Effects of Sexual Experience and Puberty on Mouse Genital Cortex revealed by Chronic Imaging

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毒害艾美耳球虫早熟株的选育及内生发育观察

为选育制备弱毒疫苗所需的毒害艾美耳球虫早熟株,运用Jeffers建立的早熟系选育方法对毒害艾美耳球虫（E．necatrix）山西分离株进行了早熟选育,并观察其内生发育。结果表明,经过海兰白雏鸡8次传代之后,Enecatrix潜隐期由146．5h缩短至139h,排卵高峰期由168h提前至156h;其虫体各个发育阶段与亲本株相似,但第二代裂殖体明显小于亲本株,且出现的高峰提前。     

The growth of children in relation to the timing of obesity development

Objective: To examine whether there is an association between the timing of the development of obesity and children's growth. Research Methods and Procedures: This study investigated 141 prepubertal obese children (76 girls) and 72 healthy non‐obese children (39 girls). The target height standard deviation score (SDS), the percentage weight for height, and the height SDS (H‐SDS) at presentation and at the age of 2 years were calculated. Patients were classified, according to whether obesity developed before or after the age of 3 years, as presenting with early‐onset or late‐onset obesity, respectively. Results: Mean age (±SD) at presentation was 9.4 (2.1) years. At the age of 2 years, the H‐SDS of the children with early‐onset obesity was 1.3 (1.0) vs. 0.9 (1.3) for the late‐onset obese (p > 0.5) and 0.4 (1.0) for controls (p < 0.001), and the children with late‐onset obesity were also significantly taller than controls (p < 0.005). At presentation, children with early‐onset obesity were significantly taller than children with late‐onset obesity [1.1 (0.8) vs. 0.6 (1.0); p < 0.001] and controls [0.2 (0.8); p < 0.001]. There was no increase in H‐SDS after the age of 2 years in the late‐onset obese children (p > 0.05). H‐SDS values were below average in 21% of the children with late‐onset obesity and in only 4% of the children with early‐onset obesity. Discussion: These findings indicate that late development of obesity is not associated with increased stature in prepubertal children; however, it may be preceded by growth acceleration in the early years of life. Growth acceleration in early life may be a predictor for future obesity.     

Serum insulin-like growth factor-I, insulin-like growth factor binding protein-3, and the pubertal growth spurt in the female rhesus monkey

While there is good evidence suggesting IGF-I links to pubertal development and crown-rump length growth among rhesus monkeys, linkages between IGF-I and other measures of morphological growth have not been established. In this study, the pubertal growth spurt in a number of morphological characteristics of female rhesus monkeys is related to serum endocrine status of insulin-like growth factor-I (IGF-I) and its binding protein, insulin-like growth factor binding protein-3 (IGFBP-3), to test the hypothesis that elevations in IGF-I and IGFBP-3 coincide with the time of greatest growth rate of different morphological characteristics. A longitudinal study of pubertal growth among four female rhesus monkeys was carried out across a 3-year period. Morphometric measurements included weight, crown-rump length, foot-length, and skinfolds at five sites (biceps, triceps, abdominal, subscapular, and suprailiac). These measures were taken as being representative of total mass, skeletal growth of the trunk and head, limb length, and body fatness, respectively. Measurements were carried out as closely as possible to 3-monthly, with interpolations being performed to standardise the data to exactly 3-monthly intervals for all individuals. Blood samples were taken at time of morphometry. Elevations in serum IGF-I and IGFBP-3 took place in a manner similar to that of humans, and across the period associated with onset of puberty. Mean 3-monthly gain in crown-rump length and foot length showed significant peaks across the measurement period, while mean 3-monthly gains in weight and sum of five skinfolds did not. Greatest foot length gain occurred on average between 3-3.5 years of age, while crown-rump length gain was greatest between 3.75-4 years of age. Periods of greatest gain in crown-rump length and foot length took place across the period of elevated serum IGF-I levels, which was between 3-4.5 years of age. Significant elevations in IGF-I and IGFBP-3 were not coincident with greatest gains in foot length or crown-rump length. Thus the hypothesis does not hold true for the two measures showing significant peaks in 3-monthly gain across the measurement period. The nature of the endocrine impact on macaque morphology remains unclear, although this may be fundamental to the understanding of the variation in the pubertal growth spurt and its influence on morphology at maturity both within and across primate species.     

The genetic architecture of correlations among growth‐related traits and male age at maturation in rainbow trout

Heritabilities and genetic correlations among growth‐related traits of two cultured strains (Rainbow Springs and Spring Valley) of rainbow trout Oncorhynchus mykiss were estimated using restricted maximum likelihood methods with a three‐generation pedigree. Heritability was high (>0·50 ± 0·03) for body mass and condition factor but moderate (0·35 ± 0·04) for age at sexual maturity in males. Body mass and age at sexual maturation were phenotypically correlated in the families of one experimental strain, Rainbow Springs, and had a positive genetic correlation (0·26 ± 0·03) across families from both test strains (Rainbow Springs and Spring Valley). This indicates that faster growing individuals were more likely to mature at 2 years of age than slower growing individuals in the two hatchery strains investigated. Microsatellite markers of body mass quantitative tract loci (QTL) were reconfirmed as being located on linkage groups B, G, N, 5 and new markers on Oi were detected. Some QTL effects were restricted to specific sampling dates suggesting temporal expression of QTL. QTL for condition factor were limited to linkage group G in both strains. Three suggestive QTL for precocious maturation mapped to similar regions as those for body mass in the Rainbow Springs families while no associations were evident in the Spring Valley families. The results suggest that these regions may play a role in the basis for genetic and phenotypic correlations between body mass and precocious maturation in this species.     

女孩性早熟患者中检出一种新的雌激素受体基因突变

对收集的16例未见血液雌激素水平升高的临床女孩性早熟患者的外周血样本,利用PCR-SSCP方法筛查了雌激素受体基因编码区的可能突变。结果在1例患者发现：其雌激素受体基因8号外显子编码精氨酸的548位密码子,1个C→T转换导致精氨酸残基被半胱氨酸所替代;这一突变使DNA序列中产生1个BtsⅠ酶切位点,通过PCR-RFLP实验证明此患者为Arg548/Cys548杂合体。为证明该突变在性早熟发生中的作用,构建了一个雌激素受体反应元件报道质粒pGL3-promoter-ERE;成功将野生型ESR1基因定点突变,并克隆于PCR3.1真核表达质粒。报道质粒和表达质粒共转染CMF-7细胞,Cys548突变能够增加萤火虫荧光素酶的产生。结果证明该突变雌激素受体在体外具有高活性特征,因而推测在体内也可能具有相应的过高活性,从而导致女孩的性早熟。     

Effects of gonadal steroids during pubertal development on androgen and estrogen receptor‐α immunoreactivity in the hypothalamus and amygdala

Perinatal development is often viewed as the major window of time for organization of steroid‐sensitive neural circuits by steroid hormones. Behavioral and neuroendocrine responses to steroids are dramatically different before and after puberty, suggesting that puberty is another window of time during which gonadal steroids affect neural development. In the present study, we investigated whether the presence of gonadal hormones during pubertal development affects the number of androgen receptor and estrogen receptor α‐immunoreactive (AR‐ir and ERα‐ir, respectively) cells in limbic regions. Male Syrian hamsters were castrated either before or after pubertal development, and 4 weeks later they received a single injection of testosterone or oil vehicle 4 h prior to tissue collection. Immunocytochemistry for AR and ERα was performed on brain sections from testosterone‐treated and oil‐treated males, respectively. Adult males that had been castrated before puberty had a greater number of AR‐ir cells in the medial preoptic nucleus than adult males that had been castrated after puberty. There were no significant differences in ERα‐ir cell number in any of the brain regions examined. The demonstration that exposure to gonadal hormones during pubertal development is associated with reduced AR‐ir in the medial preoptic nucleus indicates that puberty is a period of neural development during which hormones shape steroid‐sensitive neural circuits. © 2000 John Wiley & Sons, Inc. J Neurobiol 44: 361–368, 2000     

Metabolic and reproductive characteristics of replacement beef heifers subjected to an early-weaning regimen involving high-concentrate feeding

In an effort to better understand the consequences of early weaning (EW) for replacement beef heifers, a two-phase experiment was conducted investigating the impact on metabolic function and documenting reproductive characteristics. In phase 1, Angus×Simmental heifers (n=35) were stratified by BW and sire, and randomly assigned to either a normal weaning (NW, n=18) or EW (n=17) treatment. EW heifers were weaned at 107±3 days of age and provided access to a concentrate-based ration ad libitum with limit-fed mixed grass hay. NW heifers remained with their dams until 232±3 days of age, at which point heifers from both treatments were comingled and grazed on mixed summer pasture. Following NW, weekly blood samples were collected from all heifers for progesterone analyses used to determine the onset of puberty. Pelvic and ovarian size was measured before breeding. All heifers were subjected to an estrous synchronization protocol with timed artificial insemination (AI) at 437±4 days of age. During phase 2 of the experiment, a subset of pregnant heifers (n=16) were divided into two replicates and subjected to a glucose tolerance test, epinephrine challenge and progesterone clearance analysis. Neither age nor BW at puberty differed between EW and NW heifers. Likewise, no differences in pelvic area or ovarian size were observed. Thus, it appears that the reproductive maturity of EW and NW heifers was similar. Heifers studied during phase 2 of the experiment were restricted to those that had become pregnant to their first AI. Within this cohort, EW heifers tended to have lower overall circulating progesterone concentrations than those that were NW (P=0.14). Aspects of glucose and insulin dynamics were also altered, as EW heifers tended to have lower baseline glucose concentrations (P=0.10) despite similar baseline insulin concentrations. Compared with NW heifers, EW heifers had lower insulin area under the curve (P<0.05), which was partly the result of a tendency for lower peak insulin concentrations (P=0.11). Results of the glucose tolerance test indicate that a lesser insulin response was necessary to properly clear the glucose in the EW heifers, suggesting enhanced insulin sensitivity. Collectively, these results indicate that EW is not detrimental for the growth or reproductive development of replacement beef heifers, although some differences in glucose and insulin dynamics persist into adulthood.     

Genome‐scan analysis for genetic mapping of quantitative trait loci underlying birth weight and onset of puberty in doe kids (Capra hircus)

The objective of this study was to locate quantitative trait loci (QTL) causing variation in birth weight and age of puberty of doe kids in a population of Rayini cashmere goats. Four hundred and thirty kids from five half‐sib families were genotyped for 116 microsatellite markers located on the caprine autosomes. The traits recorded were birth weight of the male and female kids, body weight at puberty, average daily gain from birth to age of puberty and age at puberty of the doe kids. QTL analysis was conducted using the least squares interval mapping approach. Linkage analysis indicated significant QTL for birth weight on Capra hircus chromosomes (CHI) 4, 5, 6, 18 and 21. Five QTL located on CHI 5, 14 and 29 were associated with age at puberty. Across‐family analysis revealed evidence for overlapping QTL affecting birth weight (78 cM), body weight at puberty (72 cM), average daily gain from birth to age of puberty (72 cM) and age at puberty (76 cM) on CHI 5 and overlapping QTL controlling body weight at puberty and age at puberty on CHI 14 at 18–19 cM. The proportion of the phenotypic variance explained by the detected QTL ranged between 7.9% and 14.4%. Confirming some of the previously reported results for birth weight and growth QTL in goats, this study identified more QTL for these traits and is the first report of QTL for onset of puberty in doe kids.     

Impaired reproduction in adult male, but not female, rats following juvenile treatment with the aromatase inhibitor, exemestane

BACKGROUND: Exemestane is an irreversible steroidal inhibitor of cytochrome‐P450 aromatase required for estrogen synthesis. The safety of the drug in the pediatric population, particularly in males, has not previously been evaluated. Given the increased interest in treating children with aromatase inhibitors, we undertook a study in rats to assess the potential for exemestane to alter reproductive development and function when administered to juveniles. METHODS: Male and female rats were treated with exemestane at doses anticipated to produce exposures approximately 2‐ and 35‐fold the expected clinical plasma exposure in young adult males during the period of reproductive maturation. After maturation, treated rats were mated to evaluate the potential impact on reproductive function. RESULTS AND CONCLUSION: There were no effects on sexual maturation in either sex or on female reproductive function. Treatment of juvenile male rats caused increased cohabitation time and decreased copulation rates; pregnancy rates and litter size were not affected in rats that mated. Decreased testis (10–15%) and epididymis (20–30%) weights, and decreased Sertoli cell numbers were noted at all doses. This indicates that exemestane can reduce Sertoli cell proliferation during maturation. The sensitive window for this effect is expected to be limited to the period of Sertoli cell proliferation, which is completed by around postnatal day 15 in rats and before puberty in humans. Treatment beginning at a later time relative to the window for Sertoli cell proliferation or for a longer duration is not expected to have additional adverse effect as the effect was not shown to be degenerative. Birth Defects Res (Part B) 92:304–313, 2011. © 2011 Wiley‐Liss, Inc.