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Biomedical subjects

M M Anceschi

Publications and source records attributed to M M Anceschi.

At least 55 records · Page 3Linked to original sources
PubMed1993

Human papilloma virus infection and Ki-ras oncogene in paraffin-embedded squamous carcinomas of the cervix.

42 paraffin-embedded squamous cervical carcinomas were screened for the presence of human papilloma virus (HPV; 6b, 11, 16, 18) and for activation of the Ki-ras oncogene family by polymerase chain reaction. In 72% of cases we found one or more HPV types, but no mutations of the Ki-ras gene (codon 12-1 and 61-1, 61-2 and 61-3) were found. We conclude that mutations of the Ki-ras oncogene, at the positions analyzed, are not likely to be involved in the events leading to cervical carcinogenesis.

Carcinoma, Squamous Cell↗
PubMed1993

Inhibin and activin in human fetal membranes: evidence for a local effect on prostaglandin release.

Trophoblast and fetal membranes (amnion and chorion) are the tissues forming the anatomical/functional interface between the mother and the fetus. The aim of the present study was to evaluate the presence and a possible effect of inhibin and activin in human amnion and chorion. The expression of inhibin/activin alpha, beta A, and beta B subunit messenger RNA (mRNA) and the localization of immunoreactive material were evaluated in amnion and chorion collected at term pregnancy by a Northern blot analysis and by immunohistochemistry. Amnion cells expressed the mRNA of the three inhibin/activin subunits, with the beta B message the most abundantly expressed. The epithelial layer of the amnion showed an intense fluorescent staining of beta B inhibin/activin subunit, and positive signals were also observed for the alpha and beta A subunits. Inhibin/activin alpha and beta A subunit mRNAs were found highly expressed in chorion. The cytotrophoblast of the chorion showed a positive staining for the three inhibin/activin subunit antisera. The addition of activin A increased the release of prostaglandin E2 from human amnion-derived cultured cells. The effect was dose and time dependent. Inhibin A did not induce significant changes of prostaglandin E2 release from amnion cells. The present results show that amnion and chorion produce inhibin and activin subunits and that activin stimulates the release of prostaglandin E2 from cultured amnion cells, suggesting a possible role of inhibin and activin in fetal membranes.

Activins↗
PubMed1992

Perinatal AIDS.

AIDS is the major public health concern today. The short-term history of the disease adds considerable emphasis to the problem in that it has literally exploded in a few years. The pathophysiology and natural history and, what is most important, the treatment, remain enigmatic. Management of women at risk of HIV infection is colored by the nature of the illness, the subgroups of the people first infected, the mode of transmission, and the implication of vertical transmission.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Erythrocyte membrane composition in pregnancy-induced hypertension: evidence for an altered lipid profile.

OBJECTIVE: To investigate whether the increased membrane fluidity postulated as a possible contributing factor to the hypertensive states of pregnancy is related to the lipid composition of the erythrocyte membrane. DESIGN: An observational case control study. SUBJECTS: 30 women with pregnancy induced hypertension, 26 normotensive pregnant women matched for gestational age, and 10 normotensive non pregnant nulliparous women. INTERVENTIONS: Erythrocyte membranes were prepared from venous blood samples obtained from all the women. MAIN OUTCOMES MEASURES: Lipid analysis, including cholesterol to phospholipids ratio, distribution of phospholipid classes and fatty acid composition of total phospholipids in erythrocyte ghosts. RESULTS: The cholesterol/phospholipid ratio was significantly higher in the women with pregnancy induced hypertension compared with the normotensive pregnant women (mean 1.24, SD 0.31, 95% CI 1.12 to 1.35 vs mean 0.90, SD 0.09, 95% CI 0.86 to 0.94; P less than 0.01). Normotensive non-pregnant erythrocyte membrane cholesterol/phospholipid ratio was 0.88 (SD 0.11, 95% CI 0.79 to 0.96). The percentage distribution of different phospholipid classes and fatty acid composition was similar in all the four groups. CONCLUSIONS: The increased cholesterol/phospholipid ratio of the erythrocyte membrane found in pregnancy-induced hypertension represents one factor involved in the pathophysiology of this condition and a possible biochemical marker of the disease.

Adult↗
PubMed1992

Abnormal platelet lipid membrane composition in pregnancy induced hypertension.

The cholesterol:phospholipid ratio (C/PL) was measured in platelet plasma membrane in patients with pregnancy-induced hypertension [with proteinuria (PE), and without proteinuria (PIH)] and in matched normotensive gestational controls (NT). The C/PL was raised in the platelet membrane from PE (1.52 +/- 0.50, 95% CI 1.13 to 1.90) and PIH (1.38 +/- 0.34, 95% CI 1.08 to 1.67) compared with that from NT controls (0.88 +/- 0.13, 95% CI 0.80 to 0.95) (p less than 0.01, ANOVA test). No correlation was found when C/PL was regressed against total serum cholesterol levels. The abnormality of lipid composition of the platelet plasma membrane could account for some of the changes in platelet function that have been described in PIH.

Blood Platelets↗
PubMed1992

Collagen and elastin in rabbit fetal lung: ontogeny and effects of steroids.

Ontogeny of lung collagen and elastin were studied in fetal rabbit from day 25 to term. Collagen (isolated by hot trichloroacetic acid treatment) and elastin (contained in the residue) were hydrolyzed and the hydroxyproline and desmosine quantitated by hplc. Hydroxyproline slightly increased from day 25 to day 30 (204 to 244 micrograms/100g dry weight). Over the same period desmosine increased from 2.2 to 5.1 micrograms/100 mg dry weight (P < 0.01). The effect of antenatal corticosteroids on the lung of prematurely-delivered fetuses was also evaluated. Betamethasone (B) was given to pregnant does at a dose of 0.2 mg/kg 24 and 48 h before delivery of the fetuses at 26, 27 and 28 days. In treated animals elastin concentration increased significantly by about 22% on day 26 (P = 0.05), by 29% on day (P < 0.02) and by 47% on day 28 (P < 0.02). Hydroxyproline was not affected by steroid treatment at any gestational age. This suggests that steroids affect fetal lung development also via changes in connective tissue.

Animals↗
PubMed1992

CA 125 in peritoneal fluid: reliable values at high dilutions.

Forty-three samples of peritoneal fluid from women undergoing laparotomy or laparoscopy for various gynecologic diseases were examined to determine and characterize CA 125 antigen. The data were compared with the corresponding serum levels. CA 125 levels in undiluted peritoneal fluid ranged between 41-301 U/mL and were significantly higher than levels in serum, except in cases of ovarian carcinoma. However, when CA 125 of peritoneal fluid was measured at dilutions greater than 1:50, higher antigen levels were measured (1120-31,500 U/mL), with the highest CA 125 values in patients with ovarian carcinoma. Measurements at dilutions of less than 1:50 were also affected but did not show any decreased binding of the antigen. Immunoblotting analysis of serum and peritoneal fluid indicated the presence of two main bands in each. The monoclonal antibody OC 125 reacted strongly with peritoneal fluid CA 125, in agreement with the CA 125 values obtained by immunoradiometric assay using high dilutions. These data suggest that CA 125 measurements in peritoneal fluid are unreliable unless the samples are diluted 1:50 or more. Furthermore, the statistical difference found between patients with benign and malignant tumors and those with leiomyomata uteri and controls suggests that diluted peritoneal fluid could have a role in identifying abnormal antigen levels.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1991

Regulation of CA 125 production by amnion and WISH cells in culture.

Amnion and human amnion-derived WISH cells release CA 125 antigen into culture medium. CA 125 output was higher in WISH cells than in amnion cells. In this study we showed that release of the antigen is regulated, with both amnion and WISH cells responding in a similar manner to the tested agents. Release of CA 125 decreased in the presence of dexamethasone (10(-6) mol/L) or cycloheximide (0.1 micrograms/ml) and increased when colchicine (0.01 micrograms/ml) was added to the culture medium. Stimulatory and inhibitory effects were more apparent after 3 days in culture. The precise mechanisms by which some of these agents (colchicine and dexamethasone) affect CA 125 release remain unknown. We propose that amnion and WISH cells in culture represent a useful model to investigate some regulatory aspects of the production of CA 125 in normal tissues.

Amnion↗
PubMed1990

CA 125 is released by human amnion cells in culture.

CA 125 was measured in the medium of human amnion cells in primary culture after confluence. The antigen accumulated as a function of time with a median value of 1897 U/mg protein after 7 days in culture. CA 125 was detectable by immunoperoxidase staining in the cells, which supports the possibility that amnion cells play a role as a source of the CA 125 found in the amniotic fluid.

Amnion↗
PubMed1990

Multiple primer pairs polymerase chain reaction for the detection of human papillomavirus types.

A polymerase chain reaction (PCR) based on the use of multiple primers enabling the simultaneous detection of HPV-6b, -11, -16 and -18 in a single tube reaction was developed and validated on cervico-vaginal specimens, including tissues embedded in paraffin. This PCR setting proved to be specific and sensitive, allowing the detection of as few as 200 viral particles per specimen.

Base Sequence↗
PubMed1989

Ontogeny of CA 125 antigen in pregnancy: immunoradiometric determination in amniotic fluid and immunohistochemical localization in fetal membranes.

CA 125 antigen was measured in amniotic fluid, maternal blood, cord blood, and fetal urine by a commercially available immunoradiometric assay kit. The amniotic fluid was obtained from 99 normal pregnancies at various gestational ages. The mean antigen levels were 29,676, 3350, and 1680 U/ml in amniotic fluid of the first, second, and third trimesters, respectively. In maternal blood, 12.5% of pregnant women in the first trimester of pregnancy showed elevated levels of CA 125 (65 to 100 U/ml). Late in gestation, CA 125 levels in cord blood and fetal urine were always less than 65 U/ml. Immunohistochemical study of CA 125 in fetal membranes, placenta, and decidua showed the presence of antigen only in the amnion. These results suggest that CA 125 is shed into amniotic fluid directly from the amniotic membrane.

Amniotic Fluid↗
PubMed1989

Lung surfactant enhancement in utero.

Over the last 10 years the strategy for the prevention of neonatal respiratory distress syndrome (RDS) has been directed towards the acceleration of fetal lung maturity in utero by means of drugs administered to the mother, the most thoroughly investigated being glucocorticoids (GC). Many reports indicate that the administration of GC decreases the incidence of RDS in the neonate delivered between 28 and 32 weeks and weighing less than 1500 g. The type of GC and the drug-delivery interval are critical. Harmful potential side effects of GC have led to the testing of other drugs capable of accelerating fetal lung maturity, among them ambroxol and aminophylline. Ambroxol has been shown to reduce significantly RDS compared to placebo, without causing important adverse effects either on the mother or the baby. Our experimental studies on aminophylline have shown that the drug exerts only minor beneficial effects on fetal lung maturation and surfactant production. Recently we have evaluated the association of GC with inositol. The sugar alcohol dramatically affected pregnant rabbit fetal lung mechanisms, reducing GC-adverse effects such as decrease in lung DNA and protein content. In attempts to minimize the risk of neonatal RDS it is important (1) to identify pregnant women at risk for preterm labor; (2) to establish specific guidelines for the use of any prenatal drug to be administered for the prevention of RDS; (3) to assess fetal lung maturity; (4) to intensively monitor the fetus intrapartum; and (5) to prevent birth asphyxia.

Animals↗
PubMed1989

Requirements of perinatal prevention and treatment of respiratory distress syndrome.

In the last decade the strategy for the prevention of the neonatal respiratory distress syndrome (RDS) has been directed towards the acceleration of foetal lung maturation in utero by means of drugs administered to the mother, the most thoroughly investigated being glucocorticoids. Harmful potential side effects of glucocorticoids have led to testing of other drugs capable of accelerating foetal lung maturation, including ambroxol and aminophylline. More recently supplementary surfactant instilled into the trachea has been shown to improve oxygenation of premature babies and to reduce the severity of RDS. To minimise the incidence of neonatal RDS it is important to identify pregnant women at risk for preterm labour and to establish specific guidelines for the use of any prenatal drug to be administered for prevention of RDS. It is also mandatory to assess foetal lung maturity in case of preterm delivery, to monitor the foetus intensively intrapartum, to prevent birth asphyxia and to control, and promptly correct derangements of neonatal homeostasis.

Ambroxol↗
PubMed1989

The alveolar type II cells as a model for investigating the metabolism of surfactant phospholipids.

The use of type II pneumocytes in pure culture allows the investigator to directly define at the cellular level the metabolism of pulmonary surfactant. Surfactant analysis and/or secretion has been shown to be enhanced and depressed by a variety of substances, and the main metabolic pathways of the major components have been elucidated. Type II cells are also important in maintaining the in vivo homeostasis of the pulmonary alveolus, because after lung injury they proliferate and serve as stem cells for type I cells. In view of the increasing therapeutic use of surfactant supplementation in RDS and ARDS, the regulation of surfactant secretion is of particular interest, and presumably involves a receptor mediated mechanism in which surfactant associated apoproteins seem to play a pivotal role. These findings support the view that surfactant secretion is a self regulated phenomenon.

Animals↗
PubMed1988

Control of ColE1 replication: low affinity specific binding of Rop (Rom) to RNAI and RNAII.

We have studied the interactions between the three molecules Rop, RNAI and RNAII that are involved in the regulatory mechanism controlling the replication of ColE1 plasmids. We show that it is possible to purify the two RNA molecules by passing an RNA mixture through an affinity column containing Rop immobilized to a solid support. The dissociation constants of the Rop-RNAI and Rop-RNAII complexes are of the order of 10(-4) M, several orders of magnitude higher than dissociation constants of stable protein-nucleic acid complexes (10(-10) M in the lambda repressor system). Although complete RNAI molecules have higher affinity, stem-and-loop I alone can also bind Rop, suggesting that this structure plays an important role in the interaction. Rop protects the stems of RNAI and RNAII from digestion by RNases while the sensitivity of the loops to digestion by RNase T1 is not affected by high concentrations of Rop. We propose a model for Rop-RNAI/RNAII interaction in which the dimeric protein acts as an adaptor between stem structures to position the two RNAs in the correct position for loop interaction.

Bacteriocin Plasmids↗
PubMed1988

Inositol and glucocorticoid in the development of lung stability in male and female rabbit fetuses.

Inasmuch as inositol affects the development of lung surfactant, and exogenous glucocorticoids accelerate fetal lung maturation, a possible interaction of the two substances on alveolar stability of preterm rabbit fetuses of 28 days gestation was investigated. On days 26 and 27 of gestation inositol or glucose were added to the diet of does treated with betamethasone (0.2 mg/kg intramuscularly on days 26 and 27). Inositol increased lung-thorax compliance of paralyzed fetuses at all insufflation pressures studied (from 16 to 22.5 and 30 cm H2O and back to 22.5, and 16 cm H2O). At a ventilation pressure of 30 cm H2O, lung-thorax compliance of fetuses treated with inositol plus betamethasone was more than doubled as compared with controls (1.2 +/- 0.6 versus 0.5 +/- 0.2 ml/kg x cm H2O; p less than 0.001). Inositol alone had no detectable effect on compliance, whereas betamethasone tended to increase compliance (p = 0.05). According to variance analysis, the effect of inositol was statistically significant only among the males. Inositol prevented the glucocorticoid-induced decrease in lung protein and, to a lesser extent, the decrease in DNA. Inositol did not further increase the lavageable surfactant pool of the glucocorticoid-treated, ventilated fetuses, although the area occupied by lamellar bodies within type II cells was increased after inositol plus betamethasone. According to the present study, inositol modifies the physiologic and biochemical response of the immature fetal lung to a pharmacologic dose of exogenous glucocorticoid.

Animals↗