Necrobiotic Changes Research Articles

Sub-acute dermal toxicity of Jatropha curcas Linn. leaf extract coated silver nanoparticles (SNPs) in wistar rats

The application of different nanoparticles is underway in the development of phyto-medicines. Silver nanoparticles (AgNPs) are commonly used as coating agents to treat various bacterial and viral diseases. Their safety and potential toxicity necessitate further research to explore the development of nanoparticles coated herbal drugs. The Azadirachta indica (neem) 5% leaf extract and silver nitrate was used to prepare the silver nanoparticles (SNPs) with the biological reduction (green synthesis) method [1]. The application of silver nanoparticles (SNPs) coated with J. carcus leaf extract (JcLE) on Wistar rats showed no adverse sign of toxicity on hematological parameters except an increase in the neutrophil count and increased in total erythrocyte count (TEC) on 28th day. Similarly, serum biochemical values exhibited an increase in aspartate aminotransferase (AST/SGOT) and alanine transaminase (ALT/SGPT) with JcLE-coated SNPs in treated groups. The histopathology revealed that there was no alteration in skin architecture, however, minimal alteration was observed in the liver and kidney with dilatation of the central vein and sinusoidal space, fatty change in the liver, multifocal necrobiotic changes, cystic degeneration and mild focal glomerular atrophy and hyaline cast in the lumen of tubules of kidney. It indicates the proper absorption and excretion of SNPs from the body. There was no significant effect on hematological parameters in the rats treated with J. curcas leaf extract-coated SNP. However, the serum biochemical analysis revealed a toxic effect on the kidney.

Morphofunctional changes in the internal organs of laying hens affected by chronic thiamethoxam intoxication

Insecticides play an important role in agriculture, general sanitary and veterinary practices, providing protection of the plants and yield from harmful insects and preventing the spread of arthropods which cause diseases in people and animals. Therefore, the objective of our study was to analyze the morphofunctional changes in the internal organs of laying hens affected by chronic intoxication with Actara 25 WG (thiamethoxam). Identification of the toxic action of theamethoxam was carried out in 150 day-old laying hens. The chronic intoxication with the insecticide was modeled by feeding mixed feed treated with the preparation in the doses that were calculated in mg of the active compound per 1 kg of body mass. The birds of the one group were the control and received mixed feed with no supplements. The hens of the first experimental group were given mixed feed that contained the insecticide in the dose of 360 mg/kg of body mass, and hens of the second experimental group consumed mixed feed containing the preparation in the dose of 180 mg/kg per body mass. We determined that laying hens of Experimental Group 1 had significant 1.24-fold decrease in the ventriculus and significant 1.39-fold increase in the spleen. Laying hens of Experimental Group 2 were observed to have increase in the absolute mass of the heart, measuring 1.36-fold compared with the control and 1.34-fold compared with Experimental Group 1. At the same time, the absolute masses of the spleen, liver, and ventriculus in Experimental Group 2 were 1.20, 1.46, and 1.19 times lower than in Experimental Group 1. Compared with the control, the absolute mass of the liver and ventriculus, was 1.54 and 1.48 times lower, respectively. Intake of feed with thiamethoxam by laying hens of the experimental groups led to decrease in the coefficient of relative mass of the liver and ventriculus. Those results significantly correlated with the absolute mass values of those organs, indicating the toxic impact of the insecticide on laying hens, with the digestive organs being the first to react. In Experimental Group 1 chickens, we observed dystrophic-necrotic changes in the liver, round-cell infiltration of the portal tracts; dystrophic-necrotic changes in epitheliocytes of the nephrons of the kidneys’; granular dystrophy of cardiomycetes, plethora of the capillaries, and stasis and edema of the stroma in the myocardium; pericellular edemas in the brain; mucous dystrophy, desquamation of the epithelium of the mucous membrane, decrease in lymphocytes in the lymphoid structures, and atrophy of the epithelium of the glandular structure in the stomach; hyperemia and necrosis of the villus tips, and round-cell infiltration of the crypt region in the thin intestine; and reproduction of cellular elements of the connective tissue between the crypts in the thin intestine. The insecticide in the dose of 180 mg/kg of body mass caused dystrophic-necrobiotic changes in the liver and kidneys; hyperemia and edema in the myocardium; pericellular edema, swelling, and vacuolar dystrophy of neurons in the brain; necrobiotic changes in the mucous membrane epithelioctes in the proventriculus; and deformation of the villi and edema of the mucous membrane in the small intestine.

Вплив стресофакторів на стан організму людини та органів і тканин порожнини рота (огляд літератури)

Abstracts. In today’s environment, every citizen of Ukraine is exposed to varying degrees of psycho-emotional and physical stress. It is impossible to underestimate the negative impact of stressors on the tissues and organs of the oral cavity in particular, as quite often the first signs of general pathologies appear in this complex. The aim of the study is to analyse data from scientific literature sources and provide updated information on the impact of psycho-emotional stress on the development of periodontal diseases in the current conditions. Materials and Methods. The bibliosemantic method was used to clarify the state of the problem, to study the analysis of the results of previous scientific research based on the sources of literature and electronic resources. Research results and discussion. The current conditions dictated by the war on the territory of our country is cause a state of permanent stress among the population of Ukraine, which is related to the basic human instinct of survival. In general, a person can be affected by one or more groups of objective causes of stress. The citizens of Ukraine are experiencing severe stress as a result of the ongoing conflict. This includes combatants, relatives and friends of these combatants, civilians living in the area close to the hostilities, the wounded, medical workers, and internally displaced persons. The stress factor provokes the emergence and rapid development of new mental and somatic diseases, it leads to the progression of existing diseases, but the reaction to the stimulus is different for each person and is an individual manifestation. The state of the oral cavity is a very sensitive complex to any changes in the body’s homeostasis, and often the first signs of general pathologies appear in it. Among the significant risk factors that contribute to the development and aggravate the course of periodontal disease, stress is one of the most important. Long-term exposure to stress can suppress the acquired immune response, causing an imbalance between pro-inflammatory and anti-inflammatory factors. Experimental studies in rat glands have demonstrated that acute stress induces dystrophic and necrobiotic changes in the gland, resulting in a reduction in its protein synthesis function. Psychological stress can contribute to disruption of the usual lifestyle, which adversely affects hygiene. Conclusions. After analysing scientific research data and reports on the current state of psycho-somatic health of people in Ukraine in modern realities, it is obvious that the prevalence and intensity of periodontal tissue diseases may have a new negative development. The peculiarities of the development, prevention and treatment of periodontal diseases in people experiencing severe psycho-emotional and sometimes physical stress require additional study and analysis. Key words: psycho-emotional stress, stress factor, periodontium, oral cavity

Ultrastructural changes in the rat retina in the presence of long-term opioid exposure

Purpose: To determine the features of the untrastructural reorganization in the rat retina by the end of week 4 and week 6 of experimental opioid exposure. Material and Methods: Forty-eight adult male albino rats (weight, 200-250 g; age, 4.5 months) were used in this study. They received nalbuphine hydrochloride intramuscularly daily for 42 days. Particularly, the drug was administered daily at a dose of 0.212 mg/kg for weeks 1 and 2, 0.225 mg/kg for weeks 3 and 4, and 0.252 mg/kg for weeks 5 and 6. In this way, we experimentally created the conditions of chronic opioid exposure. Animals were divided into three groups. Group 1 (19 animals) received nalbuphine for 28 days, and group 2 (19 animals), for 42 days. Group 3 (control group) comprised 10 animals. Of these, 5 animals were treated with normal saline at a dose of 0.22 mg/kg intramuscularly daily for 28 days, and the rest were treated in a similar manner for 42 days. Transmission electron microscopy studies of the rat retina were conducted in a routine manner. Results: By the end of week 4 of experimental opioid exposure, there was an increase in the number of retinal microvessels with signs of hyperemia and degenerative changes in retinal pigment epithelium (RPE) cells, increase in the destruction of membranous discs of photoreceptor outer segments, necrobiotic changes in the nuclei of individual photoreceptors, axonal degeneration in the outer and inner plexiform layers, degenerative changes in retinal horizontal neurons, and the appearance of necrotic structural changes in the cytoplasm of bipolar and amacrine cells. By the end of week 6, there was a further increase in hyperemia of retinal vessels and degenerative and necrotic changes in individual RPE cells and photoreceptor outer segments. In addition, we observed destruction and shortening of mitochondrial cristae of photoreceptor inner segments, necrotic nuclear changes in individual photoreceptors, degeneration of axons of the outer and inner plexiform layers, degenerative and necrotic changes in bipolar and amacrine cells, hypertrophic Müller cell processes, degeneration of ganglion cells, and vascular hyperemia and moderate perivascular edema in the outer and inner plexiform layers. Conclusion: Therefore, in the current rat study, after a 4-week exposure to daily nalbuphine injections at a dose ranging 0.212 to 0.253 mg/kg, there was ultrastuctural evidence of destructive processes in the RPE and photoreceptor outer segments, axonal degeneration in the outer and inner plexiform layers, degenerative and necrotic changes in bipolar and amacrine cells, hypertrophic Müller cell processes, ganglion cell degeneration and hyperemia due to an impaired retinal microcirculatory ultrastructure. At week 6 of the experiment, there was evidence of increased destructive and degenerative processes in structural components of the retina.

The course of COVID-19 with the development of “shock organs — lungs and heart”

The article presents a clinical and morphological description of a case involving death upon admission to a hospital, marked by developed sepsis and septic shock caused by the addition of bacterial flora. It also presents a clinical and morphological description of the development of shock organs lungs and heart after infection with SARS-CoV-2.
 A 38-year-old patient was hospitalized diagnosed with severe coronavirus infection, leading to shock. Complications arising from the underlying disease included bilateral viral interstitial pneumonia. Virological analysis of throat and nose swap samples confirmed SARS-CoV-2 coronavirus RNA. The patients condition, evaluated on the NEWS2 scale, scored 18 points. C-reactive protein levels were measured at 117 mg/l, and procalcitonin level was 9 ng/ml. Despite treatment efforts, the patient did not survive. Sectional examination in the lungs showed focal atelectasis of various sizes, edema with a large number of red blood cells. In the alveoli, there are fibrin threads and hyaline membranes blood stasis in the microcirculatory bed. In the heart, uneven blood filling in vessels, subendocardial hemorrhages, dystrophic and necrobiotic changes in cardiomyocytes, small foci of necrosis, fragmentation of cardiomyocytes, and intermuscular edema were noted. In the described case, the patient developed an infectious-toxic shock with severe changes in the lungs and heart attributed to a SARS-CoV-2 infection. These changes were intensified because of the addition and activation of bacterial flora due to a violation of the barrier function of the lung epithelium, leading to its complete destruction.

Pathophysiological mechanisms of adaptation of the mucosa of the gastric cardia to portal hypertension

The model of before- and intrahepatic blockage of the portal system was proposed. Modeling of before-hepatic blockage of the portal system after development of toxic liver dystrophy lead to formation of the liver cirrhosis with stable portal hypertension. Gastritis with signs of hyperplastic and atrophy processes of the mucosa, formation of erosia, inflammatory infiltration of intermediate tissue and rebuilding of the glandulae were the basis of morphological changes of gastric mucosa in rats with experimental before- and intrahepatic portal blockage. Transformation of the cardiac mucosa with expressed polymorphism occured in the patients with the portal liver cirrhosis. Dystrophic and necrobiotic changes typical of hepatic gastropathy with signs of acute or chronic gastritis, formation of inflammatory infiltrates and rebuilding of the cardial mucosa into intestinal type were established microscopically. It is possible to believe that a widening of the veins leads to venous hyperemia and stasis in the portal hypertension. Therefore the morphology of the gastric mucosa was disturbed. It was accompanied bythe indurate changes and cellular destruction with erosia formation. These erosia may be a cause of rupture of the gastric mucosa in strong vomiting in Mallory-Weiss syndrome. This hypothesis needs clinic and experimental study in the future.

Morphometric assessment of age-related structural changes in the vessels of the microcirculatory bed of the prostate gland under conditions of ethanol intoxication

Vessels of the microcirculatory bed ensure the full trophism of the body at the level of capillary-tissue relations and are the first to respond to various functional and pathological conditions of organs. At the same time, morphological changes in prostate microvasculature with age under conditions of prolonged ethanol poisoning have been understudied. The purpose of this study was to determine the age-related remodelling of the prostate vessels of the microcirculatory bed in case of prolonged alcohol intoxication. Injection, histological, morphometric, and statistical methods were used. The microvasculature of the prostate gland of 80 sexually mature white male rats of different ages was studied, 40 animals served as controls, and 40 rats were injected daily for 28 days with a 30% ethanol solution at a dose of 20 ml/kg intragastrically. Morphometric analysis indicated that chronic ethanol poisoning in white rats significantly reduces the lumens of arterial microvessels and hemocapillaries, while expanding the venous vessels in the microcirculatory bed of the prostate gland. When venous congestion occurs, the density of microvessels decreases, and microcirculation bed is disturbed. This disruption is accompanied by atrophic, dystrophic, and necrobiotic changes in endotheliocytes, epithelial cells, muscle cells, stromal structures, infiltration, and sclerosing. Intragastric 28-day administration of a 30% ethanol solution at a dose of 20 ml/kg to laboratory mature white male rats leads to pronounced structural changes in the microvasculature of the prostate microcirculatory bed: constriction of arterioles, precapillary arterioles and hemocapillaries, dilation of the capillary venules and venules, which is complicated by significant venous haemorrhage, development of atrophy, dystrophy, necrosis of vascular endothelial cells, glandular epithelial cells, muscle cells, connective tissue structures, cellular infiltration, and sclerosis. Vessels of the microcirculatory bed play a leading role in ethanol-induced damage of prostate structures, which dominate in 24-month-old experimental animals

AGE FEATURES OF REMODELING OF ARTERIES OF THE PROSTATE GLAND AT ETHANOL INTOXICATION

Chronic alcohol intoxication leads to damage of almost all organs and systems, the degree of structural and functional disorders of which in this pathology is different and depends on the duration and severity of intoxication. Organs of the reproductive system are always involved in the pathological process with long-term effects of alcohol on the body. Age-related remodeling of prostate arteries in ethanol intoxication has not been studied enough.
 The aim of the study: morphologically study the age-related features of prostate artery remodeling under conditions of ethanol intoxication.
 Materials and methods. The prostate arteries of 60 white rats were morphologically studied, which were divided into 4 groups: 1 group – 15 intact animals aged 8 months; group 2 – 15 rats aged 24 months; group 3 – 15 8-month-old animals with ethanol intoxication; Group 4 – 15 24-month-old rats with the indicated simulated pathology. A 30% ethanol solution was injected intragastrically at the rate of 2 ml per 100 g of animal weight for 28 days once a day. Animals were euthanized by bloodletting under anesthesia. The external and internal diameters of small-caliber arteries, the thickness of the intima, media, adventitia, intimo-medial, intimo-adventitous, adventitio-medial, Vogenvort and Kernogan indices, and the relative volumes of damaged endotheliocytes were determined on the micropreparations of the prostate. Quantitative morphological indicators were processed statistically.
 Research results. The wall of arteries thickens, their lumen narrows, the thickness of the media and adventitia increases, and the studied indices change significantly in ethanol intoxication in the prostate. The thickness of the media in young animals with a pronounced statistically significant difference increased by 49.2 %, in old animals by 50.2 % (p<0.001), and the Wogenvoort index changed by 1.56 and 1.6 times, respectively (p <0.001). The lumen of the studied vessels in young rats was statistically significantly (p<0.001) reduced by 16.6%, in old rats by 35.0%, the Kernoghan index by 12.7 % and 13.0 % (p<0.001), which indicated a marked decrease in vascular permeability and deterioration of blood supply to the organ. The relative volume of damaged endotheliocytes in the small-caliber arteries of the prostate gland during long-term ethanol intoxication in young rats was equal to (24.80±0.18) %, and in animals of the older age group – (47.60±0.21) %. Light-optically, pronounced vascular disorders, hemoptysis, expansion of mainly venous vessels, perivisceral and stromal edema, foci of dystrophically, necrobiotically, apoptically altered endotheliocytes, epitheliocytes of glandular structures, focal infiltrates and growth of connective tissue were observed in the prostate gland during chronic alcohol intoxication. Swelling of endotheliocytes, their dystrophy, necrobiosis, desquamation and proliferation were also noted.
 Conclusions. Ethanol intoxication leads to thickening of walls of arteries of the prostate gland, narrowing of their lumen, atrophic processes in the intima, an increase of thickness of media, adventitia, disruption of the relationship between them, apoptotic, dystrophic and necrobiotic changes in endotheliocytes, endothelial dysfunction, hypoxia, dystrophy, necrobiosis cells and stromal structures, infiltration and sclerosis. The degree of structural rearrangement of prostate arteries dominates in experimental animals of the older age group.

Morphofunctional Changes in Neurons, Glial Cells and Synapses in the Sensorimotor Cortex after Severe Traumatic Brain Injury

The aim of the study was to investigate morphofunctional modifications in neurons, glial cells and synaptic terminals in the sensorimotor cortex of the brain in rats after severe traumatic brain injury (STBI).Material and methods. STBI simulation in white rats (main group, n=30) was performed on a device with a special shock mechanism. Intact animals (n=6) were included in the control group. The sensorimotor cortex (SMC) of the brain in rats was studied histomorphologically on sections stained with hematoxylin and eosin and thionin according to Nissl. Synaptophysin and GFAP were detected immunohistochemically, then morphometry was performed. On serial frontal sections of the SMC, neurons, neuroglia, and interneuronal synapses were studied in animals of the control group and in animals exposed to STBI in 1, 3, 7, 14, and 30 days after STBI simulation. The number density of neurons, neuroglia, and synaptic terminals was determined per a unit area of the section of layers I (terminals only), III, and V of the cerebral SMC. Statistical hypotheses were tested using nonparametric methods in the Statistica 10.0 program.Results. In animals of the control group, typical normochromic pyramidal neurons predominated, synaptic terminals were clearly verified; this was combined with unaltered neuropil. In animals exposed to STBI, there were signs of tinctorial, hydropic, dehydration and necrobiotic changes in neurons, reactive astrogliosis, fields of "loss" of neurons appeared; the overall numerical density of neurons and synapses decreased. The maximally increased content of pycnomorphic neurons was detected in 1 day after STBI (in layer III of the SMC, by 11.6%; in layer V of the SMC, by 18.5%). The peak in the number density of shadow cells and hyperchromic non-wrinkled neurons was noted in 3 days. The numerical density of synaptic terminals in different layers of the SMC decreased by 1.5-2 times. The altered balance of the destruction and restoration processes of the synaptic pool after STBI was evidenced by statistically significant data on the decreased and increased numerical density of terminals during 30 days of the study. There was no complete recovery of the studied parameters of neurons and synapses to control values within 30 days.Conclusion. The SMC of the brain in rats remains functioning after STBI; this occurs in the context of long-term preservation of reversibly and irreversibly damaged neurons, reactive neurogliosis, and permanent reorganization of interneuronal relationships due to activated reparative neuro- and synaptic plasticity. The data obtained will specify reorganization of the components of various neuronal complexes of the SMC (layers I, III, and V) after STBI.

Morphological changes in the kidney tissue of rats with experimental diabetes mellitus and during correction with metformin and modulators of hydrogen sulfide metabolism

Annotation. Metformin is widely used for pharmacocorrection of diabetic nephropathy in type 2 diabetes mellitus. However, the mechanisms of the protective effect of metformin on the kidneys remain unclear, in particular, the contribution of the hydrogen sulfide system to metformin’s nephroprotective effect is unknown. Therefore, the aim of our study was to assess the role of metformin and its combination with modulators of hydrogen sulfide metabolism in the correction of histological changes in the kidneys of streptozotocin-induced diabetic rats. The studies were performed on 30 white non-linear male rats, which were divided into five groups: 1 group - control; group 2 – animals with experimental diabetes, which was initiated by a single intraperitoneal injection of streptozotocin (40 mg/kg of weight) in 0.1 M citrate buffer (pH 4.5); Group 3 - animals with experimental diabetes, which were treated with metformin (500 mg/kg/day, intragastrically) from the 3rd to the 28th day; Group 4 - animals with diabetes mellitus, which, along with metformin, were administered NaHS (56 μmol/kg/day, intragastrically); Group 5 - animals with diabetes mellitus, which, along with metformin, were administered propargylglycine (442 μmol/kg/day, intragastrically). Histological examinations were performed according to generally accepted methods using an Olympus BX-41 light microscope (Olympus Europe GmbH, Japan). It was found that animals with experimental diabetes develop nephrosclerosis and glomerular hypertrophy, damage to the endothelium of kidney vessels, interstitial inflammation, and edema, and dystrophic and necrobiotic changes in the glomeruli. The administration of metformin to diabetic animals reduced the severity of nephrosclerosis, glomerular hypertrophy, destruction of vascular endotheliocytes, inflammation, and damage to the glomerular apparatus. The use of the hydrogen sulfide donor NaHS increased the nephroprotective activity of metformin, while the introduction of the hydrogen sulfide synthesis inhibitor- propargylglycine, significantly reduced the protective effect of metformin on the kidneys. The obtained results of the histological examination justify the feasibility of implementation of a hydrogen sulfide donor in order to potentiate the renoprotective effect of metformin.

The effect of passive smoking on the structure of hepatocytes and the state of the microcirculatory bed in the liver in rats

BACKGROUND: Smoking is an important societal problem that greatly threatens the health of the population.
 AIMS: To study the effect of smoking on the hepatobiliary system of rats.
 MATERIALS AND METHODS: We used 46 outbred white male rats. The control group comprised intact animals (n=10). The experimental rats in groups 1 (n=12), 2 (n=12), and 3 (n=12) were exposed to an atmosphere of tobacco smoke for 7, 14, and 21 days, respectively.
 RESULTS: The greatest changes in the liver were noted in the third group. Small foci of necrosis were detected, around which a perifocal inflammatory reaction occurred. Signs of hydropic dystrophy and the presence of acidophilic lumps around the nuclei and thrombotic masses in the vessels were found. Signs of the capillaryization of the sinusoids were revealed. In all experimental groups, the number of cells up to 10 m in diameter significantly increased. The percentage of cells with a diameter of up to 1020 m increased in the central zone in group 1; that in group 2 increased by 3 and 2.6 times in the central and peripheral zones, respectively; and that in group 3 increased by 3.4 and 2.8 times in the central and peripheral zones, respectively (p 0.001). The number of cells with a diameter of up to 2030 m decreased in group 1, that in in group 2 decreased by 1.9 and 1.5 times in the central and peripheral zones, respectively; and that in group 3 decreased by 2.7 and 2.0 times in the central and peripheral zones, respectively (p 0.001). The number of cells with a diameter of more than 30 had changed and showed the greatest changes in the peripheral zones: that in groups 1 and 2 decreased by 2.7 times, and that in group 3 decreased by 2.9 times.
 CONCLUSIONS: Under tobacco smoke intoxication in rats, dystrophic and necrobiotic changes occurred in the liver, the number of binuclear cells decreased, the number of normal hepatocytes with a diameter of 2030 m decreased, and the percentage of cells with diameters of up to 10 and 1020 m increased.

Necrobiosis lipoidica of the breast associated with Crohn’s disease: a case report

BackgroundNecrobiosis lipoidica located to the breast; without evidence of glucose intolerance, is extremely rare, and its association to Crohn’s disease is not usual.Case presentationWe report an interesting case of an association of necrobiosis lipoidica of the breast and Crohn’s disease in a 54-year-old Moroccan woman. Skin necrobiotic changes are a characteristic feature in necrobiosis lipoidica, but they are exceptional in metastatic Crohn’s disease, since there are only three published cases of necrobiotic skin lesions on the lower leg resembling erythema nodosum in metastatic Crohn’s disease.ConclusionsOn the basis of this rare observation, necrobiosis lipoidica without evidence of glucose intolerance should be recognized as a possible cutaneous manifestation or association of Crohn’s disease.

QUANTITATIVE MORPHOLOGICAL FEATURES OF THE STRUCTURAL REARRANGEMENT OF THE VENOUS BLOOD VESSELS OF THE PROSTATE GLAND IN POST-RESECTION PORTAL HYPERTENSION.

Aim: Using quantitative morphological methods to study the peculiarities of the structural reconstruction of the venous bad of the prostate at the conditions of post-resection portal hypertension. Materials and Methods: Morphologically, the venous bed of the prostate of 15 intact white rats, 30 animals with post-resection portal hypertension, 17 rats with a combination of post-resection portal hypertension with hepatargia, enteral, cardiac, and renal insufficiency was studied. Rats were slaughtered one month after the start of the experiment by bloodletting under general thiopental anesthesia. Morphometry of the venous blood vessels of the prostate gland was performed on histological specimens, during which the diameter of the postcapillary venules, the diameter of the venules, the external diameter of the venous vessels, the internal diameter of the venous vessels, the thickness of the wall of the venous vessels was determined. Also it was studied the height of endothelial cells, diameter of their nuclei, nuclear-cytoplasmic ratio in these cells, relative volume of damaged endothelial cells, density of vessels of microcirculatory bed per 1 mm² of prostate tissue. Results: It was found that resection of the left and right lobes of the liver leads to the development of postresection portal hypertension and pronounced remodeling of the vessels of the venous bed of the prostate gland, which was characterized by the expansion of the capillary venules of the prostate by 36.5%, with the occurrence of multiple organ failure by 38.5% (р<0.001 ), an increase in the lumen of veins, thinning of their wall, atrophy, dystrophy, and necrobiosis of endothelial cells, disruption of structural cellular homeostasis, endothelial dysfunction, hypoxia, dystrophic-necrotic changes in cells, stromal structures, infiltration, and sclerosis. Morphological changes in the structures of the prostate dominated when post-resection portal hypertension was combined with multiple organ failure. Conclusions: Post-resection portal hypertension in laboratory sexually mature white male rats leads to pronounced remodeling of the venous bed of the prostate gland, which is characterized by the expansion of the lumen of the vessels, thinning of their walls, atrophic, dystrophic and necrobiotic changes in endothelial cells, a violation of structural cellular homeostasis in them, endothelial dysfunction, hypoxia, dystrophic-necrotic changes in cells, stromal structures, infiltration and sclerosis. Morphological changes in the structures of the prostate dominated when post-resection portal hypertension was combined with multiple organ failure.

Therapeutic Efficacy of Selenium in Management of Hyperhomocytenemia in Cisplatin-Induced Nephrotoxicity

Nephrotoxicity is a prominent cause of global of injury and mortality. The aim here is to investigate the therapeutic role of selenium in treatment of cisplatin-induced experimental nephropathy. Animals were classified into four groups including cisplatin group in which animals were injected (intraperitoneal) with a single dose of cisplatin, while treated group in which rats injected with cisplatin and then received selenium (0.5 mg /k.g.b.w. / day) orally for ten days , control group , and selenium group in which healthy rats received selenium in a dose of 0.5 mg /k.g.b.w. / day , orally for ten days .After the experimental period, samples (blood and kidney tissues) were collected from each rat to estimate different biochemical and histological parameters using different techniques. Cisplatin significantly increased serum creatinine and urea comparing to control. However, reduction in catalase antioxidant enzyme was recorded in nephrotoxic rats, while marked increase in lipid peroxide (MDA), Advanced Oxidant Protein Product (AOPP), interleukin-1β(IL-1β), ceramide, tumor necrosis factor –α (TNF–α), metalloproteinase -9 (MMP-9)and homocysteine (Hcy) levels was detected as compared to control. Histopathological investigation revealed necrobiotic changes and deterioration in the lining tubular epithelium and tubular cystic dilatation at the cortex and inflammatory cells between the degenerated tubules. Treatment with selenium showed improvement in histopathological picture and corrective effects in all biomarkers under investigation. Nephrotoxicity induced by csplatin in rats is associated with remarkable elevation of oxidative stress, inflammatory markers, and renal histopathological lesions. While, the therapeutic effect of selenium (Se) may be attributed to` the alleviation of ROS-mediated apoptosis. These current results indicated that Se may be offer a promising dietary supplement against nephrotoxicity.

Neutrophilic dermatosis with necrobiotic changes as an unusual manifestation after the first shot of a COVID‐19 mRNA vaccine together with a high fever and liver injury

Coronavirus disease 19 (COVID‐19) mRNA vaccines sometimes cause various skin rashes. We report an unusual case of erythema nodosum‐like nodules with vesicular and pustular papules, which arose after the first shot of a COVID‐19 mRNA vaccine. A skin biopsy showed marked neutrophilic infiltration with necrobiotic changes throughout the dermis and subcutis. Immunohistochemically, CD8+ cells were much more common than CD4+ cells in the dense neutrophilic infiltrates. Many CD68+ macrophages were present around the CD8+ cells. No cases of neutrophilic dermatosis with necrobiotic changes have been reported. Thus, our findings should be added to the cutaneous adverse effects of the vaccines.

Pathological manifestations of inflammatory microthrombosis in COVID-19

Background. COVID-19 is a predominantly respiratory disease caused by the SARS-CoV-2 virus that has spread as a pandemic since 2020; characterized by high mortality and unexplored long-term outcomes.&#x0D; Aim. To describe the morphological changes in the lungs and other organs in severe forms of COVID-19.&#x0D; Material and methods. A macro- and microscopic examination of the lungs, kidneys, liver, brain and heart of 45 patients who died from complications of COVID-19 was carried out. Histological preparations were stained with hematoxylin and eosin, by the Picro-Mallory stain, as well as with fluorescent antibodies and dyes to visualize neutrophil extracellular traps.&#x0D; Results. The leading pathomorphological manifestations of COVID-19 were inflammation and microthrombosis in the lungs. At the same time, diffuse alveolar damage often developed as a manifestation of acute respiratory distress syndrome in an adult. Diffuse leukocyte infiltration of the lungs was combined with the formation of neutrophil extracellular traps in the lumens of the blood vessels. Diffuse microthrombi were found in most lung tissue samples (87%), while macroscopic thrombi were much less common (16%). In single cases, the cause of death was thromboembolism of the branches of the pulmonary artery, originating from deep vein thrombi of the lower extremities or the right atrial appendage. In the tissues of the liver, heart, kidneys and brain, moderate alterative (degenerative and necrobiotic) microscopic changes were observed, as well as morphological signs of concomitant chronic diseases.&#x0D; Conclusion. COVID-19 is characterized by pathogenically interrelated morphological manifestations of inflammation and primary pulmonary (micro)thrombosis in the form of accumulation of leukocytes both in blood clots and in the alveoli, while regional pulmonary immunothrombosis is associated with diffuse damage to the alveoli; in the heart, brain, liver and kidneys, predominantly dystrophic and necrobiotic changes occur, which are typical of secondary injuries and/or concomitant pathology.

Histopathology of organs of grass carp (Ctenopharyngodon idella) from the Ile river and the Kapshagay reservoir

The ecosystems of the Ile-Balkhash region have been subjected to anthropogenic pressure in recent years, which leads to a decrease in biodiversity, including commercial fish. In the present study, using the method of atomic absorption spectroscopy, the content of heavy metals in the surface waters and bottom sediments of the Ile River (upper reach, Panfilovsky district, Almaty region) and the southeastern part of the Kapshagay reservoir was determined. An excess of MPC among the 9 determined HMs, was found for Fe &gt; Zn &gt; Pb &gt; Cd. The accumulation of these HMs was also found in organs (gills, liver, large intestine, kidneys) of grass carp caught in different parts of the studied water bodies. With the help of histological and morphometric methods, the morpho-functional state of grass carp was assessed and destructive changes in the same organs were revealed. At the same time, it was found that the nature and quantitative indicators of histopathological changes depend on the level of HM accumulation and the place of capture. At the same time, the greatest structural changes were found in the organs of grass carp from the Ile River (upper reach) compared with fishes from the southeastern part of the Kapshagay reservoir. In the gills, hyperplasia, fusion of the plates, necrosis and edema of the gill epithelium were&nbsp;revealed. Expansion of spaces of Disse, sinusoids, dystrophy and necrosis of hepatocytes, numerous melanomacrophage accumulations were found in the liver. In the large intestine – stratification of wall tissues: muscular, serous, submucosal and mucous bases, necrosis of enterocytes. In the kidneys, wrinkling and divergence of capillaries in the vascular glomeruli, an increase in the Bowman space, dystrophic and necrobiotic changes in the epitheliocytes of the proximal and distal renal tubules were observed. It was concluded that heavy metals bioaccumulated in the tissues and organs of grass carp subsequently worsen their histopathological state and, thus, affect the health of fish. The revealed histopathological effects can be biomarkers of the state of the aquatic environment. Key words: Ile river, Kapshagay reservoir, heavy metals, grass carp, histopathology.

Protective action of polysaccharides from Laurencia papillose (Rhodophyta) against imidacloprid induced genotoxicity and oxidative stress in male albino rats.

Imidacloprid (IMI), the main component of neonicotinoid insecticides, promotes oxidative stress and genotoxicity in mammals. The aim of this experiment is to assess oxidative stress in liver cells and genotoxicity of erythrocytes for rats exposed to sub-lethal doses of IMI and the protective effects for Rhodophyta as antioxidant material versus imidacloprid. A total of 30 adult male albino rats (average body weight, 190–200 g) were divided into six groups (n=5) as follows: group 1 served as the control, group 2 received 200 mg/kg red algae, group 3 received 45 mg/kg IMI (high-dose group), group 4 received 22.5 mg/kg IMI (low-dose group), group 5 received 200 mg/kg red algae +45 mg/kg IMI, and group 6 received 200 mg/kg red algae +22.5 mg/kg IMI. After 28 d of treatment, the antioxidant activity of the crude extract of red algae was assessed in terms of free radical scavenging activity and found to be higher in TCA (75.57%) followed by DPPH (50.08%) at concentration 100 μg extract and a significant increase in lipid peroxidation and reductions in glutathione were observed in liver cells were intoxicated with high and low doses of IMI. Moreover decreases in catalase and glutathione peroxidase parameters in same previous groups which indicated oxidative stress. In addition significant increases in micronucleus frequency (MN) in the bone marrow of the rats as a genotoxicity marker which indicated DNA damage in erythrocytes cells with alterations in the histopathology of liver cells were also noted such as necrosis, inflammatory cells, infiltration, and necrobiotic changes. Whereas Rhodophyta succeeded in alleviation the oxidative damage and genotoxicity induced by the insecticide. In conclusion, IMI demonstrates hazardous effects, such as alterations in antioxidant status and mutagenicity of erythrocytes and polysaccharides from Rhodophyta has good antioxidant activity in vivo model systems against imidacloprid.

Acute Ascending Necrotizing Myelitis After COVID-19 Infection: A Clinicopathologic Report.

Neurologic manifestations of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2, COVID-19) infection are common and varied. The objective of this report was to describe clinicopathologic findings of rare acute ascending necrotizing myelitis (ANM) and briefly summarize similar COVID-19-associated longitudinally extended transverse myelitis cases. We described the clinical presentation, disease course, diagnostic workup, therapeutic measures, and pathologic findings of ANM associated with COVID-19 infection. A 31-year-old previously healthy woman developed a longitudinally extensive lower thoracic myelopathy 3 weeks after COVID-19 infection. The thoracic spinal cord lesion extended to cervical level in 1 week and to the lower medullary level in 2 more weeks. Thoracic laminectomy at T5-T6 level and cord biopsy revealed necrobiotic changes without viral particles or microglial nodules. The clinical deficit stabilized after immunomodulatory and eculizumab therapies. COVID-19 infection can cause ANM. It adds to the spectrum of reported cases of COVID-19 -associated encephalitis and myelitis.

Pathomorphological diagnostics of panleukopenia in cats (case description)

The article highlights the results of autopsy and histopathological studies of cats diagnosed with panleukopenia (FPV), confirmed by immunochromatographic rapid test. The spread of FPV among cats is declining sharply worldwide due to domestic vaccination of cats. However, the number of deaths among homeless animals is still high. The disease course usually varies from subclinical infection to acute syndrome with sudden death. Typical clinical manifestations are characterized by fever, lethargy, and anorexia. Sick cats suffer from vomiting and subsequent watery or hemorrhagic diarrhea. Homeless animals often die from complications associated with secondary bacterial infection, sepsis, and dehydration. Cats aged four months to one year are the most severely affected. Mortality varies depending on the disease course, the animal’s general condition, and timely veterinary care. The autopsy of the dead animals showed signs of catarrhal gastritis, catarrhal and hemorrhagic enterocolitis, splenomegaly, serous lymphadenitis, liver and kidneys’ acute congestive hyperemia, and pulmonary edema. Duodenum histological examination revealed villi necrosis, edema of the mucous membrane’s stroma, and desquamation of enterocytes into the intestinal lumen. Necrosis of Lieberkühn crypts and viral intracytoplasmic inclusions in enterocytes were very pronounced. Microscopic changes in the stomach and large intestine were characterized by dystrophic and necrobiotic changes of mainly the epithelial plate of the mucous membrane. Extracapillary glomerulonephritis developed in the kidneys, while focal emphysema and edema occured in the lungs. Stroma edema, delimphatization and lymphocytic necrosis were observed in the spleen and lymph nodes.