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Biomedical subjects

C Surrenti

Publications and source records attributed to C Surrenti.

At least 73 records · Page 4Linked to original sources
PubMed1990

Gastric juice immunoreactive epidermal growth factor levels in patients with peptic ulcer disease.

Immunoreactive epidermal growth factor (IR-EGF) was measured by a highly sensitive and specific radioimmunoassay in gastric juice samples obtained during endoscopy from 26 control subjects, 44 patients with duodenal ulcers, and 18 with benign gastric ulcers. In the active stage, the concentrations of the peptide were consistently reduced, compared with those found in control subjects (592.7 +/- 55.8 pg/ml), in both duodenal (262.6 +/- 21.4 pg/ml) and gastric ulcer patients (320.2 +/- 34.1 pg/ml) (p less than 0.001 and 0.01, respectively). Mean IR-EGF values distinctly lower than in the controls were still present in the gastric juice of patients with inactive duodenal ulcers (349.7 +/- 35.9 pg/ml; p less than 0.001), whereas no difference was observed in patients with healed gastric ulcers (502.2 +/- 132.3 pg/ml). Although these findings suggest a possible role for EGF deficiency in the pathogenesis of peptic ulcer disease, the pathophysiological significance of our results (if any) remains to be elucidated.

Adult↗
PubMed1990

Cellular localization of type I III and IV procollagen gene transcripts in normal and fibrotic human liver.

The authors have determined the cell types producing alpha 1 (I), alpha 2 (I), alpha 1 (III), and alpha 1 (IV) procollagen gene transcripts in adult human liver by in situ hybridization with [35S]-labeled RNA probes. The liver specimens comprised a total of 20 biopsies with normal histology and biopsies with fibrosis or cirrhosis at different clinical stages and of heterogeneous origins. In normal liver, procollagen type I, III, and IV transcripts were detected in stromal and vascular mesenchymal cells of portal tracts and central veins, as well as in some perisinusoidal cells of the lobule. In fibrotic liver, increased levels of these procollagen mRNAs were observed in the same locations, and particularly enhanced in stromal cells of fibrotic septa and portal tracts, as well as in perisinusoidal cells. Expression of alpha 1 (IV) procollagen RNA was additionally found in some vascular endothelial and bile duct epithelial cells. Although previously suggested as the major source of liver collagens, hepatocytes showed no significant procollagen transcript levels in any of our samples. Thus, procollagen synthesis does not appear to be a function of hepatocytes, but rather of mesenchymal, endothelial, and bile duct epithelial cells in adult human liver. These findings may have implications for the development of specifically targeted antifibrotic therapies.

Adult↗
PubMed1989

Effect of thiorphan on response of the guinea-pig gallbladder to tachykinins.

Tachykinins produced a concentration-related contraction of the isolated guinea-pig gallbladder, with a rank order of potency neurokinin A (NKA) greater than Arg-neurokinin B = neurokinin B (NKB) greater than substance P (SP). Only the effect of SP was potentiated by thiorphan (0.1-10 microM). A significant enhancement of the response to SP was also produced by captopril (1 microM). [Nle10]NKA-(4-10) and [beta-Ala8]NKA-(4-10), selective NK-2 receptor agonists, were active, whereas [Pro9]SP sulfone (selective NK-1 agonist) was almost ineffective. [MePhe7]NKB (selective NK-3 agonist) had some activity but only at high concentrations. Septide was almost ineffective and DiMeC7 had an action comparable to that of [MePhe7]NKB. None of the effects induced by these synthetic tachykinin analogs were significantly potentiated by thiorphan. Capsaicin (10 microM) produced a contraction which was unaffected by thiorphan. Both capsaicin and NKA-induced contractions were antagonized by Spantide at concentrations (5-10 microM) which had no effect against the atropine-sensitive contractions produced by electrical field stimulation. Capsaicin (1 microM) produced a consistent release of SP-like immunoreactivity (SP-LI) and a second application of the drug had no further effect, indicating complete desensitization. SP-LI release by capsaicin was almost doubled in the presence of thiorphan. These findings indicate that NK-2 and possibly some NK-3 receptors mediate the contractile response of the guinea-pig gallbladder to tachykinins. Both exogenous and endogenous (released by capsaicin) SP were degraded to a significant extent in this organ via a thiorphan-sensitive mechanism, the identity of which remains to be established.

Animals↗
PubMed1989

Duodenal ulcers are associated with a depletion of duodenal calcitonin gene-related peptide-like immunoreactivity in rats.

Calcitonin gene-related peptide-like immunoreactivity (CGRP-li) was decreased in duodenal samples from animals treated with ulcerogens such as dulcerozine, cysteamine or mepirizole. The degree of these experimental ulcers was inversely correlated with the levels of duodenal CGRP-li. These findings show that endogenous CGRP may play an important role in duodenal ulcerogenesis.

Animals↗
PubMed1989

Effects of calcitonin gene-related peptide (CGRP), neurokinin A and neurokinin A (4-10) on the mitogenic response of human peripheral blood mononuclear cells.

(1) We have studied the ability of some regulatory peptides to induce a mitogenic (incorporation of tritiated thymidine) response in human peripheral blood mononuclear cells (PBMC) and to modify the response produced by phytohaemagglutinin (PHA), a well known PBMC mitogen. (2) Human calcitonin gene-related peptide (hCGRP), human or salmon calcitonin (hCT, sCT), neurokinin A (NKA) and neurokinin (4-10) (up to 1 microM for each peptide) did not produce per se any significant PBMC stimulation. (3) hCGRP (0.1 nM-1 microM) produced a concentration dependent enhancement of the response to a submaximal concentration of PHA (1 microgram/ml). On the other hand, hCGRP decreased the mitogenic response to a maximal concentration of PHA (25 micrograms/ml). (4) Neither hCT nor sCT (0.1 nM-1 microM) had a significant influence on the response to PHA (1-25 micrograms/ml). (5) Both NKA and NKA (4-10) produced a concentration-dependent (1 fM-10 pM) enhancement of the response to 1 microgram/ml PHA, while these compounds had no effect on the response to 25 micrograms/ml PHA. (6) These findings suggest a potent modulatory action of CGRP and NKA, two peptides present in sensory and other nerves, on immune function which is possibly mediated via C2 receptors for CGRP and NK-2 tachykinin receptors, respectively.

Adult↗
PubMed1989

Release of substance P- and calcitonin gene-related peptide-like immunoreactivity and motor response of the isolated guinea pig gallbladder to capsaicin.

The aim of this study was to assess whether a local motor response to capsaicin could be observed in the isolated guinea pig gallbladder and to discover the mechanism involved. Capsaicin produced a contraction of this organ that exhibited desensitization, suggesting a specific action on sensory nerves. In preparations preexposed to capsaicin to produce a functional blockade of the capsaicin-sensitive sensory fibers, the contractile response to field stimulation was unaffected as compared with controls. Tachykinins (substance P and neurokinin A) produced a concentration-related contraction of this organ, neurokinin A being more potent than substance P. Spantide, a tachykinin antagonist, markedly inhibited the capsaicin-induced gallbladder contraction, leaving the atropine-sensitive response to field stimulation unaffected. Calcitonin gene-related peptide (CGRP) produced a concentration-related relaxation, which was tetrodotoxin-resistant, suggesting a direct effect on muscle cells. Repeated administration of CGRP produced desensitization. At this stage, application of capsaicin produced a contractile response much larger than in controls. Both substance P- and CGRP-like immunoreactivity were detected in the guinea pig gallbladder by radioimmunoassay and were significantly reduced after systemic capsaicin desensitization. Capsaicin induced the simultaneous release of substance P- and CGRP-like immunoreactivity from superfused isolated gallbladders. These findings indicate that capsaicin-sensitive nerves in the guinea pig gallbladder can produce a local motor response involving the release of multiple neuropeptides. In the guinea pig gallbladder, tachykinins and CGRP might act as "physiologic antagonists," as observed in other viscera from rats and guinea pigs.

Animals↗
PubMed1989

Culture of fibroblast-like cells derived from normal human liver. Identification by morphologic and immunologic criteria.

Fibroblast-like cells were isolated from liver biopsies of normal adult donors. The cells were grown in tissue culture first as a heterogeneous population, afterwards as homogeneous cultures of fibroblast-like cells. Phase contrast microscopy demonstrated that cultured human liver fibroblast-like cells grew as monolayers of slender, spindle-shaped cells in parallel arrays. By transmission electron microscopy (TEM), cultured human liver fibroblasts were seen to have morphological characteristics of in vitro fibroblasts. By immunoelectronmicroscopy, cultured fibroblast-like cells were seen to produce components of connective tissue, such as fibronectin, collagen type I, type III, and small amounts of collagen type IV. These studies demonstrate that it is possible to culture morphologically and immunologically identifiable human liver fibroblasts from normal human liver.

Adult↗
PubMed1989

Enzyme immunoassay of gastric luminal prostaglandin E2 in duodenal ulcer disease.

A highly sensitive enzyme immunoassay was used to determine gastric juice prostaglandin E2 (PGE2) levels in control subjects with or without gastritis and in both active or inactive duodenal ulcer patients. Mean pentagastrin-stimulated PGE2 concentration was significantly lower in patients with duodenal ulcer than in control subjects considered as a whole group (with or without gastritis). However, no such difference was found between duodenal ulcer patients and controls showing histologically normal gastric mucosa. On the other hand, controls with chronic superficial gastritis had PGE2 levels significantly higher than those of histologically normal subjects and duodenal ulcer patients. Therefore, it seems unlikely that an absolute gastric PGE2 deficiency is involved in the pathogenesis of duodenal ulcer disease. However, the possibility that PGE2 synthesis could be deficient in relation to the prevailing level of mucosal inflammation cannot be excluded.

Adult↗
PubMed1989

S-adenosylmethionine inhibits collagen synthesis by human fibroblasts in vitro.

Previous studies have indicated that S-adenosylmethionine (SAMe), the precursor of methyl groups and thiols, exerts an anti-inflammatory activity. In order to clarify whether this molecule also has antifibrotic properties, we evaluated its pharmacological effects on human fibroblasts in vitro. Accordingly, fibroblasts between 5 and 10 subcultures were incubated for 24 h with different SAMe concentrations (from 0.005 to 626 microM). Fibroblast proliferation measured by incorporation of labeled thymidine was not affected by SAMe in the range of the tested concentrations. Moreover, cell viability assessed by trypan-blue exclusion test was greater than 98% in all cultures, without any difference between SAMe and control cultures. Collagen synthesis estimated by HPLC measurement of hydroxyproline in both media and cells was not modified by SAMe concentrations lower than 0.05 microM. On the other hand, SAMe concentrations higher than 0.05 microM significantly (p less than 0.01) reduced collagen synthesis as compared with untreated controls. This effect was not dose-dependent. In conclusion, this study indicates that SAMe addition to fibroblasts in the range of concentrations which can be found in vivo induces a marked decrease (about 50% of control value) in collagen synthesis with no adverse effects on cell proliferation and viability. These findings suggest further investigation of the potential antifibrotic role of SAMe.

Cell Division↗
PubMed1988

A second antibody solid-phase enzyme immunoassay of prostaglandin E2 in human gastric juice.

A second antibody solid-phase enzyme immunoassay for the determination of prostaglandin E2 in human gastric juice was developed using acetylcholine esterase as label, covalently coupled to the eicosanoid. The assay was performed on 96-well microtiter plates coated with the second antibody (swine antirabbit IgG antibody). The enzyme-labeled and unlabeled prostaglandin E2 were allowed to react in a competitive manner with the immobilized specific antibody (rabbit anti-prostaglandin E2 serum). After addition of the enzyme substrate, the specifically bound acetylcholine esterase was determined at 414 nm by means of a colorimetric assay and the enzyme activity was correlated with the amount of unlabeled prostaglandin E2. According to the calibration curve, prostaglandin E2 was determined in the range of 0.5-250 pg/ml. The minimal detectable concentration of prostaglandin E2 was 1.9 +/- 0.2 pg/ml. The intraassay coefficient of variation was less than 10%. Most prostaglandins and their metabolites tested showed a cross-reactivity of less than 1%.

Chromatography, High Pressure Liquid↗
PubMed1988

Capsaicin-induced release of substance P-like immunoreactivity from the guinea pig stomach in vitro and in vivo.

Capsaicin induced a release of substance P-like immunoreactivity (SP-LI) in superfusates from gastric fundic mucosa of guinea pig in vitro and from gastric perfusates of anaesthetized guinea pigs in vivo. Tissue SP-LI from the gastric fundus was reduced (43.4%) by systemic capsaicin desensitization. These findings provide direct neurochemical evidence which supports the hypothesis for the involvement of local neuropeptide release in the 'gastric defence mechanism' played by capsaicin-sensitive nerves.

Animals↗
PubMed1988

Serum HBV DNA and intrahepatic hepatitis B core antigen (HBcAg) in chronic hepatitis B virus infection: correlation with infectivity and liver histology.

In this study we investigated the HBeAg/anti HBeAg status, the liver histological features, the intrahepatic localization of HBcAg, and the presence of serum HBV DNA in a group of 79 HBsAg-positive patients. We found a close relationship between the presence of HBV DNA and intrahepatic HBcAg in HBeAg-positive patients. Among the 56 anti-HBeAg-positive patients considered, 13 (23.2%) showed the presence of intrahepatic HBcAg and serum HBV DNA. In this group of patients, active viral replication was associated with a chronic inflammatory liver disease and particularly with CAH. Furthermore, a prevalent cytoplasmic localization of HBcAg was found in 66.6% of patients affected by CAH, showing that this peculiar distribution of HBcAg seems to be associated with a poor prognosis.

Adult↗
PubMed1987

Is determination of serum N-terminal procollagen type III peptide (sPIIIP) a marker of hepatic fibrosis?

Serum N-terminal procollagen type III peptide (sPIIIP) levels were evaluated in 58 patients affected by chronic liver disease, in order to assess the usefulness of sPIIIP as a marker of hepatic fibrosis. In 45 patients sPIIIP was also correlated to liver histology; biopsies were scored by two of the authors, without knowledge of diagnosis. Compared to normal controls, sPIIIP concentration was found to be significantly elevated in chronic active hepatitis (CAH) and in cirrhosis, but not in fatty liver. Patients affected by chronic persistent hepatitis (CPH) had values of sPIIIP higher than normal in four of 11 cases considered. A close correlation was found between sPIIIP values and histological parameters of inflammation, necrosis, and degeneration, while the relationship between sPIIIP levels and fibrosis was weaker. These data suggest that sPIIIP determination may reflect the extent of inflammatory changes in the liver; but it cannot be considered a reliable index of hepatic fibrosis.

Adult↗
PubMed1987

Cell-mediated immunity to HBcAg in chronic HBV infection.

The role of hepatitis B core antigen (HBcAg) as a possible target of cell-mediated immune response in chronic hepatitis B virus (HBV) infection has been recently emphasized. Peripheral blood leukocytes (PBLs) from 35 chronic carriers of hepatitis B surface antigen (HBsAg) were studied in vitro for their immune response to a purified preparation of HBcAg isolated from circulating Dane particles. PBLs from all the studied HBsAg-positive patients yielded a stimulation index above 3, with values ranging from 3.1 to 38.1. None of the healthy seronegative subjects, taken as control group, had a stimulation index above 2, with a mean value +/- SD of 1.28 +/- 0.35. Levels of PBL stimulation correlated with the histologic activity of liver disease, and the differences reached statistical significance. These results indicate that lymphocyte response to HBcAg may be relevant in determining liver cell damage.

Adult↗
PubMed1986

Diagnostic significance of anti-HBc IgM (RIA) in healthy HBsAg carriers and in chronic hepatitis B.

The diagnostic significance of IgM antibody against hepatitis B core antigen (anti-HBc) in healthy hepatitis B surface antigen (HBsAg) carriers and in subjects affected by chronic hepatitis B was evaluated. IgM anti-HBc was sought and found in all nine patients examined who were affected by acute HBsAg-positive hepatitis. It was also detected in 2 out of 18 patients with HBsAg-positive chronic persistent hepatitis and in 12 out of 42 patients affected by HBsAg-positive chronic active hepatitis. The absence of this marker was noted in all 26 HBsAg healthy carriers and in the subjects with HBsAg-positive cirrhosis. No relationship was found between the presence of IgM anti-HBc and the degree of inflammatory activity in the patients with HBsAg-positive chronic active hepatitis. A correlation was not found between the presence of IgM anti-HBc and the presence of hepatitis B e antigen (HBeAg) in the same patients. These data show that the absence of IgM anti-HBc may be useful in identifying healthy carriers of HBsAg. The presence of this antibody may be a suitable indication of acute HBsAg-positive hepatitis. In patients with chronic active hepatitis B the presence of IgM anti-HBc cannot be used as diagnostic tool in predicting the severity of liver disease.

Antibody Specificity↗
PubMed1985

Immune mechanisms for hepatic fibrogenesis. T-lymphocyte-mediated stimulation of fibroblast collagen production in chronic active hepatitis.

Lymphocytes can produce soluble factors capable of enhancing fibroblast proliferation and collagen synthesis. T-lymphocytes, adherent cells and undifferentiated peripheral blood mononuclear cells from patients with HBsAg-positive chronic active hepatitis and from HBsAg healthy carriers were triggered with purified HBsAg and tested for their ability to enhance collagen production by human dermal fibroblast cultures. Purified HBsAg did not induce any proliferative response in the mononuclear cell cultures. Addition of patient T-lymphocyte supernates to monolayers of fibroblast consistently resulted in a significant enhancement of collagen production. On the contrary, supernates harvested from adherent cell cultures did not demonstrate any stimulatory activity. We therefore assumed that the observed enhancement of collagen production was probably the result of lymphokine(s) produced by T-lymphocytes. This fibrogenic factor (or factors), which is released by T-cells independently of the presence in vitro of HBsAg, is stable at -80 degrees C, not dialyzable and, by Sephadex G-100 gel filtration, is present in a fraction which collects substances of a molecular weight between 50 000 and 100 000. Mononuclear cell supernates from HBsAg healthy carriers did not influence fibroblast collagen accumulation. These data emphasize the possible role that lymphokines may play in the pathogenesis of fibrosis during the natural history of chronic liver disease.

Adult↗