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POST-STROKE DYSPHAGIA: A TOPICAL DIAGNOSIS = ПОСТІНСУЛЬТНА ДИСФАГІЯ: ТОПІЧНИЙ ДІАГНОЗ
Palamarchuk A. L. POST-STROKE DYSPHAGIA: A TOPICAL DIAGNOSIS = ПОСТІНСУЛЬТНА ДИСФАГІЯ: ТОПІЧНИЙ ДІАГНОЗ. ВІСНИК МОРСЬКОЇ МЕДИЦИНИ. 2020;2(87):122-126. ISSN 0049-6804.
DOI http://dx.doi.org/10.5281/zenodo.3976570
http://www.herald.com.ua
УДК 616.321-008.17-02:616.831-005.1/.4]-079.2
DOI http://dx.doi.org/10.5281/zenodo.3976570
ПОСТІНСУЛЬТНА ДИСФАГІЯ: ТОПІЧНИЙ ДІАГНОЗ
А. Л. Паламарчук
Київський медичний університет
Summary. Palamarchuk A. L. POST-STROKE DYSPHAGIA: A TOPICAL DIAGNOSIS. - Kyiv Medical University, Ukraine; e-mail: [email protected]. Swallowing dysfunction (dysphagia) is common and disabling after acute stroke, but its impact on long-term prognosis for potential complications and the recovery from swallowing dysfunction remain uncertain. The aim of the study is to assess the basic patterns in the occurrence of post-stroke dysphagia depending on the location of the ischemia. It is shown that bilateral lesions of the cortico-nuclear pathways with the development of pseudobulbar syndrome, right-sided localization of stroke involving cortical and subcortical structures with afferent disorganization and left-sided strokes with the development of aphasia and oral apraxia, as well as stroke can be considered. The pathogenesis of post-stroke dysphagia is associated with the development of bulbar syndrome in 13.5% of cases, pseudobulbar syndrome - in 31.2% and swallowing apraxia syndrome - in 55.3%. Topical diagnosis of post-stroke dysphagia requires neuroimaging and functional tests as soon as possible after the first signs of stroke.
Key words: post-stroke dysphagia, topical diagnosis, neuroanatomy, neurophysiology
Реферат. Паламарчук А. Л. ПОСТИНСУЛЬТНАЯ ДИСФАГИЯ: ТОПИЧЕСКИЙ ДИАГНОЗ. Цель исследования: оценить основные закономерности возникновения постинсультных дисфагий в зависимости от локализации очага ишемии. Показано, что двустороннее поражение корково-ядерных путей с развитием псевдобульбарного синдрома, правосторонняя локализация инсульта с вовлечением корковых и подкорковых структур с афферентной дезорганизацией и левостороннего инсульта с развитием афазии и оральной апраксии а также инсультные поражения в мозжечке могут считаться основными причинами возникновения ПИД. Патогенез постинсультных дисфагии связан с развитием бульбарного синдрома в 13,5% случаев, псевдобульбарного синдрома - в 31,2% и синдрома апраксии глотания - в 55,3%. Топическая диагностика постинсультных дисфагии требует проведения нейровизуализационных исследований и функциональных тестов в возможно короткий срок после первых проявлений инсульта.
Ключевые слова: постинсультная дисфагия, топическая диагностика, нейроанатомия, нейрофизиологи
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Programmed cell death 4 (Pdcd4) is a tumor suppressor protein that interacts with eukaryotic initiation factor 4A and inhibits protein synthesis. Pdcd4 also suppresses the transactivation of activator protein-1 (AP-1)-responsive promoters by c-Jun. The Akt (protein kinase B) serine/threonine kinase is a key mediator of phosphoinositide 3-kinase pathway involved in the regulation of cell proliferation, survival, and growth. Because Pdcd4 has two putative Akt phosphorylation sites at Ser67 and Ser457, we investigated whether Akt phosphorylates and regulates Pdcd4. Our results show that Akt specifically phosphorylates Ser67 and Ser457 residues of Pdcd4 in vitro and in vivo. We further show that phosphorylation of Pdcd4 by Akt causes nuclear translocation of Pdcd4. Using luciferase assay, we show that phosphorylation of Pdcd4 by Akt also causes a significant decrease of the ability of Pdcd4 to interfere with the transactivation of AP-1-responsive promoter by c-Jun. ©2005 American Association for Cancer Research
Dispelling the Myths Behind First-author Citation Counts
We conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
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Akt phosphorylates Tal1 oncoprotein and inhibits its repressor activity
The helix-loop-helix transcription factor Tall is required for blood cell development and its activation is a frequent event in T-cell acute lymphoblastic leukemia. The Akt (protein kinase B) kinase is a key player in transduction of anti-apoptotic and proliferative signals in T cells. Because Tall has a putative Akt phosphorylation site at Thr90, we investigated whether Akt regulates Tall. Our results show that Akt specifically phosphorylates Thr90 of the Tall protein within its transactivation domain in vitro and in vivo. Coimmunoprecipitation experiments showed the presence of Tall in Akt immune complexes, suggesting that Tall and Akt physically interact. We further showed that phosphorylation of Tall by Akt causes redistribution of Tall within the nucleus. Using luciferase assay, we showed that phosphorylation of Tall by Akt decreased represser activity of Tall on EpB42 (P4.2) promoter. Thus, these data indicate that Akt interacts with Tall and regulates Tall by phosphorylation at Thr90 in a phosphatidylinositol 3-kinase-dependent manner. © 2005 American Association for Cancer Research
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