[The Corypheus in Russian pathological anatomy. On the occasion of the 120th anniversary of the birth of Anatoly Ivanovich Strukov]. / Korifei otechestvennoi patologicheskoi anatomii. K 120-letiyu so dnya rozhdeniya Anatoliya Ivanovicha Strukova.

The article dedicated to the 120th anniversary of the birth of Academician A.I. Strukov shows his role in the development of Russian and European pathological anatomy and describes his life and merits in the modernization of teaching pathological anatomy at medical universities. In addition, A.I. Strukov is shown as the standard of a teacher and a public figure.

[Alma mater of Russian pathoanatomy (on the occasion of the 170th anniversary of the Department of Pathoanatomy, I.M. Sechenov First Moscow State Medical University)]. / Alma mater rossiiskoi patologicheskoi anatomii (k 170-letiiu kafedry patologicheskoi anatomii Pervogo MGMU im. I.M. Sechenova).

The paper describes the history of the Department of Pathoanatomy, I.M. Sechenov First Moscow Medical University (Sechenov University) from its establishment in 1849 to the present time. It gives the names of all the heads of the Department and the features of its development in different periods of its activity.

[Costal cartilage changes in children with pectus excavatum and pectus carinatum]. / Izmeneniia rebernogo khriashcha pri voronkovidnoi i kilevidnoi deformatsii grudnoi kletki u detei.

Pectus excavatum (PE) and pectus carinatum (PC) in children are the most common congenital deformities that cause complications in the thoracic organs; however, the role of chondrocytes and cartilage canals in the pathogenesis of these conditions remains unexplored. OBJECTIVE: To investigate qualitative and quantitative changes of cartilage lacunae and canals in the costal cartilages in children with PE and PC compared to those with normal chests. SUBJECT AND METHODS: Costal cartilages were investigated in 10 children with normal chests (a control group), in 12 children with PE, and in 12 children with PC. Tissue fragments were fixed in 10% neutral formalin and embedded in compacted paraffin. Sections were stained with hematoxylin and eosin. Slides were examined by light microscopy. Cartilage lacunae, hyper- and hypolacunar zones, and cartilage canals were morphometrically examined, followed by statistical data analysis. RESULTS: There was a significant decrease in the number of cartilage lacunae and in the frequency of hyperlacunar zones and an increase in that of hypolacunar zones in the PE and PC groups. There were no significant differences in these parameters between the PE and PC groups; however, there was a tendency to the smallest number of cartilage lacunae and canals in the PC group and that to the preponderance of empty lacunae in the PE group. Only the PC group showed also negative correlations between the proportions of empty lacunae and the age of children. CONCLUSION: The pathogenesis of PE and PC in children is related to the impaired trophism of costal cartilages due to the smaller number of cartilage channels containing vessels and lacunae with chondrocytes. The development of PE and PC is associated with specific costal cartilage morphological changes that suggest that PE and PC are different manifestations of the same disease, namely connective tissue dysplasia.

[Costal cartilage structural and functional changes in children with a funnel or keeled chest]. / Strukturnye i funktsional'nye izmeneniia rebernykh khriashchei pri voronkovidnoi i kilevidnoi deformatsii grudnoi kletki u detei.

Congenital chest wall deformities (CCWDs) in children are severe diseases leading to cosmetic defects and diseases of the respiratory and cardiovascular systems. The most common of these deformities are funnel-shaped (pectus excavatum, FD) and keeled (pectus carinatum, KD) ones. The pathogenesis of CCWDs and the role of costal cartilage structural and functional changes in their pathogenesis have now been not well studied, which makes it difficult to elaborate pathogenetic approaches to correcting these diseases. Analysis of the literature has shown that structural and functional changes occur in the matrix and chondrocytes from the costal cartilage in FD. Similar costal cartilage changes are observed in KD. It is still unknown exactly which pathological processes are present in the costal cartilage and how they result in the development of one or other type of CCWDs. The role of amianthoid transformation (AT) of costal cartilages in these processes is also unknown. It is not improbable that it is AT drastically changing the native cartilage matrix, which is one of the key mechanisms leading to changes in its properties and to the subsequent development of FD or KD.

[The morphological and morphometric study of amianthoid transformation of the costal cartilage in health and in keeled chest deformity in children]. / Morfologicheskoe i morfometricheskoe issledovanie amiantoidnoi transformatsii rebernykh khryashchei v norme i pri kilevidnoi deformatsii grudnoi kletki u detei.

Amianthoid transformation (AT) is the accumulations of abnormal collagen structures (amianthoid fibers) in the hyaline cartilages, tumors, and tendons. Neither functional value of costal cartilage matrix AT, nor its role in the pathogenesis of congenital chest deformities is known now. AIM: to examine the morphological features of AT in the costal cartilage of children with the normal and keeled chest. SUBJECTS AND METHODS: Costal cartilages were studied in 6 children with the normal chest (autopsy material) and in 5 ones with keeled chest (surgical material). Tissue fragments were fixed in 10% neutral formalin and embedded in compacted paraffin. The sections were stained with hematoxylin and eosin, picrofuchsin by van Gieson, with picrosirius, toluidine blue and by the Malaurie method modified by Gallego. The specimens were examined by light, phase-contrast, dark-field, fluorescence, and polarization microscopy. The frequency of AT sites and their area were morphometrically studied and the findings were then statistically processed. RESULTS: Various types of AT in the costal cartilages were described as both the normal and keeled chest. According to their morphological features, classic, fine-fiber, twisted, and intralacunar types were identified. There were statistically significant increases in the incidence of all types (except the intralacunar one) and in the area of the fine-fiber AT type in keeled chest deformity as compared to health. There were positive correlations between the area of classic, intralacunar, and twisted types in both groups and between the area of a classic type and age in the controls. CONCLUSION: A classification of AT areas varying in structures in health and disease has been given for the first time; their relation to each other and to the presence of keeled deformity shown, which, in our opinion, suggests that AT is implicated in the pathogenesis of the disease.

[Immune granulomatous inflammation as the body's adaptive response].

Based on their studies and literature analysis, the authors offer a hypothesis for the adaptive pattern of chronic immune granulomatous inflammation occurring in infectious diseases that are characterized by the development of non-sterile immunity. The authors' proposed hypothesis holds that not every chronic inflammation is a manifestation of failing defenses of the body exposed to a damaging factor. By using tuberculosis and leprosy as an example, the authors show the insolvency of a number of existing notions of the pathogenesis and morphogenesis of epithelioid-cell and leprous granulomas. Thus, the authors consider that resident macrophages in tuberculosis maintain their function to kill mycobacteria; thereby the immune system obtains information on the antigenic determinants of the causative agents. At the same time, by consuming all hydrolases to kill mycobacteria, the macrophage fails to elaborate new lysosomes for the capacity of the pathogens to prevent them from forming. As a result, the lysosome-depleted macrophage transforms into an epithelioid cell that, maintaining phagocytic functions, loses its ability to kill the causative agents. It is this epithelioid cell where endocytobiosis takes place. These microorganisms destroy the epithelioid cell and fall out in the area of caseating granuloma necrosis at regular intervals. Some of them phagocytize epithelioid cells to maintain non-sterile immunity; the others are killed by inflammatory macrophages. The pathogenesis and morphogenesis of leprous granuloma, its tuberculous type in particular, proceed in a fundamentally similar way. Thus, non-sterile immunity required for tuberculosis, leprosy, and, possibly, other mycobacterioses is maintained.

[Functional morphology of ischemic cardiomyopathy].

OBJECTIVE: To show that ischemic cardiomyopathy (ICM) that is generally believed to be a variant of chronic heart disease (CHD) and an analogue of chronic heart failure is an initial stage and the background of all further forms of CHD. SUBJECTS AND METHODS: Sixty cardiac biopsies obtained from patients during aortocoronary bypass surgery for CHD and myocardia from 55 rabbits in which the investigators simulated atherosclerosis over time, as well as acute, transient, and recurrent coronary insufficiency after vasopressin administration were examined. A number of adequate histological, histochemical, and immunohistological procedures, electron microscopic and electron histochemical studies, and morphometry were employed. The investigators made biochemical monitoring of blood cholesterol and triglyceride levels and ECG monitoring in the animals had received intravenous vasopressin. RESULTS: The authors have indicated that CHD begins with endothelial changes in the trophic component of the microhemocirculatory bed, which gives rise to its impaired blood flow and to hypoxia at the level of the myocardial structural and functional unit--fascicules. Over time, the disease develops a set of processes that cause damage to microvessels, cardiomyocytes, stroma, lymph capillaries, and nerve endings and changes in secretion. Compensatory and adaptive responses that long mask the symptoms of damage to the vascular bed and myocardial tissue take place simultaneously. The occurring lesions result in irregular diffuse cardiosclerosis, micro- and lymphocirculatory, innervation, and conduction disturbances, and irregular cardiomyocyte damage. The authors consider this set of myocardial changes to be an initial phase of ICM that shows no clinical manifestation at all. As coronary atherosclerosis progresses, the already damaged myocardium is superimposed by the morphological changes caused by higher hypoxia at the whole organ level. Depending upon a combination of these changes, one or another form of CHD and progression of chronic CHD may prevail at a later time. CONCLUSION: ICM is a broader concept than chronic heart failure and it is a basis for the pathogenesis and morphogenesis of CHD.

[The morphology and molecular bases of damage to the stem cell niche of respiratory acini in idiopathic interstitial pneumonias].

UNLABELLED: The authors present the material of their study of the morphological and molecular biological features of damage to the stem cell niches (SCN) in the respiratory acini of the lung and the significance of their occurring changes in the pathogenesis of chronic idiopathic interstitial pneumonias (IIP), including idiopathic pulmonary fibrosis (IPF), desquamative interstitial pneumonia (DIP), cryptogenic organizing pneumonia (COP) with bronchiolitis obliterans (BO), and nonspecific interstitial pneumonia (NSIP). SUBJECTS AND METHODS: The study was performed using open transthoracic (n=181) and transbronchial (n=71) lung biopsies from 194 patients (118 cases (61%) with IPF, 35 (18%) with NSIP, 23 (12%) with DIP, 18 (9%) with COP + BO). The serial paraffin sections were stained with hematoxylin and eosin and van Gieson's picrofuchsin and immunohistochemical reactions were carried out to detect MMP-1, MMP-2, MMP-7, Apo-Cas ("Novocastra", 1:100), vimentin (Vimentin) ("LabVision" 1:100), SMA ("LabVision", 1:100), TGF-ß, TNF-α, CD34, Ost-4, and CD117 ("Dako", 1:50), CD68, and EMA ("Dako", 1:100). Biotinylated anti-mouse and anti-rabbit immunoglobulin antibodies ("Dako" LSAB + KIT, PEROXIDASE) were used as secondary antibodies. All the quantitative and semi-quantitative data obtained were processed by variation statistics. RESULTS: The compared IIPs were shown to differ in the site and degree of initial and secondary respiratory acinus damages caused by the aggressiveness of an inflammatory infiltrate and the spread of a lesion to different SCN areas involved in the regeneration of lung tissue. The mesenchymal cell with myofibroblast differentiation, which is probably associated with a mesenchymal stem cell, as evidenced by Oct-4, Vimentin, SMA, CD117, and CD34 expression by these cells, may be considered to be a marker cell of deep SCN damage. CONCLUSION: The author state that the clinical course and degree of morphological changes in IPP directly depend on the severity and depth of damage to the SCN areas of the respiratory acinus.

[Immunomorphologic features of epithelial-stromal relationships at hyperplasia and endometrial carcinoma].

The results of a immunomorphologic comprehensive study of epithelial-stromal relationships in the uterus hyperplasia and endometrial cancer suggest that the suppressor gene of cancer (PTEN) plays a key role in the process of neoplastic transformation of endometrial hyperplasia and adenocarcinoma development. For the first time the existence of two highly differentiated endometrial adenocarcinoma immunophenotype were detected The first one is a PTEN-negative endometrial aedenocarcinoma, characterized by an almost complete inhibition of tumor suppressor gene PTEN in the epithelium of the glands and stromal cell of the tumor The second type is a PTEN-positive endometrial adenocarcinoma, in which epithelial and stromal tumor suppressor gene PTEN activity has retained Based on these results we have formulated a hypothesis about the different types of endometrial hyperplasia morphogenesis and its possible transfer to cervical cancer associated with features of tumor suppressor gene PTEN.

[Causes of the people death from drunkenness and alcoholism].

We analyzed causes of 1008 people death, who abused by alcohol. Among them 2 groups were separated out: people died due to drunkenness and due to alcoholism. The structure of the death was similar in the both groups, however depended on alcoholism stages. The major cause of the death in group of drunkenness people was acute heart insufficiency, less commonly--lung pathology, and very rarely--brain vessels pathology and liver cirrhosis. In group of people, who died due to alcoholism, lung pathology was the major cause of these deaths, acute heart insufficiency was occurred less commonly, and very rare brain pathology because of delirium tremens or alcohol withdrawal syndrome, as so liver cirrhosis with complications. Hemorrhagic pancreonecrosis after alcoholic excess was found out in both groups, but it was more often in people, who died due to drunkenness. Obtained results show importance of chronic alcoholism identification as a disease with several stages including drunkenness and alcoholism.

[Hepatopathies in concomitance of chronic drug and alcoholic intoxications].

Liver biopsy specimens were morphologically investigated in 87 patients, including 30 with drug (marijuana and poppy straw) addiction, 23 with chronic alcoholic intoxication, and 25 abused narcotics and alcohol concomitantly. All the patients were not found to be infected with viruses of hepatitis B, C, G, TTV, or CMN; the clinical manifestations and biochemical blood parameters were studied over time. In patients who simultaneously used drugs and alcohol, the specific features of hepathopathy were shown to be more pronounced and more rapidly progressive changes as fatty hepatosis and diffuse liver tissue fibrosis than in those used either drugs alone or alcohol alone. This is favored by chronic inflammation and cholestasis that is accompanied by bile duct proliferation. Concomitance of these processes leads to permanent liver tissue atrophy and death and to the relatively early development of hepatic monolobular cirrhosis. The mechanisms responsible for the patho- and morphogenesis of combined toxic hepatopathy are discussed.

[Initial mechanisms of sepsis].

The author's hypothesis of the most important role of bacterial toxins (rather than not infection) in the pathogenetic basis of sepsis is discussed. This allows one to understand why sepsis is of multiple etiologies and not transmissible as an infectious agent, and why it does not induce the immunity. In the author's opinion, the hypothesis makes it possible to develop specific therapy for sepsis, rather than its symptomatic therapy.

[Structural and functional conception of alcohol disease].

A new conception of alcohol disease (AD) as a disease in which the prolonged ethanol intoxication leads to the development of changes of organs and systems--from minimal changes of the microcircular bed to the polyorganic pathology with symptoms characteristic of alcoholism is proposed. The pathogenesis of AD comprises three stages: the 1st one--episodic alcoholic intoxications; the 2nd--heavy drinking; the 3rd--alcoholism and its complications. At the 3rd stage, the morphological changes are irreversible that makes this stage incurable. At the 2nd stage, these changes appear to be reversible provided that amount of drinking will not exceed the basal metabolic level in the liver of the patient. Therefore, the author suggests that the solution of the problem of AD depends in large on the attention that general practitioners and experts will draw to treatment of alcoholism on the stage of heavy drinking.

[The role of macrophages in pathogenesis of limited inflammation].

It is shown on 250 male rats that a limiting capsule around an inflammation focus develops in the presence of bacteria as well as intoxication and possibility of infection generalization. Macrophages (Mph) phagocyte necrotic tissue in aceptic inflammation and stimulate reparation with formation of a scar. The role of Mph is more complicated in modeling of soft tissue abscess: they phagocyte bacteria inducing immune system involvement into the inflammatory process, stimulate primary cooperation of cells which produce inflammatory tissue mediators, regeneratory processes with final formation of a connective tissue capsule around a focus of purulent inflammation. When the system of phagocyting mononuclear cells is stimulated, all processes in the zone of inflammation become activated; when this system is inhibited the processes slow down.

[Pathologic anatomy of hard drinking and alcoholism]. / Patologicheskaia anatomiia p'ianstva i alkogolizma.

The analysis of 826 autopsies is presented. 654 persons in their life abused alcohol but refused treatment; they were considered as hard drinkers. 172 persons were repeatedly treated for alcoholism and were included into the group of alcoholics. The control group consisted of persons who had not abused alcohol. Morphological and morphometric methods were used. It is shown that chronic alcoholic intoxication involves all internal organs with the same trend in pathological processes in hard drinkers and alcoholics. There was progressing alteration of microcirculatory bed, fat degeneration of parenchymatous organs, atrophic and sclerotic processes, primarily in the liver, lungs, heart and brain. While in hard drinking pathological processes can be considered reversible and well compensated, in alcoholism the degree of organ damage makes these lesions irreversible. It is suggested that less severe organ damage in hard drinking is due to the effect of ethanol while grave atrophic and sclerotic processes as well as psychic dependence on alcohol are due to acetaldehyde. The key point in alcohol abuse is hard drinking (or preclinical stage of alcoholism) as there is neither psychic no physical dependence on alcohol and organ alterations are reversible under adequate treatment. The treatment should be performed first of all of the liver to enhance its basal metabolism.

[Viral inclusions of sarcoid granuloma into the epitheliocytes]. / Virusnye vkliucheniia v épitelioidnykh kletkakh sarkoidnoi granulemy.

Electron microscopy was used study the cellular composition of sarcoid granulomas in the lung of 10 patients. In 4 patients, epithelioid cells contained herpes virus virions. In these patients, the disease clinically began acutely, ran along with erythema nodosum; their treatment involved glucocorticosteroids. In the other patients, the cells of sarcoid granulomas did not contain viruses, the granulomas were at the fibrosing stage; diffuse pneumosclerosis was clinically diagnosed. It is suggested that in sarcoidosis, immunity is of not sterile character and the phagocytosis of virus aggregates with epithelioid cells demonstrates the degree of endocytobiosis. This process takes place in tuberculosis, which is a manifestation of the biological expediency of endocytobiosis as this allows infection immunity to be maintained.

[Changes in the components of the extracellular matrix and its regulators in the endometrium of women with habitual abortion]. / Izmeneniia komponentov vnekletochnogo matriksa i ego reguliatorov v éndometrii zhenshchin s privychnym nevynashivaniem beremennosti.

Biopsies of the endometrium from 93 patients with habitual abortions (HA) were studied immunohistochemically. Chronic endometritis (CE) was diagnosed in 26 patients. Decreased tenascin expression in the endometrial stroma with merozin accumulation in the glandular basal membranes, covering epithelium and vessels were found in HA combined with CE. Abnormal distribution of collagen type I and III with predominance of type I collagen and appearance of merozin. This is indicative of alteration in the endometrium maturation which may result in inadequate ovum implantation and pregnancy interruption. Stromal alterations in HA with or without chronic endometritis are under multifactorial control of various mediators. High level of MMP-9 combined with low level of TFP-beta 1 may serve a prognostic criterion of successful completion of pregnancy regardless of CE. Low level of MMP-9 may increase the risk of pregnancy interruption.

[Endocrine glands in alcohol drinkers and patient with alcoholism]. / Zhelezy vnutrennei sekretsii pri p'ianstve i alkogolizme.

Chronic alcoholic intoxication results in atrophic and sclerotic changes of the endocrine glands, as was demonstrated by 225 autopsies of subjects who suffered from heavy drinking (165 cases) and alcoholism (60 cases). Morphometry and statistical data processing showed that alcoholism leads to irreversible changes, while heavy drinking causes changes that are reversible and compensated. The testes and ovaries are the most sensitive to ethanol and acetaldehyde, while the adrenals are the least sensitive. The pancreas retains its function for a long time despite pronounced changes.