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L Matturri

Publications and source records attributed to L Matturri.

At least 91 records · Page 5Linked to original sources
PubMed1989

Densitometric evaluation of DNA contents in expanded human skin.

We studied 18 patients who underwent skin expansion. In 3 patients the prostheses had been inserted in anatomical areas previously expanded: in 3 other patients scarring tissue had been involved in the expansion. The DNA content of sections of epidermis, before and after the implantation of expanders, were analysed using an image analyzer (IBAS 2000). The preliminary data demonstrate that, at the end of the expansion, epidermis enters a phase of quiescency and is not affected by dysplastic processes.

Adolescent↗
PubMed1989

A multifactorial study (cell kinetics, cytogenetics, DNA content) of lung tumours: basic information for prognostic evaluation.

Different prognostic parameters (labeling index, chromosomal pattern, DNA content) were studied in 32 cases of lung tumour. A great variability was observed in the proliferative activity and karyotype, and there was a lack of correlation between these parameters and the histologic type. It was possible to demonstrate that a diploid DNA content does not necessarily correspond to a normal karyotype. A more precise evaluation of the prognostic significance of data obtained will be possible in correlation with an extensive follow-up of the patients studied.

Adenocarcinoma↗
PubMed1988

His bundle haemorrhage and external cardiac massage: histopathological findings.

Histological examination showed acute haemorrhage of the bifurcating His bundle and of the left bundle branch in a 35 year old man who died after being given external cardiac massage for cardiac arrest. "Hammering" of the ventricular septum crest against the central fibrous skeleton of the heart by compression of the sternum was believed to have caused the haematoma of the junctional tissue.

Adult↗
PubMed1988

Morphometric characteristics of hepatocellular dysplasia.

Morphometric study of liver biopsies from six entities (normal tissue, post-hepatitis cirrhosis, post-alcoholic cirrhosis, cancer-related cirrhosis, hepatocellular adenoma and hepatocellular adenocarcinoma) confirmed that this technique can be a valuable adjunct to histopathologic study in the examination of such specimens. As expected, measurements in cirrhotic nodules showed two populations of cells. The so-called "large dysplastic cells" had nuclear and cellular areas close to those of normal hepatocytes and should thus be considered to be hyperplastic elements, not precancerous elements. The smaller dysplastic cells had morphometric values close to those of the corresponding hepatocellular carcinomas, indicating that these cells are the truly precancerous ones. Therefore, while the study confirmed that hepatic cirrhosis is a precancerous lesion, it also showed that the term hepatocellular dysplasia must be restricted to the smaller type of cells found in such nodules.

Adenoma↗
PubMed1987

Permanent form of junctional reciprocating tachycardia involving an atrio-hisian accessory pathway: electrophysiologic and histologic correlations.

We present clinical, electrophysiologic and morphologic correlations of a patient with a permanent form of junctional reciprocating tachycardia, who died from a lung tumor. At electrophysiologic study, the tachycardia circuit was suspected to involve an atrio-Hisian accessory pathway antegradely and the AV node retrogradely; a ventriculo-atrial accessory pathway was excluded. Pathologic examination revealed a right-sided atrio-Hisian accessory pathway and an area of abnormal dispersion in the distal His bundle fibers. This case is consistently different from another previously reported case in which a concealed, serpiginous, septal atrioventricular accessory pathway was demonstrated by anatomic examination. Thus, different substrates seem to be responsible for the permanent form of junctional reciprocating tachycardia.

Aged↗
PubMed1987

Chromosomal and cell kinetic pattern in human transitional cell bladder carcinoma.

Cell kinetics in transitional cancer of the bladder was studied in 35 patients by using the in vitro 3H-thymidine labeling index. The proliferative activity was remarkably lower than that observed for other human histotypes. Analysis of the relation between cell kinetics and histologic grading showed a value for grade III tumors two-fold that of grade I and grade II tumors. Cytogenetic analysis was possible in 15 cases, and different chromosome numbers from 40 to 120 and the presence of various structural aberrations were observed. When cytogenetic features were analyzed in relation to cell kinetics, higher proliferative activities were always associated with a loss of chromosome 13 and, except for one case, with a loss of chromosome 22.

Carcinoma, Transitional Cell↗
PubMed1987

[Anisoinotropism of myocardial cells: elementary histological picture of early ischemic dys-asynergy].

Twelve autoptic hearts from victims of cardiogenic shock, within a few hours from infarction, were studied at light microscope. At the site of early ischemia, a discrepancy in contraction of myocardiocytic units along single fibers (otherwise normal) has been observed. It configurated as an asynergic contracture (with Z lines impinging upon A bands), side by side with relaxed elements (with evident I bands); frequent dehiscence of intercalated disks ensues, due to imbalanced mechanic strain. These morphologic features, only rarely seen in 20 control hearts, are consistent with pertinent knowledge in pathophysiology, and can be defined "anisoinotropism" of myocardial fibers. They seem to be the microscopic substrate for the contractile dys-asynergy, which is credited in modern clinical diagnostics among the earliest signs of cardiac ischemia. The discal injury may also imply an impairment in intercellular conductivity, with an arrhythmogenic potential (reentry). Anisoinotropism presents as the forerunner of the well known "contraction band degeneration-necrosis", by progressive coagulative denaturation of the contractile proteins, up to conglutination and cancellation of sarcomere structures. The changes described herein can be taken into consideration in histopathology of heart's acute ischemia, before the occurrence of patent pictures of initial infarction.

Adult↗
PubMed1986

Cardiac amyloidosis involving the conduction system and the aortocoronary neuroreceptors. Clinicopathologic correlates.

In a patient with cardiac primary amyloidosis with conduction disturbances and dynamic cardiocirculatory disorders, the specialized system of the heart and the hitherto neglected cardiac nerve plexus and annexed aortocoronary glomera were studied histologically. Amyloid deposition in the conduction system and in the nerves and neuroreceptors seemed to correlate with the dysrhythmic manifestations, and, respectively, with some undue responses to vasodilator therapy. The possible hazards deriving from involvement of the aortocoronary glomera in patients with amyloidosis have been pointed out accordingly.

Amyloidosis↗
PubMed1986

Renal allograft rejection: immunohistochemistry of inflammatory cellular subsets and vascular lesions.

We have examined sixty-seven surgically removed allograft kidneys to identify the different leukocyte subsets of interstitial infiltration and the early vascular lesions which characterize renal allograft rejection. Histochemical and immunohistochemical results (mouse monoclonal antibodies anti: Leu 1, Leu 3a-3b, Leu 7, Leu 2a, OK Ia-Dr, OKB2, Leu M1, Leu M3; rabbit heteroclonal antibodies anti -: IgA, IgG, IgM, C3, fibrinogen, lysozyme; lectins-ABC: RCA, WGA, UEA) and routine histochemical staining have shown an increase of T-helper and T-activated lymphocyte subsets in acute rejection. Neutrophilic leucocytes were present in hyperacute rejection; macrophages were also noted. In chronic rejection, several lymphocyte subsets, in different ratios, were identified. Monocyte/macrophage leukocytes were the most abundant cell population. IgA deposits were noted on tubular epithelia in hyperacute and chronic rejections. IgM deposits were observed in vascular walls in chronic rejection. C3 and fibrinogen deposits were seen in glomerular capillaries and in arterial walls, although in different ratios, in all cases of renal allograft rejections. We have generally seen weak reactions to IgG deposits. Histochemical analysis of lectin receptors has given different results according to the type of rejection considered. In hyperacute rejection, receptors for WGA were found both on glomerular endothelial cells and on the tubular brush border. In the latter, receptors for RCA were also found. In acute rejection, receptors for UEA and WGA were found in a lower number of cases of acute vascular rejection. In acute cellular rejection, receptors for RCA, UEA and WGA were recognized in tubular epithelia. In acute vascular rejection, as well as in chronic rejection, only receptors for WGA were present on tubular epithelia and on capillary loop endothelium. The use of anti-human lysozyme antibodies has yielded the following results: in acute and hyperacute rejection, when renal failure occurred, we saw a high ratio of lysozyme, either coarsely granular or diffuse in the proximal tubular epithelia. Lysozyme was found in myelocyte/macrophage cells within capillary loops and arterial walls, when acute necrotizing vasculitis was present. In acute rejection, proximal tubular cells were lysozyme-negative or lysozyme-positive only segmentally, especially when obliterative vasculitis by fibrointimal proliferation was present and renal function progressively failed. In most of the chronic rejections, tubular cells were lysozyme-negative.

Acute Disease↗
PubMed1986

[Myocardial mechanical injury in acute ischemia: a pathophysiologic and histopathologic review].

The recognition of histopathologic substrates of myocardial contractile damage in human acute ischemia is still very poor, notwithstanding the impressive advances in the inherent clinical diagnostic technology and concepts. The first and foremost inotropic abnormality ensuing ischemia, easily taken for atonic in origin, actually consists of a pathologic contracture of the injured myocardium, depending upon abrupt fall of ATP, and defective extrusion calcium pump with persistence of actomyosin rigor-complexes. In sustained ischemia, further membrane damage exposes the myocell to massive calcium intrusion, with eventual precipitation of it and cell death (reperfusion stone-heart). In case of transient, "hit and run" ischemia, the "stunned" myocardium undergoes prolonged contractile abnormalities. In keeping with fundamentals in pathophysiology of contraction, ischemic myofibrils in human hyperacute infarct, showed spare I bands, accounting for contracture and followed by loss of the regular cross-striation register; then, groups of adjacent sarcomeres were seen to join into true "contraction" bands, with Z lines impinging upon A bands and obliterating the I bands. Coagulative denaturation of contractile proteins follows, presenting as irregular, amorphous degeneration stripes astride irreversibly damaged myocells. As such, these cells can be passively overstretched by the nearby functioning muscle. In turn, the fixed waviness of viable, acutely ischemic myocardium was thought to configure, histologically, the loss of ATP-dependent "plasticity" of myofilaments, in a state of contracture. The "relaxant effect" of inotropic-chronotropic-positive catecholamines, favoring diastole, has been also pointed out. The present microscopic findings are cogent to clinicopathologic problems of coronary ischemia-reperfusion, and sudden death from cardiogenic shock.

Adenosine Triphosphate↗
PubMed1986

[Specific extranodal sinoatrial muscle cells in the crista terminalis. Cyto-morphometric study and anatomoclinical considerations].

To assess the occurrence, location and structure of specialized pacemaker slender cells, beyond the conventional anatomic boundaries of the sinoatrial node, cyto-morphometric evaluations were made in specimens from 10 human hearts. The morphometric analysis showed significant histocytological peculiarities of extranodal slender cells, which presented 60% to 70% smaller than those of the ordinary atrial muscle; their preferential location was at a mean distance of 12 to 14 mm from the posterior tip of the sinoatrial node, beneath the crista terminalis. These morphologic data were taken into consideration with regard to electrophysiologic recording of shifts in pacemaking, within and around the sinoatrial node. It was also remarked that the presence and action of extranodal specialized cells along the crista terminalis are consistent with clinical and pathologic evidence obtained from human cases of sick sinus syndrome, as well as from animal experiments at sinoatrial node damage.

Adult↗
PubMed1986

Kinetic pattern of human urinary transitional cell carcinoma.

The potential proliferative activity, expressed as labelling index, has been studied in 24 cases of bladder transitional cell carcinomas. The data showed a wide range of values, varying between 0.4 and 36%. The average proliferative activity was 3.2%. An analysis of the connection between the labelling index and the histological grading has also brought out the existence of a gradient of proliferative activity; average values of 1.6-2.53% and 3.49%, respectively, were found for grades I-II and grade III.

Adult↗
PubMed1986

Extranodal specialized sinoatrial cells.

To define the occurrence of specialized pacemaker and transitional (slender) cells beyond the anatomic limits of the sinoatrial node, cytomorphometric evaluations were carried out in specimens from ten human hearts. The morphometric analysis showed significant histocytologic peculiarities of the extranodal slender cells, which were 60% to 70% smaller than those of the ordinary atrial myocardium, and their location at a mean distance of 12 to 14 mm from the posterior sinoatrial nodal edge, beneath the crista terminalis. These data can help in understanding the substrates for subsidiary pacemaking in sinoatrial disease.

Female↗