This study was done to compare the accuracy of prediction of growth parameters using the Gompertz model when (1) data was collected infrequently, (2) data collection was truncated, and (3) data was missing. Initial growth rate and rate of decay were reduced by half when the model was fitted to data collected biweekly compared to data collected weekly. This reduction led to an increase in age of maximum growth and subsequently over-predicted the asymptotic body weight. When only part of the growth duration was used for prediction, both the initial growth rate and rate of decay were reduced. The degree of data truncation also affected sexual dimorphism of the parameters estimated. Using pre-asymptotic data for growth parameter prediction does not allow the intrinsic efficiency of growth to be determined accurately. However, using growth data with body weights missing at different phases of the growth curve does not seem to significantly affect the predicted growth parameters. Speculative or diagnostic conclusions on intrinsic growth should be done with data collected at short intervals to avoid potential inaccuracies in the prediction of initial growth rate, exponential decay rate, age of maximum growth and asymptotic weight.
In slowly metabolizing tissue such as tooth, bone and ocular lens, D-amino acids converted from L-amino acids accumulate with age and thus reflect the tissue turnover rate. To investigate whether D-amino acids play a role in determining the bone remodeling rate, we measured the accumulation of D-aspartic acid, which has the fastest rate of racemization, in various areas of the mandible. The level of D-aspartic acid was higher in the ramus than in the body (P < 0.01), and within the body, the level was higher in the basal area than in the alveolar area (P < 0.01). Within the alveolar area, the level of D-aspartic acid was higher in the molar region than in the incisal region (P: 0.05-0.01). No correlation was found between the accumulated level of D-aspartic acid with age, because all the specimens were obtained from elderly people with only a few years difference in age. There was also no correlation between D-aspartic acid and sex. In conclusion, we suggest that accumulation of D-aspartic acid in the mandibular bone reflects the differences in remodeling associated with occlusion. The incisal portion of the alveolar area of the mandible (above the mandibular canal), shows the greatest evidence of active remodeling.
OBJECTIVE:To compare bone mass in newborn infants of First Nations, white and Asian mothers while accounting for vitamin D status. Fifty infants born healthy at term age were measured for bone mass using dual energy x-ray absorptiometry (DXA) within 15 days of life. Vitamin D status was measured as 25(OH)D in cord plasma. White infants were separated based on 25(OH)D concentrations into sufficient and insufficient (< 32.5 nmol/L) to match for vitamin D status of the Asian infants and the First Nations group. Differences among groups were tested using ANOVA and post hoc testing with Bonferroni multiple comparisons test. There were no differences in whole body, spine or femur BMC between the white sufficient and insufficient infants. However, the Asian infants had lower (P < 0.01) spine BMC compared to the white infants and the First Nations infants were intermediate. No differences among the ethnic groups were observed for whole body or femur BMC. These data suggest that white and First Nations newborn infants have comparable bone mass. Asian infants have lower spine bone mass which is more than a factor of body size and independent of vitamin D status at birth.
Prenatal development is highly sensitive to the effects of environmental contaminants. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxicant that at very low levels causes teratogenic effects such as irregular tooth development. Variations in susceptibility to TCDD's effects have been attributed primarily to differences at the Ahr locus. There is some evidence, however, that genes at other loci may be involved in mediating TCDD's effects on various endpoints. Our hypothesis therefore was that the effect of TCDD on molar development would differ even among inbred mouse strains possessing similar Ahr alleles. To test this, geometric morphometric techniques were used to evaluate the effects of several different levels of TCDD on molar size, shape and asymmetry in the offspring of dosed females from five different inbred strains of mice bearing TCDD-sensitive Ahr alleles. The results indicated that a maternal dose of 1 microg TCDD/kg body weight on gestation day 13 altered the shape (but not the size or asymmetry) of the first two molars in mice from the C3H/HeJ and CBA/J strains of mice, but not in mice from the other strains. The C3H/HeJ and CBA/J strains appeared to be the most sensitive to the disruption of molar development via TCDD and the C57BL/6J strain appeared to be the least sensitive.
Available techniques for determining age from human cranial remains are limited. This study examines the efficacy of Meindl and Lovejoy's (1985) method of determining age based on ectocranial suture closure patterns as compared to a baseline of ages developed from a multifactorial approach employing various age determining factors from across the skull. What makes this study different is that the sample upon which this comparison is performed contains a large number of artificially deformed crania. Our hypothesis is that aging techniques that rely on suture closure patterns as markers are complicated by the results of artificial modification of the cranial vault. The study is conducted on adult, human crania from prehispanic archaeological sites in South America. Results demonstrate a significant difference between the two aging methods, more particularly when applied to deformed skulls. We conclude that when a skull is deformed age should be estimated utilizing multiple factors that exclude Meindl and Lovejoy's ectocranial suture aging technique.
A growth trial was conducted with the Ross 708 broiler chicken to corroborate the relationships between changes in the growth curve (7 to 35 days) and in vitro metabolic parameters. These in vitro parameters also included estimates of the expression of certain genes regulating proteins implicated with regulation of lipogenesis. Birds were fed diets containing 24% protein from 0 to 14 days of age, 21% from 14 to 26 days of age and 18% protein until 35 days of age. Birds were selected and killed at ages corresponding to protein changes. Dual X-ray absorptiometry (DXA) was used to approximate body composition of birds at day 35. The switch from the starter protein level of 24% crude protein to the only slightly lower protein grower diet (21% crude protein) increased both in vitro lipogenesis and malic enzyme activity. A similar observation was noted when the birds were switched to the 18% crude protein finisher diet. These same switches also elicited initial increases in malic enzyme, fatty acids synthase and acetyl CoA carboxylase gene expression that were not sustained following adaptation to the dietary change. Data also show that DXA can be used to estimate body composition of this type of bird.
Three growth models were used to examine the effects of prenatal exposure to aspirin on the postnatal development of brain parts. A total of 60 pregnant rats which were divided into three experimental groups and a control group were exposed to aspirin doses of 12.5, 25, 37.5 mg/kg, and distilled water, respectively. The brain parts of 200 rat pups starting from the first week after birth until the fifth week were weighted and the length and width of the cerebrum and cerebellum were measured to determine the parameters of the growth models. The results indicated that the three models successfully predicted the growth of the different brain parts and that aspirin decreased the total brain weight, cerebrum length and width, and decreased the cerebellum length and width at aspirin dose of 37.5 mg/kg. Further analysis is needed to investigate if aspirin effects were carried out through its role in inhibiting prostaglandin production and consequently affecting the activity of the hypothalamus-pituitary axis.
Over expression of the pro domain of myostatin (MLC-pro) interferes with myostatin function, thus promoting muscle growth. The purpose of this study was to use dual energy X-ray absorptiometry (DXA) to monitor, in vivo, the course of changes in body composition of control and MLC-pro transgenic (TG) mice between 10 and 91 days of age. MLC-pro TG (n = 32) and littermate control (n = 28) mice were produced by mating G-3 male TG mice with non-TG females. At days 10, 20 and weekly thereafter to day 62, and finally at day 91, the mice were anesthetized and scanned by DXA. By day 34, the body weight of the male TG mice was more than that of the control mice and was accompanied by a larger lean mass (LM) and a lower percentage of fat (%F) (P < 0.05). At day 91, the male TG mice had 15.6% greater body weight, 19.4% more LM, 22.4% lower %F, 11.5% more bone mineral, and 4.4% higher bone density (P < 0.05). The lower %F in the TG mice was due mainly to an increase in LM, rather than reduced FM. Measurements of the TG female mice were not different (P > 0.05) from those of control female mice. A region-of-interest analysis was used to provide a separate measure of the hind limb. By using DXA, this study determined the onset and degree of differences in body composition of MLC-pro TG and littermate control mice.
Ontogenetic growth can be described by mathematical equations constructed on the goodness of fit. Recently, the biological mechanism underlying mathematical growth equations has been explored using basic cellular properties. Here, we derive a general statistical model for understanding the genetic regulation of ontogenetic growth by integrating those biologically-proven meaningful growth equations into a quantitative trait locus (QTL) mapping framework. We can characterize the dynamic patterns of effects of QTL governing growth curves and estimate the global effect of the underlying QTL throughout the entire course of growth. The model provides the basis for deciphering genetic relationships for growth rates and the timing of life history events for any kind of organisms.
The aim of the present study was to assess body weight recovery in rats with intrauterine growth retardation (IUGR) castrated and treated with growth hormone (GH). Wistar albino rats were divided into the following experimental groups: control (C), sham-operated (SH), IUGR, IUGR castrated (IUGR+C), and IUGR castrated and injected with GH (IUGR+C+GH). IUGR was induced by partial bending of uterine vessels at day 14 of pregnancy. GH (Genotropin 3.0 mg/kg/day) was administered from weaning (21 days old) to 60 days of age. SH rats were injected only with diluent. Castration was performed at weaning. Body weight, body weight velocity and relative food intake were registered weekly. Data were analyzed by ANOVA and LSD post hoc test. The between-subjects analysis showed significant differences for sex and treatment factors. Differences in body weight were significant among treatments, being SH > IUGR > IUGR+ C+GH > IUGR+C in males, and SH > IUGR+C > IUGR+C+GH > IUGR in females. Differences in relative food intake were IUGR+C > IUGR+C+GH > IUGR > SH in males, and IUGR+C+GH > IUGR+C > IUGR > SH in females. These results indicate that nutritional rehabilitation impairs the effects of IUGR. While the absence of testosterone inhibited body weight gain, the absence of estrogens promoted catch-up growth. Castrated animals with or without GH treatment ate relatively more, suggesting the absence of an anabolic effect of gonadal steroids.
The depression of body growth rate and the reduction of body mass for chronological age and gender in growing experimental animals exposed to hypobaric air (simulated high altitude = SHA) have been associated with hypophagia because of reduced appetite. Catch-up growth during protein recovery after a short period of protein restriction only occurs if food intake becomes super-normal, which should not be possible under hypoxic conditions if the set-point for appetite is adjusted by the level of SHA. The present investigation was designed to test the hypothesis that growth retardation during exposure to SHA is due to an alteration of the neural mechanism for setting body mass size rather than a primary alteration of the central set-point for appetite. One group of female rats aged 35 d were exposed to SHA (5460m) in a SHA chamber for 27 d (HX rats). Other group was maintained under local barometric pressure conditions (NX rats). One half of both NX and HX rats were fed a protein-free diet for the initial 9 d of the experimental period. From this time on, they were fed a diet containing 20% protein, as were the remaining rats of both groups during the entire experimental period. The growth rates of both mass and length of the body were significantly depressed in well-nourished rats exposed to SHA during the entire observation period when compared to normoxic ones. At its end, body mass and body length were 24% and 21% less in HX than in NX rats. Growth rates were negatively affected by protein restriction in both NX and HX rats. During protein recovery, they reached supernormal values in response to supernormal levels of energy intake that allowed a complete catch-up of both body mass and length. The finding that energy intake during the period of protein rehabilitation in HX rats previously stunted by protein restriction was markedly higher than in HX control ones at equal levels of hypoxia demonstrates that the degree of hypoxia does not determine directly the degree of appetite and energy intake. Furthermore, the finding that catch-up growth in the stunted HX rats returns the animal only to the stunted size appropriate for the hypoxic animal supports the hypothesis that hypoxia lowers the set-point for body mass size, which is reached by inhibition of appetite. Confirmation of the hypothesis was done by assessment of the set-point of body mass by the behavioral method of the weight threshold to hoard food. It was lowered by 17.0% in HX rats.
The temporomandibular joint (TMJ) is a exceptional joint involved in growth as well as mastication. In adult mice, it provides a model for age related natural osteoarthritis (OA). The insulin-like growth factor (IGF-) system plays was tested because it plays important roles in cartilage biology and OA pathogenesis. Decalcified and paraffin embedded TMJs of 48 NMRI mice sacrificed in groups of three male and females each at the ages of 3, 4, 5, 7, 9, 10, 12, and 18 months were prepared for histopathology and immunohistochemistry for IGF-I and -II, IGF1 receptor and IGF binding proteins -1, -2, -3, -4, -5, and -6. Histopathological signs of OA were obvious in the TMJ of all animals older than 5 months, but did not show a clear age-related staging. Immunoreactivity for all IGF components was found in unchanged anterior and posterior regions of the condyle and in regions of advanced OA lesions. Receptor immunostaining was obvious in all ages. Most IGFBPs showed immunostaining patterns similar to IGFs. While the anterior and posterior zones of the condylar cartilage appear to be specialized judging by structure and IGF immunostaining pattern, probably due to metabolic or biomechanical peculiarities, the central portion undergoes early degeneration. In advanced OA stages, the IGF system seems to be upregulated to induce repair processes. According to their mainly inhibiting functions, IGFBPs may suppress anabolic IGF activities.
Although recent endeavors to discover the mechanisms of the aging process have been numerous and successful, there is still much to be learned. Genes implicated in the aging process were mapped to the canine genome and will serve as additional framework markers for the assignment of contiguous segments from the canine genome sequence to chromosomes. The 54 genes were selected because of their demonstrated contribution to longevity in other organisms or based upon their proximity to a marker, D4S1564, on human chromosome 4 (Puca et al., 2001). This effort lays the necessary groundwork for our utilization of the domestic dog as a model organism to define the genes that govern aging and longevity. Within the species, naturally diverse life expectancies and highly homogeneous populations create an ideal population structure for studying the genetic components of aging (Patronek et al., 1997).
Memory lymphocytes play a central role in the secondary immune response. The concentration of memory lymphocytes increases with age. A high level of cell surface CD44 is a marker of memory lymphocytes compared to naive lymphocytes which express a low level of CD44. Major histocompatibility complex (MHC) class I protein expression also increases with age. To explore a possible correlation between the expression of CD44 and MHC class I protein (K-b), peripheral blood lymphocytes from 27 C57BL/6 mice ranging in age from 3 months to 33 months were isolated by Ficoll-Hypaque gradient centrifugation. Single and double indirect immunofluorescence assays were then performed with rat IgG anti-CD44 and/or mouse IgG anti-K-b as first antibodies, and phycoerythrin (PE) labeled goat anti-rat IgG and/or fluorescein (FITC) labeled goat anti-mouse IgG as second antibodies. Cells were then analyzed by using a FACScan flow cytometer. As expected, the percentage of lymphocytes expressing high levels of CD44 (memory cells) increased significantly with age and the expression of K-b increased significantly with age. Interestingly, the expression of K-b in lymphocytes expressing high levels of CD44 (memory cells) was 72% more than in cells expressing low levels of CD44 (naive cells) regardless of age.
Most studies of malnutrition focus on adult size, or limited durations of malnutrition. Little is known about the impact of life-long maternal malnutrition on young, pre-weaning offspring, in part because working with such infants is difficult. We created a maternal generation of malnourished dams by feeding female Sprague-Dawley rats, from weaning, either a control diet high in protein (CT) or an isocaloric low protein diet (LPT). The offspring of matings between these dams and control fathers were weighed daily and radiographed three times before sacrifice at 22d, when several visceral organs and muscles were dissected out and weighed. We compared lengths of craniofacial and limb bones, and organ and muscle weights, between the two diet treatments. Allometric cancellation was used to assess integration of growth among organs and muscles. The offspring of LPT dams had body, organ and muscle weights smaller than the offspring of CT dams. When scaled to body mass, some organs of the LPT offspring were relatively larger. Although the CT offspring skeletons were significantly larger than the LPT skeletons, considerable variation existed in the patterns of growth between the two treatments. The CT offspring had a higher level of correlation among muscles, and most organs, than did the offspring of LPT dams. The organs that did maintain a correlation in growth, or linkage, were pairs of organs more likely to be protected (heart-lung or eye-brain) from the insult of protein malnutrition. The ability to protect some organs may be the result of their tighter developmental program, one that is more resistant to differences in available nutrition.
The body weight growth of OF1 mice, both females and males, from day of birth to 220 days old is studied herein. After comparison of different theoretical models, an extension of Koops's multiphasic functions, the tetraphasic, is proposed as the best choice in so wide a time interval in mouse development. This function has allowed us to take into account different aspects of growth. Coefficients and phases of this function are characterized. The end of the first phase was established at 17 days of age. The second phase finished at 35 days of age in females and at 39 days in males. This difference increased during the third phase: the end of it was at 173 days of age in males, and at 160 days in females. The end of the fourth phase in OF1 mice would be produced after 220 days of age. Inflexion points in every four phases, in females and males, are situated. The biggest weight increase occurred in the second phase in both sexes, specially in males (1.26 g per day). Biological meanings of every phase are also discussed. The short lifetime of rodents have allowed us to study a great number of growth phases in a short period of time. Thus the present analysis could be a good starting point for the study of growth curves in other species of mammals.
Myostatin is a potent growth and differentiation factor involved in skeletal muscle tissue formation in vertebrates. In the present study, temporal and spatial expression patterns of myostatin transcripts were investigated in chicken embryos. Myostatin mRNA was detected by RT-PCR analysis in embryos collected immediately after oviposition (stage HH1) and persisted until the fifth day of incubation (stage HH26). Whole-mount in situ hybridization revealed myostatin to be expressed in the ventral myotomal region of mature somites, thus confirming the importance of myostatin in skeletal muscle tissue formation during avian embryogenesis. A smaller myostatin transcript was also identified. This transcript appears to have resulted from an alternative splicing event from common GT-AG processing sites. Analysis of the amino acid sequence generated from this alternative transcript confirmed the presence of a truncated protein that lacks the C terminal region, including the cysteine domains characteristic of the TGF-beta super family. The temporal and spatial patterns of myostatin expression presented in this study agree with the proposed role of myostatin as modulator of muscle cell proliferation.
Growth hormone secretion is under the control of a pair of hypothalamic factors, growth hormone releasing hormone and somatostatin. The growth hormone secretagogue receptor (GHSR) and its endogenous ligand represent a novel third method regulating the release of growth hormone. Early chicken embryonic development has been proposed to be independent of GH. However, recent evidence shows that peripheral GH secretion has paracrine/autocrine functions during embryonic development. In the current study, we used the reverse-transcriptase polymerase chain reaction to determine the expression pattern of the GHSR during embryonic development and the effects of in ovo recombinant human (rh) IGF-I administration on its expression pattern. Eggs were injected once with 100 ng rhIGF-I in 10 mM acetic acid, and 0.1% BSA per embryo on embryonic day 3. Total RNA was isolated from whole embryos on embryonic day (E) 0-6 (n=6 per day), thoracic/abdominal halves of the embryos on E7- E8 (n= 6 per day) and Pectoralis muscle on E9-E20 (n= 4 per day). We found that GHSR expression was low during E0-E4, followed by an increase on E5 and remained constant through E17. GHSR expression then increased on E18 before reducing on E20. A similar pattern was found in the rhIGF-I treated embryos with the exception of a significant increase in GHSR expression on E8. These data indicate that the GHSR may be active in regulating GH secretion during early embryonic development, and upregulation of the GHSR gene following IGF-I administration may have an important role in the determination of postnatal muscle growth.
Although changes in dietary protein levels change metabolism in the broiler chicken, there is little information concerning the time course of the process of adaptation. Therefore, male Hubbard broiler chickens were fed diets containing either 12 or 30% crude protein from 7 to 28 d of age and then were switched to the opposite level for an additional 9 d. Birds were bled and killed at 0, 2, 5, 7and 9 d following the reversals. Data taken at these intervals included those involved in vitro lipogenesis (IVL), growth and feed consumption, hepatic enzyme activities and plasma hormones and metabolites. Birds fed the lower level of crude protein were smaller in growth from 7 to 28 d. Feeding these birds a higher protein diet from 28 to 37 d improved both growth and feed efficiency in comparison to controls. Lipogenesis was also greater and plasma insulin-like growth factor-I (IGF-I) less in birds fed the lower protein diet. Switching dietary treatments increased and decreased lipogenesis as birds were switched from high to low and low to high protein diets, respectively. Half-maximal changes were observed 2 d after the reversal and maximal changes 5 d after the reversal. In contrast, switching dietary treatments decreased and increased plasma IGF-I as birds were switched from high to low and low to high protein diets, respectively. Half-maximal changes were observed 2 d after the reversal. Of the three hepatic enzymes monitored, malic enzyme activity most closely followed the rapid changes in IVL. In the present study, plasma IGF-I may be a more sensitive indicator of changes in dietary protein than changes in intermediary metabolism.
The adrenal medulla in mammalian species is surrounded by a cortex that contains three distinct layers, whereas the cortex and medulla are intermingled in poultry species. The objective of the present study was to determine the distinct zonation changes in the adrenal cortex of geese in various ages using both electron and light microscopy. Adrenal glands were obtained from French Geese (Anser anser) under deep ether anesthesia at posthach day 1, 5, 10, 21 and 30 (n= 5 per day). The cytoplasm of interrenal cells located beneath the adrenal capsule (sub-capsular zone, SCZ) were stained lighter than that of interrenal cells located inside the adrenal gland (inner zone, IZ) and contained several vacuoles for each sampling day. Additionally, unlike IZ cells, SCZ cells contained nuclei that were various shapes and surrounded by irregularly arranged membranes, lipid droplets which were not surrounded by a membrane, mitochondria with mostly shelf-like cristae. The arrangement of SCZ cells appears similar to that of zona glomerulosa and also the arrangement of IZ cells to that of zona fasciculata of mammalian adrenal cortex, suggesting the significant signs of zonation in goose adrenal cortex.
