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C Lamberti

Publications and source records attributed to C Lamberti.

At least 37 records · Page 2Linked to original sources
PubMed2001

Regulation of beta-catenin function by the IkappaB kinases.

Both the beta-catenin and the nuclear factor kappaB (NF-kappaB) proteins are important regulators of gene expression and cellular proliferation. Two kinases, IKKalpha and IKKbeta, are critical activators of the NF-kappaB pathway. Here we present evidence that these kinases are also important in the regulation of beta-catenin function. IKKalpha- and IKKbeta-deficient mouse embryo fibroblasts exhibited different patterns of beta-catenin cellular localization. IKKbeta decreases beta-catenin-dependent transcriptional activation, while IKKalpha increases beta-catenin-dependent transcriptional activity. IKKalpha and IKKbeta interact with and phosphorylate beta-catenin using both in vitro and in vivo assays. Our results suggest that differential interactions of beta-catenin with IKKalpha and IKKbeta may in part be responsible for regulating beta-catenin protein levels and cellular localization and integrating signaling events between the NF-kappaB and Wingless pathways.

Animals↗
PubMed2001

Ti location in the MFI framework of Ti-Silicalite-1: a neutron powder diffraction study.

The first direct evidence that Ti atoms are not equally distributed in the 12 crystallographically independent T sites of the MFI framework is presented on the basis of neutron diffraction data collected at the HRPD instrument of the ISIS pulsed neutron source. We found strong evidence indicating that T6, T7, and T11 are the most populated sites and weak evidence that Ti may be hosted in T10. Ti occupancy can be excluded for sites T1, T2, T4, T5, T9, and T12. The occupancy of the remaining sites is doubtful. Since defective silicalite has been shown to exhibit the same preferential sites (T6, T7, T11, and T10) for Si vacancies, it may be suggested that the incorporation mechanism of the Ti atoms in the MFI framework occurs via the insertion of titanium in the defective sites. This hypothesis implies that titanium has a mineralizing effect on the MFI framework, and it is supported by independent spectroscopic data on both TS-1 and defective silicalite. The results are discussed in comparison with the known substitution mechanisms in the T-sites of MFI-type structures.

Journal Article↗
PubMed2001

Left ventricular endocardial surface detection based on real-time 3D echocardiographic data.

OBJECTIVE: A new computerized semi-automatic method for left ventricular (LV) chamber segmentation is presented. METHODS: The LV is imaged by real-time three-dimensional echocardiography (RT3DE). The surface detection model, based on level set techniques, is applied to RT3DE data for image analysis. The modified level set partial differential equation we use is solved by applying numerical methods for conservation laws. The initial conditions are manually established on some slices of the entire volume. The solution obtained for each slice is a contour line corresponding with the boundary between LV cavity and LV endocardium. RESULTS: The mathematical model has been applied to sequences of frames of human hearts (volume range: 34-109 ml) imaged by 2D and reconstructed off-line and RT3DE data. Volume estimation obtained by this new semi-automatic method shows an excellent correlation with those obtained by manual tracing (r = 0.992). Dynamic change of LV volume during the cardiac cycle is also obtained. CONCLUSION: The volume estimation method is accurate; edge based segmentation, image completion and volume reconstruction can be accomplished. The visualization technique also allows to navigate into the reconstructed volume and to display any section of the volume.

Echocardiography, Three-Dimensional↗
PubMed2001

Can APC mutation analysis contribute to therapeutic decisions in familial adenomatous polyposis? Experience from 680 FAP families.

BACKGROUND AND AIMS: In familial adenomatous polyposis (FAP), correlations between site of mutation in the adenomatous polyposis coli (APC) gene and severity of colonic polyposis or extracolonic manifestations are well known. While mutation analysis is important for predictive diagnosis in persons at risk, its relevance for clinical management of individual patients is open to question. METHODS: We examined 680 unrelated FAP families for germline mutations in the APC gene. Clinical information was obtained from 1256 patients. RESULTS: APC mutations were detected in 48% (327/680) of families. Age at diagnosis of FAP based on bowel symptoms and age at diagnosis of colorectal cancer in untreated patients were used as indicators of the severity of the natural course of the disease. A germline mutation was detected in 230 of 404 patients who were diagnosed after onset of bowel symptoms (rectal bleeding, abdominal pain, diarrhoea). When these patients were grouped according to the different sites of mutations, mean values for age at onset of disease differed significantly: patients carrying APC mutations at codon 1309 showed a disease onset 10 years earlier (mean age 20 years) compared with patients with mutations between codons 168 and 1580 (except codon 1309) (mean age 30 years), whereas patients with mutations at the 5' end of codon 168 or the 3' end of codon 1580 were diagnosed at a mean age of 52 years. Within each group of patients however large phenotypic variation was observed, even among patients with identical germline mutations. A higher incidence of desmoids was found in patients with mutations between codons 1445 and 1580 compared with mutations at other sites, while no correlation between site of mutation and presence of duodenal adenomas was observed. CONCLUSIONS: As age at manifestation and course of the disease may be rather variable, even in carriers of identical germline mutations, therapeutic decisions should be based on colonoscopic findings in individual patients rather than on the site of mutation. However, in patients with mutations within codons 1445-1580, it may be advisable to postpone elective colectomy because desmoids may arise through surgical intervention.

Adenomatous Polyposis Coli↗
PubMed2001

A semi-automatic method for left ventricle volume estimate: an in vivo validation study.

This study aims to the validation of the left ventricular (LV) volume estimates obtained by processing volumetric data utilizing a segmentation model based on level set technique. The validation has been performed by comparing real-time volumetric echo data (RT3DE) and magnetic resonance (MRI) data. A validation protocol has been defined. The validation protocol was applied to twenty-four estimates (range 61-467 ml) obtained from normal and pathologic subjects, which underwent both RT3DE and MRI. A statistical analysis was performed on each estimate and on clinical parameters as stroke volume (SV) and ejection fraction (EF). Assuming MRI estimates (x) as a reference, an excellent correlation was found with volume measured by utilizing the segmentation procedure (y) (y=0.89x + 13.78, r=0.98). The mean error on SV was 8 ml and the mean error on EF was 2%. This study demonstrated that the segmentation technique is reliably applicable on human hearts in clinical practice.

Echocardiography, Three-Dimensional↗
PubMed2000

Structure of Homoleptic Cu(I)(CO)(3) Cations in Cu(I)-Exchanged ZSM-5 Zeolite: An X-ray Absorption Study This project was supported by MURST (Cofin 98, Area 03). XAFS measurements were performed at ESRF (European Synchrotron Radiation Facitity) within the public user program. BM8 GILDA beamline is supported by INFN, INFM and CNR. The European Community is gratefully acknowledged for a TMR grant to G.T.P. We are indebted to F. Danca for skilful technical support and to M. Benfatto for critical discussion.

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Journal Article↗
PubMed2000

Neutron powder diffraction study of orthorhombic and monoclinic defective silicalite

The crystal structure of silicalite (SiO2) with a substantial amount of structural hydroxyl groups [Si(1-x)O(2-4x)(OH)4x, with 0.08<x<0.10] has been refined from neutron powder diffraction data measured using the HRPD instrument at the ISIS pulsed neutron source. Powder data were collected on the as-synthesized orthorhombic sample at 298 K, and on the deuterated monoclinic sample at 100 K. Preferential location of Si-atom vacancies was found on four out of 12 independent T sites in the orthorhombic silicalite [Si(6), Si(7), Si(10) and Si(11)], although the H atoms of the substituting hydroxyl groups could not be located because of the low statistical site occupancy on multiple sites. No significant population of D atoms or of Si vacancies was found in the tetrahedral sites of the monoclinic sample. The detected long-range order of adjacent Si atoms in defective orthorhombic [MFI] structures is compatible with a mechanism of Si vacancy clustering and with the model of hydroxyl nests assumed in the literature on the basis of IR spectroscopic evidence. Crystal data: orthorhombic, Pnma, Z = 8, a = 20.0511 (1), b = 19.8757 (1), c = 13.36823 (9) A, V = 5327.62 (5) A3, Dx = 1.798 g cm(-3), Mr = 721.01; monoclinic, P2(1)/n, Z = 4, a = 19.8352 (2), b = 20.0903 (2), c = 13.3588 (1) A, beta = 90.892 (1), V = 5322.78 (6) A3, Dx = 1.799 g cm(-3), Mr = 1442.02.

Journal Article↗
PubMed2000

Real-time 3D echocardiographic data analysis for left ventricular volume estimation.

A new computerized semi-automatic method for left ventricular chamber segmentation is presented. The left ventricle is imaged by real-time three-dimensional echocardiography. This real-time data acquisition method allows accurate evaluation of chamber size and shape, even in case there are cavities with irregular geometry. The surface detection model is based on a partial differential equation that propagates interfaces with curvature dependent speeds. The equation is solved by applying numerical methods for conservation laws. The method consists of one step only. Initial conditions are manually established on a small subset of slices of the entire volume. The solution obtained is a surface corresponding to the surface between LV cavity and LV endocardium. This mathematical model is applied to sequences of frames of human hearts (volume range: 34-109 ml) imaged by real-time 3D echocardiography. Volume estimates show an excellent correlation with those obtained by manual tracing (r=0.99).

Cardiac Volume↗
PubMed1999

Tiagabine antinociception in rodents depends on GABA(B) receptor activation: parallel antinociception testing and medial thalamus GABA microdialysis.

The effects of a new antiepileptic drug, tiagabine, (R)-N-[4,4-di-(3-methylthien-2-yl)but-3-enyl] nipecotic acid hydrochloride, were studied in mice and rats in antinociceptive tests, using three kinds of noxious stimuli: mechanical (paw pressure), chemical (abdominal constriction) and thermal (hot plate). In vivo microdialysis was performed in parallel in awake, freely moving rats in order to evaluate possible alterations in extracellular gamma-aminobutyric acid (GABA) levels in a pain-modulating region, the medial thalamus. Systemic administration of tiagabine, 30 mg kg(-1) i.p., increased nearly twofold the extracellular GABA levels in rats and increased significantly the rat paw pressure nociceptive threshold in a time-correlated manner. Dose-related significant tiagabine-induced antinociception was also observed at the doses of 1 and 3 mg kg(-1) i.p. in the mouse hot plate and abdominal constriction tests. The tiagabine antinociception was completely antagonised by pretreatment with the selective GABA(B) receptor antagonist, CGP 35348, (3-aminopropyl-diethoxy-methyl-phosphinic acid) (2.5 microg/mouse or 25 microg/rat i.c.v.), but not by naloxone (1 mg kg(-1) s.c.), both administered 15 min before tiagabine. Thus, it is suggested that tiagabine causes antinociception due to raised endogenous GABA levels which in turn activate GABA(B) receptors.

Abdomen↗
PubMed1999

Peutz-Jeghers syndrome: four novel inactivating germline mutations in the STK11 gene. Mutations in brief no. 227. Online.

The diagnosis of Peutz-Jeghers syndrome is based on the occurrence of hamartomatous gastrointestinal polyps and perioral pigment spots. In view of the development of hamartomatous polyps in several syndromes and the variability of pigment spots in Peutz-Jeghers patients, identification of affected individuals is difficult. Recently, germline mutations in the STK11 gene have been reported as a molecular cause of Peutz-Jeghers syndrome. We present four novel inactivating mutations identified by direct sequencing of all 9 exons of the STK11 gene in 4 patients suggestive of Peutz-Jeghers syndrome: three frameshift mutations (125-137del; 474-480del; 516-517insT) and one nonsense mutation (Q220X). Our data obtained in these patients and in those reported previously emphasize the diagnostic value of histological discrimination between different types of hamartomatous polyps and of molecular analysis, particularly in cases with no family history of the disease.

AMP-Activated Protein Kinase Kinases↗
PubMed1999

Histaminergic neurons modulate acetylcholine release in the ventral striatum: role of H3 histamine receptors.

To investigate whether histaminergic neurons influence the activity of cholinergic neurons, the ventral striatum was superfused through a push-pull cannula and the release of endogenous acetylcholine was determined in the superfusate. Local inhibition of histamine synthesis by superfusion with alpha-fluoromethylhistidine (FMH) gradually decreased the release rate of acetylcholine. Superfusion with histamine increased the release of acetylcholine. The releasing effect of histamine was greatly inhibited when the striatum was simultaneously superfused with the D2/D3 agonist quinpirole and the D1 antagonist (+/-)-7-bromo-1-(fluoresceinylthioureido)phenyl-8-hydroxy-3-methyl -2,3,4,5-tetrahydro-1H-3-benzapine (SKF 83566). The effect of histamine on acetylcholine release was abolished by the GABA(A) receptor antagonist bicuculline. Superfusion with the H3 receptor agonists imetit or immepip increased acetylcholine release rate in the striatum. The releasing effects of the two H3 agonists were FMH resistant, while superfusion with quinpirole and SKF 83566 abolished the H3 receptor agonist-induced acetylcholine release. Superfusion with the H3 receptor antagonist thioperamide enhanced acetylcholine release rate. The releasing effect of thioperamide was abolished after inhibition of histamine synthesis by FMH. The release of acetylcholine by thioperamide was also abolished on simultaneous superfusion with quinpirole and SKF 83566. The findings show that, in the striatum, the activity of cholinergic neurons is permanently modulated by neighbouring histaminergic nerve terminals and axons. The release of acetylcholine is also permanently inhibited by neighbouring GABAergic neurons. The enhanced release of acetylcholine by the H3 receptor agonists imetit and immepip is due to stimulation of H3 heteroreceptors, while the increase of acetylcholine release by the H3 receptor antagonist thioperamide is elicited via blockade of H3 autoreceptors. Histamine released from histaminergic nerve terminals increases the release of acetylcholine in part by inhibition of dopamine release which, in turn, decreases GABAergic transmission. A dopamine-independent way seems also to be involved in the histamine-evoked acetylcholine release.

Acetylcholine↗
PubMed1999

Histaminergic neurons modulate acetylcholine release in the ventral striatum: role of H1 and H2 histamine receptors.

To investigate whether H1 and H2 histamine receptors are implicated in the modulation of acetylcholine release by endogenous histamine, the ventral striatum of the conscious, freely moving rat was superfused by the push-pull superfusion technique with drugs and the release of acetylcholine was determined in the superfusate. Superfusion with the H1 receptor agonist 2-thiazolylethylamine (TEA, 50 micromol/l) enhanced the release of acetylcholine, while the H1 receptor antagonist triprolidine (50 micromol/l) reduced acetylcholine outflow and abolished the TEA-evoked release of the neurotransmitter. The inhibitory effect of triprolidine was not influenced either on simultaneous superfusion with 10 micromol/l (+/-)-7-bromo-1-(fluoresceinylthioureido)phenyl-8-hydroxy-3-methyl -2,3,4,5-tetrahydro-1H-benzazepine (SKF-83566, D1 dopamine receptor antagonist) and 50 micromol/l quinpirole (D2/D3 dopamine receptor agonist) or on superfusion with the GABAA receptor antagonist bicuculline (50 micromol/l). The H2 receptor antagonists ranitidine or famotidine (50 micromol/l each) greatly enhanced acetylcholine release rate in the ventral striatum. Presuperfusion with alpha-fluoromethylhistidine (FMH, 1 mmol/l), which inhibits neuronal synthesis of histamine, abolished the famotidine-induced release of acetylcholine. The releasing effect of famotidine was also abolished on simultaneous superfusion with 10 micromol/l SKF-83566 and 50 micromol/l quinpirole. The release of acetylcholine elicited by famotidine was reversed to a decreased acetylcholine outflow when the striatum was superfused with the GABA(A) receptor antagonist bicuculline (50 micromol/l) prior to famotidine. Superfusion with the H2 receptor agonist impromidine (1 micromol/l) decreased acetylcholine outflow, while the H2 agonist dimaprit (50 micromol/l) exerted the opposite effect. The releasing effect of dimaprit was not influenced by FMH (1 mmol/l), but it was abolished in the presence of SKF-83566 (10 micromol/l) and quinpirole (50 micromol/l). In the presence of bicuculline the release of acetylcholine by dimaprit was enhanced and prolonged. It seems possible that dimaprit and impromidine stimulate different subtypes of H2 receptors. The findings suggest that the release of acetylcholine in the striatum is modulated by neighbouring histaminergic neurons in a complex way. Stimulation of H1 histamine receptors, probably located on cholinergic neurons, enhances acetylcholine release. Stimulation by histamine of H2 receptors located on cholinergic or GABAergic neurons enhances the release of acetylcholine, while stimulation of H2 receptors located on dopaminergic neurons exerts the opposite effect.

Acetylcholine↗
PubMed1999

Regularization of blood motion fields by modified Navier-Stokes equations.

A technique for the regularization of incompressible fluid motion fields based on the use of modified Navier-Stokes equations is presented. It is shown that the technique belongs to the class of Tikhonov-type regularization methods. The technique was applied to an analytically known fluid-dynamic problem (Couette flow). Noisy and scattered versions of the analytical velocity field were generated, and the accuracy in reconstructing the analytical field was evaluated. It was found that accuracy depends on the value of a regularization parameter, and its optimal value depends on the entity of noise and scattering. When the optimal value is selected, the accuracy of the regularization technique is excellent, even for consistent noise and scattering levels. The technique was finally applied to echocardiographic data in order to estimate the blood velocity field within the left ventricle.

Algorithms↗