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Biomedical subjects

Ezio Gaia

Publications and source records attributed to Ezio Gaia.

9 recordsLinked to original sources
PubMed2007

Medical complications of pancreatic resections.

The sequelae of pancreas surgery are determined by the type of procedure, the extent of the parenchymal resection and the underlying disorder. In ductal carcinoma, the outcome is heavily influenced by the disease itself. Mortality rates are lower in centers which perform the most operations. In chronic pancreatitis, surgical management is essentially therapeutic for complications and palliative for the disease whose progress is closely correlated with the sequelae. Elective surgery does not appear to increase the risk of diabetes whereas distal pancreatectomy is an independent risk factor. Parenchymal resection aggravates nutritional deficiencies, such as low selenium, linoleic acid, LDL and apolipoprotein B levels, and thus increases the risk of atherogenesis. Abstinence from alcohol is an indispensable step towards the disappearance of postoperative pain.

Humans↗
PubMed2006

c-Jun N-terminal kinase upregulation as a key event in the proapoptotic interaction between transforming growth factor-beta1 and 4-hydroxynonenal in colon mucosa.

Cells of colonic mucosa are sensitive to the Smad-mediated growth-inhibitory effect of transforming growth factor-beta1 (TGF-beta1). Another important cell growth inhibitor is the polyunsaturated lipid peroxidation end product, 4-hydroxynonenal (HNE), which triggers apoptosis through c-Jun N-terminal kinase (JNK) activation. Interestingly, a close association between TGF-beta1 and HNE was found in the progression of human colon cancer, with concentration of both molecules inversely related to the malignancy. We investigated the cross talk between Smads and JNK signal transduction pathways in inducing apoptosis. To this purpose TGF-beta1 and HNE were added singly or in combination to CaCo-2 human colon adenocarcinoma cells. The cotreatment induced a marked enhancement of apoptosis and of JNK and Smad4 activities much more than either individual molecule. Cell preincubation with the JNK inhibitor SP600125 significantly prevented JNK and Smad4 enhancement and, subsequently, the cooperative proapoptotic effect was abolished. The primary role of JNK activity in TGF-beta1/HNE cooperative signaling was fully confirmed in a second set of experiments by using JNKi I, a more selective kinase inhibitor. Hence, in tumor cells becoming resistant to TGF-beta1-mediated growth inhibition, increased induction of the remaining TGF-beta1 pathways by interaction with other antiproliferative molecules, such as HNE, could help in inhibiting tumor growth.

Adult↗
PubMed2006

Epithelial microchimerism: consistent finding in human liver transplants.

BACKGROUND: Eleven liver biopsies from six male patients who received a liver transplant (LT) from female donors were examined in order to determine whether male host-derived hepatic cells were present in female grafts that exhibited minimal or important inflammatory damage. METHODS: Immunohistochemistry for epithelial cell type differentiation (anticytokeratin monoclonal antibody) and fluorescence in situ hybridization for XY chromosomes identification were performed on each slide. RESULTS: Host-derived hepatic cells were found in all except one transplant, with a frequency ranging from 2.3 to 25 per thousand of the total hepatocytes in the biopsy specimen. They were usually found as isolated cells scattered throughout the hepatic lobule; in one patient they were grouped into little clusters. Host-derived hepatic cells persisted throughout the histological follow up (up to 535 days after LT). Polyploidy for XY chromosome was observed. CONCLUSION: Hepatocytes derived from extra-hepatic stem cells are frequently found in small numbers in human liver grafts and persist over time.

Aged↗
PubMed2004

Colonoscopic screening and follow-up in patients with acromegaly: a multicenter study in Italy.

Acromegaly is an infrequent disease attributable to endogenous excess of GH and IGF-I. Human studies have associated the GH-IGF-I axis with the development of colorectal cancer; however, the question of whether colorectal cancer is a problem in acromegaly is currently unresolved. We performed a cross-sectional study to assess the risk of colonic neoplasia in patients with acromegaly. Colonoscopic screening was performed in 235 patients with acromegaly at five tertiary care hospitals in Italy between January 1, 1996, and December 31, 2001. A repeat colonoscopy was performed in 121 patients after a mean interval of 32.1 months. Colonoscopic findings in patients with acromegaly were compared with those of 233 patients with nonspecific abdominal complaints who were referred for endoscopy during the study period. A total of 65 patients (27.7%) and 36 controls (15.5%) had colonic neoplasia. In 55 patients (23.4%) and 34 control subjects (14.6%), the most important findings were adenomas (odds ratio, 1.7; range, 1.1-2.5), whereas 10 patients (4.3%) and two control subjects (0.9%) had carcinoma (odds ratio, 4.9; range, 1.1-22.4). The risk of colonic neoplasia was higher for younger patients with acromegaly compared with age-matched controls. Patients with acromegaly with or without colonic neoplasia did not differ significantly for IGF-I levels or duration of disease. A neoplastic recurrence was found in 16.5% of patients who underwent follow-up; 90% of them had had a neoplasm removed at the first colonoscopy. Acromegaly carries with it a moderate, but definitive, increase in the risk of colonic neoplasia that occurs at a younger age than in the general population. Patients who are found to harbor a colonic neoplasia are at risk for recurrence.

Acromegaly↗
PubMed2004

Analysis of the CARD15 variants R702W, G908R and L1007fs in Italian IBD patients.

CARD15 on chromosome 16 is the only IBD susceptibility gene identified among several mapped loci. Its recurrent variants R702W, G908R and L1007fs have shown significant association with Crohn's disease (CD), but not with ulcerative colitis (UC), in different Caucasian populations. We analysed these three variants in 184 CD and 92 UC Italian patients and in 177 healthy controls. L1007fs and G908R were independently associated with CD, while R702W showed a nonsignificant increase. After combining the three variants together, 32.6% of CD patients were positive vs 18.6% of the controls. The association was stronger for homozygotes and compound heterozygotes, OR 13.9 (1.8-108), and weaker but still significant for simple heterozygotes, OR 1.7 (1.0-2.9). An excess of homozygotes/compound heterozygotes also resulted from the comparison with Hardy-Weinberg expectations. Phenotype-genotype correlations were analysed first by univariate logistic regression and then by multivariate analysis, the effect of CARD15 positivity being adjusted according to the status of smoking, familiarity and sex, so as to focus on the predictivity of genetic and environmental risk factors on the clinical phenotype. Significant risk estimates of the CARD15 genotype were obtained for stricturing vs inflammatory behaviour, OR 2.76 (1.2-6.3), and for penetrating behaviour, 2.59 (1.0-6.6), and marginally significant for ileal vs colic location, OR 3.0 (0.9-9.8). Our findings indicate that the association of the CARD15 genotype with behaviour and location of disease holds also for the Italian population.

Carrier Proteins↗
PubMed2002

Germline mutations in CFTR and PSTI genes in chronic pancreatitis patients.

Mutations in the cationic trypsinogen, cystic fibrosis transmembrane conductance regulator (CFTR) and pancreatic secretory trypsinogen inhibitor (PSTI) genes have recently been associated with chronic pancreatitis. This paper investigates the frequency of CFTR and PSTI gene mutation in patients with idiopathic and alcoholic chronic pancreatitis, the clinical course of patients with these two kinds of disease, and examines the clinical differences between carriers and noncarriers of mutation. In idiopathic pancreatitis a significant increase was found in mutation frequency both in the CFTR gene (13%) and N34S mutation in the PSTI gene (3.9%), as well as an increase in familial disposition to pancreatic disorders. In alcohol-induced pancreatitis an increase in calcification, exocrine insufficiency, and diabetes mellitus was observed. In conclusions, mutations in the genes investigated are involved in causing idiopathic pancreatitis. Such mutations have no connection either with the age at onset or the clinical course of the disease.

Adult↗