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Biomedical subjects

R Clemente

Publications and source records attributed to R Clemente.

At least 37 records · Page 2Linked to original sources
PubMed1996

Fetal malformations in an epileptic pregnant woman treated with carbamazepine.

We report a case of an epileptic pregnant woman at 20 weeks of gestation treated with carbamazepine, whose fetus was affected by major malformations probably due to the drug teratogenicity. After a therapeutic abortion minor malformations were also found. After seven months the patient was pregnant again, at 14 weeks of gestation she aborted spontaneously a fetus with no malformations. During this pregnancy the patient took a reduced dosage of carbamazepine.

Abnormalities, Drug-Induced↗
PubMed1995

Role of glycosyl-phosphatidylinositol hydrolysis as a mitogenic signal for epidermal growth factor.

We have investigated the role of the hydrolysis of glycosyl-phosphatidylinositol (GPI) as one of the signalling pathways elicited after interaction of epidermal growth factor (EGF) with its specific plasma membrane receptor (EGFR). Endogenous GPI was characterized in both NIH 3T3 mouse fibroblast cells and in EGFR-transfected NIH 3T3 cells (designated EGFR T17). GPI molecules isolated from both cell lines were identical and they incorporated radioactivity from both sugar and fatty acid substrates. Incubation of EGFR T17 cells with EGF, produced a rapid and transient hydrolysis of GPI. Maximum hydrolysis occurred after a 1-min incubation with 50 nM EGF. No such effects of EGF were observed in the parental cell line. Both inositol phosphoglycan (IPG)- and EGF-induced cell proliferation was inhibited in the presence of an IPG-antibody to different extents. The relationship between GPI hydrolysis and the activity of the EGFR was studied using the tyrosine kinase inhibitors tyrphostin (RG50864) and genistein. These agents were able to significantly inhibit EGF-mediated cell proliferation, EGF-dependent hydrolysis of GPI and EGF-regulated autophosphorylation of the EGFR. It is concluded that GPI hydrolysis is one of the earliest intracellular events generated in response to EGF.

3T3 Cells↗
PubMed1995

[Microsurgical treatment of trigeminal neuralgia. A study of 50 cases].

The authors present a study of 50 patients with trigeminal neuralgia treated by posterior fossa microsurgery. Microvascular decompression of the trigeminal nerve was performed in 48 patients. In 2 cases no neuro-vascular compression was found, and a partial rhizotomy was carried out. In 98% of the cases there was postoperative abolition of the pain. Two cases of wound infection and three CSF fistulas were the operative complications. These patients were reoperated and cured. Twenty five patients were reviewed between 13 months and 8 years after surgery. Twenty one remained painfree without any drug, 3 were painfree taking 200 to 400 mg Carbamazepineper day, and 1 patient was reoperated after two years without pain because of recurrence of the neuralgia. There was no mortality or major morbidity in this series. Our results and the literature concerning this method are discussed in this article. In conclusion, microvascular decompression may be indicated in a large number of patients with essential trigeminal neuralgia due to its excellent pain control, no mortality and low morbidity.

Adult↗
PubMed1993

The diagnostic potential of fetal renal biopsy.

The feasibility of fetal renal biopsy has been investigated in order to assess the diagnostic value of the histological specimen. Two fetuses with a severe bilateral renal abnormality (multicystic dysplastic kidney, Meckel-Gruber syndrome with polycystic kidney) and one fetus with Down syndrome (no detectable structural anomaly) were sampled. Histological findings in the biopsy specimens of cases 1 and 2 were diagnostic of an early obstructive renal disease. In case 3, the findings were consistent with normal development for gestational age of the kidney. Fetal renal biopsy is technically feasible; histological examination of the samples showed a good correlation with postnatal findings. Further studies of its diagnostic value are required.

Adult↗
PubMed1992

A phosphatidylinositol-linkage-deficient T-cell mutant contains insulin-sensitive glycosyl-phosphatidylinositol.

Glycosyl-phosphatidylinositol molecules, acting as both signal transduction elements and membrane protein anchors, have been proposed to play a role during T-cell activation. The MVB2 cell line is a mutant, derived from the wild-type T-T hybrid YH.16.33, which has a defect in the biosynthesis of PtdIns-protein linkages. As a consequence, MVB2 mutants are defective in activation through the T-cell receptor. Despite the lack of glycosyl-PtdIns anchors in the mutant MVB2 cells, a comparison of the levels and structural features of the insulin-sensitive glycosyl-PtdIns between the MVB2 and YH.16.33 lineages indicates that both cell lines are identical in this respect. The time course for insulin-responsiveness coincides in both cell lines, with maximal hydrolysis 30 s after insulin addition. The ultimate localization of insulin-regulated glycosyl-PtdIns at the outer surface of the cell membrane is also similar. These data indicate that the glycosyl-PtdIns whose hydrolysis is regulated by insulin is not anchoring proteins at the cell surface of T-lymphocytes.

Animals↗
PubMed1992

Role of the glycosylphosphatidylinositol/inositol phosphoglycan system in human fibroblast proliferation.

The involvement of the glycosylphosphatidylinositol/inositol phosphoglycan (gly-PtdIns/IPG) system in the stimulation of macromolecular syntheses in human fibroblasts has been investigated. The study demonstrates that an insulin sensitive gly-PtdIns/IPG system is present in human fibroblasts, that IPG can significantly stimulate DNA, RNA, and protein synthesis, and that the action of insulin on DNA synthesis as well as that of IPG can be significantly reduced by a specific anti-IPG antibody. These results strongly support the hypothesis that the gly-PtdIns/IPG system is involved in the signal transduction pathway leading to the stimulation of cell proliferation.

Cell Division↗
PubMed1991

Glycosyl-phosphatidylinositol/inositol phosphoglycan: a signaling system for the low-affinity nerve growth factor receptor.

Nerve growth factor (NGF) exerts a variety of actions during embryonic development. At the early stages of inner ear development, NGF stimulates cell proliferation, an effect mediated through low-affinity receptors. We have studied the possibility that the glycosyl-phosphatidylinositol/inositol phosphoglycan (glycosyl-PtdIns/IPG) system is involved in transmitting this NGF signal. Endogenous glycosyl-PtdIns was characterized in extracts of cochleovestibular ganglia (CVGs) that incorporated [3H]glucosamine, [3H]galactose, [3H]myristic acid, and [3H]palmitic acid. Incubation of CVG with NGF produced a rapid and transient hydrolysis of glycosyl-PtdIns. Hydrolysis was complete at 100 ng/ml, and the half-maximal effect occurred at 25 ng/ml, overlapping with the concentration dependence of the mitogenic effect of NGF. An IPG was isolated from embryonic extracts. It had biological effects similar to those reported for the insulin-induced IPG in other tissues. It exerted a powerful mitogenic effect on CVG, comparable to that of NGF. Both the IPG- and NGF-induced cell proliferation were blocked by anti-IPG antibodies that recognized the endogenous IPG on a silica plate immunoassay. These results show that CVG possesses a fully active glycosyl-PtdIns/IPG signal transduction system and that the proliferative effects associated with NGF binding to low-affinity receptors require IPG generation.

Animals↗
PubMed1990

Asymmetric distribution of the phosphatidylinositol-linked phospho-oligosaccharide that mimics insulin action in the plasma membrane.

We have investigated the topography of a glycosyl-phosphatidylinositol implicated in insulin action by a combination of two complementary methods: (a) chemical labelling with a non-permeable (isethionyl acetimidate) and a permeable (ethyl acetimidate) probe; and (b) enzymatic modifications with beta-galactosidase (EC 3.2.1.23) or phosphatidylinositol-specific phospholipase C (EC 3.1.4.3). Using the first approach the majority of the glycosyl-phosphatidylinositol is found in the outer surface of intact hepatocytes, adipocytes, fibroblasts and lymphocytes, but not in erythrocytes which presented only a 20% of the total labelled glycosyl-phosphatidylinositol to the exterior. Upon insulin addition (10 nM), about 60% of the total glycosyl-phosphatidylinositol was hydrolysed in both hepatocytes and adipocytes but not in erythrocytes. In agreement with the extracellular localization in hepatocytes and with the proposed role of this glycolipid in insulin action, treatment of rat hepatocytes with beta-galactosidase from Escherichia coli, an enzyme that hydrolyses the oligosaccharide moiety of the glycosyl-phosphatidylinositol, cleaved 65% of the total glycophospholipid and blocked the effect of insulin (but not of glucagon) on pyruvate kinase (EC 2.7.1.40). Similar treatment with phosphatidylinositol-specific phospholipase C from Bacillus cereus hydrolysed 62% of the total glycosyl-phosphatidylinositol. From the various approaches used it is concluded that the majority of this glycophospholipid is at the outer surface in a variety of insulin-sensitive cells.

Animals↗
PubMed1988

Different phosphorylated forms of an insulin-sensitive glycosylphosphatidylinositol from rat hepatocytes.

Labeling with [3H]galactose was employed to isolate a glycosylphosphatidylinositol from rat hepatocytes which might be involved in the action of insulin. The polar head group of this glycosylphosphatidylinositol was generated by phosphodiesterase hydrolysis with a phosphatidylinositol-specific phospholipase C from Bacillus cereus. By Dowex AG1 x 8 chromatography the polar head group could be separated into three radioactive peaks eluting at 100 mM (peak I), 200 mM (peak II) and 500 mM (peak III) ammonium formate, respectively. Peak III was the most active as an inhibitor of the cAMP-dependent protein kinase. Treatment of peak III with alkaline phosphatase markedly reduced its activity on cAMP-dependent protein kinase. When peaks I, II or III were treated with alkaline phosphatase and analyzed again by Dowex AG1 x 8 chromatography, the radioactivity eluted with the aqueous fraction. The above results indicate that the polar head group of the insulin-sensitive glycosylphosphatidylinositol from rat hepatocytes exists in three different phosphorylated forms and that the biological activity of this molecule depends on its phosphorylation state.

Alkaline Phosphatase↗
PubMed1985

Diabetic gastroparesis: an abnormality of gastric emptying of solids.

Gastric emptying is delayed in subjects with gastroparesis diabeticorum. To ascertain whether solid or fluid gastric emptying is affected by visceral autonomic neuropathy, ten severe diabetics with gastroparesis and ten nondiabetic disease matched controls were studied. Subjects were screened to identify the presence or absence of autonomic neuropathy. The gastric emptying of fluids and solids was assessed by standard methodology utilizing a simultaneous dual radionuclide technique. If delayed gastric emptying was present on the initial study, metoclopramide (10mg IV bolus) was administered in a repeat study on a separate day. Screening modalities for autonomic neuropathy were markedly positive for the diabetic group, and were negative in the control group. The gastric emptying rate of fluids was normal in both groups and was not statistically different from previous standards developed using the same methodology (p = 0.53, analysis of covariance). The gastric emptying of solids was markedly delayed in the diabetic group in relation to the control group (p = .0035, analysis of covariance). Metoclopramide normalized delayed solid emptying rates without affecting fluid emptying rates.

Autonomic Nervous System Diseases↗
PubMed1984

Gastric emptying in patients with chronic renal failure receiving hemodialysis.

Patients with renal failure requiring hemodialysis often suffer from nausea and vomiting. Gastric emptying has not been studied in these patients. To determine whether an abnormality of gastric emptying might account for symptoms in these patients, two groups of ten patients each were selected, one group with symptoms of nausea and vomiting and another without symptoms. Autonomic function was assessed in all patients. Fluid and solid gastric emptying rates were quantified utilizing a dual radionuclide technique. Half-emptying times for fluid and solid test meals were not statistically different from previous standards derived using the same methods in a normal population. Patients with chronic renal failure receiving hemodialysis have no demonstrable abnormality in gastric emptying, whether symptomatic or not.

Gastric Emptying↗