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T Bani Sacchi

Publications and source records attributed to T Bani Sacchi.

At least 19 recordsLinked to original sources
PubMed2001

The vasorelaxant hormone relaxin induces changes in liver sinusoid microcirculation: a morphologic study in the rat.

This study shows that specialized contractile endothelial cells exist in rat liver sinusoids which may be involved in the local control of hemodynamics and which are sensitive to vasoactive agents, including the vasorelaxant hormone relaxin. Male rats were treated with 10 microg relaxin for 4 days; phosphate-buffered saline (PBS)-treated rats were the controls. For comparison, rats treated with relaxin together with the NO-synthase inhibitor N(omega)-nitro-l -arginine methyl ester (L-NAME), and rats treated with the vasodilator taurodeoxycholic acid or the vasoconstrictor ethanol were investigated. Liver fragments were studied morphologically and morphometrically. In the control rats, peculiar contractile cells were present in the endothelial lining. These cells had abundant myofilaments and formed cytoplasmic blebs projecting into and often occluding the lumen. In the ethanol-treated rats, sinusoids were constricted and filled with cytoplasmic blebs. In the relaxin-treated rats, sinusoids were markedly dilated and the cytoplasmic blebs nearly disappeared. Similar findings were observed in the taurodeoxycholic acid-treated rats. The effects of relaxin were blunted by L-NAME, suggesting that the relaxin action involves an NO-mediated mechanism.

Animals↗
PubMed1999

Relaxin promotes differentiation of human breast cancer cells MCF-7 transplanted into nude mice.

Previous studies showed that the hormone relaxin acts on human breast cancer MCF-7 cells in vitro by modulating cell proliferation and promoting cell differentiation toward a duct epithelial phenotype. The present study was designed to investigate whether relaxin retains these properties when acting in vivo on MCF-7 cell tumors developed in athymic nude mice. Mice bearing MCF-7 cell tumors transplanted under the mammary fat pad and estrogenized to sustain tumor growth were treated systemically with relaxin (10 microg/day) for 19 days. Vehicle-treated mice were used as controls. Thirty days later, the mice were sacrificed and tumor fragments were analyzed by light and electron microscopy and immunocytochemistry. Measurements of tumor volume were recorded weekly for the overall experimental period. The results obtained indicate that relaxin treatment promotes differentiation of tumor cells towards both myoepithelial-like and epithelial-like cells, as judged by the ultrastructural features of the cells and by the increased expression of smooth muscle actin and cadherins. Measurements of tumor size and of the number of cycling cells show that relaxin, at the doses and times of exposure used in this study, does not significantly influence tumor growth and cell proliferation.

Actins↗
PubMed1998

Histamine release from rat mast cells induced by the metabolic activation of drugs of abuse into free radicals.

BACKGROUND: The metabolic activation of morphine, cocaine and methadone into free radicals could have pathophysiological relevance in the organic injuries of drug addiction. METHODS: Isolated purified rat serosal mast cells were incubated with morphine, cocaine and methadone (10(-7) M-10(-4) M) with oxidative enzymes (prostaglandin-H-synthetase, 25 mU; rat liver homogenate fraction S 10-mix, 400 microl), and with the drugs of abuse in the presence of oxidative enzymes. Histamine and lactate dehydrogenase (LDH) were analysed with a fluorimetric and spectrophotometric assay, respectively; the generation of malonyldialdehyde (MDA) was measured by a spectrophotometric assay. RESULTS: The release of mast cell histamine and the generation of MDA are present only when mast cells were incubated with the drugs of abuse in the presence of oxidative enzymes. This release was dependent on the concentration of the drug in question and showed a maximum value at 10(-4) M. Moreover, in parallel experiments we demonstrated that, under the same experimental conditions, the release of LDH was always less than 20% of the total, suggesting that this effect is due to a selective exocytotic process. Histamine release and MDA generation were abated by the free radical scavengers: reduced glutathione, 10(-4) M GSH and alpha-tocopherol, 10(-4) M and by the spin trapper 5.5-dimethyl-1-pyrroline-N-oxide, 10(-4) M DMPO. The light and electron microscopic features are consistent with exocytotic secretion in the cases of morphine and methadone and with cell lysis in the case of cocaine. CONCLUSION: These results suggest that morphine, cocaine and methadone are activated into free radicals which produce membrane lipid perturbation and histamine release, suggesting that a massive release of mast cell histamine could be an additional risk factor in heroin and cocaine overdoses.

Animals↗
PubMed1998

Relaxin activates the L-arginine-nitric oxide pathway in vascular smooth muscle cells in culture.

The peptide hormone relaxin (RLX) has been shown to elicit a powerful vasodilatory response in several target organs. This response is mediated by the stimulation of intrinsic nitric oxide (NO) generation. The present study was designed to clarify whether RLX directly promotes the relaxation of vascular smooth muscle cells through stimulation of NO generation. Vascular smooth muscle cells from bovine aortas were incubated with RLX at concentrations ranging from 1 nmol/L to 1 micromol/L. The expression and activity of NO synthase, production of NO, and the intracellular levels of cGMP and Ca2+ were determined. The cell morphology and signal transduction mechanisms of these bovine aortic smooth muscle cells in response to RLX were also studied. RLX stimulated the expression of immunoreactive inducible NO synthase and increased significantly and in a concentration-related fashion inducible NO synthase activity, NO generation, and intracellular cGMP levels. Concurrently, RLX significantly decreased cytosolic Ca2+ concentrations and caused changes in cell shape and the actin cytoskeleton that were consistent with cell relaxation. The signal transduction mechanisms leading to the enhanced expression of inducible NO synthase protein and activity caused by RLX involve the activation of tyrosine kinase, phosphatidylcholine-phospholipase C, and the transcription factor nuclear factor-kappaB, similar to bacterial endotoxins and proinflammatory cytokines. This study suggests that RLX is an endogenous agent capable of regulating vascular tone by activation of the L-arginine-NO pathway in vascular smooth muscle cells.

Analysis of Variance↗
PubMed1995

Effects of relaxin on the endometrial stroma. Studies in mice.

The current study was designed to elucidate the effects of relaxin, administered systemically to mice in combination with estrogen and medroxyprogesterone, on the endometrial stroma, with use of structural, ultrastructural, and immunocytochemical methods. Female, sexually mature virgin mice were placed into 4 groups and treated with estrogen, estrogen + progestin, estrogen + relaxin, and estrogen + progestin + relaxin in sequence. The results obtained show that relaxin causes a striking increase in the protein-synthesizing machinery of endometrial stromal cells, leading them to resemble closely the decidualized cells of rodent pregnant uterus. Relaxin also induces in the same cells the expression of laminin, which is regarded as a reliable marker of decidual transformation of endometrial stromal cells in mice, and which is needed for trophoblast to adhere to and invade the endometrial stroma. Moreover, relaxin seems to synergize with the steroids in promoting a growth response of the endometrial stromal cells. The above findings allow for relaxin to be regarded as an agent capable of promoting decidual transformation of endometrial stromal cells and, possibly, to participate in the events that lead to blastocyst implantation.

Animals↗
PubMed1994

Differentiation of breast cancer cells in vitro is promoted by the concurrent influence of myoepithelial cells and relaxin.

Our previous studies showed that relaxin promotes differentiation of MCF-7 breast adenocarcinoma cells. In the current investigation, we aimed to elucidate whether the effect of the hormone is potentiated when MCF-7 cells are grown together with myoepithelial cells, thus creating a microenvironment reminiscent of the organised tissue architecture of the mammary parenchyma in vivo. The findings obtained reveal that most MCF-7 cells cultured alone have an undifferentiated, blast-like phenotype, only a minority showing a more differentiated phenotype with more organelles and rudimentary intercellular junctions. When co-cultured with myoepithelial cells more MCF-7 cells acquire ultrastructural features consistent with a more differentiated phenotype, such as a rich organellular complement, apical microvilli and intercellular junctions. When relaxin was added to the co-cultures, the ultrastructural signs of differentiation could be observed in even more MCF-7 cells and became more pronounced than in the absence of the hormone, judged by the appearance of a clear-cut polarisation of cytoplasmic organelles, an almost continuous coat of apical microvilli and numerous intracellular pseudolumina.

Adenocarcinoma↗
PubMed1992

Structural changes of the exocrine pancreas in a patient with cholecystolithiasis.

The exocrine pancreas has been studied histologically, morphometrically, and ultrastructurally in a patient with cholecystolithiasis in comparison with three control patients free from gastrointestinal or pancreatic diseases. In the gallstone-bearing patient, acinar cells undergo a significant increase in the average cell area and average zymogenic area (i.e., the portion of acinar cell cytoplasm occupied by zymogen granules). In addition, these cells showed cytological signs of enhanced synthesis of secretory proteins and increased formation and release of zymogen granules. The findings concerning centroacinar/ductular cells are consistent with a significant increase in their number and average cell area that is associated with ultrastructural signs of enhanced functional activity.

Adult↗
PubMed1992

Are pancreatic VIPomas paraneuron neoplasms? A clue to the neuroectodermal origin of these tumors.

Three pancreatic vasoactive intestinal polypeptide (VIP)-producing tumors associated with the watery diarrhea-hypokalemia-achlorhydria syndrome were studied histologically, ultrastructurally, and immunocytochemically. All the tumors contained varying numbers of cells arranged in pseudoglandular structures. The cells showed a polar organization, with apical tuft of microvilli and basal VIP-containing, synaptic vesicle-like granules. Based on the morphology of the VIPoma cells typical of recepto-secretory cells, together with the ability to synthesize and release a peptide that in normal conditions is expressed exclusively by neurons, and the absence of VIP-producing endocrine cells in normal pancreas and gastrointestinal mucosa, the hypothesis is drawn that the pancreatic VIPomas reported here are paraneuron neoplasms, which possibly originate from neuroectodermal ancestors.

Adult↗
PubMed1992

Immunocytochemical and ultrastructural abnormalities of islet tissue in patients with VIP-producing tumors of the pancreas.

Nontumoral endocrine pancreas from three patients with malignant vasoactive intestinal polypeptide (VIP)-omas and the Verner-Morrison (watery diarrhea, hypokalemia, and hypoachlorhydria) syndrome was studied immunocytochemically, ultrastructurally, and morphometrically. Compared with normal islets from control subjects, those of the VIPoma-associated pancreas showed a decrease of immunoreactive insulin in B-cells associated with cytological features indicative of enhanced insulin synthesis and secretion and an increase in the number of immunoreactive somatostatin- and pancreatic polypeptide-containing cells, in the absence of ultrastructural signs of modified secretory activity. No substantial alterations of A-cells were observed. In addition, images of diffuse de novo formation of ducts and islet tissue were often found. Possible mechanisms involved in determining the above changes are discussed.

Adult↗
PubMed1990

Histamine release by platelet aggregation.

Coincubation of rat serosal mast cells with human platelets leads to a significant release of histamine. which dose-dependently increases when platelet aggregation is induced by various concentrations of arachidonic acid. In turn, histamine enhances platelet aggregation induced by different agonists, this effect being mimicked by pyridyl-ethyl-amine (PEA), blocked by mepyramine and amplified by ranitidine. The data suggest the existence of a platelet-derived histamine releasing factor (PDHRF) and indicate the presence of platelet H1 and H2 receptors, capable of modulating platelet aggregation.

Animals↗
PubMed1989

A malignant tumor of the pancreas producing glucagonoma syndrome: immunocytochemistry and ultrastructure of liver metastases and comparison with the primary tumor.

In this study, liver metastases from a patient with a pancreatic glucagonoma producing the syndrome have been investigated histologically, ultrastructurally, and immunocytochemically. A comparison has also been made between the metastases and the primary pancreatic tumor investigated in a parallel study. In the metastatic tissue, glucagon-, pancreatic polypeptide (PP)-, and somatostatin-containing cells were found together with a majority of cells without any immunoreactivity. Glucagon-positive cells were much more numerous than PP- and somatostatin-immunoreactive cells. As in the primary tumor, double immunogold staining of ultrathin sections demonstrated the co-existence of glucagon and PP immunoreactivities in most of the granulated cells, but PP immunolabeling was often faint, so that it probably could not be revealed by the PAP method in light microscopical sections. Such a finding, together with the histological and ultrastructural features, is consistent with an ontogenic and phylogenetic primitiveness of the metastatic cell population.

Adenoma, Islet Cell↗
PubMed1989

A malignant tumor of the pancreas producing glucagonoma syndrome: coexistence of glucagon and pancreatic polypeptide (PP) in the tumor cells.

A malignant tumor of the pancreas producing the glucagonoma syndrome and associated with high plasma levels of glucagon and pancreatic polypeptide was studied histologically, ultrastructurally, and immunocytochemically. The histologic and ultrastructural features were closely similar to those of previously reported malignant glucagonomas. However, immunolabeling with specific antisera revealed that, in addition to cells having only glucagon- or only pancreatic polypeptide-immunoreactivity, other cells were also present, showing a co-existence of both peptides. These findings indicate that the tumor contains a cell population with a phenotype similar to that of intestinal L-cells rather than to pancreatic A-cells.

Adenoma, Islet Cell↗
PubMed1989

The endocrine pancreas in patients with insulinomas. An immunocytochemical and ultrastructural study of the nontumoral tissue with morphometrical evaluations.

The nontumoral endocrine pancreas was studied immunocytochemically and ultrastructurally in 12 patients with isolated insulinomas. Changes affecting hormone content and secretion of B-, A-, and D-cells were found in the islets of insulinoma-bearing patients when compared with controls, in terms of a significant decrease of the insulin-immunoreactive tissue areas and an increase in the glucagon- and somatostatin-immunoreactive ones. Conversely, only in two of the patients examined were PP-immunoreactive tissue areas augmented. Diffuse ducto-endocrine proliferation (nesidioblastosis) was also a common feature in the tumor-associated pancreas. Both morphometry and qualitative features revealed that islet cell hyperplasia occurs in the presence of insulinoma. Ultrastructural examination revealed that the functional activity of B-cells is substantially depressed in the insulinoma-bearing patients, whereas it is maintained or even enhanced in the other cell types. The islet content in immunoreactive insulin decreases along with duration of hypoglycemic symptoms. The present findings indicate that, in the presence of an insulinoma, the endocrine pancreas undergoes changes that can be regarded as an adaptive response to the chronic excess of insulin and are possibly responsible for the patients' postoperative clinical course.

Adenoma, Islet Cell↗
PubMed1988

Effects of relaxin on the microvasculature of mouse mammary gland.

The effects of RLX on the microvasculature of the mouse mammary gland are reported. RLX (pure porcine standard NIH-RXN-P1) at a dose of 3 GPU was administered subcutaneously to virgin adult mice ovariectomized 12 days before. The mammary glands were removed 18-20 h after RLX injection and their examination by light microscopy did not reveal any substantial growth-response to the hormone. Histology and morphometry indicated striking dilation of microvessels, especially capillaries, and electron microscopy revealed an increase in the micropinocytotic vesicles, thus suggesting enhanced transendothelial transport of substances. Such phenomena, which were independent of a release of granules by mast cells, may represent an important component of the mammotrophic action of RLX.

Animals↗