BIOSYNTHESIS OF TESTOSTERONE AND OESTROGENS IN VITRO BY THE TESTICULAR TISSUE FROM PATIENTS WITH KLINEFELTER'S SYNDROME

1971 ◽  
Vol 66 (4) ◽  
pp. 737-744 ◽  
Author(s):  
Dinesh C. Sharma ◽  
J. Lester Gabrilove
Keyword(s):  
Normal Control ◽  
Testicular Tissue ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Positive Form ◽  
Control Subjects ◽  
End Products ◽  
Testis Tissue

ABSTRACT Testis tissue from patients with the chromatin positive form of Klinefelter's syndrome was incubated with 17α-hydroxyprogesterone and testosterone. The ratio of oestrogen to testosterone in the end products of the incubation utilizing 17α-hydroxyprogesterone as substrate was 5 to 10 times the ratio obtained in similar investigations employing testis from normal control subjects. An increased conversion into oestrogen of testosterone utilized as substrate was also observed in the in vitro studies of testis obtained from the patients with Klinefelter's syndrome. These data lend support to the thesis that in the chromatin positive form of Klinefelter's syndrome there is an increased conversion of testosterone into oestrogen in the testis.

Plasma Inhibitory Activity against Tumour Necrosis Factor in Fulminant Hepatic Failure

1996 ◽  
Vol 90 (1) ◽  
pp. 77-80 ◽  
Author(s):  
Helen M. Keane ◽  
Nick Sheron ◽  
John Goka ◽  
Robin D. Hughes ◽  
Roger Williams
Keyword(s):  
Tumour Necrosis Factor ◽  
Normal Control ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Tumour Necrosis ◽  
Neutralization Capacity ◽  
Control Subjects ◽  
Significant Difference ◽  
Necrosis Factor

1. Soluble tumour necrosis factor receptors released into the circulation inhibit the effects of excess tumour necrosis factor-α and represent an important protective response. 2. In this study we have measured the levels of tumour necrosis factor and soluble tumour necrosis factor receptors p55 and p75 in the plasma of 10 patients with fulminant hepatic failure and 10 healthy control subjects. The capacity of the plasmas at varying dilutions to inhibit the biological activity of 1000 pg/ml of recombinant tumour necrosis factor in a tumour necrosis factor cytotoxicity assay in vitro was also determined. 3. The mean plasma levels of tumour necrosis factor in patients with fulminant hepatic failure (48.4 ± 10.9 pg/ml) were significantly increased compared with normal control subjects (6.1 ± 1.04 pg/ml, P < 0.01). Plasma soluble tumour necrosis factor receptors p55 and p75 were also significantly elevated in patients with fulminant hepatic failure (18.16 ± 9.94 ng/ml and 16.06 ± 9.93 ng/ml respectively) when compared with normal control subjects (1.28 ± 0.24 ng/ml and 1.62 ± 0.91 ng/ml, P < 0.001). 4. Fulminant hepatic failure plasma had a much lower capacity to inhibit tumour necrosis factor bioactivity in vitro, with a statistically significant difference between the inhibitory capacity of the fulminant hepatic failure and normal plasma seen at plasma dilutions of 1:5 and 1:20 (P < 0.05). 5. The reduced tumour necrosis factor neutralization capacity observed in fulminant hepatic failure, despite the increased levels of soluble tumour necrosis factor receptors, suggests enhanced susceptibility to the potential deleterious effects of tumour necrosis factor in fulminant hepatic failure.

In Vitro Cell-Mediated Immunologic Assay for Cow's Milk Allergy

PEDIATRICS ◽  
1980 ◽  
Vol 66 (3) ◽  
pp. 399-402
Author(s):  
Azaria Ashkenazi ◽  
Stanley Levin ◽  
Dalia Idar ◽  
Ayala Or ◽  
Ian Rosenberg ◽  
...  
Keyword(s):  
Normal Control ◽  
Acute Gastroenteritis ◽  
Milk Protein ◽  
Cow’S Milk ◽  
Milk Allergy ◽  
Cow's Milk ◽  
Control Subjects ◽  
Β Lactoglobulin ◽  
In Infants And Children

The production of a lymphokine, the leukocyte-migration-inhibition factor (LIF), by peripheral blood lymphocytes in response to an in vitro challenge with bovine β-lactoglobulin was assayed in infants and children suspected of having allergy to cow's milk protein. of the patients studied, 24 had cow's milk allergy, 24 were normal control subjects, 18 had recovered from milk allergy, 10 were newborns, and 10 were babies suffering from acute gastroenteritis. All patients with milk allergy demonstrated significant LIF production in response to β-lactoglobulin (23.5% ± 6.4%). In the normal control subjects, LIF was 3.1% ± 4.3% (P &lt; .0005). Only two of the 24 control subjects and two of the ten newborns had high-normal values bordering on the positive. None of the ten babies with acute gastroenteritis gave a positive response. Most of the children who had recovered from milk allergy and were ingesting cow's milk had negative assays. This cell-mediated immune assay is shown to be a reliable test for the diagnosis of sensitivity to milk protein in infants and children, and for determining dietary treatment and when this treatment can be safely terminated. In most cases, its use should eliminate the need for the potentially dangerous and ethically questionable provocation test, as well as the need for repeated intestinal biopsies.

FAMILIAL CONGENITAL MUSCULAR DYSTROPHY WITH GONADAL DYSGENESIS

1957 ◽  
Vol 24 (3_Suppl) ◽  
pp. S203 ◽  
Author(s):  
H. H. Bassee
Keyword(s):  
Congenital Muscular Dystrophy ◽  
Clinical Signs ◽  
Testicular Tissue ◽  
Pubic Hair ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Medical Department ◽  
Internal Genitalia ◽  
Embryonic Life ◽  
Ovarian Agenesis

Abstract In the medical department, Hammerfest Hospital, seven individuals in one family were observed, suffering from cataract and generalized weakness in the striated musculature. Five of the patients were under ten years of age. The two eldest ones were sister and brother, 22 and 26 years of age, respectively. The woman could hardly walk even with support. She had clinical signs of ovarian agenesis, increased urinary excretion of gonadotrophic hormones, and high tolerance to insulin. The diagnosis was verified by laparotomy demonstrating thin, white, fibrous ovaries and infantile internal genitalia. The brother could hardly walk, had fairly long extremities, cubitus valgus, and widely separated nipples. The pubic hair presented a feminine appearance and the testicles were infantile and soft. No increase in urinary gonadotrophic hormones were found. The amount of neutral 17-ketosteroids was low and the output of oestrogens increased in urine. The histological examination of testicular tissue showed a thick, fibrous capsule and scanty testicular canals with a few Sertolian cells. Most of the preparation, however, merely consisted of a hyaline substance. In the vascular stroma were seen large heaps of Leydig cells, similar to what is seen in Klinefelter's syndrome. The ovarian agenesis may either have been caused by a virus infection during early embryonic life or be due to heredity. The latter suggestion is supported by the presentation of two sibs with ovarian agenesis and Klinefelter's syndrome.

OESTRADIOL-17β AND TESTOSTERONE IN RAT TESTIS TISSUE: EFFECT OF GONADO-TROPHINS, LOCALIZATION AND PRODUCTION IN VITRO

1974 ◽  
Vol 60 (3) ◽  
pp. 409-419 ◽  
Author(s):  
F. H. de JONG ◽  
A. H. HEY ◽  
H. J. van der MOLEN
Keyword(s):  
Intravenous Injection ◽  
Testicular Tissue ◽  
Prolonged Treatment ◽  
Seminiferous Tubules ◽  
Interstitial Tissue ◽  
Tissue Concentrations ◽  
Hypophysectomized Rats ◽  
Trophic Hormone ◽  
Testis Tissue

SUMMARY Concentrations of oestradiol-17β and testosterone were estimated in testicular tissue from intact and hypophysectomized rats. Within 30 min after intravenous injection of human chorionic gonadotrophin (HCG) or follicle-stimulating hormone (FSH) to intact animals the tissue concentrations of both steroids were not significantly changed. Prolonged s.c. administration of HCG (5 days) caused an increase in the tissue levels of both steroids, which was further increased when the prolonged treatment was followed by an intravenous injection with this trophic hormone. FSH had no influence on tissue concentrations of oestradiol-17β or testosterone in hypophysectomized rats. Assay of separated seminiferous tubules and interstitial tissue indicated that oestradiol-17β and testosterone were mainly localized in the interstitial tissue. Incubations of these constituents showed that oestradiol-17β was produced in the seminiferous tubules, while testosterone was produced in the interstitial compartment.

In vitro analysis of the proliferative potential of T cells from patients with brain tumor: glioma-associated immunosuppression unrelated to intrinsic cellular defect

1992 ◽  
Vol 76 (2) ◽  
pp. 251-260 ◽  
Author(s):  
Daniel W. McVicar ◽  
Donna F. Davis ◽  
Randall E. Merchant
Keyword(s):  
T Cells ◽  
Brain Tumor ◽  
T Cell ◽  
Normal Control ◽  
Phorbol Ester ◽  
Cell Populations ◽  
Glial Tumors ◽  
Control Subjects ◽  
Steroid Dependent

✓ Patients harboring a malignant brain tumor have been described as being highly immunosuppressed, as evidenced by reduced numbers of T cells and the decreased ability of their lymphocytes to produce interleukin-2 (IL-2). In order to determine whether an intrinsic abnormality exists in the T lymphocytes of glioma patients and to evaluate what role corticosteroids may play in glioma-associated immunosuppression, in vitro T cell proliferative function in the presence of recombinant IL-2 (rIL-2) was examined in age-matched groups of normal control subjects, steroid-free patients with glial tumors, steroid-dependent patients with glial tumors, and steroid-dependent patients with nonglial cerebral tumors. The results demonstrated that, when enriched T cell populations of all brain-tumor patients were stimulated with rIL-2 and phytohemagglutinin (PHA), there were no statistically significant differences between any groups. In contrast, when T cell populations were stimulated with mitogenic combinations of phorbol ester, calcium ionophore, and rIL-2, those from steroid-dependent patients with glial tumors had a significantly lower response than those from normal control subjects, suggesting that a population of T cells capable of responding to phorbol ester/ionomycin and not PHA stimulation is inhibited by corticosteroid therapy in glioma patients. In addition, T cells of four brain-tumor patient/age-matched control subject pairs were stimulated with either phorbol ester/ionomycin or PHA for 24 hours; three of the four patients expressed low-affinity IL-2 receptor levels as high or higher than their respective control subjects, suggesting that IL-2 receptor expression in these patients may be quantitatively normal once the T cell number is corrected. Taken together, these results show that the decreased PHA responsiveness that has been previously reported in lymphocytes of glioma patients is not due to a cellular abnormality within the potentially responsive cells, but rather reflects the reduced proportion of T cells within their peripheral blood which, as a consequence, reduces the level of IL-2 production attained upon activation.

THE EFFECT OF OESTROGEN ADMINISTRATION ON PLASMA TESTOSTERONE, FSH AND LH LEVELS IN PATIENTS WITH KLINEFELTER'S SYNDROME AND NORMAL MEN

1974 ◽  
Vol 77 (4) ◽  
pp. 765-783 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
R. M. Lequin ◽  
Th. J. Benraad
Keyword(s):  
Normal Subjects ◽  
Plasma Testosterone ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Testosterone Levels ◽  
Control Subjects ◽  
Dose Dependent Decrease ◽  
Normal Males ◽  
Normal Men ◽  
Dose Dependent

ABSTRACT In 6 eugonadal males and 6 patients with Klinefelter's syndrome the effect of increasing amounts of ethinyloestradiol (EE) (15, 30 and 150 μg daily for 7 days) on plasma levels of LH, FSH and testosterone was studied. Control levels of LH and FSH in the Klinefelter patients were significantly higher than in the normal males, whereas plasma testosterone levels were significantly lower. In 3 of the 6 Klinefelter patients plasma gonadotrophin levels were clearly elevated despite normal plasma testosterone concentrations. After EE administration a dose-dependent decrease of plasma FSH and testosterone levels was observed in both the control subjects and the Klinefelter patients, whereas the LH decrease was dose-dependent in the Klinefelter patients, but not however, in the eugonadal males. Despite significant testosterone suppression plasma LH and FSH levels in the Klinefelter patients remained supranormal when compared with the levels of the control subjects. Amounts of EE, roughly equivalent to the physiological oestrogen production (15 μg of EE daily) in men, decreased plasma LH and testosterone levels in the normal males, not however, in the Klinefelter patients. The suppression of plasma testosterone by EE in both the normal subjects and the Klinefelter patients could readily be overcome by exogenous gonadotrophin administration, favouring the concept that the EE induced testosterone decrease is predominantly gonadotrophin mediated. It is concluded that small amounts of oestrogens play a role in the pituitary-gonadal axis in normal males. Although higher doses are needed to modulate this axis in Klinefelter's syndrome, the hypothalamic-pituitary-gonadal feedback in this disorder is still operative, though at a higher setting.

SUGGESTION OF ABNORMAL TESTICULAR STEROIDOGENESIS IN SOME OLIGOSPERMIC MEN

1978 ◽  
Vol 87 (2) ◽  
pp. 400-412 ◽  
Author(s):  
Luis J. Rodriguez-Rigau ◽  
David B. Weiss ◽  
Keith D. Smith ◽  
Emil Steinberger
Keyword(s):  
Normal Control ◽  
Normal Volunteer ◽  
Testicular Biopsy ◽  
Testicular Tissue ◽  
Biosynthetic Activity ◽  
Testicular Steroidogenesis ◽  
17 Hydroxyprogesterone ◽  
Tissue Specimens ◽  
Steroid Dehydrogenase

ABSTRACT Androgen biosynthesis in the testis may be analyzed in some detail by means of techniques of in vitro incubation of small testicular biopsy specimens with suitable radiolabelled precursors. Sixty-six tissue specimens from 33 patients who underwent bilateral testicular biopsies because of infertility were incubated in vitro with [3H]pregnenolone in order to investigate the possibility of abnormalities in their steroid biosynthetic activity. As a normal control, testicular tissue obtained by testicular biopsy from a young normal volunteer was used. The distribution of metabolites in the incubates of testes from 8 infertile men differed greatly from the remaining 25 patients and the normal control. The major steroids formed from pregnenolone by the testes of those 8 men were 17-hydroxypregnenolone, dehydroepiandrosterone, 20α-dihydropregnenolone and 20α-dihydro-17-hydroxypregnenolone. Very small amounts of Δ4-3 oxo products (progesterone, 17-hydroxyprogesterone, androstenedione and testosterone) were formed suggesting a deficiency of 3β-hydroxy-steroid-dehydrogenase activity in the testes of these 8 men, possibly related to the derangement of their spermatogenic function.

IN-VITRO SYNTHESIS OF ANDROGEN FROM PREGNENOLONE IN THE TESTES OF THE GOAT (CAPRA HIRCUS) AND IDENTIFICATION OF 5-PREGNENE-3β,17α,20α-TRIOL AS AN INTERMEDIATE IN THE METABOLIC PATHWAY OF PREGNENOLONE

1980 ◽  
Vol 84 (3) ◽  
pp. 381-390 ◽  
Author(s):  
MAKOTO MORI ◽  
SACHIKO MATSUKURA ◽  
KAZUHIKO KAWAKURA ◽  
BUN-ICHI TAMAOKI
Keyword(s):  
Time Course ◽  
Microsomal Fraction ◽  
Testicular Tissue ◽  
The Other ◽  
Capra Hircus ◽  
Cytosol Fraction ◽  
In Vitro Synthesis ◽  
Intermediary Metabolite ◽  
End Products

When [4–14C]pregnenolone was aerobically incubated in vitro in the presence of NAD+ and NADPH with cell-free homogenates of testicular tissue of adult domestic goats (Capra hircus), progesterone, 17α-hydroxypregnenolone, 17α-hydroxyprogesterone, 17α,20α-dihydroxy-4-pregnen-3-one, dehydroepiandrosterone, androstenedione and testosterone were identified as its known metabolites. Time-course studies on this metabolism showed that the production of 17α,20α-dihydroxy-4-pregnen-3-one and testosterone constantly increased up to the end of incubation, suggesting that these are both end-products of pregnenolone metabolism in this system. The other metabolites behaved as intermediates and were ultimately converted, in part, to testosterone by the testicular homogenates, indicating that testosterone was synthesized through both 4-ene and 5-ene-pathways. Furthermore, besides these metabolites, 5-pregnene-3β,17α,20α-triol was also identified as an intermediary metabolite, formed from pregnenolone through 17α-hydroxypregnenolone in the presence of NADPH, and further convertible into 17α,20α-dihydroxy-4-pregnen-3-one by the microsomal fraction and into 17α-hydroxypregnenolone by the cytosol fraction in the presence of NAD+ and NADP It was not, however, significantly transformed into C19-steroids. Furthermore, 17α,20α-dihydroxy-4-pregnen-3-one, which was formed either from 5-pregnene-3β,17α,20α-triol or from 17α-hydroxyprogesterone, remained almost unchanged without conversion to C19-steroids when incubated with the caprine testicular homogenates.

URINARY TESTOSTERONE, OESTROGEN PRODUCTION RATE AND URINARY OESTROGEN IN CHROMATIN POSITIVE KLINEFELTER'S SYNDROME

1970 ◽  
Vol 63 (3) ◽  
pp. 499-504 ◽  
Author(s):  
J. L. Gabrilove ◽  
G. L. Nicolis ◽  
R. U. Hausknecht
Keyword(s):  
Urinary Excretion ◽  
Production Rate ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Positive Form

ABSTRACT In seven patients with the chromatin positive form of Klinefelter's syndrome, the urinary excretion of testosterone was markedly decreased. In contrast the oestrogen production rate and the urinary excretion of oestrogen were normal. These findings indicate that there is an altered conversion of androgen to oestrogen in patients with this disorder.

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