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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentrations of aldosterone in the plasma and adrenal glands, the concentrations of sodium and potassium in the plasma and the hematocrit were estimated from birth to day 6 after birth in premature mice removed by Caesarean section on day 19 of pregnancy in comparison with newborn mice delivered spontaneously vaginally on day 20 of pregnancy. In premature mice, the plasma aldosterone concentrations increased twice: at birth after reanimation, then at 6 h after birth. The first increase at birth resulted probably from ACTH stimulation. Several factors could be involved in the peak at 6 h after birth: ACTH stimulation, the decrease in the level of sodium in the plasma and the increase in the hematocrit due to kidney immaturity of premature mice. The results suggest that the renin-angiotensin-aldosterone system is able to respond to stimulations in the first 6 h after birth in premature mice. The rise in the level of plasma aldosterone which has been found at birth in newborns delivered spontaneously vaginally on day 20 of pregnancy (control animals) did not result from variations of plasma electrolytes, plasma volume and ACTH; this rise has been induced by labor of the parturition which caused the aldosterone release from adrenal glands.
Steroids 1982 Sep
PMID:Plasma and adrenal aldosterone levels in premature mice at birth and during neonatal development. 718 5

In the present paper, we report that injection of testosterone propionate (500 microg) during the critical window of rat development (postnatal day 5) induces temporary appearance of aged interstitial cells in developing ovaries (days 7 and 10). Aged interstitial cells showed large size (> or = 12 microm), enhanced androgen receptor (AR) and low estrogen (ER) and luteinizing hormone receptor (LHR) expression. Although normal mature interstitial cells (large size and strong ER and LHR expression) appeared later (day 14), and ovaries of androgenized rats were similar to normal ovaries between days 14 and 35, ovaries of adult androgenized females showed only aged and no mature interstitial cells. Androgenization on day 10 caused the development of aged interstitial cells on day 14, but adult ovaries were normal. Long lasting postnatal estrogenization (estradiol dipropionate for four postnatal weeks) caused in developing and adult ovaries a lack of interstitial cell development beyond the immature state. Immature interstitial cells were characterized by a small size (< or = 7 microm) and a lack of AR, ER and LHR expression. Because the critical window for steroid-induced sterility coincides with the termination of immune adaptation, we also investigated distribution of mesenchymal cells (Thy-1 mast cells and pericytes, ED1 monocyte-derived cells, CD8 T cells, and cells expressing OX-62 of dendritic cells) in developing and adult ovaries. Developing ovaries of normal, androgenized and estrogenized females were populated by similar mesenchymal cells, regardless of differences in the state of differentiation of interstitial cells. However, mesenchymal cells in adult ovaries showed distinct behavior. In normal adult ovaries, differentiation of mature interstitial cells was accompanied by differentiation of mesenchymal cells. Aged interstitial cells in ovaries of androgenized rats showed precipitous degeneration of resident mesenchymal cells. Immature interstitial cells in ovaries of estrogenized rats showed a lack of differentiation of resident mesenchymal cells. These observations indicate that an alteration of interstitial cell differentiation during immune adaptation toward the aged phenotype results in precipitous degeneration of resident mesenchymal cells and premature aging of ovaries in adult rats, and alteration toward immature phenotype results in a lack of differentiation of mesenchymal cells and permanent immaturity of ovaries in adult females.
Steroids 2002 Mar
PMID:Changes of ovarian interstitial cell hormone receptors and behavior of resident mesenchymal cells in developing and adult rats with steroid-induced sterility. 1185 52

When patients present with acute weight training injuries, familiarity with the demands of the activity can help physicians get the most out of the patient history. Probable risk factors for injury include errors in technique (described in a sidebar), skeletal immaturity, and anabolic steroid abuse. Common acute injuries in weight training include sprains, strains, tendon avulsions, and compartment syndrome. Possible nonmusculoskeletal problems include retinal hemorrhage, radiculopathy, and various cardiovascular complications. Treatment of acute musculoskeletal injuries varies, but usually includes sports medicine mainstays such as prompt RICE. Chronic weight training injuries will be described in part 2 of this series.
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PMID:Weight training injuries: part 1: diagnosing and managing acute conditions. 2008 81