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Biomedical subjects

J C Porter

Publications and source records attributed to J C Porter.

At least 163 records · Page 9Linked to original sources
PubMed1978

Clinical and endocrinological evaluation of patients with congenital microphallus.

Eight patients with congenital microphallus were investigated. Plasma luteinizing hormone, follicle-stimulating hormone, testosterone and androstenedione levels were obtained in all cases. In addition, the response to the administration of human chorionic gonadotropin, luteinizing horomone-releasing hormone and adrenocorticotropic hormone, the assessment of testicular histology by electron microscopy and the measurement of dihydrotestosterone formation by preputial skin were determined in some patients. The results of these studies were compared to similar studies in 6 normal prepubertal boys, 4 boys with bilateral cryptorchidism, 1 male infant with anorchia and 1 adult with hypogonadotropic hypogonadism. The clinical and endocrinological findings in the 8 patients with microphallus can be divided into 2 distinct categories. In 5 patients the disorder is familial, gonadotropin levels are low and there is a normal response to stimulation with chorionic gonadotropin. The data are compatible with the possibility that 3 (possibly 5) of the 8 patients with microphallus have hypogonadotropic hypogonadism. In the other group the cases are sporadic, serum luteinizing hormone and follicle-stimulating hormone levels are elevated and plasma testosterone failed to increase after short-term treatment with chorionic gonadotropin. In these patients a primary testicular disorder appears to be responsible. Experimental and clinical evidence suggests that microphallus results from defective testicular function during the second and third trimesters of pregnancy, either as the result of defective gonadotropin secretion or defective androgen synthesis.

Adolescent↗
PubMed1978

Studies on the subsynaptosomal localization of luteinizing hormone-releasing hormone and thyrotropin-releasing hormone in the rat hypothalamus.

In the current investigation, subcellular particles (synaptosomes) of hypothalamic homogenates were isolated by differential centrifugation and discontinuous sucrose density gradient fractionation and found to be rich in LHRH, TRH, and the neuronal marker, norepinephrine (NE). Of the total quantity of LHRH, TRH, or NE in the nuclei-free homogenate, 52-65% was recovered in synaptosomes, whereas the cytosol, myelin/microsomes, and mitochondria contained only 1-12%. To determine the subsynaptosomal localization of LHRH and TRH, purified synaptosomes were lysed and the resulting suspensions were fractionated on discontinuous sucrose density gradients. LHRH (30-40%) was found to be localized primarily in subsynaptosomal particles which banded at sucrose densities between 0.6-1.0 M. Electron micorscopic analysis of these particles revealed the presence of dense-cored granules (70-80 nm diameter) and synaptosomal membrane remnants. Norepinephrine was found in two pools within the isolated nerve endings: 15-25% of synaptosomal NE was associated with the synaptic vesicles (45-55-nm diameter); about 40% was in the cytosol. TRH was present primarily as a soluble component of the nerve ending. No apparent association of TRH with dense-cored granules was demonstrable in this study; however, there may be some TRH in synaptic vesicles.

Animals↗
PubMed1978

Regulation by plasma lipoproteins of progesterone biosynthesis and 3-hydroxy-3-methyl glutaryl coenzyme a reductase activity in cultured human choriocarcinoma cells.

The regulation of both the activity of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG CoA) reductase [mevalonate-NADP+ oxidoreductase (CoA-acylating) EC 1.1.1.34] and the secretion of progesterone by human plasma lipoproteins has been investigated in human choriocarcinoma cells in culture. HMG CoA reductase activity was computed from the rate of formation of [14C]mevalonolactone from [14C]HMG CoA. The activity of HMG CoA reductase was expressed as nanomoles of mevalonolactone formed/min . mg solubilized cell protein. An inverse relationship was found between the presence of lipoprotein in the culture medium and the activity of HMG CoA reductase in these cells. In cells maintained in the presence of lipoprotein-enriched culture medium containing 840 micrograms cholesterol/ml, the average activity of HMG CoA reductase was 0.25 nmol/min . mg protein. After removal of lipoprotein, the activity of HMG CoA reductase increased to 1.3 nmol/min . mg protein. The average activity of HMG CoA reductase in cells maintained in lipoprotein-deficient culture medium was 1.5 nmol/min . mg protein but fell to 0.3 nmol/min . mg protein after addition of lipoprotein to the medium. When cells were maintained in the presence of lipoprotein, the rates of section of progesterone and pregnenolone into the culture medium were 2-8 times greater than the rates of secretion of these steroids by cells maintained in the absence of lipoprotein. On the basis of these results, it is concluded that lipoproteins control the rate of cholesterol biosynthesis in cultured choriocarcinoma cells by regulating the activity of HMG CoA reductase, and control the rate of synthesis of progesterone by providing the precursor, cholesterol. We suggest that progesterone synthesis by the trophoblast of the human placenta may also be regulated by the uptake of lipoprotein from maternal blood.

Cells, Cultured↗
PubMed1977

Inhibition of prostaglandin-enhanced release of LH by antiserum to luteinizing hormone releasing hormone.

Prostaglandin E2 (PGE2), PGF2alpha, PGF2beta was infused into a lateral ventricle of the brain of adult male rats, after pretreatment with normal rabbit serum (NRS) or anti-LH-RH serum, and the concentration of LH in arterial plasma was determined. I.v. administration of anti-LH-RH serum 2.5 min prior to the infusion of 2 microgram or 20 microgram of PGE2 significantly inhibited the PGE2-induced rise of plasma LH. Intraventricular infusion of 20 microgram of PGF2alpha or PGF2beta into NRS-pretreated animals caused a marked increase in the plasma LH concentration; whereas, prior i.v. administration of anti-LH-RH serum blocked the PG-induced rise in plasma LH levels. It is concluded that PGE2, PGF2alpha, and PGF2beta stimulate the release of LH primarily by enhancing the release of LH-RH.

Animals↗
PubMed1977

Relationship between luteinizing hormone releasing hormone concentration in hypophysial portal blood and luteinizing hormone release in intact, castrated, and electrochemically-stimulated rats.

The concentration of luteinizing hormone releasing hormone (LHRH) in hypophysial portal plasma was determined in pentobarbital anesthetized,intact and castrated rats of both sexes, including proestrous rats following electrochemical stimulation of the medial preoptic area (MPOA). Mean LHRH levels in portal plasma obtained between 1400--1700 h from estrous and diestrous rats and from rats ovariectomized for 8 weeks were similar and ranged from 50--55 pg/ml, but the LHRH levels in proestrous rats were less than 12 pg/ml. In addition, hypophysial portal plasma collected during 1100 to 1400 h from animals orchidectomized for 8 weeks and from intact male rats contained mean LHRH concentrations that ranged from 50--65 pg/ml and 30--35 pg/ml, respectively. Electrochemical stimulation of the MPOA in the female rat on the afternoon of proestrus resulted in a marked increase in the concentration of LHRH in portal plasma. LHRH levels in portal plasma during the 0 to 30, 30 to 60, 60 to 90, 90 to 120, and 120 to 150-min periods after electrochemical stimulation of the MPOA were 105 +/- 24.2, 61 +/- 10.8, 51 +/- 8.2, 36 +/- 5.3, and 32 +/- 4.1 pg/ml, respectively. LHRH levels in portal plasma from the unstimulated rats were not detectable (less than 12 pg/ml) in most of the animals. In another group of proestrous rats, the effect of rabbit anti-LHRH serum or normal rabbit serum (NRS) on the release of LH after electrochemical stimulation of MPOA was examined. Pretreatment of proestrous rats with anti-LHRH serum blocked the release of LH due to MPOA stimulation, whereas pretreatment with NRS did not inhibit LH release. On the basis of these findings, it is concluded that electro-chemical stimulation of the MPOA in proestrous rats increases LHRH levels in portal blood and that the enhanced secretion of LHRH stimulates the release of LH from the pituitary gland.

Animals↗