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Biomedical subjects

A Ganguly

Publications and source records attributed to A Ganguly.

At least 127 records · Page 7Linked to original sources
PubMed1977

Effect of bedrest on circadian rhythms of plasma renin, aldosterone, and cortisol.

Previous studies of normal men after 5 d of bedrest showed that circulatory instability on head-up tilt or standing is preceded by increased plasma renin activity (PRA) at bedrest. In the present study, the circadian rhythms of PRA, aldosterone, and cortisol have been observed in five normal men on a constant diet. In ambulatory controls, PRA and aldosterone increased normally after standing. On the third morning of bedrest, PRA was higher than before, and at noon, PRA was higher than in standing controls. The nocturnal peaks of PRA resulting from episodic renin secretion during sleep were higher after bedrest. Plasma aldosterone was also increased by bedrest. The findings are compatible with the theory that intermittent beta-adrenergic nerve activity during sleep is increased after bedrest, but other factors, such as loss of body sodium and a lower plasma volume, may also be involved.

Adult↗
PubMed1976

Cushing's syndrome in a patient with an empty sella turcica and a microadenoma of the adenohypophysis.

A patient with Cushing's syndrome and an empty sella turcica is presented. A pituitary microadenoma was removed by the transsphenoidal approach. The Cushing's syndrome was alleviated, and the function of the other pituitary trophic hormones has remained normal eight months after surgery. It is emphasized that an empty sella turcica does not rule out a pituitary tumor. The therapeutic implications are discussed.

Adenoma↗
PubMedDate not supplied

Aberrant mRNA splicing associated with coding region mutations in children with carnitine-acylcarnitine translocase deficiency.

This report describes three infants with genetic defects of carnitine-acylcarnitine translocase (CACT), an inner mitochondrial membrane carrier that is essential for long-chain fatty acid oxidation. Two of the patients were of European and Chinese origin; the third was from consanguineous Turkish parents. CACT activity was totally deficient in cultured skin fibroblasts from all three patients. Patient 1 was heterozygous for a paternal frameshift mutation (120 del T in exon 1) and a maternal lariat branch point mutation (-10 T --> G in intron 2). Patient 2 was heterozygous for the same lariat branch point (-10T --> G intron 2) mutation, derived from the father, and a maternal frameshift mutation (362 del G in exon 3). Patient 3 was homozygous for a frameshift mutation (306 del C in exon 3). All of the three frameshift mutations give rise to the same stop codon at amino acid residue 127 which is predicted to cause premature protein truncation. In addition, cDNA transcript analysis showed that these coding sequence mutations also increase the amount of aberrant mRNA splicing and exon skipping at distances up to 7.7 kb nucleotides from mutation sites. The data suggest that the stability of mRNA transcripts is decreased or the frequency of aberrant splicing is increased in the presence of CACT coding sequence mutations. These results confirm that CACT is the genetic locus of the recessive mutations responsible for the fatal defects of fatty acid metabolism previously associated with deficiency of translocase activity in these three cases.

Carnitine Acyltransferases↗
PubMedDate not supplied

Impaired aldosterone secretion from dispersed adrenal capsular cells of chronically alpha-MSH-treated rats.

To investigate the chronic effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on aldosterone secretion, synthetic alpha-MSH (8 micrograms/day) was infused in Sprague-Dawley rats by miniosmotic pumps for 5 days. Saline was infused in equivalent volume for 5 days using the same type of pumps in the control group of rats. Aldosterone secretion from the capsular cells of the two groups was examined in the basal state and in response to various stimuli of aldosterone secretion. Aldosterone secretion in vitro from the alpha-MSH-treated rats was significantly impaired in response to all stimuli tested including cyclic AMP, suggesting an intracellular defect in aldosterone synthesis in that group. These results are similar to those observed after chronic adrenocorticotropin administration.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMedDate not supplied

Fibulin-2 exhibits high degree of variability, but no structural changes concordant with abdominal aortic aneurysms.

We used conformation sensitive gel electrophoresis and direct sequencing of PCR products to screen for mutations in the cDNA for fibulin-2, an extracellular matrix protein, from 11 patients with abdominal aortic aneurysms and two controls. When compared with the published reference sequence, a total of 14 single-base sequence variations were detected. Seven of the changes were neutral in that they did not result in an amino acid substitution. There were five missense changes at sites not conserved between human and mouse, and two missense changes at sites conserved between human and mouse. All but two of the sequence variants studied were also present in an additional set of 102 control alleles analyzed. One of these two changes was a missense mutation, but it did not segregate with abdominal aortic aneurysms in the family, whilst the other change was neutral. In conclusion, fibulin-2 has a large number of sequence variations in comparison with our previous analyses of type III collagen, and these variations will be useful in association studies. There was an excellent overall agreement between direct sequencing of PCR-products and conformation sensitive gel electrophoresis.

Adult↗
PubMedDate not supplied

Adrenal steroid responses to ACTH in glucocorticoid-suppressible aldosteronism.

To investigate adrenal responses to adrenocorticotrophin (ACTH), we infused graded doses of ACTH (1.25 to 20.0 mIU/30 minutes) in normal subjects, patients with low-renin essential hypertension (LREH), primary aldosteronism (PA), and glucocorticoid-suppressible hyperaldosteronism (GSH). Plasma aldosterone, cortisol, corticosterone, and 18-hydroxycorticosterone were measured. The results revealed a greater increase in the plasma aldosterone and 18-hydroxycorticosterone levels evoked by ACTH in the GSH group than in any other group, which suggested enhanced responsiveness of the aldosterone-producing cells to ACTH and a probable adrenal abnormality.

18-Hydroxycorticosterone↗
PubMedDate not supplied

GnRH antagonist treatment affects nuclear size and membrane associated indentations in rat Leydig cells.

In semi-thin preparations of rat testis treated with GnRH antagonist (Ac-D2Nal 1, D4ClPhe 2, DTrp 3, DArg 6, DAla 10; GnRH code- 103-289-10, National Institutes of Health, USA) for a period of 5 weeks, Leydig cells showed a reduction of 18% in the mean nuclear area as compared to the controls. The number of cells with nuclear membrane indentations increased by more than 40% as compared to the controls. Nuclear condensation was evident in the form of dark, electron-dense patches of heterochromatin present all along the rough, uneven boundary of the nuclear wall. In some cells, indentations in the nucleus appeared in the form of deep grooves extending into the core of the nucleus. Shrinkage in the cytoplasm of the cells was very much apparent. Circulating levels of LH and testosterone were very low. LH decreased from 29.6 +/- 2.9 ng/ml to 0.55 +/- 0.018 ng/ml and testosterone from 7.8 +/- .29 ng/ml to 0.5 +/- .02 ng/ml. The mean nuclear area of Leydig cells from other groups of rats treated with estradiol 17-beta (1 microgram/rat per day), testosterone (60 micrograms/rat per day) or combinations of testosterone and estradiol or GnRH antagonist and testosterone in the same regime and for the same period remained unaltered. On the other hand, cells appeared normal when testosterone was supplemented (60 micrograms/rat/day) in rats treated with GnRH antagonist. The mean nuclear area of the Leydig cells recovered significantly (p less than 0.001), but was not completely restored.

Animals↗
PubMedDate not supplied

Adverse effects of chronic GnRH antagonist administration on seminiferous epithelium in adult rats.

Seminiferous epithelium in adult rats was studied by light and electron microscopy after 5 weeks of chronic administration of GnRH antagonist (Ac-D2 Nal 1, D4ClPhe 2, DTrp 3, DArg 6, DAla 10; GnRH code-103-289-10, National Institutes of Health, USA). In these rats, the epithelium showed significant accumulation of vacuoles in more than 80% of the tubules, along with germ cell degeneration and nuclear pyknosis. Disruption in the process of spermatogenesis was also very much evident. In most of the tubules studied (greater than 90%), germ cell development was arrested beyond the pachytene spermatocyte stages. The vacuoles in the seminiferous epithelium were different sizes and when magnified were seen to consist of a thickened outer margin of solid nonfibrous coat within the Sertoli cell cytoplasm. Associated changes in the interstitium showed increased intertubular space but no inflammatory type of response. In actual cell counts, the decrease in the average number of macrophages was 32% and in Leydig cells 23%, while the total number of all types of cells in the interstitium was 30% less than that of the controls. Following the treatment, weights of testis, epididymis, seminal vesicle, and ventral prostate were drastically reduced. Rats treated with testosterone supplementation (60 micrograms/rat day) to GnRH antagonist recovered testicular and epididymal weights to approximately 57% and seminal vesicle and ventral prostate weights by 82.9 and 84%, respectively. Normalcy returned to the tubular epithelium and the interstitial cell counts were restored to original levels.

Animals↗