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Results 5 cases central gaugliocytoma and 2 cases colloid cyst were located at middle line of ventricle,6 cases medulloblastoma were located at the top of the fourth ventricle or super cerebellum vermis,5 cases ependymoma were located at one lateral ventricle,3 cases ependymoma were located at the fouth ventricle,2 cases papilloma of choroid plexus werre located at triangle area of lateral ventricle,2 cases meningioma were located at triangle area of lateral ventricle,1 cases astrocytoma were located at lateral ventricle anterior horn.

结果 5例中央性神经细胞瘤和2例胶样囊肿发生于中线室间孔区;6例髓母细胞瘤分别发生于小脑上蚓部和四脑室顶部近中线区;5例室管膜瘤发生在单侧脑室,年龄分别为28~36岁;3例室管膜瘤发生在四脑室,年龄分别为7~13岁;2例脉络丛乳头状瘤发生侧脑室三角区,年龄13~15岁;2例脑膜瘤发生在侧脑室三角区,年龄为15~71岁,1例巨细胞型星形细胞瘤发生在右侧脑室底部,年龄为30岁。

Up to now, problems of the cell differentiation mechanism and immunological rejection of xenogenic resource ESCs meeted during clinical application were still not resolved.

目前异体来源的ESCs在临床应用上还需要攻克细胞分化机制、免疫排斥等问题,而治疗性克隆获得的ESCs虽可以解决免疫排斥问题,但其技术复杂、离分化完全的功能细胞距离较远。

We find that there are two types of CRF immunoreactive neurons in the cerebral cortex. Type I cells were mainly distributed in layers II -III. Morphologically this type of cells is interneuron and is the true CRF neuron in general meaning.

我们的研究显示,皮层中有两种类型的CRF阳性神经元,其中CRF阳性Ⅰ型细胞主要分布在皮层的Ⅱ-Ⅲ层,形态学特征显示这些细胞为抑制性中间神经元,且为真正的CRF神经元。

Type II cells were mainly distributed in layer V of cortex. It appeared that these cells receive the CRF immunostaining fibers terminals afferent from other cells rather than synthesize CRF by themselves. It is probable that type II cells receive afferent fibers from both extracortex and type I cells within layers II -III cortex. Considered that Type I cells morphologically are inhibitory interneuron, we presumed that type I in layer II -III could inhibit activity of type II cells in layer V.

CRF阳性Ⅱ型细胞主要分布在皮层第Ⅴ层,形态学特征显示这类细胞更像是接收来自其它神经元的CRF纤维投射而非自身分泌CRF,证据显示Ⅱ-Ⅲ层CRF神经元纤维可进入第Ⅴ层,考虑到皮层的CRF神经元形态上为抑制性中间神经元,这些结果提示Ⅱ-Ⅲ层CRF神经元能够抑制第Ⅴ层神经元的活动。

The presence of isolated single cells is very suggestive of infiltrative carcinoma, but I have seen aspirates from pure DCIS that contain these isolated cells.

此例中细胞单一、分散更支持是侵润性的癌,但是我曾经在一例乳腺导管原位癌的穿刺涂片中也看到这样孤立单一的细胞。

Itamin D from the skin and diet is metabolized in the lier to 25-hydroxyitamin D (Figure 1), which is used to determine a patient's itamin D status1,2,3,4; 25-hydroxyitamin D is metabolized in the kidneys by the enzyme 25-hydroxyitamin D-1-hydroxylase (CYP27B1) to its actie form, 1,25-dihydroxyitamin D.1,2,3,4 The renal production of 1,25-dihydroxyitamin D is tightly regulated by plasma parathyroid hormone leels and serum calcium and phosphorus leels.1,2,3,4 Fibroblast growth factor 23, secreted from the bone, causes the sodium–phosphate cotransporter to be internalized by the cells of the kidney and small intestine and also suppresses 1,25-dihydroxyitamin D synthesis.5 The efficiency of the absorption of renal calcium and of intestinal calcium and phosphorus is increased in the presence of 1,25-dihydroxyitamin D (Figure 1).2,3,6 It also induces the expression of the enzyme 25-hydroxyitamin D-24-hydroxylase (CYP24), which catabolizes both 25-hydroxyitamin D and 1,25-dihydroxyitamin D into biologically inactie, water-soluble calcitroic acid.2,3,4

从皮肤和食物来的维生素D在肝中代谢为25-羟基维生素D(图1),被用来决定病人体内维生素D情况的1,2,3,4;25-羟基维生素D在肾中被25-羟基维生素D1羟化酶(CYP27B1)转变为有活性的1,25-二羟基维生素D 。1,2,3,4由肾产生1,25-二羟基维生素D是被血浆甲状旁腺激素和血清钙,磷水平紧密调节。1,2,3,4由骨分泌的成纤维细胞生长因子23使钠磷协同转运蛋白被肾和小肠细胞内化及抑制1,25-二羟维生素D合成。5 在1,25-二羟基维生素D作用下肾和小肠吸收钙及磷的效率增高(图1)。2,3,6 它也包括25-羟四- 24 -羟化酶的表达(CYP24),且将1,25二羟基维生素D和25羟基维生素D异化成无生物活性,水溶性的维生素D3-23羧酸。2,3,4

Then the animals were sacrificed and the surface preparation and the section of cochleae stained by MyosinⅥwere observed.Other cochlea were observed with SEM.

分别于术后第3.5个月分别行听性脑干反应检查后取双侧耳蜗标本做基底膜铺片和耳蜗冰冻切片MyosinⅥ染色观察有无新生毛细胞样细胞出现,部分耳蜗作扫描电镜观察。

Kanic acid was injected into guinea pigs' cochleae and the excitotoxicity model was established. After a week the recombinant plasmid was transferred into SGCs of guinea pigs' cochlea treated with HAT. The following week the expression of NT-3 was examined by the immunohistochemical method, and the morphology of SGNs was observed under the electronic microscope after 4 weeks, in the mean time the changes of auditory brain-stein response were examined.

通过耳蜗灌注海人酸(kainic acid, KA)建立豚鼠耳蜗兴奋性损伤模型,在给KA 1周后利用HAT携带重组质粒进行耳蜗灌注以转染耳蜗螺旋神经节细胞,免疫组化法观察转染后1周NT-3的表达及4周后电镜下螺旋神经节细胞形态学变化,同时观察对听觉脑干诱发电位(auditory brain-stem response, ABR)的影响。

To detect the changes in 〓 induced by KCl (40mM) depolarizing stimulation, the rising rate of 〓 was bigger than in control, and the amplitude of 〓 increased no more significantly in DRG cell of arthritic rat than in control.

关节炎大鼠DRG细胞动作电位时程增加,可能通过促进DRG细胞中枢末梢〓的内流而增加递质的释放,放大了伤害性信息。

Pathohistologic examination revealed normal glomeruli but vacuolar degeneration of tubular epithelial cells, and part of them disrupted and desquamated, and also tubular dilatation. Only mild pathological changes were seen in the intervention groups.

肾脏病理检查可见LPS组肾小球大致正常,而肾小管上皮细胞空泡变性,部分上皮细胞崩解、脱落,管腔扩张,两个UT干预组肾小管病理变化均较LPS组减轻,不同剂量组间形态差异无显著性。

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