The adolescent brain and age-related behavioral manifestations

PIP: 43 determinants of low birth weight were analyzed from 895 published papers in the English and French literature from 1970-1984 The assessment was limited to singleton births of women living at sea level with no chronic illness; rare factors and complications of pregnancy were excluded The 43 factors were categorized as genetic and constitutional, demographic and psychosocial, obstetric, nutritional, maternal morbidity during pregnancy, toxic exposure and antenatal care The existence and magnitude of a causal effect on birth weight, gestational age, prematurity and intrauterine growth retardation were determined by a set of methodological standards In developed countries, the most important factor was cigarette smoking, followed by nutrition and pre-pregnancy weight In developing countries the major determinants were racial origin, nutrition, low pre-pregnancy weight, short maternal stature, and malaria Pre-pregnancy weight, prior premature birth or miscarriage, diethylstilbestrol exposure and smoking were major determinants of gestational duration, but the majority of prematurity was unexplained in both developed and developing countries There is a need for future research on the effect of maternal work, prenatal care, and certain vitamin and mineral deficiencies on intrauterine growth, and the effect of genital tract infection, prenatal care, maternal employment, stress and anxiety on prematurity

Determinants of low birth weight: Methodological assessment and meta-analysis

Steroidogenesis entails processes by which cholesterol is converted to biologically active steroid hormones. Whereas most endocrine texts discuss adrenal, ovarian, testicular, placental, and other steroidogenic processes in a gland-specific fashion, steroidogenesis is better understood as a single process that is repeated in each gland with cell-type-specific variations on a single theme. Thus, understanding steroidogenesis is rooted in an understanding of the biochemistry of the various steroidogenic enzymes and cofactors and the genes that encode them. The first and rate-limiting step in steroidogenesis is the conversion of cholesterol to pregnenolone by a single enzyme, P450scc (CYP11A1), but this enzymatically complex step is subject to multiple regulatory mechanisms, yielding finely tuned quantitative regulation. Qualitative regulation determining the type of steroid to be produced is mediated by many enzymes and cofactors. Steroidogenic enzymes fall into two groups: cytochrome P450 enzymes and hydroxysteroid dehydrogenases. A cytochrome P450 may be either type 1 (in mitochondria) or type 2 (in endoplasmic reticulum), and a hydroxysteroid dehydrogenase may belong to either the aldo-keto reductase or short-chain dehydrogenase/reductase families. The activities of these enzymes are modulated by posttranslational modifications and by cofactors, especially electron-donating redox partners. The elucidation of the precise roles of these various enzymes and cofactors has been greatly facilitated by identifying the genetic bases of rare disorders of steroidogenesis. Some enzymes not principally involved in steroidogenesis may also catalyze extraglandular steroidogenesis, modulating the phenotype expected to result from some mutations. Understanding steroidogenesis is of fundamental importance to understanding disorders of sexual differentiation, reproduction, fertility, hypertension, obesity, and physiological homeostasis.

The molecular biology, biochemistry, and physiology of human steroidogenesis and its disorders.

Mammalian ovaries consist of follicles as basic functional units. The total number of ovarian follicles is determined early in life, and the depletion of this pool leads to reproductive senescence. Each follicle develops to either ovulate or, more likely, to undergo degeneration. The dynamics of ovarian follicle development have interested endocrinologists and developmental biologists for many years. With the advent of assisted reproductive techniques in humans, the possibility of regulating follicle development in vivo and in vitro has gained clinical relevance. In this review, we focus upon key branching points during the development of ovarian follicles as well as factors involved in determining the eventual destiny of individual follicles. We discuss inconsistencies in the literature regarding the definitions of follicle recruitment and selection and propose to name the two major steps of follicle development as initial and cyclic recruitment, respectively. Because some of these disparities have arisen due to differences in the animal systems studied, we also compare the development of the ovarian follicles of both humans and rats. We also review the status of knowledge of several puzzling clinical issues that may provide important clues toward unlocking the mechanisms of follicle development.

https://redlara.com/images/arq/LOC1_recrutamento.pdf

Initial and cyclic recruitment of ovarian follicles.

I. Introduction II. Mechanisms of Estrogen Action A. “Genomic” and “nongenomic” mechanisms B. Steroid hormone actions on gene expression C. Subtypes of estrogen receptors D. Steroid hormone actions on putative receptors on membranes E. Rapid actions of steroids on neuronal excitability F. Steroid hormone actions via second messengers G. Neuroprotective effects of estrogens H. Summary III. Areas of the Brain Affected Outside of the Hypothalamus A. Studies of hypothalamic and extrahypothalamic actions of estrogens B. Estrogens and the cholinergic system C. Estrogens and the serotonergic system D. Catecholaminergic neurons E. Spinal cord F. Hippocampus G. Glial cells, endothelial cells, and the blood-brain barrier H. Summary IV. Effects of Estrogens on Learning and Memory V. Estrogens, Neuroprotection, and Alzheimer’s Disease VI. Conclusions

Estrogen actions in the central nervous system.

The concentrations of the adrenal steroids dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), and Δ4-androstenedione (Δ4-A) have been measured by RIA before and after sexual maturation in plasma of rodents, domestic animals, and primates to determine whether these species exhibit an adrenarchal process comparable to man. The average concentrations of DHA and DHAS were less than 60 ng/dl and 5 μg/dl, respectively, in plasma of sexually mature rodents and domestic animals, and a significant increase in the plasma DHA level after sexual maturation was seen only in the rabbit and dog. The concentrations of DHA, DHAS, and Δ4-A in 21 rhesus monkeys from 0–3 yr of age were 2021 ± 235 ng/dl (mean ± SE), 357 ± 60 μg/dl, and 107 ± 9 ng/dl, respectively, and did not increase during sexual maturation. By contrast, DHA, DHAS, and Δ4-A levels in plasma of chimpanzees were 5.9-fold, 3.3-fold, and 4.8-fold greater, respectively, in 7- to 22- compared to 0- to 3-yr-old animals. Temporally, the increase i...

Adrenarche: A Survey of Rodents, Domestic Animals, and Primates

Endometriosis: role of ovarian steroids in initiation, maintenance, and suppression.

The dominant ovarian follicle

MUCH MORE is known about ovarian function in small mammals, especially laboratory rodents, than about the factors regulating cyclic ovarian function in primates. However, recent results, including our own, have enhanced the understanding of ovarian function in primates, bringing new and significant findings that now justify an assembly of knowledge on the regulation of the primate ovarian cycle. In this review, the major consideration is given to aspects of folliculogenesis in primate species. Where important similarities or differences in fundamental issues have been described in other mammals, limited discussion has been given to comparative aspects of follicular maturation. Consequently, we encourage readers of this subject to rely upon several scholarly reviews (1–7) that have recently developed comparative topics more fully than is either appropriate or intended here. Accordingly, we have restricted our attention to the dynamics of follicle growth during the primate ovarian cycle to focus on recent f...

Folliculogenesis in the Primate Ovarian Cycle

To identify factors regulating the initiation of follicle growth in adult primates, the ovarian cycle of sexually mature rhesus monkeys was interrupted by surgical ablation of the preovulatory follicle or functioning corpus luteum (CL). In 10 of 10 animals, cautery of the largest visible follicle on Day 8–12 of the cycle blocked ovulation, and in all but one abolished the expected midcycle surges of gonadotropin secretion. In 8 monkeys of this group, surges of LH and FSH release occurred 12.4 ± 0.9 days (d) (mean ± SE) after cautery, coincident with elevations in serum estrogens, and succeeded by typical luteal phase patterns of circulating progesterone (P). No gonadotropin or estrogen surges were observed during the next 32 days of sampling in the remaining pair, despite visible new vesicular follicles. Removal of the CL in 5 of 5 monkeys 4–6 days after the midcycle LH surge was followed by a reduction in serum P to less than 0.25 ng/ml within 24 h and by the onset of menses within 3–4 days. After luteec...

Gary D. Hodgen

Papers

Adrenarche: A Survey of Rodents, Domestic Animals, and Primates

Endometriosis: role of ovarian steroids in initiation, maintenance, and suppression.

The dominant ovarian follicle

Folliculogenesis in the Primate Ovarian Cycle

Regulation of folliculogenesis in the cycling rhesus monkey: selection of the dominant follicle.