundant expression was noticed as early as embryonic d 12. In contrast, the level of pituitary GHRH mRNA peaked on d 8 and declined sharply afterwards. Interestingly, unlike those of pituitary GHRH and GHRHR, the higher expression levels of GH appeared much later (from d 16 to 20). The differential expressions of GHRH, GHRHR, and GH in the developing embryonic pituitaries not only imply that pituitary-derived GHRH (or pituitary adenylate cyclase-activating polypeptide) and GHRHR may have a paracrine/autocrine role in the expansion of undifferentiated somatotroph precursor cells, but also suggest that GHRHR is likely to be involved in the somatotroph differentiation occurring at the later developmental stages.
Insect angiotensin converting enzyme (ACE) is a zinc metallopeptidase capable of inactivating a variety of small to medium size peptide hormones by cleavage of C-terminal dipeptides and dipeptideamides. High levels of ACE activity are found in the hemolymph and in reproductive tissues of insects, where the enzyme is considered to have an important role in the metabolism of bioactive peptides. Therefore, inhibiting ACE activity is expected to interfere with the peptidergic endocrine system and to have detrimental effects on growth, development and reproduction. We will review the studies showing that ACE inhibitors do indeed disrupt growth and reproduction in various insect species. We will also present some new genetic and pharmacological data that strengthens our conclusion that ACE should be considered as a potential target for the development of new insect growth regulators.
Physical activity during the growth period appears to be necessary for normal growth and development of the skeleton, musculature and oxygen-carrying organs. Compared with the adult, the child (in relation to body size) has poor maximal strength and low anaerobic capacity. Muscular endurance and aerobic performance are more comparable to what is found in adults, but even as regards these qualities the child is immature and not on the same level as the adult. The growth period appears to be particularly favourable for learning new movement patterns. In arranging training and competitive sport for children or growing adolescents, attention must be paid to their special physical qualifications and also to the need for versatility in the choice of exercise.
The growth and development of children born of vegan mothers and reared on a vegan diet has been studied longitudinally: All of the children were breast-fed for the first 6 mo of life and in most cases well into the second year of life. The majority of children grew and developed normally but they did tend to be smaller in stature and lighter in weight than standards for the general population. Energy, calcium, and vitamin D intakes were usually below the recommended amounts. Their diets, however, were generally adequate but a few children had low intakes of riboflavin and vitamin B-12. Most parents were aware of the need to supplement the diet with vitamin B-12. It is concluded that provided sufficient care is taken, a vegan diet can support normal growth and development.
Data on growth and development are presented for eight litters of captive-born Phenacomys intermedius. Neonates from litters of four averaged 2.26 g at birth, significantly heavier than neonates from litters of five (1.96 g). Weights on day one showed a statistically significant decrease of 0.20 g per increase in litter size of one neonate. In general, large litters had lower growth rates. Growth of Phenacomys intermedius can be described by the equation Y = 1.17 + 0.62 X and the geometric growth constant is K = 0.079. Pinnae unfolded at 3.7 days, lower incisors erupted at 7.0 days, and eyes opened at 14.6 days. Data on growth and development are compared to other species of Phenacomys and to other microtines.
Growth and development were followed in 7 preterm newborn infants who received fluoroquinolones in the neonatal period. Quinolones were used as a "life saving" therapy in cases of sepsis caused by bacterial agents sensitive only to these drugs. Two other groups of neonates matched for gender, birth weight and gestational age served as controls. Although the quinolone group had more severe illness, no statistically significant differences were observed in growth and development between the groups. No osteoarticular problems or joint deformities were observed in the quinolone group. Therefore, quinolones could be a therapeutic option for newborns with sepsis caused by multiply resistant organisms.