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Biomedical subjects

C Marchetti

Publications and source records attributed to C Marchetti.

At least 55 records · Page 3Linked to original sources
PubMed1999

Morphologic characteristics of initial lymphatics of the healthy and diseased human gingiva.

Investigation was performed on healthy and inflamed human gingivae. In the healthy mucosa lymphatic vessels generally appeared as flattened channels with a reduced lumen. Only in very inflamed tissue were some more evident vessels with a distended wall detectable. Ultrastructurally, most of the vessels had the characteristics of capillaries and they were delimited by a thin and irregular endothelial wall with large intercellular spaces. These observations indicate that in the gingival tissues, which are continuously exposed to inflammatory agents and need a really efficient draining system, the pathway of interstitial exudation and cell migration may include both the lymphatic vessel system and the intercellular spaces of the permeable junctional epithelium.

Gingiva↗
PubMed1999

Calcitonin gene-related peptide rapidly downregulates nicotinic receptor function and slowly raises intracellular Ca2+ in rat chromaffin cells in vitro.

Although calcitonin gene-related peptide (CGRP) modulates muscle-type nicotinic acetylcholine receptors (nAChRs) via intracellular second messenger-mediated phosphorylation, the action of this peptide on neuronal-type nAChRs remains unknown. Using neuronal nAChRs of rat chromaffin cells in vitro we studied the effect of CGRP, which is physiologically present in adrenal medulla, on membrane currents and [Ca2+]i transients elicited by nicotine. Our main novel observation was that CGRP (either bath-applied or focally applied for a few seconds or even co-applied with nicotine for a few milliseconds) selectively and rapidly blocked nAChRs (a phenomenon unlikely caused by intracellular messengers in view of its speed) without affecting GABA receptors. The inhibitory effect of CGRP was independent of [Ca2+]i or membrane potential and not accompanied by baseline current changes. Like the competitive antagonist N,N,N-trimethyl-1-(4-trans-stilbenoxy)-2-propilammonium, CGRP induced a rightward, parallel shift of the nicotine dose-response curve; during co-application of these blockers the nicotine dose-ratio value was the sum of the values obtained with each antagonist alone. The block by CGRP was insensitive to the receptor antagonist hCGRP8-37 but mimicked by CGRP1-7. Persistent application of CGRP slowly increased [Ca2+]i, a phenomenon independent from external Ca2+, thus implying Ca2+ release from internal stores, and suppressed by hCGRP8-37. CGRP1-7 had no significant effect on [Ca2+]i. We propose that the 1-7 amino acid sequence of CGRP was responsible for the direct, rapid block of nAChRs, whereas the full-length peptide molecule was necessary for the delayed rise in internal Ca2+ potentially able to trigger phosphorylation-dependent modulation of nicotinic receptor function.

Animals↗
PubMed1999

Dexamethasone-induced thymocyte apoptosis: apoptotic signal involves the sequential activation of phosphoinositide-specific phospholipase C, acidic sphingomyelinase, and caspases.

Glucocorticoid hormones (GCH) have been implicated as regulators of T-lymphocyte growth and differentiation. In particular, it has been reported that GCH can induce thymocyte apoptosis. However, the molecular mechanisms responsible for this GCH-induced death have not been clarified. In this work, the biochemical events associated with apoptosis induced by Dexamethasone (Dex), a synthetic GCH, in normal mouse thymocytes, have been analyzed. Results indicate that Dex-induced thymocyte apoptosis is attributable to an early ceramide generation caused by the activation of an acidic sphingomyelinase (aSMase). Caspase activity plays a crucial role in Dex-induced apoptosis and is downstream the aSMase activation in that inhibition of the early ceramide generation inhibits caspase activation and thymocyte death. Moreover, Dex treatment rapidly induces diacylglycerol (DAG) generation, through a protein kinase C (PKC) and G-protein-dependent phosphatidylinositol-specific phospholipase C (PI-PLC), an event which precedes and is required for aSMase activation. Indeed, PI-PLC inhibition by U73122 totally prevents Dex-induced aSMase activity, ceramide generation, and consequently, caspase activation and apoptosis. All these effects require Dex interaction with GCH receptor (GR), are countered by the GR antagonist RU486, and precede the GCH/GR-activated transcription and protein synthesis. These observations indicate that GCH activates thymocyte death through a complex signaling pathway that requires the sequential activation of different biochemical events.

Animals↗
PubMed1999

Immunolocalization of gelatinase-A (matrix metalloproteinase-2) in damaged human temporomandibular joint discs.

The fibrous tissue of the articular disc of the dysfunctional temporomandibular joint undergoes deep and variable structural modifications. Here the concurrence of morphological changes and the expression of matrix metalloproteinase-2 (MMP-2) in damaged discs from individuals suffering joint dysfunction was investigated. Microscopic, ultrastructural and immunocytochemical investigations were made on variously damaged articular discs and on one control sample. Disaggregation of collagen fibres, an increase in cellular components and calcification of large areas of tissue were observed in the damaged discs. These modifications were accompanied by a positive immunoreaction pattern for MMP-2. Fibroblast-, chondroblast- and osteoblast-like cells displayed a positive cytoplasmic reaction. In samples displaying evidence of synovial hyperplasia, some cells of the synovial protrusions were MMP-2 immunoreactive. No MMP-2 staining was observed in the control sample. These findings demonstrate that structural modifications of the articular disc could be specific responses to changes in the function of the temporomandibular joint. Variations in extrinsic stimuli may activate intrinsic factors, such as MMPs, that induce structural modifications in the discal tissue.

Adult↗
PubMed1999

Pathways of cadmium influx in mammalian neurons.

The influx of the toxic cation Cd2+ was studied in fura 2-loaded rat cerebellar granule neurons. In cells depolarized with Ca2(+)-free, high-KCI solutions, the fluorescence emission ratio (R) increased in the presence of 100 microM Cd2(+). This increase was fully reversed by the Cd2+ chelator tetrakis(2-pyridylmethyl)ethylenediamine, indicating a cadmium influx into the cell. The rate of increase, dR/dt, was greatly reduced (67+/-5%) by 1 microM nimodipine and enhanced by 1 microM Bay K 8644. Concurrent application of nimodipine and omega-agatoxin IVA (200 nM) blocked Cd2+ permeation almost completely (88+/-5%), whereas omega-conotoxin MVIIC (2 microM) reduced dR/dt by 24+/-8%. These results indicate a primary role of voltage-dependent calcium channels in Cd2+ permeation. Stimulation with glutamate or NMDA and glycine also caused a rise of R in external Cd2+. Simultaneous application of nimodipine and omega-agatoxin IVA moderately reduced dR/dt (25+/-3%). NMDA-driven Cd2(+) entry was almost completely prevented by 1 mM Mg2+, 50 microM memantine, and 10 microM 5,7-dichlorokynurenic acid, suggesting a major contribution of NMDA-gated channels in glutamate-stimulated Cd2+ influx. Moreover, perfusion with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate caused a slow increase of R. These results suggest that Cd2+ permeates the cell membrane mainly through the same pathways of Ca2+ influx.

Animals↗
PubMed1999

Orbital (desmoid type) fibromatosis.

A case of extra-abdominal fibromatosis (EF) of the orbit is described in a 35-year-old man presenting with progressive exophthalmos, right ptosis and diplopia. MRI showed an orbital mass of intermediate signal in T1-weighted images (WI) and low signal in T2WI, which enhanced non-homogeneously after contrast injection. The histological diagnosis of EF was made and the lesion was surgically removed. No recurrence occurred in 40 months of follow-up.

Journal Article↗
PubMed1999

Semirigid fixation of the mandible in bimaxillary orthognathic surgery: stability after 18 months.

The stability of osteosynthesis with the use of semirigid mandibular fixation was evaluated in 15 patients who underwent bimaxillary procedures for correction of Class III malocclusion. All patients received rigid fixation (4 miniplates and screws) in the maxilla. Cephalometric evaluation was performed before the operation, immediately after the operation, and at least 18 months after the operation. At the 18-month follow-up, a mean mandibular relapse of 2.2 mm, associated with an additional advancement of the maxilla of 0.27 mm, was observed. The dental relationship was substantially correct. Stability of mandibular fragments in this sample of patients depended on the stability of the maxilla. In addition, neither clinical damage to the temporomandibular joint nor lesions to the neurovascular bundle were detected.

Adult↗
PubMed1998

Expression of CD38 increases intracellular calcium concentration and reduces doubling time in HeLa and 3T3 cells.

CD38 is a bifunctional ectoenzyme, predominantly expressed on hematopoietic cells during differentiation, that catalyzes the synthesis (cyclase) and the degradation (hydrolase) of cyclic ADP-ribose (cADPR), a powerful calcium mobilizer from intracellular stores. Due to the well established role of calcium levels in the regulation of apoptosis, proliferation, and differentiation, the CD38/cADPR system seems to be a likely candidate involved in the control of these fundamental processes. The ectocellular localization of the cyclase activity, however, contrasts with the intracellular site of action of cADPR. Here we demonstrate that ectocellular expression of human CD38 in CD38(-) HeLa and 3T3 cells results in intracellular CD38 substrate (NAD+ + NADH) consumption and product (cADPR) accumulation. Furthermore, a causal relationship is established between presence of intracellular cADPR, partial depletion of thapsigargin-sensitive calcium stores, increase in basal free cytoplasmic calcium concentration, and decrease of cell doubling time. The significant shortening of the S phase in CD38(+) HeLa cells, as compared with controls, demonstrates an effect of intracellular cADPR on the mammalian cell cycle.

3T3 Cells↗
PubMed1998

Dissociation between recency and span: neuropsychological and experimental evidence.

This article reports dissociations between verbal span and the recency portion of the serial position curve in immediate free recall, in 2 neuropsychological case studies and in 3 experiments with normal participants. Patient A. N. presented with an impaired serial verbal span while showing an intact recency effect. The opposite pattern was observed in patient G. C., who despite a poor recency showed normal span in verbal serial recall tasks. Experiments 1 and 2 showed a recency effect with visually and auditory presented lists and written recall was resistant to the effects of articulatory suppression and of irrelevant speech, but was disrupted by the suffix effect. Experiment 3 showed that in contrast with recency, memory span was affected by articulatory suppression and irrelevant speech during presentation but not by a suffix. These findings are not consistent with the idea that span and recency measure aspects of the same memory system. Moreover, in clinical practice, they should not be used as equivalent alternatives.

Adult↗
PubMed1998

Heart transplantation 1985-1998: 13-years experience at Angelo De Gasperis Cardio-Thoracic Department-Milan.

BACKGROUND: After 13 years of transplant experience in our center, we analyzed the results in the overall population and in particular subgroups of heart transplant recipients. We tried to identify risk factors for both early (3 months) and late (over 3 months) mortality after heart transplantation. METHODS: The data on 461 patients transplanted from November 1985-June 1998 were reviewed. To study risk factors for mortality, the results for 313 patients operated on from June 1985-June 1995 were studied and analyzed with a multivariate logistic regression and Cox's proportional hazard model. Seventy pre-, intra- and postoperative variables were considered including patient demographics, clinical status, hemodynamic parameters, donor characteristics, donor-recipient HLA mismatches, complications, and immunosuppressive protocols. We also compared results for patients transplanted from 1985-1991 (Group 1) and from 1992-1998 (Group II) to assess improvements due to changes in indications and in perioperative treatments. RESULTS: Overall mortality in the entire population was 20.2% (93/461). The 30-day, 3-month and late mortality rates were 8.0%, 10.2%, 11.1%, respectively. Group II mortality rates were 6.5%, 8.5% and 6.8%, respectively, despite a significant increase in Status I patients (20.6% in Group I vs 49.0% in Group II, p = 0.0001). The main causes of death were graft failure (24.7%), cardiac allograft vasculopathy (18.3%), and infection (16.1%). The mean follow-up of the 414 recipients who survived more than 3 months was 54.0 +/- 37.3 months. Actuarial survival was 87.4%, 79.2% and 68.9% at one, 5 and 10 years, respectively. The difference in the 5-year actuarial survival rates between Group I and Group II patients was statistically significant (73.5% vs 83.9%, p = 0.0135). The transpulmonary gradient, right atrial pressure and mid-high doses of donor inotropic support were identified as independent risk factors for early mortality. The number of moderate rejections at biopsy and early posttransplant infections were identified as independent risk factors for late mortality. The results of patients transplanted while on ventricular assist devices, urgent and elective patients and combined heart and kidney transplants were also reported. CONCLUSIONS: The overall results of our 13-year experience are very satisfying in relation to early and late mortality, with a significant favorable trend between patients transplanted in the early era (1985-1991) and those transplanted in the recent era (1992-1998). Pulmonary hypertension and elevated preoperative right filling pressure appear to indicate a significantly increased risk of early death and only marginally influence late survival, which is principally influenced by severe postoperative complications. Good results were achieved in combined heart and kidney transplantation and among patients who deteriorated during the waiting period and were supported with ventricular assist devices. The early and late outcomes for urgent (status I) and elective (status II) heart transplant patients were comparable.

Adolescent↗
PubMed1998

Multicenter evaluation of the Paragon CZE 2000 capillary zone electrophoresis system for serum protein electrophoresis and monoclonal component typing.

Serum protein electrophoresis and typing of monoclonal components (MCs) are routine but time-consuming and technically demanding assays. We evaluated capillary electrophoresis (Paragon CZE 2000) for automation of the two assays. CZE and cellulose acetate electrophoresis gave similar data on 794 samples. Within-run and between-run CVs were < 2% for albumin and gamma-globulins and 4-7% for alpha 1-, alpha 2-, and beta-globulins. Bilirubin, hemoglobin, triglycerides, and fibrinogen were found not to interfere. No carryover by capillaries was detected. The detection limit for MC was < 0.5 g/L. MC assessment by immunosubtraction on 403 samples identified the monoclonal type in all samples with peak concentrations > 10 g/L; only 50% of MCs that could not be quantified by densitometric scan were typed.

Antibodies, Monoclonal↗
PubMed1998

Plasma apolipoproteins A-I and B in survivors of myocardial infarction and in a control group.

The values of apolipoproteins (apo) A-I and B were determined in a population sample of hospital outpatients with a standardized method to verify if the cutpoints calculated in a cross-sectional study in the US are usable with other populations. We also tested the apolipoproteins' ability to discriminate between healthy people and survivors of myocardial infarction. In the studied population the apo A-I value corresponding to the HDL-cholesterol decisional centile is 1.12 g/L for males and 1.17 g/L for females; the apo B value corresponding to the LDL-cholesterol decisional centile is 1.23 g/L for males and 1.14 g/L for females. These values are quite close to the cutpoints proposed for the American population (1.20 g/L for both apolipoproteins). In comparison with the LDL- and HDL-cholesterol decisional concentrations, the cutpoints for apolipoproteins allow a correct classification of a greater percentage of postmyocardial infarction patients (16% higher for apo B and 5% for apo A-I). Standardized assays coupled with a reference database allow a better clinical use of apolipoprotein measurements.

Adult↗
PubMed1998

[Massive hepatic necrosis secondary to treatment of hepatocellular carcinoma by percutaneous alcoholization].

Fatal complications of percutaneous ethanol injection for the treatment of hepatic tumors are rare events. We report a case of massive hepatic necrosis after treatment by percutaneous ethanol injection of a 4 cm diameter hepatocellular carcinoma, which resulted in the death of the patient. The mechanism of this complication was probably an intratumoral aterioportal shunt, which allowed ethanol to spread through the blood vessels.

Aged↗
PubMed1997

Deoxycholic acid and SCFA-induced apoptosis in the human tumor cell-line HT-29 and possible mechanisms.

Short chain fatty acids (propionate and butyrate) and deoxycholic acid (DCA) are able to induce apoptosis in HT-29 colonic tumor cell line, but DCA induces a much higher level of apoptosis than butyrate and propionate. Mixtures of DCA with butyrate or propionate enhance the effect of the single components. Apoptosis is not affected by the PKC, PTK or de novo mRNA and protein synthesis inhibitors, so that the involvement of these enzymes and processes is ruled out. In contrast, DCA-induced apoptosis is directly related to [Ca2+]i concentration as demonstrated by the apoptosis inhibition caused by [Ca2+]i chelator BAPTA/AM.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1997

Endothelin and nitric oxide synthase in lymphatic endothelial cells: immunolocalization in vivo and in vitro.

BACKGROUND: Endothelin (ET) is an endothelium-derived multifunctional peptide that produces a potent, long-lasting vasoconstriction. Nitric oxide (NO), besides being the most important endothelium-derived relaxant factor in blood vessels, is supposed to be involved in regulating the interactions among endothelium, adhesive molecules, and leukocytes. METHODS: We investigated the possible occurrence and distribution of ET and constitutive nitric oxide synthase (NOs), the enzyme that generates NO from L-arginine, in bovine lymphatic vessels and primary culture of lymphatic endothelium by using immunocytochemistry. RESULTS: Specific immunostaining with both ET and endothelial constitutive NOs antisera was detectable at light and electron microscopic levels in the endothelial cell layer of lymphatic vessels, whereas no immunostaining could be observed in the muscular and adventitial layers. The immunoreaction showed a diffuse pattern throughout the cytoplasm of endothelial cells. Primary cultures of endothelial cells isolated from lymphatic vessels also displayed cytoplasmic ET- and NOs-like immunoreactivities. The endothelial nature of cell monolayers was confirmed by the positive reaction to the von Willebrand factor, a reliable marker of endothelial cells, and by ultrastructural features of cultured cells. CONCLUSIONS: These findings suggest that the endothelium is a major source of ET and NO in lymphatic vessels. Interestingly, the lymphatic endothelium maintains the capability of producing such vasoactive sustances also in vitro, thus suggesting that lymphatic endothelial cells in culture may be used in studies concerning the role of the endothelium in the generation of vasoactive molecules. According to previous functional studies, the occurrence of ET and NOs immunoreactivities in lymphatic vessel endothelium supports the view that lymphatic endothelium may play an important role in the regulation of lymphatic vascular tone and in the production of vascular contractile activity promoting lymph flow.

Animals↗
PubMed1997

Evidence for gene conversion in the generation of extensive polymorphism in the promoter of the growth hormone gene.

The human growth hormone gene (GH-N) is located in a cluster of five highly homologous genes that are coordinately expressed in pituitary (GH-N) and in placental tissues (the chorionic-somatomammotropin-like gene, the GH-variant gene and the two chorionic somatomammotropin genes). Sequence analysis from position -162 to position +100 of the GH-N gene has revealed eight nucleotide polymorphisms with no significant difference in frequency between patients affected by isolated growth hormone deficiency and controls. Remarkably, all these variations are located at positions where the GH-N differs from at least one of the other four homologous genes. The analysis of the twelve GH-N haplotypes originating from the combinations of the eight polymorphisms has revealed that not only single variations, but also nucleotide combinations are identical to those of the other placental genes. These findings suggest that whole stretches of the GH-N gene promoter have been replaced by homologous DNA stretches copied from one of the other four loci by repeated gene-conversion-like events, where the GH-N gene has acted as the recipient and the placental genes as donors of the converted sequences. The presence of a Chi-like element also indicates that the GH-N promoter represents a hot spot of gene conversion. Three of these variations cause, in addition, an amino-acid substitution in the GH-gene-derived transcriptional activator gene whose coding sequence overlaps the GH-N promoter. Thus, a DNA region that serves two distintic functions representing the proximal promoter of a gene and the 5' coding region of another gene displays an unusually high degree of polymorphism that has probably arisen because of gene conversion.

Base Sequence↗