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Fiorella Calabrese

Publications and source records attributed to Fiorella Calabrese.

43 records · Page 3Linked to original sources
PubMed2003

C-JUN and CPP32 (CASPASE 3) in human pancreatic cancer: relation to cell proliferation and death.

INTRODUCTION: There is strong evidence that tumor growth is not only a result of uncontrolled cell proliferation but also of decreased apoptosis. AIMS: To ascertain the expression of c-Jun in specimens of pancreatic duct cancer and to evaluate its correlation with CPP32, apoptotic index, and proliferation index (MIB-1). METHODS: Tissue samples were collected from 23 patients with pancreatic duct cancer who had not received chemotherapy nor radiation therapy before surgery. In these specimens we determined the expression of c-Jun protein, CPP32, and MIB-1 by immunohistochemical method. Apoptosis was studied by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling method. RESULTS: CPP32/caspase3 was expressed in 83% and c-Jun in 87% of primary lesions. Three of 23 samples were completely negative for c-Jun, and 4 of 23 were negative for CPP32. Three of 4 specimens negative for CPP32 showed low or negative c-Jun. A significant correlation was found between CPP32/caspase3 and c-Jun (r = 0.51; p < 0.01) and between c-Jun and MIB-1 (r = 0.57; p < 0.004). No correlation was found between CPP32, c-Jun, MIB-1, and apoptotic index. CONCLUSIONS: The positive correlation between the expression of c-Jun and CPP32 and the absence of both in the same specimens suggest that a common factor or common factors induce the expression of both genes. Pancreatic cancer tissue with an increased percentage of proliferating tumor cells showed also a strong expression of c-Jun, which supports the hypothesis that this oncogene may be involved in the growth of pancreatic cancer. We hypothesize that under different extracellular stimuli both death and proliferation are activated in neoplastic cell, probably under the control of transcription factor AP-1.

Adult↗
PubMed2002

Recurrence of idiopathic pulmonary hemosiderosis in a young adult patient after bilateral single-lung transplantation.

BACKGROUND: Idiopathic pulmonary hemosiderosis (IPH) is a rare disease of unknown etiology characterized by hemoptysis, diffuse pulmonary infiltration, and anemia. Diagnosis requires a detailed clinical history and transbronchial lung biopsy (TLB). METHODS AND RESULTS: A 19-year-old man developed progressive dyspnea, hemoptysis, and anemia. The chest x-rays showed bilateral opacities. IPH was diagnosed on the basis of clinical findings and TLB. The patient was treated with corticosteroidal therapy. His respiratory function worsened, and he underwent lung transplantation in 1997. The pathological examination on native lungs confirmed the previous histologic diagnosis. In 2000, the patient again developed hemoptysis, fever, and hypoxemia. A recurrence of the disease was established by TLB. CONCLUSIONS: This is the first report of recurring IPH. The possibility of recurrent IPH raises the question whether these patients should be disqualified from lung transplantation. This question is unanswerable because incidence of recurrence, time course, and impact on the graft function are presently unknown and unpredictable.

Adult↗
PubMed2002

Molecular diagnosis of myocarditis and dilated cardiomyopathy in children: clinicopathologic features and prognostic implications.

Myocarditis is the most common cause of heart failure in children. We investigated viral etiology of myocarditis/dilated cardiomyopathy (DCM) in children and correlated molecular findings with pathologic and clinical data. Polymerase chain reaction (PCR) or reverse transcription (RT)-PCR were used to analyze 59 endomyocardial biopsies from 48 consecutive young (<18 yrs) patients (pts) with clinical and histologic diagnosis of myocarditis and DCM, employing primers designed to amplify specific sequences of various DNA and RNA viruses. Nucleic acids were successfully extracted in 41 pts and viral genomes were found in 20 (49%): 12 out of 26 pts (46%) with myocarditis, 6 out of 13 (46%) pts with DCM, and both patients with endocardial fibroelastosis. Enteroviruses were more common in DCM (72%), whereas adenoviruses and enteroviruses shared the same rate (36%) in myocarditis. The mumps virus genome was detected in the two pts with endocardial fibroelastosis. More diffuse inflammatory infiltrates and myocyte damage as well as more impaired left ventricular end diastolic volume and shortening fraction were noted in viral positive cases. PCR positive pts had a worse outcome, resulting in transplantation or death. Three out of 8 pts with viral myocarditis who underwent cardiac transplantation had recurrent PCR-proven graft viral infection. Viral myocarditis/DCM appeared to be a more severe disease than nonviral forms. Enteroviruses were more common in DCM, whereas adenoviruses were as frequent as enteroviruses in myocarditis. Persistence of viral infection was associated with disease deterioration. Viral myocarditis relapsed after transplantation.

Adolescent↗
PubMed2002

Lone hepatitis C virus myocarditis responsive to immunosuppressive therapy.

OBJECTIVES: This study analyzes the causal role of hepatitis C virus (HCV) in patients with lone myocarditis, and its susceptibility to immunosuppression. BACKGROUND: Prevalence of HCV in lone myocarditis, its mechanism of damage, and possible treatment are still unknown. METHODS: Among 48 consecutive patients with myocarditis serologically screened for HCV and other cardiotropic viruses, 3 patients had anti-HCV antibodies. Clinical manifestation was heart failure in two cases, and left bundle-branch block with moderate cardiac dysfunction was present in patient 3. The three patients underwent two-dimensional echocardiography, coronary angiography, and endomyocardial biopsy. Nested polymerase chain reaction (PCR) for positive and negative strands of HCV on sera and myocardial samples, and PCR for the most common cardiotropic viruses were performed. HCV in the myocardium was detected by TORDJI-22 antibody. RESULTS: At histology, a lymphocytic myocarditis associated with myocytes positively stained by TORDJI-22 was shown in all. Cardiac autoantibodies were detected in all cases. Nested PCR showed both positive and negative strands of HCV RNA in serum and myocardium; other viral genomes were absent. Patients were treated with prednisone and azathioprine for 6 months, with recovery of cardiac volumes and function. At 4-week control biopsy, myocarditis progressed to a healed phase, though HCV RNA was still detectable in the serum and myocardium. Cardiac improvement was maintained at the 12-month overall follow-up. CONCLUSIONS: HCV can be detected in the myocardium of as many as 6% of patients with lone myocarditis; HCV myocarditis can benefit from immunosuppression despite persistence of viral genome, suggesting an immunomediated mechanism of damage.

Adult↗
PubMedDate not supplied

Twenty years of progress and beckoning frontiers in cardiovascular pathology: cardiomyopathies.

In the last 20 years, with the advent of cardiac transplantation and the availability of molecular biology techniques, major advancements were achieved in the understanding of cardiomyopathies. Novel cardiomyopathies have been discovered (arrhythmogenic right ventricular, primary restrictive, and noncompacted myocardium) and added in the update of WHO classification. Myocarditis was also included with the name "inflammatory cardiomyopathy." Adenoviruses and parvoviruses were found to be frequent cardiotropic viruses in addition to enteroviruses. The extraordinary progress accomplished in molecular genetics of inherited cardiomyopathies allowed to establish hypertrophic and restrictive cardiomyopathies as sarcomeric ("force generation") diseases, dilated cardiomyopathies as cytoskeleton ("force transmission") disease, and arrhythmogenic right ventricular cardiomyopathy (ARVC) as cell junction disease. If we consider also cardiomyopathy as ion channel disease (long and short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia), because they are diseases of the myocardium associated with electrical dysfunction, then a genomic/postgenomic classification of inherited cardiomyopathies may be put forward: cytoskeletal cardiomyopathy, sarcomeric cardiomyopathy, cell junction cardiomyopathy and ion channel cardiomyopathy.

Adenovirus Infections, Human↗
PubMedDate not supplied

Arrhythmogenic right ventricular cardiomyopathy/dysplasia: is there a role for viruses?

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a primary heart muscle disease characterized structurally by progressive fibrofatty replacement of the right ventricle and clinically by life-threatening ventricular arrhythmias with left bundle branch block morphology. Recently, there has been a great deal of interest on ARVC/D as a cause of sudden death in young people, and it has been reported as the most common cause of exercise-related sudden death among competitive athletes in Italy. An autosomic dominant familial occurrence has been recognized, and four disease-causing genes have been recently identified in the dominant forms: ryanodinic cardiac receptor 2, desmoplakin, plakophilin 2, and transforming growth factor (TGF)-beta3. Furthermore, plakoglobin has been identified as the first gene responsible for the recessive variant of ARVC/D associated with palmoplantar keratosis and woolly hair (Naxos disease). However, although much progress has been made in molecular genetics, up to today, the pathogenesis of the disease is still unclear. The occurrence of myocyte apoptosis has been documented, suggesting that recurrent bouts of apoptosis may account for progressive atrophy of the myocardium, which is then replaced by fibrofatty tissue. Considering the frequent finding of myocarditis at histology, an inflammatory theory has been advanced, and infective mechanisms have been postulated to contribute to the onset and the progression of the disease. Cardiotropic viruses have been detected in some ARVC/D cases, and they have been proposed as possible etiologic agents. Several etiopathogenetic theories are herein presented in detail with particular attention to the inflammatory/infective one and its possible links between this and the genetic/dystrophic theories are discussed.

Animals↗