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Experimental studies and chemical analysis have been made on Ligustium chuanxiong in its period of growth, generation and growth of organs, content and accumulation of nutritive elements, accumulation of dry matters, fertilizer consumption, etc.
More than 100 patients with central precocious puberty are participating in this international multicenter study using monthly i.m. injections of the slow-release GnRH agonist Decapeptyl-Depot. In 15 patients, Decapeptyl-Depot treatment could be discontinued after 2 years of therapy. Gonadal suppression was promptly reversible in all of them, as shown by prepubertal low gonadotrophin and sex steroid levels. Of the remaining 90 patients, 40 have been treated for more than 3 years, including 33 girls and 7 boys. Plasma levels of LH, FSH, estradiol and testosterone dropped to the prepubertal range after one month of Decapeptyl-Depot and remained there for the whole period of therapy. At start of therapy, mean chronologic age of these 40 children was 6.6 +/- 1.4 (SD) years, mean bone age 10.2 +/- 1.9 years. Mean predicted adult height increased in the boys from 173.6 +/- 13.8 (SD) cm at start of therapy to 184.6 +/- 17.0 cm after 3 years. Predicted adult height increased in girls from 158.0 +/- 12.2 to 161.0 +/- 7.5 cm. Undue side effects were not seen, long term tolerance was good. It is concluded that Decapeptyl-Depot injected i.m. every 4 weeks suppresses the pituitary gonadal axis in children with central precocious puberty without clinical or biochemical escapes, and leads to an increase in predicted adult height by more than 3 cm in all boys and in 53% of the girls after three years of treatment.
Chickens were infected concurrently with 10 and 20 metacercariae/eye of Philophthalmus megalurus and Philophthalmus gralli. After 14 and 34 days of growth, the adults were removed and worm lengths, return rates, stage of development, and distribution within the host recorded. In a second experiment, chickens infected on day 1 with 10 metacercariae/eye of P. megalurus were concurrently infected with a similar dose of P. gralli on day 14. At day 34, the worms were removed and evaluated for the same parameters as in the first study. The effect of concurrent infections on worm length of P. gralli but not P. megalurus was significant when compared to single species control groups. In all cases recovery rates of P. megalurus in concurrent infections were significantly lower than controls, whereas P. gralli adults were recovered at lower rates only in 20-metacercariae--14-day infections. Maturation of eggs was delayed in both species in concurrent infections at the higher infection levels. Normal distribution was disrupted more for P. gralli at the higher infection levels and longer growth periods. Philophthalmus megalurus adults rarely left their normal habitat in the conjunctival sac. A delayed infective dose of P. gralli affected both species by disrupting normal distribution patterns, delaying egg development, and, in the case of P. megalurus, reducing the recovery rate. The possible role of crowding and antagonistic effects is discussed.
BACKGROUND: High-frequency ultrasound is effective for noninvasive phenotypic analysis of cardiovascular development and function in mutagenized fetal mice. However, lacking is a normative database of echocardiographic variables for monitoring growth and cardiovascular function. METHODS: C57BL/6J fetal mice were scanned in utero using an ultrasound system with a 15-MHz linear phased-array transducer. Pregnant mothers were anesthetized with 1% isoflurane mixed with 100% oxygen. Quantitative variables for monitoring fetal growth and cardiac function were obtained in several imaging planes and modalities. RESULTS: Fetal growth measurements increased linearly. Inflow velocities showed significant A-wave dominance. The E wave progressively increased during development. Cardiac function was best assessed through M-mode analysis, but short-axis images were difficult to obtain. Spectral Doppler was readily obtained and the myocardial performance index was calculated. CONCLUSIONS: These results provide an essential foundation for the evaluation of cardiovascular defects in mutagenized and transgenic mice.
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Maternal malnutrition in humans and also in the rat interferes with normal placental growth as reflected by a lower weight, smaller placental size, and reduced DNA content. The affected placentas also have a reduced peripheral villous mass and villous surface. Biochemical studies have revealed a reduced polysome/monosome ratio and higher levels of alkaline ribonuclease activity. However, the rate of protein synthesis in a cell free system, expressed per milligram of rRNA, is not impaired. The composition of the placenta is also altered by malnutrition. Reduced concentrations of ash, hydroxyproline, and fat have been described in human placentas and reduced glycogen and putrescine concentrations have been described in the rat placenta. The functional implications of some of these changes are still unclear. In malnourished women a reduced estriol and pregnanediol excretion have been reported. Malnourished rats near term have a reduced maternal-fetal transfer of alpha-aminoisobutyric acid and glucose, but is is still unclear to what extent the reduced transfer is due to placental factors or preplacental factors such as reduced placental blood flow, also present in malnourished animals.
Carbonic anhydrase III is a cytosolic protein which is particularly abundant in skeletal muscle, adipocytes, and liver. The specific activity of this isozyme is quite low, suggesting that its physiological function is not that of hydrating carbon dioxide. To understand the cellular roles of carbonic anhydrase III, we inactivated the Car3 gene. Mice lacking carbonic anhydrase III were viable and fertile and had normal life spans. Carbonic anhydrase III has also been implicated in the response to oxidative stress. We found that mice lacking the protein had the same response to a hyperoxic challenge as did their wild-type siblings. No anatomic alterations were noted in the mice lacking carbonic anhydrase III. They had normal amounts and distribution of fat, despite the fact that carbonic anhydrase III constitutes about 30% of the soluble protein in adipocytes. We conclude that carbonic anhydrase III is dispensable for mice living under standard laboratory husbandry conditions.
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Thirty]six neonates in whom hypothyroidism was diagnosed after thyroid stimulating hormone screening were reassessed at 1 year. All had grown satisfactorily and the mental development scores were normal in all except two. Treatment was withdrawn in 32 and persistent hypothyroidism was confirmed in 31 cases. Thyroid stimulating hormone concentrations were raised in one-third of cases before the withdrawal of treatment and this was associated with generally lower concentrations of serum thyroxine (T4) and smaller doses of L-thyroxine than in those cases with normal concentrations of thyroid stimulating hormone. In treating congenital hypothyroidism, serum T4 concentrations should be monitored regularly and the dose of thyroxine adjusted to maintain serum T4 in the upper part of the reference range.
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In the absence of long-term results of experimental therapies, a common sense approach toward dealing with the growth of patients who have CAH is desirable. First, an effort can be made to decrease the replacement cortisol dose during the first year of life. Doubling, rather than tripling, the basal dose at times of stress could be helpful. The use of adjunctive therapy for infections could result in fewer fevers. After 1 year of age, mean parental height could be used to establish at which centile the child should theoretically grow. The dose of cortisol could be adjusted to maintain the bone age between +/- 1 SD. Plasma androstenedione levels should not rise above 50 ng/dL, and 17-hydroxyprogesterone should not be totally suppressed but be maintained between 500 and 1000 ng/dL. Compliance with therapy should be encouraged, particularly for adolescent patients. In the final analysis, a realistic expectation for patients would be a height between the 50th and third percentile of the normal growth curve and, in some cases, slightly below the third percentile when the genetic potential is slight.
83 children suffering from malabsorption and disorders of metabolism were investigated with regard to body growth and weight gain. Though at first the increase of weight in comparison to body height was more rapid, the norm was obtained by the time the children were starting school. The period of retardation depended on the severity of disease and the diet being strictly kept to. It is most important that the circumference of the head was normal, though the other proportions of the body were too small for the age. These findings are parallel with normal intellectual development.
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Energy partitioned to maintenance plus activity, tissue synthesis, and storage was measured in 41 children in early recovery [W/L (wt/length) less than 5th percentile] from severe protein-energy malnutrition and in late recovery (W/L = 25th percentile) to determine energy requirements during catch-up growth. Metabolizable energy intake was measured by bomb calorimetry and metabolic collections. Energy expended (means +/- SD) for maintenance and activity estimated by the doubly labeled water method was 97 +/- 12 kcal/kg FFM (fat-free mass) in early recovery and 98 +/- 12 kcal/kg FFM in late recovery (p greater than 0.5). Energy stored was 5-6 kcal/g of wt gain. Tissue synthesis increased energy expenditure by 1 +/- 0.7 kcal/g gain in both early and late recovery. From these data a mathematical model was developed to predict energy requirements for children during catch-up growth as a function of initial body composition and rate and composition of wt gain. The model for predicting metabolizable energy requirements is [(98 x FFM + A (11.1 B + 2.2 C)], kcal/kg.d, where FFM is fat-free mass expressed as a percentage of body wt, A is wt gain (g/kg.d), B and C are percentage of wt gain/100 as fat and FFM, respectively. The model was tested retrospectively in separate studies of malnourished children.
Activated lymphocytes must increase in size and duplicate their contents (cell growth) before they can divide. The molecular events that control cell growth in proliferating lymphocytes and other metazoan cells are still unclear. Here, we utilized transgenesis to provide evidence suggesting that the basic helix-loop- helix-zipper (bHLHZ) transcriptional repressor Mad1, considered to be an antagonist of Myc function, inhibits lymphocyte expansion, maturation and growth following pre-T-cell receptor (pre-TCR) and TCR stimulation. Furthermore, we utilized cDNA microarray technology to determine that, of the genes repressed by Mad1, the majority (77%) are involved in cell growth, which correlates with a decrease in size of Mad1 transgenic thymocytes. Over 80% of the genes repressed by Mad1 have previously been found to be induced by Myc. These results suggest that a balance between Myc and Mad levels may normally modulate lymphocyte proliferation and development in part by controlling expression of growth-regulating genes.
CONTEXT: Despite recent studies that failed to show catastrophic effects of prenatal cocaine exposure, popular attitudes and public policies still reflect the belief that cocaine is a uniquely dangerous teratogen. OBJECTIVE: To critically review outcomes in early childhood after prenatal cocaine exposure in 5 domains: physical growth; cognition; language skills; motor skills; and behavior, attention, affect, and neurophysiology. DATA SOURCES: Search of MEDLINE and Psychological Abstracts from 1984 to October 2000. STUDY SELECTION: Studies selected for detailed review (1) were published in a peer-reviewed English-language journal; (2) included a comparison group; (3) recruited samples prospectively in the perinatal period; (4) used masked assessment; and (5) did not include a substantial proportion of subjects exposed in utero to opiates, amphetamines, phencyclidine, or maternal human immunodeficiency virus infection. DATA EXTRACTION: Thirty-six of 74 articles met criteria and were reviewed by 3 authors. Disagreements were resolved by consensus. DATA SYNTHESIS: After controlling for confounders, there was no consistent negative association between prenatal cocaine exposure and physical growth, developmental test scores, or receptive or expressive language. Less optimal motor scores have been found up to age 7 months but not thereafter, and may reflect heavy tobacco exposure. No independent cocaine effects have been shown on standardized parent and teacher reports of child behavior scored by accepted criteria. Experimental paradigms and novel statistical manipulations of standard instruments suggest an association between prenatal cocaine exposure and decreased attentiveness and emotional expressivity, as well as differences on neurophysiologic and attentional/affective findings. CONCLUSIONS: Among children aged 6 years or younger, there is no convincing evidence that prenatal cocaine exposure is associated with developmental toxic effects that are different in severity, scope, or kind from the sequelae of multiple other risk factors. Many findings once thought to be specific effects of in utero cocaine exposure are correlated with other factors, including prenatal exposure to tobacco, marijuana, or alcohol, and the quality of the child's environment. Further replication is required of preliminary neurologic findings.
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