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E Ragazzoni

Publications and source records attributed to E Ragazzoni.

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

[Medical nephropathies: what has changed in 20 years].

The authors analyse the series of patients with medical nephropathy undergoing renal biopsy between 1973 and 1993 in order to make a diagnostic and prognostic comparison between the first (ID) and second (IID) decade. Clinical indications for biopsy, which became more precise during the second decade, led to the diagnosis of fewer patients with normal histology; the introduction of ME and IF allowed non-significant histological conditions to be reduced during IID; echo-guided biopsy has led to a reduced number of post-biopsy complications in IID compared to ID. Epidemiological analysis reveals the reduction of focal glomerulosclerosis in IID in favour of glomerulonephritis with IgA deposits in correlation with the use of IF; the increase in mebranous glomerulonephritis secondary to increased antigenic stimuli; reduced acute post-infective glomerulonephritis and membrane-proliferative glomerulonephritis owing to an improved prophylaxis of sources of infection. Among the patients undergoing renal biopsy and commencing dialysis an increase was observed in IID in the number of cases of membranous glomerulonephritis or caused by IgA deposits. There was an increased interval between biopsy and the start of dialysis in IID compared to ID, in spite of fewer patients receiving immunosuppressive therapy. This was probably due to the increased number of pathologies with a slower evolution, thus justifying the postponement of the start of dialysis.

Adult↗
PubMed1995

A possible role for nitric oxide but not for prostaglandin E2 in basal and interleukin-1-beta-induced PRL release in vitro.

In previous experiments we have shown that nitric oxide (NO) was able to modulate CRH and ACTH release from cultured rat hypothalamic and anterior pituitary cells, in vitro. Now, we show experimental evidence of an involvement of NO in basal and interleukin-1 beta-induced prolactin (PRL) release. L-NG-nitro-arginine, an inhibitor of nitric oxide synthetase, and hemoglobin, a NO scavenger, impaired basal and interleukin-1-beta-induced PRL release, while molsidomine, a NO donor, was able to release PRL and to amplify interleukin-1-beta-induced PRL release, confirming a modulatory role for nitric oxide in pituitary hormone secretion. On the other hand, no evidence regarding a possible role of prostaglandin E2 (PGE2) in IL-1beta-induced PRL release came out from our experiments.

Animals↗
PubMed1995

Effects of vindesine on hypothalamic-pituitary-adrenal axis.

Vindesine, a cell-cycle-specific agent currently employed in the treatment of some neoplasias, was able to produce a remarkable dose-dependent adrenocortical activation, but it was unable to increase plasma corticosterone in hypophysectomized rats in vivo. In addition, vindesine was able to increase ACTH release in vitro when tested on isolated pituitary cells in culture suggesting a direct involvement of the pituitary gland in the increase of adrenal secretion in vivo.

Adrenocorticotropic Hormone↗
PubMed1994

Effects of lipopolysaccharide on hypothalamic-pituitary-adrenal axis in vitro.

The possible involvement of lipopolysaccharide (LPS) and interleukin-1 beta (IL-1 beta) and their eventual interplay in CRH and ACTH release from cultured hypothalamic and pituitary cells respectively, have been studied. IL-1 beta was able to activate the hypothalamo-pituitary-adrenal axis at both hypothalamic and pituitary sites; LPS showed no direct action at hypothalamic level but it was able to inhibit basal and IL-1 beta-induced ACTH release: this could be responsible for a blunting of the adrenal cortex response that normally occurs in septic shock syndrome.

Adrenocorticotropic Hormone↗
PubMed1994

Peptide histidine isoleucine-like immunoreactivity release from the rat gastric fundus.

1. Longitudinal muscle strips from the rat gastric fundus were subjected to in vitro electrical field stimulation (EFS) under non-adrenergic non-cholinergic (NANC) conditions to study the release of peptide histidine isoleucine-like immunoreactivity (PHI-LI) and the correlation between PHI-LI release and NANC relaxation. 2. Different radioimmunoassay (RIA) systems employing C-terminal- and N-terminal-specific anti-PHI sera were used to determine the relative contributions of PHI and its C-terminally extended forms, peptide histidine glycine (PHI-Gly) and peptide histidine valine [PHV(1-42)], to the PHI-LI released by the rat gastric fundus. 3. In the presence of atropine (1 microM) and guanethidine (5 microM), EFS (120 mA, 1 ms, 0.25-32.0 Hz, trains of 2 min) induced frequency-dependent relaxations of 5-hydroxytryptamine (3 microM) pre-contracted strips. 4. EFS at frequencies of 8-32 Hz evoked significant increases in PHI-LI outflow. The increases in PHI-LI outflow evoked by 16-Hz EFS were abolished by tetrodotoxin (3 microM) and by a calcium-free medium, indicating an active release process from intramural nerves. 5. The EFS-induced release of PHI-LI measured with the N-terminal-specific antiserum was significantly greater than that detected with the C-terminal-specific antisera. 6. Sephadex G-25 gel permeation chromatographic analysis was performed on the PHI-LI release in response to 32-Hz EFS. A C-terminal-specific antiserum revealed one peak co-eluting with the rat PHI standard. When PHI-LI was measured with the N-terminal-specific antiserum, two peaks were found that co-eluted with the rat PHV(1-42) and rat PHI-Gly/PHI standards, respectively. 7. The present data suggest that the extended forms of PHI are the primary components of the PHI-LI released by NANC inhibitory neurones in the rat gastric fundus and support a NANC inhibitory neurotransmitter role for PHI and its extended forms in this tissue.

Animals↗
PubMed1994

[The morphological and histochemical characteristics of the interprismatic structures and the human enamel. A light microscopy study (corrected)].

Inter-rod structures of human enamel were investigated at the light microscopic level in order to define their morphology as well as the presence and distribution of both organic and inorganic molecules inside them. The histologic procedure employed in the present study allowed us to obtain 100 (microns) thick sections from permanent teeth without previous decalcification and paraffin or resin embedding. Three inter-rod structures were identified in the innermost area of the enamel on the basis of their morphologic aspect, namely the endings of dentinal tubules, the spindles and structures with a spherical or ovoidal shape never described before and by us denominated spheroids. Both spindles and spheroids were connected to one or more dentinal tubules which cross the dentin-enamel junction. Measurements performed on all the specimens led to establish the real dimensions of the inter-rod structures. Histochemical staining carried out with selective dyes showed that spindles and spheroids were quite alike similar to each other as far as chemical composition and molecule distribution are concerned. Both structures contained calcium salts, glycosaminoglycans, glycoproteins, but not collagen. The endings of dentinal tubules among the rods showed histochemical characteristics similar to those of spindles and spheroids. On the basis of the above findings, spindles and spheroids could have a dentinal origin, and so likely derived from the metabolic activity of odontoblasts during the tooth-germ development. Whether they are embryonic vestigia without a functional role or are receptors which transmit signals to nerve endings in dentin and pulp remains to be clarified.

Dental Enamel↗
PubMed1994

[Cost methodologies in dialysis in relation to the Italian National Health Service].

This work analyses the economic aspects of dialysis in Italy in relation to government resources allocated to the health service in general. The authors illustrate the procedures used to estimate the resources required by the dialytic programme. The costs of dialytic programmes in different cities and at different periods in the history of the Italian health service are compared. A concrete example is outlined of the economic management of dialysis and the authors demonstrate how the results were obtained using cost analysis.

Health Care Costs↗
PubMed1992

Antipyrine metabolism in patients with liver metastases from colorectal cancer.

BACKGROUND: The influence of cancer on antipyrine metabolism is under debate. METHODS: To assess the functional activity of a liver with solid metastases from primary colorectal cancer, antipyrine metabolism was studied after the drug was administered orally (18 mg/kg body weight) to 55 healthy volunteers, 62 patients with well-compensated cirrhosis, and 42 patients with small (Class A) or massive (Class B) metastatic liver involvement. RESULTS: In patients with cancer, antipyrine clearance (0.472 +/- 0.177 ml/min/kg) was similar to that in healthy volunteers (0.456 +/- 0.198 ml/min/kg) and significantly higher than in those with cirrhosis (0.259 +/- 0.17 ml/min/kg, P less than 0.001). There was no difference in antipyrine pharmacokinetics between Class A and B involvement. In the entire population, antipyrine clearance was correlated with serum albumin levels (r = 0.294, P = 0.0002) and prothrombin activity (r = 0.416, P = 0.001). This positive correlation was not present when only the neoplastic group was considered. No correlation was found between antipyrine clearance and alkaline phosphatase levels. In patients with cancer, no relationship was found between antipyrine clearance and carcinoembryonic antigen and lactic dehydrogenase levels. CONCLUSIONS: These results show that patients with livers largely replaced by solid metastases are able to metabolize antipyrine to the same extent as healthy subjects.

Adult↗
PubMed1992

Release of vasoactive intestinal polypeptide from the rat gastric fundus.

1. Auxotonic responses and release of vasoactive intestinal polypeptide-like immunoreactivity (VIP-LI) induced by electrical field stimulation (EFS) were studied in longitudinal muscle strips from the gastric fundus of reserpinized rats suspended between parallel platinum electrodes in Krebs solution containing atropine (1 microM), 5-hydroxytryptamine (3 microM) and bovine serum albumin (50 mg l-1). 2. EFS (supramaximal voltage, 1 ms, 0.25-32.0 Hz, trains of 2 min) induced frequency-dependent relaxations. 3. EFS at frequencies greater than or equal to 8 Hz also produced significant increases in VIP-LI release. 4. VIP-LI release induced by EFS at 16 Hz no longer occurred in the presence of tetrodotoxin (1 microM) or a Ca(2+)-free medium. 5. Detection of VIP-LI upon activation of inhibitory non-adrenergic, non-cholinergic neurones indicates that VIP meets the 'detectable release' criterion for an inhibitory neurotransmitter in the rat gastric fundus.

Animals↗
PubMed1992

Interleukin-1 beta and interleukin-6 specifically increase the release of prostaglandin E2 from rat hypothalamic explants in vitro.

It has previously been shown that the cytokines interleukin-1 beta and interleukin-6 (IL-1 beta and IL-6) stimulate directly the release of corticotrophin-releasing-hormone-41 from the rat hypothalamus in vitro, while IL-1 beta can also stimulate the release of somatostatin. These effects can be antagonized by drugs which block prostaglandin (PG) synthesis. PGs are also involved in the control of hypothalamic neuropeptides by other neurotransmitters. In the present study, we have characterized the production of PGs from the rat hypothalamus in vitro, and investigated the effects of IL-1 beta and IL-6, as well as the neurotransmitters norepinephrine, acetylcholine and 5-hydroxytryptamine, on the acute release of PGs, using a well-validated acute hypothalamic incubation system. The rate of release of PGs [PGE2, PGF2 alpha, 6-keto-PGF1 alpha (6KPGF1 alpha) and thromboxane B2 (TXB2) in the medium was found to stabilize after 60 min of preincubation and thereafter remain constant, with TXB2 being the predominant species. Twenty-minute incubation in the presence of human recombinant IL-1 beta or IL-6, in the dose range 1-100 U/ml, had no effect on the release of PGF2 alpha, 6KPGF1 alpha or TXB2; however, the release of PGE2 was significantly increased by both IL-1 beta and IL-6. The effect of IL-1 beta was antagonized by both indomethacin and dexamethasone. None of the other neurotransmitters tested had any effect on the release of any of the PGs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Hydroxyurea: relationship between toxicity and centrally-induced adrenal activation.

The anticancer drug hydroxyurea (HU) at doses of 300-800 mg/kg/day causes a dramatic lethality (up to 100% after a 5-day treatment) in hypophysectomized as well as in adrenalectomized rats drinking physiological saline + 5% glucose. Mortality in controls was less than 10% over a 5-day period. Adrenal stimulatory or replacement therapies protect pituitary- or adrenal-ablated rats against HU toxicity. They also counteract white blood cell changes induced by the drug. HU (30-800 mg/kg) induces a dose-dependent increase of plasma corticosterone in normal rats after single or repeated treatments that is not observed in hypophysectomized animals. HU also increases plasma levels of epinephrine, although this finding cannot account for the rise in plasma corticosterone; indeed, it is secondary to a strong rise in plasma corticosterone. The stimulation of the hypothalamic-hypophyseal-adrenal axis induced by HU is responsible for the drug-induced adrenocortical activation. This activation appears to be a valuable defence mechanism protecting intact rats against HU lethality, and its failure causes the dramatic HU lethality in pituitary- or adrenal-ablated animals.

Adrenal Glands↗
PubMed1988

Effects of the benzazepine SCH 23390 on prolactin release from isolated pituitary.

The benzazepine, SCH 23390 (10(-5) M), is able to block D2 anterior pituitary receptors and their interaction with a maximal concentration of dopamine (10(-7) M) in an experimental setting involving superfused pituitary slices and prolactin release by lactotrophs as a functional model of such receptors; this finding which correlates nicely with binding studies and drug-induced hyperprolactinaemia supports a SCH 23390 D1 dose-related selectivity; given at doses higher than those inducing behavioural changes, the compound may affect D2 receptor-driven functions, e.g. prolactin secretion.

Animals↗
PubMed1985

Possible adrenal involvement in hydroxyurea toxicity defense mechanisms.

Changes in blood biochemistry, resembling adrenocortical hyperfunction, induced by oral administration with hydroxyurea (HYD) at a dosage of 800 mg/Kg/d for 5 days (K+ and total protein decrease, total cholesterol increase) are not modified or enhanced (total protein) by adrenalectomy. Adrenalectomy dramatically enhanced the decrease of WBC and neutrophils normally induced by HYD. Replacement therapy with corticosterone attenuated and/or delayed the above changes. Normally-functioning adrenocortical tissue may play a role in protection against HYD haematological toxicity in the rat and the drug-induced hypothalamus pituitary mediated adrenocortical activation seems to represent a mechanism capable of counteracting drug toxicity.

Adrenalectomy↗
PubMedDate not supplied

Neuramide stimulates adrenocorticotropin but not prolactin release from rat pituitary.

Neuramide (NMD), a substance found in crude preparations of porcine stomach extract, is a viral inhibitor that also has putative immunostimulatory effects. The effects of NMD on stress-hormone (ACTH and prolactin-PRL) release were assessed in in vivo and in vitro studies. In the former, blood levels of corticosterone and PRL were measured in NMD-treated male rats. In vitro experiments were performed to evaluate the effects of NMD and three of its fractions (obtained with high performance liquid chromatography) on ACTH and PRL release from perfused rat pituitary slices. NMD increased plasma corticosterone levels in vivo and produced dose-dependent increases in in vitro pituitary release of ACTH. No effects on PRL secretion were observed in vivo or in vitro. The stimulatory effects on ACTH release were caused by the NMD fraction with a molecular weight of > 5000 < 10000 Da.

Adrenocorticotropic Hormone↗