Patologia polska最新文献

A rare case of the malignant form of Gorlin's cyst is reported in a 42-year-old woman. The neoplasm developed in the right maxilla, infiltrated the anterior wall and roof of the sinus and grew into the nasal cavity. Based upon literature data we characterized various clinical and histological forms of Gorlin's cyst (calcifying odontogenic cyst).

Immunohistochemical and flow cytometric multiparameter analysis of proliferating cell nuclear antigen (PCNA) was performed on fifteen formalin fixed, paraffin embedded lymph nodes with malignant lymphoma (eleven non-Hodgkin's lymphomas, four Hodgkin's lymphomas), and fifteen lymph nodes with metastatic carcinomas. A general concordance between PCNA measurement by both methods has been observed: the percentage of positively stained cells in tissue sections correlated well with the percentage of cells expressing this antigen in cell suspensions (r = 0.76). Both diploid and aneuploid tumors expressed PCNA, and a correlation between PCNA and the percent cells in S-phase was evident in both: in PCNA-positive tumors the mean percent of cells in S-phase was 16.5%, and in PCNA-negative tumors, 5.9%. The data indicate that PCNA can be detected in formalin-fixed tissues by either classic immunohistochemical analysis or by flow cytometry.

The genetic basis of the limited lifespan and apparently programmed number of divisions in normal, diploid cells is discussed. Two different mechanisms may underlie a programmed inhibition of cell divisions before they age and die: 1. A genetic mechanism involving the CpG sequence in promotor regions of genes. Inactive, but gradually activated basic function genes such as ribosomal and energy metabolism genes, when inactive have their CpG promotor sequences methylated. During each cell division a proportion of 5-methyl cytosines will be oxidatively deaminated leading to C to T transitions. After a certain number of divisions all methylated CpG islands will be mutated with consequent loss of viability and cell death. 2. An epigenetic mechanism involving the methylated promotor sequences of silent growth control genes. After a certain number of divisions with incomplete maintenance methylation, the growth control genes will be derepressed with consequent cessation of proliferation, decline of metabolic activity, ageing, and death.

In 42 children 4 to 16 years old with ulcerative colitis by using peroxidase method and monoclonal antibodies we evaluated the presence of immunoglobulin A, M, G, E in the mucosa of the large and small intestines. It was found that the distribution of immunoglobulins in the acute phase was similar in the intestinal segments studied, which supports the opinion that the whole intestine has a common immune system playing a major role in the pathogenesis of the disease.

A unique case of a surgically treated primary amyloid tumour of the mediastinum has been reported in a 40-year-old man. Immunohistochemical examinations revealed the presence of transthyretin and amyloid AA within the amyloid masses.

The effect of haemorrhage (1 ml per 100 g b. w.) on the vasopressin and oxytocin storage in the hypothalamus and neurohypophysis of melatonin-treated male rats was determined. Melatonin treatment (100 micrograms/100 g b. w., once daily over 8 days) resulted in a known decrease of vasopressin as well as oxytocin content both in the hypothalamus and neurohypophysis. Haemorrhage decreased the neurohypophysial vasopressin and oxytocin storage in animals injected with vehicle solution or otherwise not treated. In melatonin-treated rats, however, bleeding did not affect the actual (i.e., decreased by melatonin) vasopressin and oxytocin content in the hypothalamo-neurohypophysial system. The results demonstrate that melatonin may be involved in mechanisms determining the rate of the response of vasopressinergic and oxytocinergic neurones to bleeding.

Variability in microvessel changes of blood vessel density has prompted us to undertake quantitative morphometric studies of infarcted areas in human brain. In the initial study, brains were obtained at autopsy from 10 patients (ages 45-85). Samples were collected from infarcted hemisphere and controls from the contralateral hemisphere. Formalin fixed, paraffin embedded and thereafter routinely processed sections were stained after Pickworth and with HE. Altogether 6,520 microvessels, representing 10,801 microscopic fields were counted. The Wilcoxon Range test was used for statistical analysis. In 9 of 10 patients in infarcted brain hemispheres, there was a marked increase in microvessel density (p < 0.01), when compared with contralateral brain hemisphere. In addition, a positive correlation was also found between the time of survival and both total density and density of non-perfused blood vessels. To gain a deep insight into the enhanced activity of microvessels, immunocytochemical studies were performed, which have shown, that the vascular endothelial cells in infarcted brain were reactive to two monoclonal antibodies, one, E-9, directed against an activation/proliferation associated endothelial cell specific protein and the other recognizing adhesion molecule VCAM-1. Pan-endothelial Mab PECAM/CD31 was used in those studies for controls and confirmed the obtained results. Our findings strongly support the concept of angiogenesis in the infarcted area. If correlated with morphometric results, it may indicate an important role of microvessels in pathobiology of ischemic stroke.

Two hundred cases of adenomyosis have been studied in order to clarify the origin and significance of intravascular endometrial tissue in adenomyosis. A tumor-like intravascular proliferation of the adenomyotic stroma (IVSP) has been found in 17.5% of the cases. An endolymphatic proliferation (35 cases) was occasionally accompanied by an intravenous proliferation (3 cases). IVSP originated from a perivascular stromal proliferation (PVSP) and occurred only in deep adenomyosis. IVSP was focal and showed no atypia. It was significantly most frequent in patients 50-53 years of age and more frequent in patients up to 53 years than in those over 53. The frequency of occurrence of PVSP and IVSP was related to the histologic features of adenomyosis and the endometrium and was highest in hyperplastic adenomyosis and in adenomyosis accompanied by hyperplasia of the endometrium. The study suggests that PVSP and IVSP develop in the areas of adenomyotic stroma stimulated by estrogen and nonresponsive to progesterone. The differential diagnosis of tumor-like and sarcomatous IVSP, and histogenesis of adenomyosis are discussed.

Encountered in orthopedics cases of accelerated bone union and abundant formation of the callus in patients after craniocerebral injuries as well as cases of extraskeletal ossification in neural diseases give rise to a question whether neural damage affects in any way the course of osteogenesis. The present study was carried out in an attempt to answer this question in an animal model. The study included 120 inbred WAG rats in which heterotopic induction of osteogenesis was performed by intramuscular placement of decalcified and lyophilized implants of rat cortical bones. By producing various neural damages their effect on the course of osteogenesis was evaluated. The rats were divided into four groups of 30 subjects each. In group I cerebral cortical damage was induced by intracortical injection of kainic acid solution, in group II paraplegia was produced by transverse dissection of the spinal cord on the level of Th 10-11, in group III denervation of the hind limb was performed by dissection of all supplying peripheral nerves, group IV consisted of controls. An attempt was made to evaluate changes in the course of osteogenesis while observing advancing with the passage of time changes in histological patterns of the preparations obtained from the site of bone implantation at 3, 5, 10, 20 and 40 days after the operation. While analyzing the histological pattern I paid attention to features characteristic for the process of osteogenesis such as: formation of granulation around bone grafts, penetration of mesenchymal cells into transplants, differentiation of mesenchymal cells into osteogenic cells, formation of bone tissue and development of bone marrow. The rate of development of these features in the consecutive preparations reflected the dynamics of induced osteogenesis. Analysis of the results showed that experimentally induced neural damage affects the course of osteogenesis. In case of cerebral cortical injury and peripheral neurotomy the formation of granulation around bone grafts was very abundant, whereas penetration of mesenchymal cells into the implants and differentiation of mesenchymal cells into chondroblasts occurred more rapidly than in other animal groups. In contrast, spinal cord injury resulted in a markedly decreased dynamics of osteogenesis which was manifested by weaker cell reaction around the implants and delayed differentiation of mesenchymal cells into chondroblasts. The effect was seen on the 20th day. In the final stage of the study--at 40 days--the effect of neural damage on the course of osteogenesis was reduced and the histological pattern was similar in all animal groups.(ABSTRACT TRUNCATED AT 400 WORDS)