Characteristics of pulmonary microvascular structure in postnatal yaks

Yaks are typical plateau-adapted animals, however the microvascular changes and characteristics in their lungs after birth are still unclear. Pulmonary microvasculature characteristics and changes across age groups were analysed using morphological observation and molecular biology detection in yaks aged 1, 30 and 180 days old in addition to adults. Results: Our experiments demonstrated that yaks have fully developed pulmonary alveolar at birth but that interalveolar thickness increased with age. Immunofluorescence observations showed that microvessel density within the interalveolar septum in the yak gradually increased with age. In addition, transmission electron microscopy (TEM) results showed that the blood–air barrier of 1-day old and 30-days old yaks was significantly thicker than that observed at 180-days old and in adults (P < 0.05), which was caused by the thinning of the membrane of alveolar epithelial cells. Furthermore, Vegfa and Epas1 expression levels in 30-day old yaks were the highest in comparison to the other age groups (P < 0.05), whilst levels in adult yaks were the lowest (P < 0.05). The gradual increase in lung microvessel density can effectively satisfy the oxygen requirements of ageing yaks. In addition, these results suggest that the key period of yak lung development is from 30 to 180 days.

Expression of COX-2, HMGB-1 and CD68 in lung tissue in sheep fibrinous bronchopneumonia

This study aimed to determine the expression of some cytokines, such as cyclooxygenase-2 (COX-2), High Mobility Group Box-1 (HMGB-1) and CD68, in the lung tissue of sheep with fibrinous bronchopneumonia by immunohistochemical methods. Forty sheep which had suffered from respiratory problems were brought for necropsy to the Faculty of Veterinary Medicine, Department of Pathology, Aksaray University, between November 2014 and December 2017. After necropsy, lung tissues grossly diagnosed with fibrinous bronchopneumonia were processed histologically, and stained histopathologically and immunohistochemically. Bacteriological culture was also applied to the lung tissues to isolate the agents. In histopathological examinations, congestion, red consolidation and grey consolidation stages were detected in the lung tissues. In such cases, we observed fibrin masses accumulated in some alveolar lumens, as well as inflammatory cell infiltrations of various extent in alveolar and bronchiolar lumens. In the interalveolar septum, a thickening was observed due to a fibrin mass and thrombotic vessels. Immunohistochemically, it was determined that COX-2 and HMGB-1 cytokines showed positive reactions, especially in bronchial, bronchiolar and alveolar epithelia, as well as goblet cells and macrophages. CD68 was found to be expressed in alveolar macrophages. COX-2 and HMGB-1, which have been implicated in the inflammatory response, were also shown to be expressed in fibrinous bronchopneumonia in sheep for the first time. Thus, these cytokines are thought to play a role in the pathogenesis of the disease. Moreover, their increased expression suggests that it may be helpful in the diagnosis of the disease.

Histochemical Examination on Periodontal Tissues of Klotho-Deficient Mice Fed With Phosphate-Insufficient Diet

To elucidate which of elevated serum concentration of inorganic phosphate (Pi) or disrupted signaling linked to αklotho/fibroblast growth factor 23 (FGF23) is a predominant regulator for senescence-related degeneration seen in αKlotho-deficient mice, we have examined histological alteration of the periodontal tissues in the mandibular interalveolar septum of αKlotho-deficient mice fed with Pi-insufficient diet. We prepared six groups of mice: wild-type, kl/kl, and αKlotho−/− mice with normal diet or low-Pi diet. As a consequence, kl/klnorPi and αKlotho−/−norPi mice showed the same abnormalities in periodontal tissues: intensely stained areas with hematoxylin in the interalveolar septum, dispersed localization of alkaline phosphatase–positive osteoblasts and tartrate-resistant acid phosphatase–reactive osteoclasts, and accumulation of dentin matrix protein 1 in the osteocytic lacunae. Although kl/kllowPi mice improved these histological abnormalities, αKlotho−/− lowPi mice failed to normalize those. Gene expression of αKlotho was shown to be increased in kl/kl lowPi specimens. It seems likely that histological abnormalities of kl/kl mice have been improved by the rescued expression of αKlotho, rather than low concentration of serum Pi. Thus, the histological malformation in periodontal tissues in αKlotho-deficient mice appears to be due to not only increased concentration of Pi but also disrupted αklotho/FGF23 signaling.

ПАТОМОРФОЛОГІЧНІ ЗМІНИ ЛЕГЕНЕВОЇ ТКАНИНИ ЗА ІНФЕКЦІЙНОГО ПЕРИТОНІТУ КОТІВ

The article presents the results of pathoanatomical, pathohistological and histochemical researches of the lung tissue for exudative form of the spontaneous infectious peritonitis of cats. The results of researches allow us to analyze pathoanatomical, microstructural changes in lung tissue of cats in various forms of peritonitis infectious and to define the mechanism of the pathological process that cause lethal consequence.The pathoanatomical research of dead bodies of 4 cats has been carried out: a 3 year–old cat and 1 year and 2 month–old cat and 1 year and 5 month–old with symptoms of exudative pleurisy; a 2 year–old cat with clear signs of exudative peritonitis and pleurisy. Peritoneal fluid and lung tissue fragments for cytological and pathohistological examination were selected. At pathoanatomical autopsy accumulation in the thoracal, abdominal cavities and pericardial space fluid with the flakes of fibrin were revealed, thickening of the serous membranes, layering them fibrin. At the pathohistological research in lung tissue noted the consequences of hemodynamic disturbances in the form of multiple perivascular hemorrhage, interstitial pneumonia, atelectasis and emphysematous cells and signs of fibrinous pleurisy in the state organization have been noted. The hardest changes were developed in the structures of the vascular system and are characterized by the damage of vascular endothelium, the development of productive meso– and periarteritis, syndrome of disseminated intravascular coagulation, stasis and hemolysis of erythrocytes in small vessels of interalveolar septum leading to the oppression of hemocirculation. In lungs, the mononuclear–macrophage infiltration prevailed, especially in periarteritis zone, indicating the presence of productively–necrotic vasculitis.The development of the syndrome disseminated intravascular coagulation led to the formation of multiple micro–blood clots, aggregated cells in vascular channel, the presence of which has led to the development of thrombi and then hemorrhages. The blockade microcirculation, in their turn, led to tissue hypoxia, acidosis and, as a result, distrophic changes in the past. The discovered processes in the vascular system of the lung tissue caused the insufficient flow of blood, irreversible changes of homeostasis and a sharp decline in adaptive capacity.

Filaments in Fibroblast in Pulmonary Alveolar Wall

A small number of fibroblasts (alveolar septal cells, pulmonary interstitial cells, mesenchymal cells) are present in the alveolar areas of the adult lungs. These cells, like fibroblasts elsewhere, may be important in production and maintenance of connective tissue fibers found throughout the lung. Very little attention has been given to these cells in studies of the lungs. Therefore their precise structure and function are not clear. This report demonstrates filaments in the fibroblasts in the alveolar ducts and alveolar walls of the mouse lungs.The lungs were inflated with 2% glutaraldehyde, post-fixed with 1% osmium tetroxide and processed for electron microscopy. The cell body and processes of the alveolar fibroblast are located in the interalveolar septum (Fig. I).