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F Dray

Publications and source records attributed to F Dray.

At least 91 records · Page 5Linked to original sources
PubMed1982

Specific binding of [3H]prostaglandin E2 to rat brain membranes and synaptosomes.

There is saturable, reversible and specific binding for [3H]prostaglandin E2 (PGE2) to rat brain membranes. This binding is of high affinity, selectively distributed with a maximum in the hypothalamus, the amygdala and the posterior pituitary, and is associated subcellularly with the synaptosomal fraction. This specific PGE2 binding has the characteristics expected for receptors, so opening new perspectives which might clarify the role of PGs in the brain.

Amygdala↗
PubMed1982

In vitro prostaglandin synthesis by various rat renal preparations.

Prostaglandin synthesis by eight different structures from the rat kidney (while cortex, cortical tubules, glomeruli, outer medulla, papilla, glomerular cultured epithelial and mesangial cells, cultured interstitial medullary cells) was measured in vitro after incubation with [14C] arachidonic acid using high-performance liquid chromatography followed by RIA with four specific anti-prostaglandin antibodies (prostaglandin E2, prostaglandin F2 alpha, 6 keto-prostaglandin F1 alpha, thromboxane B2). Prostaglandin production by the whole cortex and cortical tubules was very low. The order of abundance for isolated glomeruli was thromboxane B2 great than prostaglandin E2 greater than prostaglandin F2 alpha greater than 6 keto-prostaglandin F1 alpha. Mesangial cells synthesized prostaglandin E2 at a markedly high rate, in decreasing order: prostaglandin F2 alpha, thromboxane B2 and 6 keto-prostaglandin F1 alpha. The same order of abundance was observed for epithelial cells. The papilla synthesized essentially prostaglandin E2 and prostaglandin F2 alpha, whereas the main product for the outer medullar was 6 keto-prostaglandin F1 alpha. Cultured interstitial cells synthesized mainly prostaglandin E2 and to a lesser extent prostaglandin F2 alpha. Unidentified peaks eluting between 6 keto-prostaglandin F1 alpha and thromboxane B2 were also observed chiefly with glomeruli but they were absent with the medullary preparations. They disappeared after incubation with indomethacin or aspirin and represented for glomeruli the greatest percentage of conversion of [14C] arachidonic acid. These results show that the prostanoid profile varies markedly with the different regions and cells of the rat kidney.

Animals↗
PubMed1982

Biotin-responsive immunoregulatory dysfunction in multiple carboxylase deficiency.

The immunoregulatory system has recently been shown to require prostaglandins (PG) for its activation in man. We report here an impairment of immunoregulatory function, due to defective PGE monocytic production, in a 12-month-old boy with multiple carboxylase deficiency (MCD). The abnormal immune-response was corrected in vitro by adding PGE to the medium. Moreover, PGE deficiency and immunoregulatory dysfunction responded to biotin administration in vivo. It is suggested that the PGE deficiency in MCD could result from an impaired activity of a biotin enzyme, acetyl CoA carboxylase, since the product of this enzyme reaction, malonyl CoA, is required for prostaglandin synthesis.

Biotin↗
PubMed1982

The in vitro production of prostanoids by cultured bovine articular chondrocytes.

Bovine articular chondrocytes, cultured as cell suspensions and monolayers, produced prostaglandin (PG) E2 and PGI2 (assayed as 6 keto PGF1 alpha), rather less PGF2 alpha and irregular quantities of thromboxane (Tx) B2. Addition of foetal calf serum to the medium greatly stimulated PG production (a sixfold increase in PGE2 and a twofold increase in 6 keto PGF1 alpha). Prostanoid production by cell suspensions grown in serum-free medium generally plateaued after 24 hours. In the presence of 20% foetal calf serum, prostanoid production in long-term monolayer cultures increased during the first 6 days of culture. Levels of PGE2 and TxB2 then decreased, while 6 keto PGF1 alpha levels remained high. Indomethacin (10(-6)M) inhibited chondrocyte PG production both in the presence and absence of added arachidonic acid (10(-4)M). Prostanoids produced by chondrocytes may play a role in the modulation of cartilage metabolism in vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Respective roles and interactions of T-lymphocyte and PGE2-mediated monocyte suppressive activities in human newborns and mothers at the time of delivery.

Recently the concept of a poorly functional humoral immune response in the newborn was proposed. Data have been presented indicating that the impaired newborn B cell maturation, as shown in vitro in a pokeweed mitogen-induced B cell maturation system, is due both to an immaturity of lymphocyte subsets and to an increased suppressive T activity. In the present work, we present evidence that there exists a predominance of a naturally occurring T lymphocyte suppressive activity in the cord blood in that the removal of the suppressive activity by irradiation allows a normal maturation of newborn B cells. Such normal maturation of newborn B cells can also be obtained using mixed cultures of adult T cells and newborn B cells. Newborn suppressor T cells belong to both EA gamma (+) and EA gamma (-) fractions, and it is not known whether these two groups do or do not belong to different subsets. The PGE2-dependent monocyte suppressive activity does not play any role in the suppression observed in newborns since newborn monocytes are poorly suppressive and since they produce a smaller amount of PGE2 than adult monocytes. Some observations suggest, on the contrary, that the suppressive T lymphocytes can regulate the level of the PGE2-dependent monocyte suppressive activity. It should be noticed that similar observations about T lymphocyte and PGE2-dependent monocyte suppressive activities have been made at the same time using mothers' cells. These observations suggest the possibility that such changes in B cell immune regulation may result from an interaction between maternal and fetal lymphoid cells.

B-Lymphocytes↗
PubMed1982

Use of an anti-human leukocyte interferon monoclonal antibody for the purification and radioimmunoassay of human alpha interferon.

Mouse monoclonal antibody directed against human leukocyte alpha interferon (IFN-alpha) was coupled to Sepharose and used as an immunoadsorbent to purify human IFN-alpha. Leukocyte and lymphoblastoid (Namalva) IFNs were retained by the immunoadsorbent with a specificity of 80 to 100% and 40 to 60%, respectively. Human IFN-beta or -gamma and mouse IFN were not retained. The purified IFN-alpha retained its antiviral and anticellular properties as well as its ability to induce the 2-5A synthetase in human cells with a specific activity similar to that of the crude IFN. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of radioactively labeled IFN showed that it consisted of several proteins in the molecular weight range of 17,000 to 27,000. 125I-labeled IFN-alpha with a high specific activity (2,000 Ci/mmol) was used in a radioimmunoassay for the titration of IFN-alpha.

Antibodies, Monoclonal↗
PubMed1982

Origin of prostaglandins in human semen.

The prostaglandins, PGE-1, PGE-2, PGF-1 alpha, PGF-2 alpha, 19-OH-PGE-(1 + 2), 19-OH-PGF-alpha were estimated by RIA in the semen of (a) normal men of proven fertility (total semen or split ejaculate); (b) men 1 year after vasectomy; and (c) men with agenesia of the vas deferens and seminal vesicles. PG concentrations in the semen of vasectomized men were largely within the normal ranges. In men with agenesia of the vas deferens and seminal vesicles, PG concentrations were 10(2) - 10(5)-fold less than that measured in normal subjects. The patterns of 19-OH-PGs and PGF-alpha in the five fractions of a split ejaculate followed in general the fructose profile. These data suggest that prostaglandins mostly originate in the seminal vesicles.

Alprostadil↗
PubMed1982

Lack of prostaglandin E2-mediated monocyte suppressive activity in newborn and mothers.

An excess of adult blood adherent cells (monocytes) inhibits mitogen, antigen and allogeneic cell-induced lymphocyte proliferations. This inhibition is dependent on the number of the adherent monocytes in the cultures and is substantially reduced (by 60%) by indomethacin or anti-PGE2 antiserum. Newborn monocytes exert only a weak inhibitory effect and produce about eight times less PGE2 than adult monocytes. The production of PGE2 and the suppression can be induced by incubating newborn monocytes with mixed leucocyte culture supernatants. Both monocytes from mothers at the time of delivery and from newborn infants, usually exert a poor suppressive activity related to a low production of PGE2. We strongly suggest that the expression of the PGE2-mediated suppression by monocytes is under the control of activated short-lived suppressor lymphocytes.

Adult↗
PubMed1982

Very low levels of 6-keto-prostaglandin F1 alpha in human plasma.

Two stable derivatives of PGI2, its nonenzymatic hydrolysis product (6-keto-PGF1 alpha) and an enzymatic metabolite (6, 15-diketo-PGF1 alpha), were determined in human plasma and urine. These compounds were measured by RIA after separation on rp-HPLC. Previous purification of the samples on rp-HPLC markedly enhanced the specificity of the RIA determinations of those compounds in plasma and urine. The PGI2 derivative 6-keto-PGF1 alpha was detected in both plasma (4.7 +/- 3.2 pg/ml, mean +/- S.D., n=34) and urine (166 +/- 61 pg/ml, n=9). No gender differences of the plasma or urinary levels of 6-keto-PGF1 alpha were found. The PGI2 metabolite 6,15-diketo-PGF1 alpha was not measurable in plasma or urine (less than 1 and less than 10 pg/ml, respectively, n=4). Thus this compound may not be a major endogenous metabolite of PGI2 in man. When [3H]PGI2 was added to citrated blood immediately after venipuncture, it was recovered entirely as [3H]6-keto-PGF1 alpha after rp-HPLC. Therefore any circulating PGI2 would be measured as 6-keto-PGF1 alpha by our method. The results obtained suggest that PGI2 could be present in human venous blood under physiological conditions, but only in very low concentrations. (J Lab Clin Med 99:388, 1982.)

6-Ketoprostaglandin F1 alpha↗
PubMed1982

[The bioavailability of natural progesterone given by mouth. Measurement of steroid concentrations in plasma, endometrium and breast tissue].

The effects of two galenic processes (micronisation and addition of oil) on the bioavailability of progesterone administrated orally were studied. After ingestion of progesterone (200 mg), mean plasma progesterone rapidly rises up to the 2nd hour and reaches levels of the normal luteal phase (12.6 +/- 2.6 ng/mg). It then decreases progressively up to the 8th hour. Daily administration of progesterone (300 mg) for 8 days significantly increases the endometrial concentration of the steroid (18.3 +/- 2.9 ng/ml) and efficiently corrects the tissular hormone deficiency. The breast tissue uptakes and concentrates equally progesterone. After oral administration of the natural hormone, progesterone concentrations are considerably increased in the three tissue compartments studied (normal glands: 25.0 +/- 9.7 ng/g; benign tumor: 38.0 +/- 9.1 ng/g; adipose tissue: 160.2 +/- 65.4 ng/g). These pharmaco-kinetic results correspond to the requirements of general substitutive hormone therapy. They justify the use of natural oral progesterone therapy, providing the amount given is modified according to immediate clinical tolerance.

Administration, Oral↗
PubMed1981

Radioimmunoassay of prostaglandins in the semen of fertile men.

Specific antisera and iodinated tracers, as well as strict conditions of sample storage PG extraction and purification, were used to estimate prostaglandins (microgram/ml) in the semen of fertile men: 19-OH-PGE (1 + 2) (350), 19-OH-PGF-alpha (22), PGE-2 (15), PGE-1 (6.2), PGF-2 alpha (2.3), PGF-1 alpha (1.3), 6-keto-PGF-1 alpha (less than 1), PGD-2, 13,14-dihydro-15-keto-PGF alpha and TXB-2 (less than 0.1). Only PGE-2 (50 pg/ml) was detectable in rat seminal fluid.

Alprostadil↗
PubMed1981

Importance of perinatal testosterone in sexual differentiation in the male rat.

Testosterone secretion in the male rat was high during the late fetal and immediate postnatal periods. It then showed a rapid decrease 3h after birth and remained low until puberty. Male rats from mothers given daily injections of an antibody to testosterone during the week before delivery displayed an LH peak when they were adult, orchidectomized and implanted with oestradiol. However, the amplitude of the peak was far smaller than in female rats from the same mothers treated in the same manner. Thus, the critical period during which testosterone triggers hypothalamic sexual differentiation is very close to birth, possibly starting at the end of the fetal period.

Animals↗