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俄羅斯遠東地區城市家飼犬外寄生硬蜱之蜱滋生病原體的分子檢測

為了解決YD1080 災情的問題，作者丹尼爾 這樣論述：

研究背景: 蜱滋生感染症在俄羅斯遠東地區成為主要公衛考量，其中有關蜱媒介立克次體菌、疏螺旋體、邊蟲及艾立克體等致病原皆常被臨床醫師所忽略。而立克次體菌及其他病原體皆已存在於各種病媒蜱及鄉村地區之野生哺乳類動物，然而卻無任何研究探討這些致病原於城市環境之家飼動物狀況。研究目的: 本研究於2021年6月至8月自俄羅斯遠東地區之哈巴羅夫斯克市(Khabarovsk)進行家飼犬外寄生蜱隻採集，並依其形態特徵進行蜱種確認，並進行立克次體菌、伯氏疏螺旋體、血小板邊蟲及犬艾立克體等病原體在蜱隻之感染篩檢。研究方法: 本研究之蜱隻乃採集自哈巴羅夫斯克市三個地區之獸醫院，採集得之蜱隻依其形態學主要特徵於立體解

剖顯微鏡下確認蜱種。而每一蜱隻則使用核酸萃取試劑組(DNeasy Blood & Tissue Kit)進行核酸(DNA)萃取，隨後運用巢式/半巢式聚合酶鏈反應技術(nested/seme-nested PCR)分別針對立克次體菌之gltA/ompB/ompA/17kd基因、血小板邊蟲及犬艾立克體之16SrRNA及伯氏疏螺旋體之OspA and 5S-23S intergenic spacer基因進行蜱隻之感染篩檢。而陽性樣本則進一步送定序。研究結果: 總計有140蜱隻採集自24隻家飼犬，並確認三屬四種株之硬蜱，包括11隻 (7.9%) 全溝硬蜱(Ixodes persulcatus)、62隻

(44.3%) 嗜群血蜱(Haemaphysalis concinna) 、10 隻(7.1%) 日本血蜱(Haemaphysalis japonica) 、55隻 (39.3%) 森林革蜱(Dermacentor silvarum)及2隻 (1.4%) 破損無法確認蜱種。其中包括66 隻(47.2%) 雄蜱、70 隻(50.0%) 雌蜱、3 隻(2.1%) 稚蜱及1隻 (0.7%)因蜱體破損而無法確認。經立克次體菌基因篩檢後發現共有32隻(22.8%)蜱感染立克次體菌，其中包括12隻(8.6%)嗜群血蜱(H. concinna)、9 隻(6.4%) 全溝硬蜱(I. persulcatus)

、 8隻 (5.7%) 森林革蜱(D. silvarum)及 3隻 (2.1%) 日本血蜱(H. japonica)。而全部陽性感染樣本則包含10 隻(7.1%) 雄蜱及22隻 (15.7%)雌蜱，並沒有任何稚蜱檢測到Rickettsia感染。依據定序結果顯示陽性樣本分別與Rickettsia heilongjiangensis 或 Candidatus Rickettsia tarasevichiae兩基因種株具有100%基因相似度，無任何樣本檢測到疏螺旋體、邊蟲及艾立克體感染。討論: 本研究結果確認所有曾發現於俄羅斯遠東地區之蜱種，並以嗜群血蜱(H. concinna)為主要蜱種，而四種蜱

種皆可檢測到立克次體菌感染，整體陽性率與鄰近國家(例如:中國及南韓)相似，因此，本研究首次確認俄羅斯遠東地區城市犬類宿主之外寄生硬蜱存在感染R. heilongjiangensis 及 Candidatus Rickettsia tarasevichiae兩種立克次體菌之基因種株。

在創傷性腦損傷模型中檢查熱處理過的人血小板沉澱裂解物的神經保護和神經修復功效

為了解決YD1080 災情的問題，作者Ouada Nebie 這樣論述：

Traumatic brain injury (TBI) remains a global health challenge nowadays, impacting over 50million people per year globally. This situation is partly linked to the fact that TBI is among thecentral nervous system disorders whose management mostly requires long-term care. It incurs asubstantial econo

mic burden to health systems and costing the global economy more than $400million. In either high, middle, or low-income countries, TBI is associated with significanteconomic and societal changes that deserve attention. The disease is described as one of the mostcomplexes, inducing some disproportio

nate effects between the countries. Unfortunately, theintervention strategies are still facing several limitations at the global level despite all the healthsciences’ progress. These obstacles are the surge of neuroinflammation, leading to progressiveneuronal degeneration and cognitive deficit. Effo

rts are made to stop this “silent killer”, but thereis a failure to manage the long-term burden of TBI efficiently until now.Nowadays, there is growing evidence that platelet lysates are full of bioactive compounds, andthey could constitute a powerful natural neuroprotective agent. Few studies have

already showntheir therapeutic potential in stroke, amyotrophic lateral sclerosis, and Parkinson's disease. Thus,we hypothesized that the delivery of human platelet lysate at an injured area in the brain couldprovide a suitable environment for recovery.The current project is intending to develop an

innovative approach for the treatment of TBI. Weaim to give the proof-of-concept of the interest of using heat-treated human platelet pellet lysate(HPPL) as a neuroprotective agent in TBI using experimental models.We used cells and animal models of TBI to achieve our goal. We first prepared HPPL fro

m nonpathogen-reduced platelet concentrates (PCs) and pathogen-inactivated PCs (I-HPPL) accordingto a previously established procedure. We evaluated their safety and functionality using cellmodels relevant to TBI, including viability assays, wound healing, anti-inflammatory activity,protein expressi

ons, and anti-ferroptosis effect. The safety assessment of the platelet biomaterialwas done using neuronal and endothelial cells and its neuroprotective potential with primaryneurons, dopaminergic cells line and, a ferroptosis inducer.Mouse TBI models were used to assess the therapeutic potential of

HPPL. We targeted it impacton motor function, neuroinflammation, oxidative stress, and synaptic loss. Behavior tests, geneexpression, fluorescent staining, ELISA, Western blot, and proteomics have been used during theinvestigation.19The in vitro experiment performed to investigate the platelet lysa

te’s safety demonstrated clearlythat HPPL/I-HPPL contain bioactive molecules and did not affect cell’s viability or induced stress.Moreover, HPPL and I-HPPL did not affect synaptic and neuronal protein expression and revealedanti-ferroptosis potential. This finding leads to further investigation of

HPPL's beneficial effect invivo. HPPL administration to TBI mice improved their motor function, mitigated the inflammationand oxidative stress. HPPL also decreased the synaptic proteins lost.HPPL is safe and exerted neuroprotective activity in vitro. It successfully reversed the motordeficit, inflam

mation, and stress triggered by brain injury in mice.