胞脈受損 的英文怎麼說
中文拼音 [bāomàishòusǔn]
胞脈受損
英文
impairment of uterine collaterals-
The brain artery can be blocked by blood clots and deprive the brain cells of nutrients and oxygen. alternatively, bursting of a brain artery causes a devastating cerebral haemorrhage with disruption of brain tissue
腦動脈可被血凝塊堵塞，令腦細胞缺乏養分和氧氣另外腦動脈也可爆裂而導致腦出血，使腦組織受損。This paper is to study the object of mn - zn ferrite powder, which is an important non - metallic magnetic materials, because of their narrow hysteresis loop, high magnetic permeability and high resistivity, high curie temperature and the low loss characteristics are widely used in many electronic industrial fields
這種磁性微粒經局部注射或經動脈導管注入瘤體后，在交變磁場作用下吸收電磁波轉化為熱能使腫瘤區升溫達所需的治療溫度（ 41 46 ） ，以殺死腫瘤細胞，而不含磁微粒的正常組織不受損，正逐漸成為醫學上腫瘤熱療技術的研究對象。Experimental results confirmed this assumption : during the interstimulus interval ( isi ) ranged from 33 to 83 ms, with the isi luminance approximated to the mean luminance of the stimulus grating, a novel okn elicited by the intermittent display of stationary gratings was observed and recorded. it can be labeled as " intermittent - display - grating induced okn " ( idg - okn ). in the second part, considering that the biphasic visual impulse resp onse is the feature of the magnocellular ( m - cell ) pathway, and the m - type ganglion cells are damaged in the primary open - angle glaucoma ( poag ), we presumed that idg - okn of poag could differ strikingly from that of normal subjects
結果顯示，當間歇刺激間隔（ interstimulusinterval ， isi ）在33 83ms范圍內， isi期間亮度近似為刺激光柵平均亮度，我們觀察並記錄到這種新型的靜止光柵誘發的oknintermittent - display - gratinginducedokn （ idg - okn ） （ magnocellular ）路特性，而且原發性開角青光眼（ primaryopen - angleglaucoma ， poag ）是m型視網膜神經節細胞受損，因此我們推測，基於雙相視覺脈沖反應的idg - okn在poag病人與正常人比較中很可能出現顯著差2間歇刺激，對11隻poag眼和14隻正常眼進行對比眼動實驗。To make clear the hypothesis, a middle cerebral artery occlusion ( mcao ) and hypoxia and glucose - deprivation ( hgd ) ischemic models were used in in vivo and in vitro study, respectively. we first studied the cellular localization of kvl. 2 and the co - localization of kvl. 2 protein and vegf receptors flk - 1 and flt - 1, observed the effect of mcao on kvl. 2 expression and phosphrylation in the rat brain in vivo, then investigated the effect of vegf on ischemia / hypoxia cell damage and tyrosine phosphorylation of kvl. 2 in sh - sy5y cells. finally, in order to further elucidate the relationship between vegf ' s neuroprotection and its regulation on kvl. 2 phosphorylation, we used a specific antisense oligodeoxynucleotide ( odn ) to knockdown the expression of endogenous vegf to observe its role in ischemia / hypoxia cell damage and regulation of kvl. 2 phosphorylation
為了驗證上述假設，本文分別在整體和離體水平，採用大腦中動脈缺血（ middlecerebralarteryocclusion ， mcao ）和體外氧?糖剝奪（ hypoxiaandglucose - deprivation ， hgd ）缺血模型，首先了解了kv1 . 2蛋白的細胞定位及與vegf受體flk - 1和flt - 1的共存情況，觀察了整體mcao后缺血再灌不同時間大鼠腦內kv1 . 2蛋白的磷酸化水平變化，然後通過外源性給予vegf蛋白，在sh - sy5y細胞株上觀察其對缺血細胞存活率及kv1 . 2蛋白磷酸化水平的影響，最後利用vegf反義脫氧寡核苷酸（ oligodeoxynucleotide ， odn ）特異阻斷內源性vegf蛋白的表達，觀察內源性vegf蛋白在缺血細胞損傷及調節kv1 . 2蛋白磷酸化中的作用，以進一步明確vegf缺血保護效應與其調節kv1 . 2蛋白磷酸化之間的關系。分享友人