Structure changes of human brain gray matter neurons and astrocytes in acute local ischemic injury.

The purpose to identify key morphological features of the Astrocytes and Neurons in the acute local cerebral ischemia human cortex. Subjects and Methods: Left middle cerebral artery ischemic stroke died persons (n = 9) brain tissue samples from 3 zones: 1st - contiguous to the tissue necrotic damage site zone, 2nd - 5-10 cm distant from the previous one, 3rd - the damage site symmetrical zone of the contralateral hemisphere. For GFAP, MAP-2, NSE, p53 detection indirect immunoperoxidase immunohistochemical staining method has been used. Also, the samples were Nissl and Hematoxylin-Eosin stained. Results: The most pronounced changes in the quantity and morphological structure of astrocytes and neurons are found in directly adjacent to the necrotic core region of theleft middle cerebral artery ischemic stroke brain. This indicates the prevalence of the inflammation processes around the area of nerve tissueischemic destruction. Morphological changes of neurons and astrocytes, apoptosis, enhanced neuron-astrocyte interaction found in the area bordering on necrotic core (5-10 cm from it), as well as ischemic hearth symmetrical sites of the contralateral hemisphere. This interaction is essential for the neuroplasticityrealization in the local ischemic brain injury. Conclusion: The results obtained were shown the nerve tissue morphological characteristics changes occur in local cerebral cortex ischemic injury not only in the lesion, but also in the contralateral hemisphere. These changes are probably related to the implementation of neuroplasticity.

[The changes of plasma levels of soluble TNF-alpha and TNF-R1 ratio is a prognostic marker and key element of the stroke pathogenesis].

The goal of the present study was to investigate the plasma levels of sTNF-alpha, sTNF-R1 in acute stroke patients, to study the relation between ones, the neurological stroke severity and functional disability. The investigations comprised 60 ischemic stroke patients, 25 patients form control group. Plasma levels of sTNF-alpha, sTNF-R1 were detected by means of ELISA. The conclusion of interaction of sTNF-alpha and tmTNF-R1 increases inflammatory and apoptotic brain tissue damage on the first day of stroke is drawn. On the 7-th and 21-st days of stroke sTNF-alpha realize a neuroprotective effect. The interaction sTNF-alpha and sTNF-R1 blockade of damage expansion. As the result, prognostic significance of sTNF-alpha/sTNF-R1 is showed.

[To the Fas-induced neurons apoptosis mechanisms in stroke pathogenesis].

The goal of the present study was to investigate the plasma levels of proteins regulating Fas-induced apoptosis in acute stroke and to relate ones to brain damage and clinical features. By means of ELISA soluble Fas receptor (sFas) and soluble Fas ligand (sFasL) plasma levels were detected. Fas protein (CD95) expression on CD3 lymphocytes surfaces was detected using flow cytometry. It is summarized, that Fas-induced apoptosis play significant role in stroke pathogenesis. As the result, prognostic significance of sFasL plasma level is showed. Fas induced apoptosis mechanisms seems to be perspective target for search new therapy stroke patients.

[Guillain-Bare syndrome in a patient with tuberculous]. / Sindrom Giiena­Barre u bol'noi tuberkulezom.

The article reports on the rarest case of Guillain-Barré syndrome in the form of acute motor-sensory polyneuropathy in a female patient with tuberculous meningitis, disseminated pulmonary tuberculosis, and tuberculous pleurisy. In the neurological status at the exit from the coma, the patient was diagnosed with tetraplegia, bulbar syndrome, and respiratory disorders. Further, within a week, pronounced muscle atrophy appeared. Active etiotropic, pathogenetic therapy, including plasmapheresis, gave a dramatic effect with a significant improvement in the condition and a gradual regression of neurological disorders. The differential diagnosis was carried out primarily with critical illness polyneuropathy. The authors emphasize the rarity of the presented case: to date, such a combination of pathologies has never been described in the literature.

Cellular composition of the thymus in Wistar rats in experimental intracerebral hemorrhage.

The time course of changes in cellular composition of the thymus after experimental intracerebral hemorrhage was studied in rats with various prognostic resistance to emotional stress. Increased migration of T lymphocyte precursors to the subcapsular zone, activation of T lymphocyte differentiation in the thymus, reduced number of mitotic cells, destruction and intensive migration of thymocytes from the thymus were observed. The severity of changes in cell composition in all layers of the thymus after experimental intracerebral hemorrhage was different in rats resistant and predisposed to emotional stress. Predisposition to emotional stress and stress before surgical modeling of intracerebral hemorrhage affected the severity of changes in the thymus. It is shown that autoimmune and adaptation mechanisms, which are closely interrelated, play an important role in the pathogenesis of the intracerebral hemorrhage.

[IL-1beta, IL-10, INF-gamma, TNF-alpha, S100beta, AMA-M2 and cell immune response in stroke].

Clinical data showed a role for stress, inflammatory, innate immune and adaptive immune mechanisms is stroke. Absolute and relative count of lymphocytes decrease, CD3 HLA DR+ and immunoregulatory balance (CD4+/CD8+) increase, concentration of IL-1beta, INF-gamma, TNF-alpha, S100beta, AMA-M2 increase, IL-10 decrease were detected in peripheral blood of 25 patients with stroke. It is explained that the products of brain cell stroke destruction (AMA-M2) play in autoimmune stroke progress mechanisms the same role as neurospecific proteins as S100beta. It is concluded that both stereotype and autoimmune mechanisms are involved in the development of stroke.

[Morphological characteristics of the Wistar rat thymus in experimental intracerebral hemorrhage].

The purpose of the present investigation was to study thymus structure in 108 Wistar rats possessing different prognostic resistance to an emotional stress under the conditions of experimentally modeled intracerebral hemorrhage. It was demonstrated that after the intracerebral hemorrhage, the thymus underwent changes that were associated with both the stereotyped response to stress and the development of an immune response against the damaged brain tissue: relative thymus mass and the cortico-medullary index were shown to decrease, while the volumetric fractions of the capsule and connective tissue septa were increased. The reaction of the vascular bed included stasis, diapedesis and perivascular edema. These changes were more expressed in the rats predisposed to an emotional stress.

[Neurohumoral response and Fas-ligand-induced apoptosis in peripheral blood of patients with acute ischemic stroke]. / Neirogumoral'nyi otvet i aktivnost' Fas-liganda perifericheskoi krovi v ostrom periode ishemicheskogo insul'ta.

OBJECTIVE: To identify an effect of the neurohumoral response on the severity and orientation of Fas-ligand-initiated processes in the acute period of IS. MATERIAL AND METHODS: The study included 155 patients with IS in the territory of the left and right middle cerebral arteries, the control group consisted of 28 people. The National Institutes of Health Stroke Scale (NIHSS), the Hospital Anxiety and Depression Scale (HADS), and the Daily Life Stress scale were used. Concentrations of sFas, sFasL, cortisol (K), adrenaline (A), norepinephrine (NE), adrenocorticotropic hormone (ACTH) in the blood plasma of patients with IS were measured by enzyme-linked immunosorbent assay on days 1, 7 and 21 and once in the control group. CD3CD95+ lymphocytes phenotyping was performed using flow cytometry. RESULTS AND CONCLUSION: The hypothalamic-pituitary-adrenal axis dominance is associated with the activation of the apoptosis-inducing properties of peripheral blood in the first week after the IS onset and their decrease towards the end of the acute period, which is clinically represented by the increased levels of anxiety and depression, an unfavorable outcome of the acute period of IS.

[Immune mechanisms in the development of hemorrhagic stroke].

The role played by immune mechanisms in intracerebral hemorrhage (ICH) was evaluated based on the studies of thymus structure and cell composition in rats showing different degree of tolerance to emotional stress. A new experimental ICH model is proposed. It is concluded that both stereotype and autoimmune mechanisms are involved in the development of ICH.

[Apoptosis as a systemic adaptive mechanism in ischemic stroke]. / Apoptoz kak sistemnyi adaptivnyi mekhanizm pri ishemicheskom insul'te.

This paper presents a literature review considering the role and mechanism of apoptosis in the pathogenesis of ischemic stroke (IS). The authors introduce a new concept: the functional request of the patient as a set of external (the nature and intensity of rehabilitation measures, characteristics of everyday life, diet, etc.) and internal (genetic factors, internal picture of the disease, availability of rental and other psychological facilities and etc.) attributes. This concept allows a new angle in understanding the pathogenesis of IS and creates fundamental and clinical potential for more successful approaches to therapy and rehabilitation after IS.

[The brain after ischemic stroke: a clinical/histological study]. / Golovnoi mozg posle ishemicheskogo insul'ta: kliniko-gistologicheskoe issledovanie.

AIM: To analyze the histological features of changes in the brain tissue after ischemic stroke. MATERIAL AND METHODS: Brain tissue samples obtained in autopsy from 9 people died as a result of a left middle cerebral artery ischemic stroke from 3 to 7 days after admission were studied. Tissue samples were taken from 3 areas of the brain: 1) contiguous to the tissue necrotic damage site zone, 2) 5-10 cm distant from the previous one, 3) the contralateral hemisphere zone symmetrical to damage site. Samples were Nissl and hematoxylin-eosin stained. Detection of p53 protein, NSE, GFAP was performed by indirect immunoperoxidase immunohistochemistry. RESULTS: A decrease in the total number of neurons and glial elements, their spatial redistribution, change in cell structure and their functional activity was found. The changes of the artery wall and impaired regional blood flow were detected. The more intense NSE reactivity; p53-positive neurons, reduced neuron-astrocytes distance were identified in zones 2 and 3. CONCLUSION: Ischemic stroke is accompanied by severe histological changes. These changes with varying degrees of severity occur both in the areas adjacent to necrotic core, and in remote areas, and it is a substrate for neuroplasticity.

[A role of the Fas system in the pathogenesis of ischemic stroke]. / Rol' sistemy Fas v patogeneze ishemicheskogo insul'ta.

The Fas system can promote several biological effects due to their activation after ischemic stroke: apoptosis, inflammation, proliferation, differentiation. Fas interacts with adapter proteins activating a number of signaling pathways, including MAPK, NFKB, JNK, ERK, phosphorylation of cytoskeletal proteins, and caspase-dependent apoptosis. Fas expressed by neuronal progenitor cells from the subventricular zone does not induce apoptosis in healthy adult humans. During motion and differentiation of these cells, Fas regulates their morphological structure by the phosphorylation/dephosphorylation of cytoskeletal elements. An increase in the Fas and Fas ligand expression is observed in response to stroke injury. Fas responsible not only for cell death and inflammation but also for neuronal plasticity which occupies a central place in the processes of sanogenesis.