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Biomedical subjects

L R Lee

Publications and source records attributed to L R Lee.

25 records · Page 2Linked to original sources

Effects of progesterone on pulsatile luteinizing hormone (LH) secretion and LH subunit messenger ribonucleic acid during lactation in the rat.

In ovarian-intact lactating rats, removal of the suckling stimulus leads to restoration of pituitary LH beta mRNA levels and pulsatile LH secretion after 72 h, which correlates with a sharp decrease in plasma progesterone concentrations to basal levels. In contrast, in ovariectomized lactating rats, the increase in pituitary LH function is observed by 24 h after pup removal. To determine if progesterone secretion from the ovary participates in the delayed recovery of LH secretion, we treated lactating rats with the progesterone antagonist RU 486 and determined the effects on the time course of recovery of pulsatile LH secretion and LH subunit mRNA after pup removal and on pituitary responsiveness to GnRH. In ovarian-intact lactating rats treated with RU 486, pulsatile LH secretion was observed in about 40% of the rats within 24 h after pup removal (LH interpulse interval, 43.7 +/- 8.3 min) and in about 90% of the rats within 48 h after pup removal (LH interpulse interval, 46.1 +/- 3.6 min). The mean plasma LH level in the RU 486-treated rats was 10.1 +/- 2.2 ng/ml 24 h after removal of pups (control, less than 5 ng/ml) and had increased to 35.1 +/- 6.4 ng/ml 48 h after pup removal (control, 9.1 +/- 2.5 ng/ml). However, RU 486 treatment had no significant effect on LH mRNA subunit levels. To determine whether progesterone acts at the pituitary to block GnRH stimulation of LH secretion, we tested the effects of RU 486 on LH secretion in response to 2- and 5-ng pulses of GnRH. Pituitary responsiveness was tested 24 h after pup removal. We found that both doses of GnRH were effective in stimulating pulsatile LH secretion, and treatment with RU 486 had no significant effect on this response. We conclude from these studies that progesterone secretion from the ovary contributes to the inhibition of LH secretion that occurs after pup removal, since antagonizing progesterone's action resulted in an earlier restoration of pulsatile LH secretion. The increase in LH secretion occurred in the absence of any significant changes in responsiveness of the pituitary to GnRH stimulation or in LH subunit mRNA levels. Therefore, the primary site of action of progesterone would appear to be at the hypothalamus to suppress pulsatile GnRH secretion.

Animals↗

Response of food intake and body weight to estradiol in old female rats.

Changes in food intake and body weight were studied in old ovariectomized prolonged vaginal cornification female rats (27.6 +/- 3.3 (SD) months of age) implanted subcutaneously with 100%, 50% and 33% estradiol benzoate (E2)-cholestrol mixture-filled silastic capsules and were compared with similarly treated young ovariectomized female rats (4.7 +/- 0.8 months of age). Serum E2 concentration was higher in old rats than young rats in the 100% E2-filled capsule implanted group. In this group, food intake suppression by E2 was larger in old rats than in young rats. However, no age-related difference was observed, when food intake decrease was adjusted for serum E2 level by analysis of covariance. Therefore a high food intake suppression in old rats than in young rats is caused by high serum E2 concentration in old rats. Suppression of body weight increase did not show any age-related difference when adjusted for serum E2 level either.

Aging↗

Effects of septal lesion on lordosis response induced by estradiol in middle-aged and old female rats.

Long-Evans female rats were divided into three age groups: 10 young rats (5 months of age), 7 middle-aged rats (10-13 months of age) and 6 old rats (21-27 months of age). The rats were ovariectomized and immediately implanted subcutaneously with a silastic capsule filled with estradiol benzoate (E2). Lordosis response was compared in each animal before and after the septal lesion. Serum E2 levels were 197 +/- 27 pg/ml (mean +/- SEM), 192 +/- 81 pg/ml and 405 +/- 83 pg/ml in young, middle-aged and old rats respectively. When serum E2 levels were adjusted by analysis of covariance, LQ (lordosis quotient) was 42, 36 and 61 in young, middle-aged and old rats respectively before the septal lesion and 98, 68 and 88 respectively after the septal lesion. The extent of potentiation of lordosis after the septal lesion was less in middle-aged and old rats than young rats. These results indicate that an enhanced lordosis response in aged rats is partly due to high circulating E2 levels and partly due to disinhibition of the septal region on lordosis.

Aging↗

Pain relief associated with a religious visitation: a case report.

A 68-year-old black woman tolerated partial colectomy for resection of a carcinoma with minimal postoperative discomfort and without the need of any analgesia. She attributed her positive experience to the presence of protective angels. Psychologic interviews and testing revealed her to be fully in touch with reality. Her experience, as well as those of similar patients reported in the medical literature, has biological, sociocultural, and psychological components. The role of religious belief in the pain experience has received scant attention, but it constitutes a challenging area for future research.

Adenocarcinoma↗

Regional differences of neuron loss of rat brain in old age.

DNA content was measured in four areas of the brain (cerebral hemisphere, cerebellum, diencephalon, and lower brain stem) of young adult (5-month-old) and aged 24- to 30-month-old Long-Evans rats. There was no change in DNA content in all four areas in old age. The number of brain cells was counted in three areas of the brain (cerebral hemisphere, cerebellum and brain stem) with an ultrasonic separation method. In old age, there was significant loss in the total number of brain cells in the cerebellum but no cell loss in the cerebral hemisphere and the brain stem. The neuron number was significantly decreased and the glia/neuron ratio was increased in the cerebellum and cerebral hemisphere, but neither of them changed in the brain stem in old age. The cerebellum showed significantly more neuron loss than the cerebral hemisphere in old age. DNA content in individual brain cells in the cerebral hemisphere, cerebellum and brain stem does not change in old age; thus, calculation of brain cell number from DNA content in the brain of old rats is justified.

Aging↗