Morpho-functional basis of endothelial dysfunction in diabetes mellitus

The diabetes mellitus (DM) inevitably progresses and leads to complications, among which the main place is occupied by micro- and macroangiopathies. The presence of endothelial damage in DM can be established even before macroscopically significant damage to the vessel. At the same time, there is no summary ED characteristic for diabetes. The aim of the study is to make a comprehensive evaluation of ED in DM -1 and DM-2 types.Materials and methods of research. 60 persons, including 53 DM type 1 and type 2, with a severe course (state of decompensation) participated in the present study. We used the method of estimating ED by the number of circulating desquamation endothelial cells (CECs) at the stages of decomposition with simultaneous determination of NO2- and NO3- metabolites of nitric oxide.Results and discussion. In patients with diabetes, the level of CECs increased in 3-5 times and ranged from 1800 to 11,200 cells / ml. The average amount of CECs in patients with diabetes was 3358.5 ± 366.3 cells / ml.Conclusions: Endothelium is involved in the pathological process at DM. This is evidenced by a significant increase in CECs in the blood plasma. The use of this method allows to detect ED before clinically considerable vascular impairment and reflects the severity of the course and duration of DM

ЕКСПЕРИМЕНТАЛЬНЕ ВИЗНАЧЕННЯ ОПТИМАЛЬНИХ ПАРАМЕТРІВ РОБОТИ ТЕЛЕКОНФЕРЕНЦІЇ НА МОБІЛЬНИХ ПРИСТРОЯХ

The article considers the problem of ensuring the availability and integrity of wireless subscribers in cellular and other wireless corporate networks. The article aims to determine the threshold values for the moment of failure of video transmission, quantitative parameters, artifacts, and the number of errors for the image. Show the dependence of the integrity of data transmitted in real-time on the characteristics of the environment. Two approaches were used to assess the quality of video information: qualitative (image recognition assessment) and quantitative (error measurement). Because the research program was written in the Kotlin programming language, a library written in Java or Kotlin was required. After searching the library, it turned out that only three libraries meet such parameters as reliability, relevance, and availability of documentation: Jaffree, Xuggler, and VLCJ. After gathering information, it was found that the most common screen extensions for desktops are 1366 × 768 and for phones—360 × 640. An error occurred that RTP did not support more than one connection. Also, the RTSP protocol could not pass the experiment on codecs other than MP4V. The experiment stopped earlier than necessary without error. Judging by the indicators, this was a very high CPU load. All other protocols were successfully tested, and results were obtained. During the experiments, we encountered various video anomalies. The worst was the video playback problem with the MJPG codec. Other anomalies were also identified: frame delay, incorrect frame rendering, white noise, and white noise mixed with frames. It is clear how up to 128 kbps experiments are successful and then begin to stop the video stream without error information. According to the results of experiments, the H.264 codec performs best.В статті розглянута проблема забезпечення доступності та цілісності безпроводових абонентів у стільникових та інших безпроводових корпоративних мережах. Метою статті є визначення порогових значень для моменту зриву передавання відеосигналу, кількісні параметри, артефакти і кількість помилок для зображення. Показати залежність цілісність даних, переданих в режимі реального часу, від характеристик середовища. Для оцінки якості відеоінформації були застосовані два підходи: якісний (оцінка розпізнавання зображення) і кількісний (вимірювання кількості помилок). Оскільки програма для проведення дослідження була написана на мові програмування Kotlin, то була потрібна бібліотека написана на Java або Kotlin. Після проведення пошуку бібліотеки виявилося, що бібліотек які задовольняють таким параметрам як: надійність, актуальність та наявність документації, лише три: Jaffree, Xuggler і VLCJ. Після збору інформації було встановлено, що найпоширенішими розширеннями екрану для настільних комп’ютерів є 1366×768 і для телефонів — 360×640. Виявилася помилка, що протокол RTP не підтримував більше одного підключення. Також протокол RTSP не зміг пройти дослід на інших кодеках крім MP4V, дослід припинявся раніше ніж потрібно без помилки, судячи по показникам причиною цьому була дуже велика загрузка процесора. Всі інші протоколи успішно пройшли дослід і були отримані результати. Під час проведення дослідів, ми зіткалися з різними аномаліями відео. сама найгірша була, проблема з відтворення відео у кодека MJPG. Також були виявлені інші аномалії: затримка кадрів, некоректне відмальовування кадрів, білий шум і білий шум в перемішку з кадрами. Добре видно як до 128 кбіт/с досліди проходять успішно, а потім починаються припинення відеопотоку без інформації про помилку. За результатами дослідів найкраще себе проявляє кодек H.26

Inactivation of mouse transmembrane prolyl 4-hydroxylase increases blood brain barrier permeability and ischemia-induced cerebral neuroinflammation

Hypoxia-inducible factor prolyl 4-hydroxylases (HIF-P4Hs) regulate the hypoxic induction of > 300 genes required for survival and adaptation under oxygen deprivation. Inhibition of HIF-P4H-2 has been shown to be protective in focal cerebral ischemia rodent models, while that of HIF-P4H-1 has no effects and inactivation of HIF-P4H-3 has adverse effects. A trans membrane prolyl 4-hydroxylase (P4H-TM) is highly expressed in the brain and contributes to the regulation of HIF, but the outcome of its inhibition on stroke is yet unknown. To study this, we subjected WT and P4htm(-/- )mice to permanent middle cerebral artery occlusion (pMCAO). Lack of P4H-TM had no effect on lesion size following pMCAO, but increased inflam-matory microgliosis and neutrophil infiltration was observed in the P4htm-/- cortex. Furthermore, both the permeability of blood brain barrier and ultrastructure of cerebral tight junctions were compromised in P4htm(-/-) mice. At the molecular level, P4H-TM deficiency led to increased expression of proinflammatory genes and robust activation of protein kinases in the cortex, while expression of tight junction proteins and the neuroprotective growth factors erythropoietin and vascular endothelial growth factor was reduced. Our data provide the first evidence that P4H-TM inactivation has no protective effect on infarct size and increases inflammatory microgliosis and neutrophil infiltration in the cortex at early stage after pMCAO. When considering HIF-P4H inhibitors as potential therapeutics in stroke, the current data support that isoenzyme-selective inhibitors that do not target P4H-TM or HIF-P4H-3 would be preferred.Peer reviewe

Inactivation of mouse transmembrane prolyl 4-hydroxylase increases blood brain barrier permeability and ischemia-induced cerebral neuroinflammation

Hypoxia-inducible factor prolyl 4-hydroxylases (HIF-P4Hs) regulate the hypoxic induction of > 300 genes required for survival and adaptation under oxygen deprivation. Inhibition of HIF-P4H-2 has been shown to be protective in focal cerebral ischemia rodent models, while that of HIF-P4H-1 has no effects and inactivation of HIF-P4H-3 has adverse effects. A trans membrane prolyl 4-hydroxylase (P4H-TM) is highly expressed in the brain and contributes to the regulation of HIF, but the outcome of its inhibition on stroke is yet unknown. To study this, we subjected WT and P4htm(-/- )mice to permanent middle cerebral artery occlusion (pMCAO). Lack of P4H-TM had no effect on lesion size following pMCAO, but increased inflam-matory microgliosis and neutrophil infiltration was observed in the P4htm-/- cortex. Furthermore, both the permeability of blood brain barrier and ultrastructure of cerebral tight junctions were compromised in P4htm(-/-) mice. At the molecular level, P4H-TM deficiency led to increased expression of proinflammatory genes and robust activation of protein kinases in the cortex, while expression of tight junction proteins and the neuroprotective growth factors erythropoietin and vascular endothelial growth factor was reduced. Our data provide the first evidence that P4H-TM inactivation has no protective effect on infarct size and increases inflammatory microgliosis and neutrophil infiltration in the cortex at early stage after pMCAO. When considering HIF-P4H inhibitors as potential therapeutics in stroke, the current data support that isoenzyme-selective inhibitors that do not target P4H-TM or HIF-P4H-3 would be preferred.Peer reviewe

Bacterial extracellular vesicles – brain invaders? A systematic review

IntroductionKnowledge on the human gut microbiota in health and disease continues to rapidly expand. In recent years, changes in the gut microbiota composition have been reported as a part of the pathology in numerous neurodegenerative diseases. Bacterial extracellular vesicles (EVs) have been suggested as a novel mechanism for the crosstalk between the brain and gut microbiota, physiologically connecting the observed changes in the brain to gut microbiota dysbiosis.MethodsPublications reporting findings on bacterial EVs passage through the blood–brain barrier were identified in PubMed and Scopus databases.ResultsThe literature search yielded 138 non-duplicate publications, from which 113 records were excluded in title and abstract screening step. From 25 publications subjected to full-text screening, 8 were excluded. The resulting 17 publications were considered for the review.DiscussionBacterial EVs have been described with capability to cross the blood–brain barrier, but the mechanisms behind the crossing remain largely unknown. Importantly, very little data exists in this context on EVs secreted by the human gut microbiota. This systematic review summarizes the present evidence of bacterial EVs crossing the blood–brain barrier and highlights the importance of future research on gut microbiota-derived EVs in the context of gut-brain communication across the blood–brain barrier