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A Mazzone

Publications and source records attributed to A Mazzone.

At least 19 recordsLinked to original sources
PubMed2006

Comparison between intravenous iloprost and vasoactive drugs in limb ischemia IIB severe. A retrospective analysis.

AIM: Peripheral arterial vascular disease is caused by atherosclerosis. The severity of peripheral arterial disease is closely associated with the risk of myocardial infarction, ischemic stroke, and death from vascular causes. Approximately 1/3 of patients with peripheral disease have typical claudication. The goals of treatment for patients with claudication are to relieve their exertional symptoms, increase walking capacity, and globally improve their quality of life. In the peripheral arterial disease IIB stage, with claudication < 100 meters, no useful medical therapy is available. Aim of this investigation is to analyse, in a retrospective way, two groups of patients treated with vasodilator drugs or iloprost. METHODS: Data from 99 patients were registered: 79 patients were treated regularly with iloprost, administered for 10 days, 4 times a year. The 2nd group of 20 patients was treated with buflomedil 600 mg/die or pentoxifilline 1200 mg/die. The end point was the pain-free walking distance (PFWD) evaluated with treadmill test at basal conditions and at 3, 6, 12, 18 months. RESULTS: Treatment groups showed no difference as for occurrence of by-pass surgery or endovascular procedures during follow-up. Improvement in PFWD was significantly more evident in patients treated with iloprost as compared with the control (P = 0.02). Even considering the PFWD variations at any follow-up step vs basal value, we always observed a statistically significant difference with iloprost, P < 0.0001. CONCLUSIONS: The study suggests that iloprost may be effective in improving walking distance in severe IIB stage peripheral arterial vascular disease.

Adult↗
PubMed2005

Altered expression of aquaporin 4 and H(+)/K(+)-ATPase in the stomachs of peptide YY (PYY) transgenic mice.

BACKGROUND INFORMATION: The hormone PYY (peptide YY), synthesized by endocrine cells in the pancreas, ileum, colon and stomach has widespread inhibitory effects on gastrointestinal and pancreatic fluid secretion. Transgenic mice expressing a viral oncoprotein under the control of the PYY gene 5'-flanking region develop well-differentiated colonic endocrine tumours producing mainly PYY and enteroglucagon. In the present study, we investigated the expression of AQP4 (aquaporin 4) water channel and H(+)/K(+)-ATPase in stomachs from both control and transgenic mice. RESULTS: Semi-quantitative RT (reverse transcriptase)-PCR showed an increase in the AQP4 transcript compared with control mice. Quantitative Western-blot analysis of stomachs from control and transgenic mice confirmed a significant increase in the 30 kDa AQP4 protein in transgenic mice. In control mice, AQP4 is specifically expressed in the basolateral membrane of gastric parietal cells, located in the basal region of the fundic glands. This particular location suggests that parietal cells in the base region of gastric pits might have a major role in water transport when compared with the more superficial parietal cells. Interestingly, immunofluorescence studies on transgenic mice revealed that the quantitative increase of AQP4 expression was actually due to an increase in the number of AQP4-expressing epithelial cells rather than to a higher expression of AQP4 in parietal cells. In fact, immunofluorescence experiments using the specific antibody raised against the AE2 isoform of Cl(-)/HCO3- exchanger specifically expressed in parietal cells confirmed that the number of parietal cells was comparable in both PYY and control stomachs. Moreover, in transgenic mice, a parallel significant decrease in the expression of H(+)/K(+)-ATPase was observed, as revealed by RT-PCR, quantitative immunoblotting and immunofluorescence. CONCLUSIONS: In the present study, we demonstrate that the sustained inhibition of gastric secretion due to tumours producing PYY/enteroglucagon in transgenic mice is associated with an increase in AQP4 expression and a down-regulation of H(+)/K(+)-ATPase in parietal cells that acquire the characteristics of basal parietal cells. The absence of H2 receptors-mediated signalling due to the inhibition of histamine release from ECL (enterochromaffin-like) cells by PYY may be in part responsible for the observed increase in the number of parietal cells expressing AQP4.

Animals↗
PubMed2005

Unusual presentation of a transparietal cavernous hemangioma of the esophagus.

Hemangiomas are tumors of vascular origin and represent less than 3% of benign neoplasm of the esophagus. We herein report a case of a 55-year-old man, who presented transitory dysphagia and weight loss. A malignancy could not be excluded by a complete work-up, including esophagogram, endoscopic biopsies, CT scan, esophageal endoscopic ultrasonography, PET and thoracoscopic biopsies. Only after partial esophagectomy with laparoscopic gastric mobilization was histological diagnosis obtained. In fact, on microscopic observation of the specimen, the neoplasm appeared to be a cavernous hemangioma of the esophageal submucosa with transparietal extension.

Deglutition Disorders↗
PubMed2004

Increase in peripheral benzodiazepine receptors on monocytes in fibromyalgia.

OBJECTIVE: The aim of this study is to evaluate the expression of Peripheral Benzodiazepine Receptors (PBRs) on leukocytes in patients affected by primary fibromyalgia and to argue their possible role in pain perception and in modulation of immunologic process. METHODS: The expression of PBRs has been evaluated by flow cytometry on monocytes, on lymphocytes and on granulocytes in twenty patients with primary fibromyalgia, with indirect immunofluorescence methods. RESULTS: Upregulation of leukocyte PBRs expression has been demonstrated in fibromyalgia. A statistically significant difference has been documented only in monocytes. The monocyte PBRs expression was 26.74 +/- 14.84 MIF in fibromyalgia versus 17.45 +/- 8.54 MIF in controls (P < 0.023). Upregulation of PBRs expression, although not statistically significant, was also observed in lymphocytes and granulocytes. CONCLUSIONS: The monocyte PBRs overincrease in fibromyalgia may be due to abnormalities in the regulation of pain or to inflammation. It might perhaps explicate the possible mechanisms of therapeutic response to benzodiazepine in fibromyalgia.

Adult↗
PubMed2002

Effects of iloprost on adhesion molecules and F1 + 2 in peripheral ischemia.

BACKGROUND: Iloprost has beneficial effects on microcirculation by preventing platelet and leukocyte reciprocal activation, which is known to lead to endothelial damage and acute thrombosis. This drug also reduces inflammatory system activation by decreasing alpha M beta 2 integrin expression on the phagocyte membrane, might have a role in the protection and restoration of endothelial integrity and might interact with coagulation cascade activation. DESIGN: Forty patients were enrolled: 29 with systemic sclerosis (SSc) and 11 with peripheral artery disease (PAD). Iloprost was administered for 5 days in the first group and for 21 days in second group of patients. To ascertain whether iloprost modifies the parameters of endothelial and coagulation cascade activations, the plasma concentrations of S-ICAM-1 and F1 + 2 were detected in patients at baseline, after 5 days and, in PAD patients only, after 21 days of iloprost therapy. S-ICAM-1 is the endothelial counter receptor for alpha M beta 2 integrin and is a marker of endothelial cell activation; and F1 + 2 is a marker of coagulation cascade activation. RESULTS: After infusion of iloprost a significant decrease of S-ICAM-1 was observed in both the SSc (P < 0.002) and PAD patients (P < 0.004). Similarly, a significant decrease of F1 + 2 was observed in the SSc (P < 0.0004) and PAD patients (P < 0.003). CONCLUSIONS: The study provides evidence that iloprost reduces endothelial cells and coagulation cascade activations. Both of these mechanisms are responsible for improvement in microvascular functional capacity and for the long-term clinical benefit observed. After iloprost infusion, the SSc patients showed marked reductions in F1 + 2 and S-ICAM-1 concentrations that were statistically more significant relative to the PAD patients.

Adult↗
PubMed2001

Possible involvement of aquaporin-7 and -8 in rat testis development and spermatogenesis.

Fluid secretion and reabsorption are of central importance in male reproductive (MR) physiology. However, the related molecular mechanisms are poorly known. Here, potential roles for AQP7 and AQP8, two aquaporin water channels abundantly expressed in the MR tract, were investigated by studying their expression and distribution in the developing testis of the Wistar rat. By semiquantitative RT-PCR and immunoblotting, first expression of AQP7 was noted at postnatal day 45 (P45), with levels increasing substantially at P90 and remaining at high levels thereafter. AQP8 began to be expressed at P15, rapidly increased until P20, and remained fairly stable thereafter. Immunohistochemical analyses demonstrated AQP7 in elongated spermatids, testicular spermatozoa, and residual bodies at P45 with increased signal intensity thereafter. AQP8 was observed in primary spermatocytes from P20 to P30 and, in elongated spermatids, residual bodies and Sertoli cells at P30 and thereafter. The ontogeny and distribution of AQP7 and AQP8 in rat testis suggest involvement in major physiologic changes in testis development and spermatogenesis.

Animals↗
PubMed2001

Increased production of inflammatory cytokines in patients with silent myocardial ischemia.

OBJECTIVES: The aim of the study was to examine the inflammatory cytokines in patients with myocardial ischemia to evaluate whether silent ischemia patients exhibit any particular cytokine pattern. BACKGROUND: Silent myocardial ischemia is frequently observed in patients with coronary artery disease. Various endogenous mechanisms control a patient's perceived intensity of pain. Among them, the inflammatory process and the related cytokine production are known to modulate the threshold for activating the primary afferent nociceptors. METHODS: Seventy-eight patients with reproducible exercise-induced myocardial ischemia were studied: 34 symptomatic patients, with rest and/or stress angina; 44 asymptomatic patients, with no symptoms during daily life activities or during positive exercise stress test. Venous blood samples were taken from all patients to evaluate the expression of CD11b receptors both on neutrophils and monocytes. Frozen plasma samples (at -80 degrees C) were used to quantify the anti-inflammatory (interleukin-4 and -10, transforming growth factor-beta) and the proinflammatory cytokines (tumor necrosis factor-alpha, interferon-gamma, interleukin-1beta and -6). RESULTS: In asymptomatic patients lower CD11b receptor expression and higher concentration of anti-inflammatory cytokines were observed. Proinflammatory cytokine production was similar in the two groups. CONCLUSIONS: The data suggest that an "anti-inflammatory pattern" of cytokine production correlates with silent ischemia and that the immune and inflammatory system activation may be crucial for angina symptoms.

Aged↗
PubMed2001

Expression and immunolocalization of the aquaporin-8 water channel in rat gastrointestinal tract.

A remarkable amount, of water is transported in the gastrointestinal (GI) organs to fulfil the secretory and absorptive functions of the GI tract. However, the molecular basis of water movement in the GI epithelial barriers is still poorly known. Important clues about the mechanisms by which water is transported in the GI tract were provided by the recent identification of multiple aquaporin water channels expressed in GI tissues. Here we define the mRNA and protein expression and the cellular and subcellular distribution of aquaporin-8 (AQP8) in the rat GI tract. By semi-quantitative RT-PCR the AQP8 mRNA was detected in duodenum, proximal jejunum, proximal colon, rectum, pancreas and liver and, to a lesser extent, in stomach and distal colon. Immunohistochemistry using affinity-purified antibodies revealed AQP8 staining in the absorptive epithelial cells of duodenum, proximal jejunum, proximal colon and rectum where labeling was largely intracellular and confined to the subapical cytoplasm. Confirming previous results, AQP8 staining was seen at the apical pole of pancreatic acinar cells. Interestingly, both light and immunoelectron microscopy analyses showed AQP8 reactivity in liver where labeling was associated to hepatocyte intracellular vesicles and over the plasma membrane delimiting the bile canaliculi. A complex pattern was observed by immunoblotting with total membranes of the above GI organs incubated with affinity-purified anti-AQP8 antibodies which revealed multiple bands with molecular masses ranging between 28 and 45 kDa. This immunoblotting pattern was not modified after deglycosylation with N-glycosidase F except the 34-kDa band of liver that, as already reported, was partially down-shifted to 28 kDa. No bands were detected after preadsorption of the anti-AQP8 antibodies with the immunizing peptide. The cellular and subcellular distribution of AQP8 suggest physiological roles for this aquaporin in the absorption of water in the intestine and the secretion of bile and pancreatic juice in liver and pancreas, respectively. The large intracellular expression of AQP8 may indicate its recycling between the cytoplasmic compartment and the plasma membrane. The cytoplasmic localization observed may also relate to the involvement of AQP8 in processes of intracellular osmoregulation.

Animals↗
PubMed2001

Expression and localization of the aquaporin-8 water channel in rat testis.

Spermatogenesis and sperm maturation and storage are accompanied by significant movements of water, and multiple aquaporin transmembrane water channels (AQPs) have been recognized in the male reproductive tract. Nevertheless, the involvement of aquaporins in male reproductive physiology is mostly unknown. Here the expression and localization of AQP8 in rat spermatogenesis is defined and compared to that of AQP7, another aquaporin expressed in male germ cells. AQP8 mRNA was found in testis but not in epididymis, whereas the AQP7 transcript was present in both locations. By immunoblotting, the AQP8 protein was detected as a 25-kDa band and a 32- to 40-kDa diffuse component corresponding to the core and glycosylated protein, respectively. Membrane fractionation revealed AQP8 both in microsomal and plasma membrane-enriched fractions of rat testis while no apparent bands were detected in epididymis. AQP7 appeared as a 23- to 24-kDa band and was found both in testis and epididymis. By immunofluorescence, AQP8 labeling was found intracellularly as well as over the plasma membrane of germ cells throughout spermatogenesis. AQP7 was present in spermatids and spermatozoa and was predominant over the plasma membrane. AQP8 may be involved in the cytoplasmic condensation occurring during differentiation of spermatids into spermatozoa and in the generation of seminiferous tubule fluid.

Animals↗
PubMed2001

Increased concentrations of inflammatory mediators in unstable angina: correlation with serum troponin T.

OBJECTIVE: To measure plasma interferon gamma, monocyte chemotactic protein-1 (MCP-1), and interleukin 6 and to assess their correlation with cardiac troponin T in unstable angina. DESIGN: Blood sampling in patients undergoing coronary arteriography for known or suspected ischaemic heart disease. PATIENTS: 76 patients divided in three groups: 29 with unstable angina (group 1), 28 with stable angina (group 2), and 19 without ischaemic heart disease and with angiographically normal coronary arteries (group 3). MAIN OUTCOME MEASURES: Plasma interleukin 6, interferon gamma, MCP-1, and troponin T in the three groups of patients. RESULTS: Interleukin 6 was increased in group 1 (median 2.19 (range 0.53-50.84) pg/ml) compared with the control group (1.62 (0.79-3.98) pg/ml) (p < 0.005), whereas interferon gamma was higher in group 1 (range 0-5.51 pg/ml) than in the other two groups (range 0-0.74 pg/ml and 0-0.37 pg/ml; p < 0.005 and p < 0.001, respectively). Patients with unstable angina (group 1) and positive troponin T had higher concentrations of interferon gamma than those with negative troponin T (0-5.51 pg/ml v 0-0.60 pg/ml, p < 0.001). Plasma MCP-1 was also higher in group 1 (median 267 (range 6-8670) pg/ml) than in the other two groups (134 (19-890) pg/ml and 84.5 (5-325) pg/ml; p < 0.005 and p < 0.001, respectively), and among group 1 patients with a positive troponin T assay than in those with normal troponin T (531 (14.5-8670) pg/ml v 69 (6-3333) pg/ml; p < 0.01). There was no difference in plasma interleukin 6 in group 1 patients between those with and without raised troponin T. CONCLUSIONS: The inflammatory cytokines interferon gamma and MCP-1 are increased in patients with unstable angina, particularly in those with raised concentrations of troponin T, suggesting that they are probably related to myocardial cell damage or to plaque rupture and thrombus formation.

Adult↗
PubMed2001

Cigarette smoking and hypertension influence nitric oxide release and plasma levels of adhesion molecules.

Progression of atherosclerosis is currently believed to involve interactions between leukocytes and vascular endothelium. Epidemiological risk factors for atherosclerosis such as hypertension and smoking are known to cause endothelial dysfunction, which is an early event in the atherosclerotic process; they also may be considered in the light of their effects on adhesion molecule expression and release. Little is known about the additive effect between these two risk factors on endothelial adhesion molecule expression and nitric oxide release. Soluble adhesion molecules and the nitric oxide were quantified in smoking hypertensive patients in comparison to those from patients with hypertension alone. Cotinine, a stable metabolite of nicotine, has been used to identify smokers. One hundred and three hypertensive patients were selected: 51 smokers (plasma cotinine levels >25 ng/ml) and 52 non-smokers. Plasma concentrations of soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble endothelial leukocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-I) were quantified with ELISA methods. Plasma concentration of nitric oxide metabolites was measured by HPLC, whilst plasma concentration of cotinine was measured by RIA. Significant increases of sICAM-1 and sVCAM-1 were demonstrated in smokers (p<0.001 and p<0.05, respectively). In the same patients, a positive significant correlation between sVCAM-1 and plasma cotinine levels was observed (p<0.002). Nitric oxide metabolites were reduced significantly (p<0.04) in smokers. In conclusion, our data show that the two risk factors, smoking and hypertension, are additive risk factors in generating endothelial dysfunction and vascular damage, which plays a key role in atherogenesis.

Arteriosclerosis↗
PubMed2001

[Leukocytes-endothelial interaction in vascular pathology: from host defence mechanism to promoter of vascular injury].

Leukocytes play a key role in the defense of human organism from bacterial and fungal infections, taking part in the host defense mechanism against viral and neoplastic diseases. The purpose of this article is to underline the interaction between leukocytes and endothelial cells in atherosclerosis vascular damage. Actually, new evidences suggest a primary role for leukocytes, adhesion molecules, citokines and proteases to promote vascular endothelial cell injury by inflammatory process, the first step in atheromatic plaque formation.

Arteriosclerosis↗
PubMed2000

Kaposi's sarcoma.

Explore the source record for details and available documents.

Castleman Disease↗
PubMed2000

Increased expression of peripheral benzodiazepine receptors on leukocytes in silent myocardial ischemia.

OBJECTIVES: The purpose of this study was to evaluate benzodiazepine receptor expression on leukocytes from patients with symptomatic or silent myocardial ischemia. BACKGROUND: Silent myocardial ischemia is frequently observed in patients with coronary artery disease. Pain can be effectively controlled by various endogenous mechanisms. Benzodiazepines and their receptors play key roles in pain, in interactions with peptide opioids, in inflammation and in the response to stress. METHODS: The study group consisted of 57 patients with reproducible exercise-induced myocardial ischemia. The presence of a constant behavior in the anginal pain perception during both exercise-induced ischemia and daily life was the most important inclusion criterion. Venous blood samples were taken from all patients to evaluate the expression of peripheral benzodiazepine receptors by flow cytometry. The study cohort was classified into two groups: 24 patients who had anginal pain both at home and during the exercise stress test and 33 patients who were asymptomatic during both daily life and exercise-induced ischemia. RESULTS: Flow cytometry analysis showed increased expression of peripheral benzodiazepine receptors on all types of leukocytes in the asymptomatic patients. The difference was statistically significant for lymphocytes (p < 0.005), monocytes (p < 0.001) and granulocytes (p < 0.001). CONCLUSIONS: These data show that expression of peripheral benzodiazepine receptors was higher in patients with silent myocardial ischemia than in symptomatic patients.

Activities of Daily Living↗
PubMed2000

Lymphangioma of the spleen in an elderly patient.

Splenic cystic lymphangioma is a very rare condition, and is classified among cystic proliferations of the spleen. It is considered to be the result of a developmental malformation of the lymphatic system and can involve the spleen alone or be a part of multiorgan disease. It is usually seen in children, often found incidentally. We describe a case of cystic lymphangioma of the spleen in an elderly woman putting emphasis on the rarity of the case in old age, and on the problems of differential diagnosis with the other cystic proliferations of the spleen, in particular hydatid disease, in the absence of histologic information.

Aged↗
PubMed1999

Neutrophil function and opioid receptor expression on leucocytes during chronic naltrexone treatment in humans.

We report that neutrophil function was impaired in former heroin addicts on chronic naltrexone maintenance. Of the subjects, 62.5% had elevated plasma ACTH, 25% had elevated plasma cortisol and one subject had increased urinary cortisol. All subjects showed enhanced expression of opioid receptors on monocytes, neutrophils and lymphocytes. In vitro, incubation with therapeutically relevant concentrations of naltrexone induced a slow increase of neutrophil cytoplasmatic free Ca(2+)concentrations ([Ca(2+)]()E2>i) and slowed down the [Ca(2+)]()E2>i rise induced by N-formyl-methionyl-leucyl-phenylalanine. Neither naltrexone nor its metabolite beta-naltrexol affected human neutrophil function in vitro. We conclude that impairment of neutrophil function during chronic naltrexone may be related to opioid receptor overexpression. With this regard, the possible role of naltrexone-induced [Ca(2+)]()E2>i changes deserves further investigation. 1999 Academic Press.

Adolescent↗
PubMed1999

Plasma levels of interleukin 2, 6, 10 and phenotypic characterization of circulating T lymphocytes in ischemic heart disease.

The purpose of this study was to assess lymphocyte receptors expression in patients with ischemic heart diseases, as well as to measure the plasma levels of interleukin (IL) 2, 6 and 10. T Lymphocytes are found in large numbers in human atherosclerotic plaques, indicating that immune and inflammatory mechanisms are important factors in the pathogenesis of atherosclerosis. Recent data have also implicated T lymphocytes in the pathogenetic mechanism of unstable angina and ischemic heart disease. Three groups of patients were studied: 42 with an acute ischemic syndrome (AIS), 36 with stable angina (SA) and 39 healthy controls. To characterize lymphocyte phenotype, flow cytometry was performed in whole-blood samples. IL-2, IL-6 and IL-10 were measured using the ELISA method. Double fluorescence evaluation showed an increase in CD8+/CD11b+ cells (cytotoxic T lymphocytes) and in CD11b+/CD16+CD56+ cells (NK lymphocytes) in the AIS group and in SA group as compared to the control group (P < 0.05 and P < 0.001, respectively). IL-2 was increased in the AIS and SA groups compared to the control group (AIS 4.5 +/- 0.5 pg/ml; SA 6.3 +/- 0.6 pg/ml; controls 2.4 +/- 0.8 pg/ml, P < 0.05), whereas IL-6 was higher in the AIS group than in the other two groups (AIS 10.8 +/- 1.8 pg/ml; SA 1.8 +/- 0.8 pg/ml; controls 1.2 +/- 0.6 pg/ml, P < 0.0001). These data show that patients with ischemic heart disease have an increase in circulating cytotoxic T lymphocytes and in IL-2 plasma levels, irrespective of their clinical presentation, compared to normal control subjects, whereas IL-6 is elevated only in patients with AIS.

Angina Pectoris↗