Biomedical subjects

M M Anceschi

Publications and source records attributed to M M Anceschi.

63 records · Page 4Linked to original sources

PubMed1985

Regulation of CTP: phosphocholine cytidylyltransferase activity in type II pneumonocytes.

Phosphatidylcholine synthesis by rat type II pneumonocytes was altered either by depleting the cells of choline or by exposing the cells to extracellular lung surfactant. Effects of these experimental treatments on the activity of a regulatory enzyme, CTP:phosphocholine cytidylyltransferase, were investigated. Although choline depletion of type II pneumonocytes resulted in inhibition of phosphatidylcholine synthesis, cytidylyltransferase activity (measured in cell homogenates in either the absence or presence of added lipids) was greatly increased. Activation of cytidylyltransferase in choline-depleted cells was rapid and specific, and was quickly and completely reversed when choline-depleted cells were exposed to choline (but not ethanolamine). Choline-dependent changes in enzymic activity were apparently not a result of direct actions of choline on cytidylyltransferase and they were largely unaffected by cyclic AMP analogues, oleic acid, linoleic acid or cycloheximide. The Km value of cytidylyltransferase for CTP (but not phosphocholine) was lower in choline-depleted cells than in choline-repleted cells. Subcellular redistribution of cytidylyltransferase also was associated with activation of the enzyme in choline-depleted cells. When measured in the presence of added lipids, 66.5 +/- 5.0% of recovered cytidylyltransferase activity was particulate in choline-depleted cells but only 34.1 +/- 4.5% was particulate in choline-repleted cells. An increase in particulate cytidylyltransferase also occurred in type II pneumonocytes that were exposed to extracellular surfactant. This latter subcellular redistribution, however, was not accompanied by a change in cytidylyltransferase activity even though incorporation of [3H]choline into phosphatidylcholine was inhibited by approx. 50%. Subcellular redistribution of cytidylyltransferase, therefore, is associated with changes in enzymic activity under some conditions, but can also occur without a resultant alteration in enzymic activity.

Animals↗

PubMed1985

Platelet-activating factor metabolism in human amnion and the responses of this tissue to extracellular platelet-activating factor.

It was found previously that platelet-activating factor (PAF, 1-0-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is undetectable in human amniotic fluid obtained before labor but is present in the majority of samples of amniotic fluid obtained after labor. In the present investigation, the amount of PAF in amnion tissue and the ability of this tissue to produce PAF and respond to PAF were investigated. Amounts of PAF in amnion obtained either during the second trimester of gestation or at term (before labor) were similar. After labor, however, the amount of PAF in amnion increased to 2.5-times that in amnion before labor without any discernible changes in the amounts of two related glycerophospholipids viz., 1-0-alkyl-sn-glycero-3-phosphocholine and 1-0-alkyl-2-acyl-sn-glycero-3-phosphocholine. The Ca2+-ionophore A23187, in the presence of Ca2+, caused an increase in the amount of PAF in amnion tissue disks but PAF did not appear to be released into the incubation medium. The stimulation of PAF formation by A23187 and Ca2+ was not affected by the addition of indomethacin. Addition of PAF to disks of amnion tissue resulted in an increase in the concentration of prostaglandin E2 in the incubation medium. An increase in prostaglandin E2 formation of similar magnitude was induced by A23187. Based on these results it is concluded that PAF can be synthesized in amnion tissue and net production is stimulated by Ca2+. In addition, amnion is receptive to extracellular PAF and exhibits, as one response, an increased production of prostaglandin E2.

Amnion↗

PubMed1984

The choline-depleted type II pneumonocyte. A model for investigating the synthesis of surfactant lipids.

When type II pneumonocytes from adult rats were maintained in a medium that lacked choline, the incorporation of [14C]glycerol into phosphatidylcholine was not greatly diminished during the period that the cells displayed characteristics of type II pneumonocytes. Cells that were maintained in choline-free medium that contained choline oxidase and catalase, however, became depleted of choline and subsequent synthesis of phosphatidylcholine by these cells was responsive to choline in the extracellular medium. Incorporation of [14C]glycerol into phosphatidylcholine by choline-depleted cells was stimulated maximally (approx. 6-fold) by extracellular choline at a concentration (0.05 mM) that also supported the greatest incorporation into phosphatidylglycerol. The incorporation of [14C]glycerol into other glycerophospholipids by choline-depleted cells was not increased by extracellular choline. When cells were incubated in the presence of [3H]cytidine, the choline-dependent stimulation of the synthesis of phosphatidylcholine and phosphatidylglycerol was accompanied by an increased recovery of [3H]CMP. This increased recovery of [3H]CMP reflected an increase in the intracellular amount of CMP from 48 +/- 9 to 76 +/- 16 pmol/10(6) cells. Choline-depleted cells that were exposed to [3H]choline contained [3H]CDP-choline as the principal water-soluble choline derivative. As the extracellular concentration of choline was increase, however, the amount of 3H in phosphocholine greatly exceeded that in all other water-soluble derivatives. Choline-depletion of cells resulted in an increase in the specific activity of CTP:phosphocholine cytidylyltransferase in cell homogenates (from 0.40 +/- 0.15 to 1.31 +/- 0.20 nmol X min-1 X mg of protein-1). These data are indicative that the biosynthesis of phosphatidylcholine is integrated with that of phosphatidylglycerol and are consistent with the proposed involvement of CMP in this integration. The choline-depleted type II pneumonocyte provides a new model for investigating the regulation of CTP:phosphocholine cytidylyltransferase activity.

Animals↗

PubMed1984

Beta-adrenergic stimulation of prostaglandin production by human amnion tissue.

Arachidonic acid is released from specific glycerophospholipids in human amnion and is used to synthesize prostaglandins that are involved in parturition. In an investigation of the regulation of prostaglandin production in amnion, the effects of isoproterenol on discs of amnion tissue maintained in vitro were examined. Isoproterenol caused a large but transitory increase in the amount of cyclic AMP in amnion discs and this was accompanied by a sustained stimulation of the release of arachidonic acid (but not palmitic acid or stearic acid) and prostaglandin E2. The dependencies of cyclic AMP accumulation, arachidonic acid mobilization and prostaglandin E2 release on the concentration of isoproterenol were similar, each response was maximal at 10(-6) M isoproterenol and was inhibited by propranolol. Dibutyryl cyclic AMP stimulated the release of prostaglandin E2 from amnion discs. Although prostaglandin E2, when added to amnion discs caused an accumulation of cyclic AMP, it did not appear to mediate isoproterenol-induced accumulation of cyclic AMP since the latter effect was insensitive to indomethacin in concentrations at which prostaglandin production was inhibited greatly. These data support the proposition that catecholamines, found in increasing amounts in amniotic fluid during late gestation, may be regulators of prostaglandin production by the amnion.

Amnion↗

PubMed1983

The renin-aldosterone system and electrolyte balance during tocolytic therapy.

The effects of short and long-term tocolytic therapy, with salbutamol on renin activity, aldosterone levels, sodium and potassium concentration in urine, blood, and red blood cells in 44 pregnant women were studied. No significant changes were observed in renin activity and aldosterone levels between the 1st and 5th days of i.v. or p.o. therapy and in 24-h sodium urinary excretion. Serum potassium levels significantly decreased by the 2nd and 4th h from start of i.v. infusion of salbutamol, returning to preinfusion levels within 24-36 h, whereas no concomitant increase in red cell potassium levels was detected. Urinary potassium excretion showed significant decrease within 24 h from start of i.v. therapy, returning to control levels after 48 h. No change in sodium concentration in blood and red blood cells was observed.

Administration, Oral↗

PubMed1982

Renin activity, aldosterone levels and urinary sodium and potassium excretion under tocolytic therapy with salbutamol.

The effects of long-term therapy with salbutamol on renin activity, aldosterone levels and urinary sodium and potassium excretion in pregnant women are studied. Salbutamol was given intravenously in a first group of 18 patients in preterm labor, orally in a second group of 9 patients, whereas a third group of 17 patients was taken as control. No significant changes were observed in renin activity and aldosterone levels between the first and the fifth day of intravenous or oral therapy and in 24-h sodium urinary excretion. Only potassium excretion showed a significant decrease (P less than 0.01) within 24 h from the start of the intravenous therapy, returning to control levels after 48 h. From these results, no replacement of potassium seems to be necessary in patients undergoing tocolytic therapy with betamimetic drugs.

Adult↗

PubMedDate not supplied

Unusual case of caudal duplication (dipygus).

We report the case of a dipygus diagnosed by sonography in the second trimester that had 6 lower extremities, double external male genitalia, a megabladder, 3 dilated ureters, and a polycystic right and a pelvic left kidney. This complex malformation represents a rare type of caudal duplication.

Adult↗

PubMedDate not supplied

Immunochemical and immunohistochemical evaluation of lung permeability in ventilated newborn rabbits.

These experiments were designed to quantify the vascular-to-alveolar leakage albumin in the neonatal lung and to analyze the distribution of leaking airspaces in the lung parenchyma. Immediately after delivery, newborn rabbits with gestational age 27-29 days received an intravenous injection of human albumin as a marker and were ventilated for 15 min with standardized tidal volume (10 ml/kg). After the period of ventilation the lungs were either lavaged via the airways or fixed for histological studies. The median amount of albumin in lung lavage fluid, determined by immunodiffusion, was 4.8% of the injected dose after 27 days, 1.3% after 28 days, and 0.4% after 29 days of gestation; it was inversely correlated with the compliance of the respiratory system (r = -0.78; p less than .001). Immunohistochemical examination of lung section revealed that the leak was not diffuse; even in animals with gestational age 27 days it involved only a median of 48% of total alveoli. The median amount of alveoli containing the label fell to 6% after 28 days and to 0% after 29 days gestation, correlating inversely with the compliance of the respiratory system (r = -0.53; p less than 0.01). We suggest that our experimental model is useful for histological demonstration of serum proteins leaking into the airpaces under experimental conditions and for evaluating the effect of therapeutic regiments on neonatal lung permeability.

Animals↗

PubMedDate not supplied

Semiquantitative PCR in the diagnosis of HIV infection: correlation to clinical stage and serological status.

Authors utilized the polymerase chain reaction (PCR) technique to detect the presence of HIV DNA in 31 subjects (12 seropositive patients, 4 seronegative, at risk persons and 15 seronegative, not at risk controls). PCR was highly sensitive (enabling the detection of as few as 10 proviral genomes) and specific. By comparison to known amounts of HIV DNA, it was possible to obtain semiquantitative evaluation. No correlation was found between the proviral amount and the clinical stage of the disease or the p24 antigenemia.

Adult↗