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The vascular adventitia is involved in the pathological process of intimal hyperplasia, and oxidative stress caused by increased NADPH oxidase activity may be one of the mechanisms.

血管外膜参与了内膜病变形成的病理过程;NADPH氧化酶活性升高导致的氧化应激可能是外膜损伤致内膜病变的机制之一。

Adventitia consisted mainly of serosa structure, but the connective tissue was at the oviduct propria side.

外膜大部分为浆膜结构,在输卵管系膜侧为结缔组织的外膜

METHODS We used a dermatome to obtain thin endocardium,midcardium and epicardium transmural strips from left ventricular free wall of canine(weight 15-18 kg) and standard microelectrode techniques to record and measure the transmembrane action potential duration.

结果:①胺碘酮延长内、外膜层心肌细胞的动作电位时程,当基础周长为1 000 m s时,使用胺碘酮后心内膜层肌细胞的APD90由(254±38)m s延长为(274±37)m s(P.01),外膜层肌细胞的APD90由(205±37)m s延长为(229±16)m s(P.01);但其明显缩短中层肌细胞的APD,其APD90由(331±50)m s缩短为(290±62)m s(P.01)。

Mu opioid receptor was not observed in the wrist, funnel, abdomen of mantle, mouth, craw, stomach theca, intestine, rectum, sialoid gland, liver. Weak positive mu opioid receptor immunoreaction was found in inner epidermis, ectoblast, connective tissue of the esophagus and the keratolytic of the stomach and positive immunoreaction in epidermis of back of mantle and membrane of wrist.

结果表明,短蛸腕、漏斗、外套膜腹面、口球、嗉囊、胃盲囊、肠、直肠、前唾液腺、后唾液腺、肝胰脏均呈μ受体阴性,但食道内上皮、外膜、结缔组织和胃角质层有μ受体分布,外套膜背面、腕间膜的上皮或近上皮部位呈μ受体阳性。

After disposal,schwann cells, myelin sheath and axon of nerve fibers were eliminated,but the basement membrane tube of schwann cells and three-dimensionalsupports of extracellular matrix of epineurium and perineurium werereserved.

经脱细胞处理后,去除了Schwann细胞、神经纤维的髓鞘和轴突,保存了由Schwann细胞基底膜管以及神经外膜和束膜的细胞外基质构成的三维支架结构。

Grew on the normal temperature, it was shown that the deposits of calcium antimonate being the indicator for Ca(superscript 2+) localization mainly concentrated within the vacuoles and intercellular spaces and there was also some Ca(superscript 2+) deposits in cell walls. But when Garyota urens L. was treated by the temperature of 2℃ for 48 h, the level of Ca(superscript 2+) increased in cytoplasm and plasma membrane, but decreased in vacuoles and intercellular spaces considerably. At the same time, the ultrastructure of chloroplasts suffered from chilling: the membrane of chloroplasts had been damaged, the layer of thylakoids was exiguous and unclear, the photosynthetic rate decreased evidently. And when Garyota urens L. was treated by the temperature of 2℃ for 120 h, the deposits of Ca(superscript 2+) mainly concentrated within the cytoplasm, nucleus and plasma membrane and there was also some Ca(superscript 2+) deposits in vacuoles, and the ultrastructure of some cells was simultaneously damaged severely: Chloroplasts structure, vacuole membrane and nuclear membrane had been damaged fully, the structure within the cell had become unclear, and the cell only have respiration.

研究结果表明,未经低温处理的董棕幼苗叶肉细胞,焦锑酸钙沉淀颗粒大量出现在液泡和细胞间隙中,细胞壁中也可见少量沉淀,而细胞基质中则看不到焦锑酸钙沉淀;经2℃ 48 h低温处理后,细胞基质和细胞膜上焦锑酸钙沉淀增加,而液泡和细胞间隙中的焦锑酸钙沉淀则显著减少,并且超微结构已初步显示出寒害的特徵,叶绿体外膜部分破损,类囊体片层稀疏且排列不规则,光合速率明显下降等;经2℃ 120 h低温处理后,细胞间隙内的焦锑酸钙沉淀极少,有的也紧贴在细胞外壁上,而细胞基质和细胞膜上则分布有非常多的焦锑酸钙沉淀,在核基质和液泡中也可见到少量的焦锑酸钙沉淀,并且超微结构遭到了显著破坏,叶绿体结构完全被破坏,核膜与液泡膜严重破损,内部结构模糊,细胞只表现为呼吸作用,不进行光合作用。

Transmembrane action potentials were recorded simultaneously from endocardium, epicardium, together with a transmural ECG, in arterially perfused left ventricular preparations by use of 2 separate intracellular floating microelectrodes. The stimulus-response- interval of the epicardium and the incidence of ventricular tachycardia were observed as well.

灌流全程同时采用浮置玻璃微电极法同步记录内膜下心肌、外膜下心肌跨膜动作电位和跨壁ECG,并观察心外膜下心肌的刺激反应间期(Stimulus-response-interval, SRI)和室性心动过速的诱发率。

At the BCL of 500ms, 1000ms and 2000ms,the VWtimes increased markedly with the BCL prolonging, and the degree of increasing was even obviously when heart rate was slow (BCL=2000ms or 1000ms). The enlargement of VWs was a most important reason to increase the incidence of ventricular arrhythmias; 2)At the BCL of 500ms, 1000ms or 2000ms,the VWtimes of the premature stimulates S2 was at endomembrane were wider than at the outermembrane. We supposed that premature stimulates come from endomembrane was easier inducing VF compared with outermembrane;3The VWtime of unidirectional block was wider than reentry's, we can see that reporlarization dispersion changed dynamicly. 4The QRS polar of the premature stimulates was opposite the primary beats ,which suggesting that excitation of inducing premature beats was coming from epicardial. That is to say electrotonic potential take part in the creation of reentry;5With the ratio of the Tp-e/QT increasing the occurrence of VF was upgrading. So the ratio was an effective method to estimate the event of SCD.6 The VWtimes of S3 were broaden than S2's. But we can not study penetratingly, which is the contents of our future studies.

在BCL为500ms、 1000ms和2000ms刺激条件下,随着刺激周长的增加单向传导阻滞时间易损窗呈增大趋势;并且在心率较慢时(BCL为2000ms和1000ms)增大最明显,是LQTS患者室性心律失常发生率增加的原因之一;2)在BCL为500ms、 1000ms和2000ms刺激条件下,S2位于内膜侧时时间易损窗大于在外膜侧时的,推测来自于内膜侧的期前刺激易于诱发室性心律失常;3)折返激动时间易损窗小于在单向传导阻滞时间易损窗,折返易发生于S2刚进入单向传导阻滞区间时,这说明复极梯度的不均一是动态变化的;4心电图上倒置QRS波与正常S1刺激所引起QRS波极性相反,提示不同位置S2刺激引发的室性早搏的兴奋均来自于外膜侧,说明了电紧张电位扩布参与了折返的产生;5)Tp-e/QT可以反应跨膜复极离散度,随着Tp-e/QT比值的增加PVT的发生增多,其可以用来预测室性心律失常的发生。6)随着期前刺激数目的增加时间易损窗增大。

Results Gelatinase activity of ascending aortic aneurysm was significantly increased compared with that of normal ascending aortic aorta.

结果 正常动脉壁外膜无或极少有明胶酶活性;动脉瘤壁的中膜与外膜明胶酶活性明显增强。

Some cell dropped into the cavity and became free. Thrombosis or part organization could be seen. The internal elastic layer became thin, disappear or broken. In internal and middle layer existed fibroblasts, fibrocytes and collagen. Some of the wall indicated hyaline change, soomth muscle cell decreased greatly. The massive inflammatory cells invaded the middle and external layer. There were many foam cells in the capsule tissue. Cytoplasm was filled with fatty tissue and cholesterol. some cavities were full of thrombosis. Some thrombosis was fibrosis, the bottom was organization. The surface of the thrombosis existed red blood cell and librae.(2)Elatic fibrila staining: the internal elastic menbrane almost completely disappeared, the intact internal elastic menbran could be seen in the new small vessels.

动脉瘤管壁厚薄明显不均,全层或局部区域显著变薄向外膨出,内皮细胞空泡变性或坏死脱落,部分内皮细胞剥离并突入管腔成游离状,可见血栓形成及部分血栓机化;内弹力板变薄、消失或突然中断;在内膜及中膜部位主要为纤维母细胞、纤维细胞和大片胶原;部分动脉瘤壁呈均质状玻璃样变,平滑肌细胞明显减少;中膜和外膜可见大量的炎性细胞浸润;瘤壁组织有纤维母细胞、纤维细胞、大片胶原成分及较多泡沫细胞,胞浆内充满脂类物质及胆固醇结晶;部分动脉瘤腔内充满血栓,有的血拴已经纤维化,血栓基部机化,血栓表面有红细胞和纤维素。

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