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J Molcho

Publications and source records attributed to J Molcho.

13 recordsLinked to original sources

Spectrophotometric determination of meconium concentration in amniotic fluid.

When a fetus is acutely distressed, for example as a result of strangulation by the umbilical cord, the bowel content, meconium, may be passed into the amniotic fluid. Assessment of meconial contamination of the amniotic fluid is important in the management of late pregnancy. Fresh or increasing meconium content is an indication for urgent delivery. 'Old' meconium is usually distinguished from 'new' by visual inspection of the stained amniotic fluid; a more objective method could have advantages. We consider the effects of meconium staining of amniotic fluid on the spectrophotometric properties of the liquor. The absorption spectra of meconial amniotic fluids reveal an excess absorption band, centred around 410 nm. Quantification of the band height is proposed and it is shown that the height is linearly related to meconium concentration, with a proportionality factor, or sensitivity, of 0.046 +/- 0.009 (mean +/- s.d.) proportionality factor, or sensitivity, of 0.046 +/- 0.009 (mean +/- s.d.) optical density (OD) units per g l-1. This sensitivity factor may be used to estimate meconium concentration in samples of amniotic fluid.

Amniotic Fluid

Electrical accidents during pregnancy.

Electrical accidents during pregnancy are relatively infrequent, and reports are rare. Six pregnant women who suffered an electrical injury during pregnancy are presented here. For all, the current path through the body was from hand to foot. Changes that occurred in fetal movements and development as well as the outcome of the pregnancies, are presented. After delivery, the placenta and cord were carefully examined in all cases. From an analysis of the published cases and the present findings, it seems that there are no specific clinical and pathological signs of fetoplacental damage. Medical examination, shortly after the accident, may reveal a dead fetus. However, when it is found alive, oligohydramnios or growth retardation may develop later, and a close follow-up seems advisable. Pregnant women should be warned to notify their attending physician in all cases of electrical shock, no matter how apparently minor.

Adult

Calcium-independent phosphatidylinositol response in gonadotropin-releasing-hormone-stimulated pituitary cells.

This paper describes the effect of gonadotropin-releasing hormone (GnRH, gonadoliberin) on phospholipid metabolism in cultured rat pituitary cells. The cells were incubated with [32P]Pi to label endogenous phospholipids (10-60 min) and then stimulated with GnRH for up to 60 min. Cellular phospholipids were separated by two-dimensional t.l.c. and the radioactivity was determined. Phosphatidylinositol (PI), a minor constituent of cellular phospholipids (7.7%), was the major labelled phospholipid, accounting for 45% of the total radioactivity, at early periods after pulse labelling. On the other hand, phosphatidylcholine, the major cellular phospholipid (37%), was labelled only to 32% of the total radioactivity. The remaining label was distributed among phosphatidylethanolamine (4.2%), cardiolipin (3.4%), phosphatidic acid (PA, 2.5%), and phosphatidylserine (1.8%). GnRH doubled 32P labelling of PA and PI significantly at 1 and 5 min of incubation respectively in the presence or absence of extracellular Ca2+. Labelling of other phospholipids was not affected by GnRH treatment. The half-maximal stimulating dose (ED50) for PI labelling and lutropin release was 0.75 nM and 0.5 nM respectively, and the stimulatory effect was blocked by the potent GnRH antagonist [D-Glp1,pClPhe2,D-Trp3,6]GnRH. GnRH-stimulated PA and PI labelling could not be demonstrated after 1 and 45 min of incubation respectively, or when the prelabelling was conducted for 60 min rather than 10 min. These results suggest heterogeneous compartmentalization of gonadotroph PA and PI pools and that increased PI turnover might be a transducing signal for Ca2+ gating that follows gonadotroph GnRH-receptor activation.

Animals

Gonadotropin-releasing hormone stimulates phosphatidylinositol labeling and prostaglandin E production in Leydig cells.

The direct effects of gonadotropin releasing hormone (GnRH) upon testicular function include a rapid (integral of 20 min) receptor-mediated increase in phosphatidylinositol (PI) turnover. Incubation of rat interstitial cells with the super-agonist [D-Ala6]desGly10-GnRH N ethylamide (GnRHa) resulted in increased incorporation of [32P]Pi into PI (2-fold at 20 min). The effect on phospholipid turnover was followed by increased prostaglandin E (PGE) and testosterone production (3 h; with ED50 values of 0.5 and 0.75 nM respectively). It is concluded that increased PI turnover and PGE production might be involved in mediating the direct testicular effects of GnRH and its agonists.

Animals

Stimulation of prostaglandin E and testosterone production in rat interstitial cells by a gonadotropin-releasing hormone agonist.

The early direct effects of a GnRH agonist analog [D-Ala6]des-Gly10-GnRH N ethylamide (GnRHa) on rat testicular interstitial cells include increased production of prostaglandin E (PGE) and testosterone (T) at 3 h (ED50 values of 0.5 and 0.75 nM, respectively). On the other hand, LH action on testicular function, which is mediated by increased cAMP, involves an increase in T production at 30 min followed by increased PGE formation at 3 h. GnRHa at concentrations of 10(-12)-10(-8) M had no effect on basal or LH-stimulated cAMP production during a 4-h incubation test. The stimulatory effect of GnRHa on PGE, but not on T production, was abolished by the prostaglandin synthesis inhibitor indomethacin (1.5 microns). We conclude that cAMP does not play a role in mediating the direct testicular effects of GnRH on PGE and T production; that PGE is not involved in mediating GnRH-induced T production; and, finally, that increased PGE and T production might be involved in mediating the direct inhibitory and stimulatory testicular effects of GnRH and its agonist analogs.

Animals

Intrinsic fluorescence of the amniotic fluid.

The intrinsic fluorescence of clear amniotic fluid from third-trimester pregnancy is reported. The fluorescence intensity peaked at 405 nm when excited by ultraviolet light in the range of 310 to 360 nm. All of the 33 samples tested fluoresced, and their emission spectrum had the same shape, varying only in magnitude. Changing sample temperature (20 to 50 C) and sample pH (7.2 to 7.7) had little effect on the emission spectrum. The same fluorescence, with higher intensity, was observed when some newborn urine was tested. The fluorescence of amniotic fluid may provide a new tool to determine fetal age, fetal organ maturation, and fetal distress.

Amniotic Fluid