[Ultrastructural characteristics of thyroid medullary carcinoma]. / Ul'trastrukturnye osobennosti medulliarnogo raka shchitovidnoi zhelezy.

17 thyroid medullary carcinomas (TMC) were studied electron microscopically (EM). Two cell groups were revealed regardless of their histological structure: EM differentiated (with signs of C-cell differentiation) and non-differentiated (without these signs). There is no correlation between histological structure of the tumor and the degree of its EM differentiation. In patients who lived 5 years maximum after the diagnosis there were different histological types but EM the tumors had relatively monomorphous structure with domination of non-differentiated cells (more than 70%), high content of dark cells (50% and more) and low content of desmosomes (less than 30%). The prognosis is more favourable the higher is content of EM differentiated cells, the better desmosomes are developed and the lower is content of dark cells. The scope of surgery and local metastases do not influence the prognosis while distant metastases (stage IV) deteriorate the prognosis.

[Histological variants of thyroid medullary carcinoma]. / Gistologicheskie varianty medulliarnogo raka shchitovidnoi zhelezy.

A total of 114 medullary carcinomas of the thyroid were studied clinically and histologically. Females and subjects aged over 40 years predominated among the patients (2-fold more than others). Five- and ten-year survival was 74 and 46.2%, respectively. The histological variants were as follows: solid, follicular, papillary, small-cell, clear-cell, oncocytic, and mixed medullary-follicular and medullary-papillary. The survival of these patients did not depend on the histological variant or the degree of tumor cell atypia.

[Spindle-cell variant of thyroid medullary carcinoma with favourable prognosis]. / Veretenokletochnyi variant medulliarnogo raka shchitovidnoi zhelezy s blagopriiatnym prognozom.

A case of a favourable outcome of spindle-cell medullary carcinoma of the thyroid is reported. Electron-microscopically, there was no correlation between histological and ultrastructural differentiation. The tumor consisted mainly of ultrastructurally differentiated cells with endocrine granules which may be the cause of the favourable prognosis.

[Status of the myocardial ventricles in thromboembolism of the pulmonary arteries and their branches (based on early autopsy material)]. / Sostoianie miokarda zheludochkov pri tromboémbolii legochnykh arterii i ikh vetvei (na materiale rannikh vskrytii).

Ventricle myocardium of 16 patients who had died from acute thromboembolism (TE) of the pulmonary arteries was studied. The most important factor in the development of myocardial alterations is the degree of a vascular occlusion by the thrombus. Chronic lung and heart diseases as well as patient age may considerably aggravate the structural changes of the cardiomyocytes. Relatively low activity of catabolic enzymes in the myocardium of patients with TE correlates with a small size of embolic damage, the presence of chronic lung and heart diseases and with advanced age.

[Changes in the dehydrogenase activity of the cardiomyocytes in experimental acute massive pulmonary embolism]. / Izmenenie aktivnosti degidrogenaz kardiomiotsitov pri ostroi massivnoi émbolii legochnoi arterii v éksperimente.

A study of the activity of SDG, LDG, NAD-D in several structures of the heart was carried out in acute compensated massive embolism of the pulmonary artery. TV-histophotometry demonstrated heterogeneity of metabolic processes in the myocardium in the control and experimental group. The animals with pulmonary artery embolism showed diverse hemodynamic changes in the lesser and greater circulation. Loads to right cardiac compartments were accompanied by an elevation of SDG, NAD-D in the interventricular septum.

[Lesions of ventricular cardiomyocytes in experimental massive pulmonary embolism]. / Povrezhdeniia kardiomiotsitov zheludochkov pri éksperimental'noi massivnoi émbolii legochnykh arterii.

The damage of ventricular myocardial cells during acute experimental massive pulmonary embolism (MPE) was studied by light, polarization and electron microscopy on anaesthetized dogs. In cases, when MPE was followed by heart failure, the deep ir reversible damage of myofibrils took place, and the relative volume of myofibrils decreased in both ventricles. The damage of right ventricular myocardium, which works against increased postload during MPE, may be reason of right ventricular insufficiency.

[Clinico-experimental study of histoenzymological changes in the ventricular myocardium in pulmonary embolism]. / Kliniko-éksperimental'noe issledovanie gistoénzimologicheskikh izmenenii v miokarde zheludochkov pri legochnoi émbolii.

The SDH and LDH activity in ventricular myocardium was studied in early autopsies of 16 patients, which died from acute pulmonary thromboembolism, and also in 17 dogs with experimental pulmonary embolism. In general the data of histoenzymological study of experimental and sectional material were identical. We revealed some factors, which correlated with low activity of catabolic enzymes in ventricular myocardium of the patients with pulmonary embolism: small volume of embolic occlusion (the thromboembolism of lobar and segmental pulmonary arteries); the presence of prior chronic cardiopulmonary disease; the advanced age and the female sex. Preexisting cardiopulmonary disease, as well as age and sex changes of myocardial metabolism, may assist the development of heart failure by relatively small volume of embolic obstruction.

[The functional-morphological state of the myocardium in experimental massive embolism of the pulmonary artery]. / Funktsional'no-morfologicheskoe sostoianie miokarda pri éksperimental'noi massivnoi émbolii legochnoi arterii.

A comparative study of hemodynamic and structural-metabolic changes in the myocardium of the right (RV) and left ventricles (LV) in acute massive pulmonary artery embolism was made in 19 mongrel dogs. In the control group the activity of SDH, MDH, GDH, NADH-DH in LV were higher than in RV. The numeral density and relative area of mitochondrial profile surface in LV was higher that in RV. A significant increase in afterload on RV causes intensification of cell respiration, a rise in numeral density and relative area of mitochondrial profile surface. Weakening of LV work leads to contrary structural-metabolic changes. Thus, contrary changes in hemodynamic loads on RV and LV in acute compensative massive pulmonary artery embolism correlated with contrary changes in their cell metabolism.