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RU
Провели морфометрический сравнительный анализ яичек и придатков яичек молодых 1,5—3-летних хряков с правильным семенем и старых 4—8-летыих хряков, показывающих различного рода расстройства в составе семени. Отметили, что наиболее сильными изменениями в яичках старых неплодных хряков были: уменьшение их массу, дегенерация эпителия семенных канальцев с одновременным утолщением основной мембраны, образование сперматоцелей и отрофия семенных канальцев с разрастанием интерстициальных клеток. В придатках яичек наблюдали гиперплазию эпителия протока, образование интраэпителиальных кист, реже дегенерацию эпителия протока. Другие часто встречаемые у остальных видов старические изменения яичек были здесь слабо выражены либо не появлялись.
EN
There were performed comparative examinations concerning the testicles and epididymis of young boars (aged from 1.5 to 3 years) characterized by a normal semen and old boars, aged from 4 to 8 years showing different disturbances in the content of their semen. It was foud that the changes in the testicles of old boars characterized a decreased mass of the testicles of old sterile boars, degeneration of epithelial cells of the seminal tract and callosity of the basal membrane, spermatocoele and atrophia of the semen canal with interstitial hyperplasia. Hyperplasia in the epithelium of the epididymis tract, the presence of cysts and less often degeneration of the epithelium were observed. Other changes often seen in old testicles were mild or were not present at all.
EN
The article presents atherosclerotic and inflammatory changes in brain vessels and perivascular tissue leading to ischemic and hypoxic changes which, in consequence, produce strokes and brain hemorrhages. The aim of the study was to examine the morphology of the brain vessels of seven elderly animals from 7-21 years of age (three monkeys, a likaon, wolf and two pigs). The brain vessels of the investigated animals demonstrated atherosclerotic changes such as: fibroid changes and amyloidal angiopathy (CAA) in the cortical and leptomeningeal vessels of the three monkeys, likaon and wolf brain. Fibroid arteritis was present in the meningeal arteries of the two sows. These atherosclerotic and inflammatory processes in the CNS vessels led to strokes and hemorrhages. Subarachnoid (Cebus apella) and intraventricular (Lemur mongoz) hemorrhages were noted in two of the monkey’s brains and fibrinotic arteritis produced massive mesencephalon hemorrhaging in the two 7-year old sows. The advanced stages of infarct necrosis were characterized by a predominance of vacuolated macrophages with proliferating mesodermal and glial components. Small post infarct and post hemorrhages lesions in nervous tissue produced scarring, with astrocytes, whereas large foci liquefied and formed cysts, marked by the presence of macrophages with hemosyderin in their margins. No atheromatosis changes were observed in the brain vessels.
EN
The aim of the study was the examine atrophy and degenerative brain changes of nine elderly animals (three monkeys, two wild cats, a likaon, a bear, a fox and horse) and to find an animal model for researching Alzheimer disease in humans. Brain hemispheres were dissected into hemispheric slabs 4.0-4.8 mm thick. Tissue samples from the brains were fixed in 10% neutral formalin, and embedded in paraffin, and then stained with hematoxylin an eosin, Nissl method, and monoclonal antibody 4G8 mAb against b-polipeptyde and neurofibrillary tangles (NFT) were stained with anti-tau monoclonal antibody. The examined animals revealed various degrees of brain atrophy neuron loss in layer III-VI in particular, lipofuscin deposit, status lacunaris, degenerative changes in the white matter, and gliosis. Lafora-like bodies were observed in licaon, horse and bear brains. The monkeys, cats, licaon, foxes, with the exception of the horse developed brain parenchymal amyloidosis-b. Two types of plaque were present, with the diffuse form being predominant. Congophilic amyloid angiopathy was observed in all the animals with the exception of the horse. NFT and amyloidosis-b was observed only in the bear brain and the latter is a good model for Alzheimer's pathology.
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