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The aim of this paper is to summarize some of our quantitative descriptive and experimental studies, to discuss them in view of the literature data, and to present a synthesis of the topic. The results of stereological analysis of some tissue components of the rat thyroid gland have been compared with the results of topological studies on the parafollicular cells of various mammalian species. Localization of the parafollicular cells in the central regions of the thyroid gland lobes, where the follicular cell activity seems to be greater than in the periphery of the lobes, has led to the hypothesis that the parafollicular cells regulate (stimulate and/or suppress) the activity of the follicular cells. Long-term application and antithyroid drugs to mice and rats has shown that excessive concentrations of thyrotropin provoke hyperplasia of both the follicular cells and the intrathyroid mast cells and, transiently, of the parafollicular cells. This and some of the literature data are congruent with the hypothesis that the parafollicular and mast cells also stimulate the follicular cells by their paracrine secretions. Long-term application of antithyroid drugs to mice and rats has shown that excessive concentrations of cular cells but also probably stimulation of the follicular cells, as judged by the stereological measurements. The biological meaning of the spatial integration of follicular and parafollicular cells seems to be a functional coordination of both epithelial cell lines, supported by intrathyroid mast cells.

In coronary artery disease (CAD), the disruption of the tunica media immune privilege manifests as increased leukocyte infiltration and the formation of vasa vasorum. We aimed to characterize the immune privilege status of the tunica media in human coronary arteries (CAs) with atherosclerotic plaques, by comparing the abundance and composition of immune-cell infiltrates within the individual arterial-wall layers, and by evaluating vasa vasorum neovascularization of the tunica media. The tissue samples were obtained from 36 symptomatic patients with diffuse CAD (aged 60-72 years) who underwent coronary endarterectomy. T and B cells, macrophages and endothelial cells in the CAs were detected by immunohistochemistry. Morphological analysis of CAs showed significant atherosclerotic changes in all specimens. In the media, we observed damage and loss of smooth muscle cells, destruction of the extracellular matrix architecture, and fibrosis. There were 43.3% of immune cells in the intima, 50% in the adventitia, and 6.7% in the media. In the media, 51.1% of the immune cells were T cells (p ˂ 0.001 compared to B cells and macrophages; ANOVA, Scheffe post hoc analysis), 23.5% were B cells, and 25.4% were macrophages. The number of vasa vasorum in the media was 1 in 38.9% of CAs, 2-3 in 36.1%, and ≥4 in 25% of CAs. Our results indicate that, in atherosclerotic CAs, the immune privilege of the media is disrupted by the infiltration of T and B cells, macrophages, and the presence of vasa vasorum.

Sixty-one patients with locally advanced squamous cell carcinomas of oral cavity and oropharynx were treated with chemotherapy, intravenously applied, in addition to radiation and/or surgery. An attempt was made to synchronize the tumor cell population by application of low doses of Vinblastine and the subsequent chemotherapy was based on the uptake of 99m-Tc --labelled Bleomycin in the tumor as an indication of synchronization. Increased number of mitoses in aspiration biopsy specimens and shift in the DNA distribution pattern on DNA histograms were taken as indicative of synchronization. A 50--100% regression of the tumor was achieved in 19 out of 38 patients with residual or recurrent tumors. The results were better in those patients, who received chemotherapy based on individual Tc-Bleomycin uptake curves. In 23 patients with previously untreated T3 tumors of oral cavity and oropharynx the results were somewhat better, but there was not statistically significant improvement on attempts with synchronization in this small series. There were no serious complications connected with chemotherapy.

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The aims of the study were to investigate the histopathologic characteristics of atherosclerotic lesions and to evaluate the role of apoptosis or programmed cell death in diffuse coronary atherosclerosis. The study included 59 patients who underwent coronary artery bypass grafting coupled with coronary endarterectomy because of diffuse coronary atherosclerosis. Histopathologic analysis of endarterectomy sequesters showed atheroma with confluent extracellular lipid core-type IV lesions in 13 cases (22%); atheroma with lipid core and a cap of fibromuscular layers-type V lesions in 9 cases (15.3%); predominantly calcified fibrous tissue-type VII lesions in 13 cases (22%); and predominantly fibrous tissue-type VIII lesions in 24 cases (40.7%). TUNEL-positive cells were observed in 4 endarterectomy sequesters (6.8%) of subjects with diffuse coronary atherosclerosis. TUNEL-positive cells were demonstrated in the area of mononuclear infiltrates as well as in the vessel wall. The percentage of TUNEL-positive cells in mononuclear infiltrates was 0.5%. Intense mononuclear infiltrates in tunica intima were found in 50% of sequesters, and they consisted of macrophages (40%), T-lymphocytes (17%), and B-lymphocytes (14%). In the area of infiltrates the proportion of MIB-1-positive cells was 2.7%, which was higher than in the intima outside the area of infiltrates (0.5%). In conclusion, apoptosis, which is confined to mononuclear infiltrates, is most likely involved in the development of diffuse coronary atherosclerosis; however, the percentage of apoptotic cells was low (0.5%). A higher proportion of apoptotic cells in the area of infiltrates compared to the rest of the intima was associated with a higher proportion of MIB-1-positive cells. Atherosclerotic lesions in diffuse coronary atherosclerosis were advanced, with a predominance of type VII to VIII lesions.

BackgroundType 2 diabetes is an important risk factor for the development of coronary artery disease (CAD). Focal or diffuse inflammation is often present in the vessels of patients with CAD. Mast cells are frequently present in the plaques as well as in the inflammatory infiltrates in the atherosclerotic vessel wall. In the study we wanted to examine whether there are differences in the morphology, number and distribution of mast cells and in their ability to modify the atherosclerotic process in coronary arteries (CA) in the diabetic vs. the hypertensive population of patients with CAD.MethodsCoronary artery endarterectomy specimens were obtained from patients with diabetes or hypertension as the only risk factor for CAD. The specimens were stained with haematoxylin-eosin and Sulphated Alcian Blue for mast cells and with immunofluorescent methods for fibrinogen-fibrin and IgG deposits in the vessel wall. Both morphological and stereological assessments were conducted for mast cells and mononuclear cell infiltrates.ResultsThe histological analysis of the vessel wall of diabetic patients in comparison with hypertensive patients showed a damaged endothelial cells layer and deposits of fibrin-fibrinogen and IgG in the tunica intima and media. The stereological count revealed a diminished numerical density of mast cells and a significantly higher volume density of the mononuclear cells. Mast cells displayed cytoplasmic vacuolization, extracellular extrusion of granule and pyknotic nuclei.ConclusionThis preliminary study suggests that the impaired mast cells might be the reason for more extensive inflammatory and immunologic atherosclerotic changes in the CA vessel wall of CAD patients with type 2 diabetes.Trial registration134/88;C3-0564-381-92

BACKGROUND AND PURPOSE: To investigate the histopathologic characteristics of atherosclerotic lessions in diffuse coronary artery disease and to evaluate the possible inflammatory role of chronic infection with Chlamydia pneumoniae (CP).MATERIALS AND METHODS: For 10 patients (males, mean age 61 years) who were surgically treated for grave diffuse coronary artery disease, histomorphological analyses of endarterectomized segments of the coronary arteries were performed. Serological analyses for the detection of CP antibodies in peripheral blood were done, preoperatively.RESULTS AND CONCLUSIONS: Diffuse and concentric atherosclerotic changes from VI to VIII stage according to the Stary classification were found. Immunohistochemical methods revealed infiltrates of T-lymphocytes (80% of cases), B-lymphocytes (40% of cases) and macrophages (80%). Using the nuclear marker for proliferation activity MIB-1, single MIB-1 positive cells were found in 40% of cases. Features of arteriologenesis and vasculitis of newly formed arterioles (as well as thickening of the wall of newly formed arterioles) were found in the vessel wall of 8 patients, 7 of them had chronic infection with CP (preoperative micro-immunofluorescent test results: 1:32<IgG ≥1:512 and IgA≥32), one had passed CP infection (1:32 ≤IgG<1:512, IgA negative). These features were absent in 2 patients, both recovered from CP infection and had not the chronic CP infection at the time of surgery. DNA of Chlamydia pneumoniae was detected using the polymerase chain reaction (PCR) method in the vessel wall of 3 patients who were chosen randomly for this method. This study suggests an inflammatory and proatherogenic role of CP in a high grade atherosclerotic coronary artery wall in diffuse coronary artery disease.