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Biomedical subjects

V Gallo

Publications and source records attributed to V Gallo.

108 records · Page 6Linked to original sources
PubMed1981

[Alpha fetoprotein in non-neoplastic liver diseases].

Seric alfa-FP has been studied in acute and chronic hepatitis and in hepatocellular carcinoma. Sixty five normal subjects, 62 cirrhoses, 10 active chronic hepatitis, 12 chronic persistent hepatitis, 4 primary biliary cirrhoses and 9 hepatomas have been examined for seric alfa-FP. Abnormal seric alfa-FP (> 10 ng/ml) values agree with literature data. It is likely that hepatocellular regeneration due to viral or inflammatory disorders, can produce formation of alfa-FP and other abnormal proteins fro a depression mechanism of sue regulator gene.

Adult↗
PubMed1981

[Assay of the carcinoembryonic antigen (CEA) in acute and chronic liver diseases and hepatocellular carcinoma].

Carcinoembryonic antigen (CEA) has been studied with a radioimmunoassay technique with an antiserum obtained from hepatic metastases of colonic cancer (Sorin Biomedica, Saluggia). The normal range of seric CEA varies from 0 to 10 ng/ml; 10 ng/ml is the higher value found in a smoker healthy subject. Seric CEA than 10 ng/ml has been found in 27% of cirrhoses, 39% of acute viral hepatitis (HBsAg+), 13.3% of chronic active hepatitis, 7.7% of chronic persistent hepatitis, 36% of alcoholic hepatitis and 100% of hepatomas. The diminished hepatic clearance of the antigen, or the derepression of its regulator gene, or the formation of CEA-like substances may cause the increase of seric CEA in hepatic diseases. The antiserum obtained from hepatic metastases of colonic carcinoma may explain the positivity in all the patients with hepatoma.

Acute Disease↗
PubMed1981

Enhancement by GABA of glutamate depolarization-induced release from cerebellar nerve endings.

Cerebellar synaptosomes were superfused in the presence of D-[3H]aspartate (to label the glutamate 'reuptake pool') and [14C]glutamine (to label the 'new synthesis pool'). The depolarization-induced release of D-[3H]aspartate and of newly synthesized [14C]glutamate were potentiated by low concentrations of GABA (2--20 microM) or muscimol. The effect was probably mediated by the interaction of GABA with presynaptic GABA receptors localized in 'glutamergic' nerve endings, since it was antagonized by the GABA antagonists picrotoxin and bicuculline.

Animals↗
PubMed1981

Glutamate as a putative transmitter in the cerebellum: stimulation by GABA of glutamic acid release from specific pools.

The aim of the present paper was to determine whether the release of glutamate from putative "glutamergic" terminals in the cerebellum is influenced by gamma-aminobutyric acid (GABA). In a group of preliminary experiments, we present biochemical evidence in favour of a neurotransmitter role of glutamate in the cerebellum: (1) endogenous glutamate was released from depolarized cerebellar synaptosomal preparations in a Ca2+-dependent away; (2) [14C]glutamate was synthesized from [14C]glutamine in cerebellar synaptosomes, and the newly synthesized [14C]glutamate was released released in a Ca2+-dependent way; (3) the elevation of cyclic GMP elicited by depolarization of cerebellar slices in the presence of Ca2+ was partly reversed by the glutamate antagonist glutamic acid diethyl ester, which probably prevented the interaction of endogenously released glutamate with postsynaptic receptors. GABA and muscimol at low concentrations (2--20 micrometers) potentiated the depolarization-induced release of D-[3H]aspartate (a glutamate analogue which labels the glutamate "reuptake pool") from cerebellar synaptosomes. The effect was concentration dependent and was largely prevented by two GABA antagonists, bicuculline and picrotoxin. The stimulation of D-[3H]aspartate release evoked by muscimol was linearly related to the logarithm of K+ concentration in the depolarizing medium. GABA did not affect the overall release of endogenous glutamate, but potentiated, in a picrotoxin-sensitive manner, the depolarization-evoked release of [14C]glutamate previously synthesized from [14C]glutamine. Since nerve endings are the major site of glutamate synthesis from glutamine, GABA and muscimol appear to exert their stimulatory effect at the level of "glutamergic" nerve terminals, probably after interacting with presynaptic GABA receptors. The possible functional significance of these findings is briefly discussed.

Animals↗
PubMed1980

A reevaluation of veratridine as a tool for studying the depolarization-induced release of neurotransmitters from nerve endings.

The effect of veratridine on neurotransmitter release was studied using rat brain synaptosomes superfused at 37 degrees C. Veratridine (5-75 microM) caused a concentration-dependent release of [3H]GABA from prelabeled synaptosomes in the presence of 2.7 mM Ca2+. In the whole range of veratridine concentrations, the release of [3H]GABA elicited by the drug was substantially increased rather than decreased in the absence of Ca2+ or with Ca2+ concentrations of 0.45 and 0.9 mM. The release of the amino acid was inhibited more by 5.4 mM than by 2.7 mM Ca2+. The effect on endogenous (chemically measured) GABA was similar to that on [3H]GABA. The inhibitory effect of Ca2+ on the veratridine-induced release of [3H]GABA was consistently seen in a variety of experimental conditions except one, namely when the experiment was run at room temperature (22-23 degrees C) rather than at physiological temperature (37 degrees C). In fact, at 22-23 degrees C the release of GABA evoked by the alkaloid was somewhat potentiated by Ca2+. At 37 degrees C, glutamate appeared to behave similarly to GABA, whereas the veratridine-induced release of [3H]noradrenaline and [3H]dopamaine was largely Ca2+-dependent. The mechanism of the release of transmitters elicited by veratridine is discussed. It is concluded that the evoked release of GABA and glutamate is due more to the veratridine-induced depolarization (Na+ influx) than to the accompanying influx of Ca2+, and it is suggested that the inhibitory effect of Ca2+ on the overall release of amino acids is due to the antagonism exerted by the divalent cation on the veratridine action at the Na+ channel. In contrast, in the case of catecholamines, the influx of Ca2+ would have a prominent role in triggering exocytotic release, whereas the depolarization itself would have slight or no importance.

Animals↗
PubMed1979

[An application of the dispersion theory in haematology (author's transl)].

A comparative study concerning dispersion theory has been carried out of patients affected by bronchiogenic cancer and normal subjects about neutrophil granulocytes frequencies. The results of this study can be drawn as follows: the patients affected by bronchiogenic cancer show the coefficient of divergence significantly higher than 1. Therefore we should think they have perhaps a quicker granulocytopoietic biorhythm than normal subjects. However the question is still debatable although the results are very suggestive.

Blood Cell Count↗
PubMed1978

[Stauffer's syndrome. Report of a clinical case].

The clinical case of a 52-year-old man with hypernephroma, abnormal hepatic function tests and no evidence of liver metastasis or abnormal histology is described. Liver function tests returned to normal values after nephrectomy. This case presents the features of the syndrome described by Stauffer in 1961 and can be added to the eighty or so cases reported since then.

Adenocarcinoma↗
PubMed1977

Localization of carcinoembryogenic antigen (CEA) in normal, inflammatory and neoplastic colonic mucosa by immunofluorescence.

To evaluate the role of tissutal carcinoembryonic antigen (CEA) in different types of colonic mucosae specimens from normal, inflammatory and neoplastic tissues were examined in immunofluorescence (IFL) with a monospecific CEA antiserum. Neither the pattern of IFL nor the amount of antigen in the tissue (defined as the antiserum dilution beyond which CEA staining was no longer visible), could reliably distinguish any histological entity a consistent overlap being observed between positive and negative results in malignant and non malignant mucosa. No correlation was found betwen IFL and the level of serum CEA. It is concluded that the tissutal localization of CEA by immunohistochemistry plays no role in the differential diagnosis of different types of colonic mucosa.

Carcinoembryonic Antigen↗
PubMedDate not supplied

Alpha-fetoprotein and tissue polypeptide antigen in non neoplastic hepatic disorders.

In order to evaluate the behaviour of alpha-fetoprotein (AFP) and Tissue Polypeptide Antigen (TPA) in non neoplastic chronic hepatic diseases 60 patients suffering from chronic hepatitis have been studied, 28 of them with different ethiology cirrhosis, 4 with primary biliary cirrhosis (CBP), 18 with chronic active hepatitis (ECA), 5 with chronic persistent hepatitis (ECP), 3 suffering from alcoholic and 2 drug-induced hepatitis. In each case the diagnosis was biopsy-proved. We have found that TPA clearly shows an increase in about 90% of cirrhosis and in about 50% of ECA. Moreover, the group with non-A, non-B (NANB) cirrhosis and chronic hepatitis has shown a statistically significant correlation between TPA and alanine aminotransferase (ALT). On the other hand, AFP hants' shown statistically significant variations. The reasons of the TPA increase must probably be looked for in the marked sensitivity of this protein to non neoplastic tissues in rapid regeneration, in addition to the sensitivity to neoplastic tissues. Further studies will be carried out to evaluate the usefulness of TPA to tracing possible cytolitic relapses or any resumption of activity in hepatic cirrhosis.

Adult↗
PubMedDate not supplied

Effects of verapamil on platelet aggregation and serum thromboxane synthesis in vitro and in vivo.

The aim of this study was to evaluate the in vitro effects of verapamil on platelet aggregation and serum thromboxane formation. We also studied the in vivo effects of verapamil retard on platelet aggregation and serum thromboxane formation. The incubation of verapamil with PRP produced a dose-dependent decrease of in vitro platelet aggregation for all the agents used. Potentiation by verapamil of antiaggregating activity of prostacyclin was also demonstrated; in fact when verapamil and prostacyclin were added simultaneously a synergistic inhibition of platelet aggregation by ADP was observed. In whole blood verapamil partially inhibited thromboxane production only at a higher concentration. In vivo verapamil significantly decreased platelet aggregation induced by ADP and epinephrine while no changes were observed after arachidonic acid. No significant changes occurred in serum TXB2 levels. The observations suggest a potential role for verapamil in antithrombotic therapy as an antiplatelet agent.

Dose-Response Relationship, Drug↗