Biomedical subjects

N Finato

Publications and source records attributed to N Finato.

22 records · Page 2Linked to original sources

PubMed1995

Microscopic thymoma and myasthenia gravis.

A rare case of microscopically sized thymoma is described in a 56 year old man suffering from myasthenia gravis. Histological examination of the surgically removed thymus showed the presence of several epithelial thymoma-like islands. As controls, 100 thymuses obtained from consecutive necropsies were sampled: 4% of these cases showed epithelial islands. This case is further proof that "microscopic thymoma" is a true pathological entity and suggests that every thymus removed from myasthenic patients in which there is no macroscopic evidence of thymoma should be examined microscopically on serial sections.

Humans↗

PubMed1995

Structure analysis of breast lesions using neighborhood graphs.

The College of American Pathologists divides proliferative lesions of the breast into three categories, but the diagnostic criteria for classification are not easy to apply. Therefore, many morphologic, immunohistochemical and morphometric features were studied in order to clarify this subdivision; however, the reported results are not very satisfactory. We also attempted to identify and differentiate the architectural features useful for the diagnosis of proliferative breast lesions. The morphologic characteristics of proliferative lesions of the breast were considered amenable to a graph theoretical approach. From a set of images of mammary ducts acquired from a hematoxylin-eosin-stained section, a hierarchy of graphs was built. The main graphs representing the structure are: (1) neighborhood graph, (2) planar graph, derived from (1) and (3) a dual graph. A simplified prototype of a system for structure analysis of the lesions was implemented and tested. Forty duct images classified by two expert pathologists were acquired and subjected to the system. The data obtained were analyzed, and some significant graph features validating our approach to the structure representation of the lesions were discovered. This approach can also be applied to other, similar classification problems and may help in understanding the biologic significance of proliferative lesions of the breast.

Breast Neoplasms↗

PubMed1994

Structural basis of end-stage failure in ischemic cardiomyopathy in humans.

BACKGROUND: Ischemic cardiomyopathy is characterized by myocyte loss, reactive cellular hypertrophy, and ventricular scarring. However, the relative contribution of these tissue and cellular processes to late failure remains to be determined. METHODS AND RESULTS: Ten hearts were obtained from individuals undergoing cardiac transplantation as a result of chronic coronary artery disease in its terminal stage. An identical number of control hearts were collected at autopsy from patients who died from causes other than cardiovascular disease, and morphometric methodologies were applied to the analysis of the left and right ventricular myocardium. Left ventricular hypertrophy evaluated as a change in organ weight, aggregate myocyte mass, and myocyte cell volume per nucleus showed increases of 85%, 47%, and 103%, respectively. Corresponding increases in the right ventricle were 75%, 74%, and 112%. Myocyte loss, which accounted for 28% and 30% in the left and right ventricles, was responsible for the difference in the assessment of myocyte hypertrophy at the ventricular, tissue, and cellular levels. Left ventricular muscle cell hypertrophy was accomplished through a 16% and 51% increase in myocyte diameter and length, whereas right ventricular myocyte hypertrophy was the consequence of a 13% and 67% increase in these linear dimensions, respectively. Moreover, a 36% reduction in the number of myocytes included in the thickness of the left ventricular wall was found. Collagen accumulation in the form of segmental, replacement, and interstitial fibrosis comprised an average 28% and 13% of the left and right ventricular myocardia, respectively. The combination of cell loss and myocardial fibrosis, myocyte lengthening, and mural slippage of cells resulted in 4.6-fold expansion of left ventricular cavitary volume and a 56% reduction in the ventricular mass-to-chamber volume ratio. CONCLUSIONS: These results are consistent with the contention that both myocyte and collagen compartments participate in the development of decompensated eccentric ventricular hypertrophy in the cardiomyopathic heart of ischemic origin.

Cardiomyopathy, Dilated↗

PubMedDate not supplied

Changes in DNA content of myocardial cells after cardiac explantation.

To evaluate the changes in DNA content of myocardial cells, image cytometric measurement was performed on a series of specimens obtained from 7 explanted hearts with respect to different fixation times after cardiac explantation. Prior to fixation, the tissue samples were stored at 4 degrees C or at room temperature. When the tissue samples were stored at room temperature, the integrated optical density decreased after 48 hours from cardiac explantation. Meanwhile, the coefficient of variation of integrated optical density and the sum of intermediate ploidies of myocyte nuclei increased. However, no significant changes were found when tissue samples were kept at 4 degrees C. This study indicates that no significant changes in DNA content are found within two days from cardiac explantation.

Cardiomyopathies↗