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At postnatal 1st week immunopositive reaction of NGF was detected mainly in sustentacular cells and the spermatogonia also showed positive staining. NGF positive staining in the testes was observed in interstitial cells, spermatogenetic cells, sustentacular cells and Leydig cells at 3rd week. After the postnatal 5th week, NGF-positive immunostaining was also detected in intersitial cells and spermatogenetic cells, but the intensity of reaction was weaker than that at 1st and 3rd weeks.

免疫组化定位分析显示:睾丸组织的神经生长因子蛋白表达于小鼠出生后的各个时期内,1周龄睾丸组织免疫阳性反应主要位于支持细胞,精原细胞也有着色;3周龄睾丸组织的间质细胞、各级生精细胞、支持细胞、管周肌样细胞表达均呈现阳性;5周后的睾丸组织内神经生长因子呈低水平表达,主要表达于间质细胞和生精细胞内。

The results showed that NaCl stress decreased the seedlings fresh mass and dry mass significantly. Under NaCl stress, the relative contents of Na(superscript +) and Cl(superscript -) in cells increased significantly, but the increment somewhat differed with different tissues. In root and stem, epidermal cells had the greatest increment, followed by cortex cells, and stelar cells; while in leaf, epidermal cells had the greatest increment, followed by cortex cells, spongy tissue cells, and palisade tissue cells.

结果表明:NaCl能显著降低长春花幼苗的鲜质量和干质量;对根、茎和叶片横切面X射线微区分析表明,NaCl胁迫导致长春花体内各组织细胞中Na和Cl相对含量显著增加,但在各器官、组织中分布稍有不同:与对照相比,根和茎中都是表皮细胞中增加幅度最大,中柱细胞次之,皮层细胞最低;在叶片中亦是表皮细胞增加幅度最大,依次是皮层细胞、海绵组织细胞及栅栏组织细胞

D. The function of stimulating xenogenous lymphocyte proliferation was the same between peripheral DCs and ascites PCs. E. The percentage of CD3〓CD56〓 cells was the same in CIK cells co-culture with DCs transfected with SKOV3 RNA, CIK cells co-culture with DCs, and CIK cells. F. The expansion rate of CIK cells can be accelerated by co-culturing with loaded or unloaded DCs. However, the expansion rate between loaded or unloaded group is the same. F. The strongest cytotoxicity against SKOV3 cell line was achieved by CIK cells co-cultured with DCs loaded with SKOV3 lysate.

结果:1、腹水可获得0.83±0.24×10〓个AMC/ml,单核细胞有0.74±0.25×10〓个/ml;2、卵巢癌患者外周血可获得0.87±0.20×10〓个AMC/ml,单核细胞有0.92±0.17×10〓个/ml;3、除CD86外周血单核细胞来源DC表达较高以外,其他表面分子在不同来源DC间没有统计学差异;4、不同来源DC的异基因刺激能力没有差异;5、与负载或未负载卵巢癌抗原的DC共培养并不能提高CIK细胞群中CD3〓CD56〓细胞的数量;6、CIK细胞增殖显著,培养14天时可扩增19.18±4.70倍,培养21天时可扩增35.82±4.36倍;7、与未负载或负载DC共培养的CIK细胞在培养第14天后增殖速率大于单纯CIK细胞

The pattern of aerenchyma formation could originate by the combination of cortical cell autolysis and enlarged intercellular space. The process occurred in some stages: cortical cells stopped expansion and the intercellular space became larger at the initial stage. Cortical cells to collapse and autolysis were found with the disintegration of cell contents. After the evacuation of cell contents, cortical cells became shrinking and invaginated.

形成过程大体分为:皮层细胞生长停止,细胞间隙增大;皮层细胞衰老,并发生自溶,内含物解体;解体物逐渐撤走,皮层细胞开始收缩、内陷,当细胞内含物全部撤走,相邻细胞的残留细胞壁叠合即在两侧形成通气空腔;径向上相邻的皮层细胞逐步发生凹陷和细胞壁叠合,结合方形的细胞间隙一起构成通气组织。

RESULTS: NK cells represent a unique subset of lymphocytes that have no restriction by MHC antigens and have the ability to lyses certain tumor cells without the requirement for prior immune sensitization of the host. In addition, NK cells can also produce cytokines and regulate the function of other immune cells. So, it is emerging to apply NK cells as therapeutic agents against a broad range of malignancies. In this respect, the anti-tumor activity of NK cells is the key factor of NK-cell-based immunotherapy.

结果:NK细胞是一种独特的淋巴细胞,对靶细胞的识别无MHC限制性,无需预先致敏即可直接杀伤肿瘤细胞,也可分泌细胞因子调节其他免疫细胞的功能,是机体天然免疫的主要承担者,也是获得性免疫的核心调节细胞,故NK细胞在抗肿瘤免疫中的地位越来越受到重视,随之增强NK细胞肿瘤杀伤活性的研究也逐步深入。

Results There was a similar distributive pattern of Neul, PPCA and β-gal in the inner ear. Neul intense staining was observed in the cochlear spiral ganglion cells, spiral limbus, spiral ligament, vestibular ganglion cells, cristae, maculae hair cells, and weak staining in inner hair cells, outer hair cells, supplying cells of the organ of Corti and stria vascularis. The intense staining of PPCA and β-gal were observed in the spiral ganglion and vestibular ganglion cells, and weak staining in the spiral limbus, spiral ligament, stria vascularis and organ of Corti. The inner ear exhibited no staining when Neul, PPCA and β-gal were deficient, respectively.

Neul最强的染色主要在螺旋神经节细胞、螺旋韧带、螺旋缘、前庭神经节细胞及壶腹嵴、球囊和椭园囊感觉毛细胞,较弱的染色分布于血管纹和Corti器内、外毛细胞及支持细胞;PPCA和β-gal在螺旋神经节和前庭神经节细胞有较强的染色,血管纹、螺旋韧带、螺旋缘和Corti器内、外毛细胞及支持细胞呈较弱的染色反应;各自酶缺乏时内耳免疫染色消失。

The histopathologic changes included lymphocyte and monocyte infiltration,hyperplasia of synovial cells and small vessels,interstitial fibrosis,hyaline degeneration and cartilaginous metaplasia.The immunohistochemical observations showed that the high expressions of IL-1 and IL-6 were significantly different between the pathologic plicae and the control groups(P<0.01).The positive expressions of IL-1 and IL-6 were the synovial cells and monocyt-lymph cells in the pathologic synovial plicae.The positive expressions of MMP-1 and TIMP-1 have significant difference between the experiment and control group(P<0.01,P<0.05).The expression of MMP-1 was positive in synovial lining cell,monocyte,fibroblast,endothelial cell in small vessel and chondrocyte.The TIMP-1 expression was detected in the synovial lining cells and a small quantity fibroblast.

结果 正常滑膜皱襞和病理性滑膜皱襞在滑膜细胞增生及小血管增生、间质纤维化及玻璃样变、软骨化生组织学改变方面,差异均有显著性(P<0.01);IL-1、IL-6在病理性滑膜皱襞内的增生滑膜细胞、单核及淋巴细胞和在正常滑膜皱襞内的表达差异均有显著性(P<0.01); MMP-1、TIMP-1在病理性滑膜皱襞和正常皱襞内的阳性表达,差异具有显著性(P<0.01,P<0.05),MMP-1在增生滑膜衬里层细胞、单核和纤维母细胞、血管内皮细胞和软骨化生的软骨细胞呈阳性表达;TIMP-1只在滑膜衬里层细胞和少量纤维母细胞有表达。

RESULTS MTT assay showed that hydroquinone inhibited the growth of cells in a concentration-dependant manner and the survival number of XRCC1-deficient cell was less than that of the two control groups. Comet assay revealed that different concentrations of hydroquinone caused more severe DNA damage in XRCC1-deficient cell line than in control cells and there were no significant difference in the two control groups.

结果 MTT结果显示,不同浓度10~100μmolL^(-1氢醌作用的XRCC1缺陷细胞,490 nm波长处吸光度值低于对照组细胞,提示缺陷细胞细胞存活率比正常细胞低;彗星实验结果显示,不同浓度的氢醌对XRCC1缺陷细胞DNA损伤比对照组细胞更严重,而2个对照组细胞之间没有明显差异。

BMSCs were isolated, depurated, cultivanted, and identified,then incubated with the concentration of 25μg Fe per milliliter at 37℃in 5% CO2. The labeled cells were stained by Prussian blue/trypan blue,and observed under fluorescent microscope.2. The labeled cells of different density (1×104/ml,5×104/ml,1×105/ml,5×105/ml,1×106 /ml,5×106/ml)were imaged by MRI with T1WI, T2WI and T2*WI sequences;and the same density (5×104/ml,1×105/ml)labeled cells were imaged by T2*WI sequences at different time.Then the signal intensities were measured and statistically analyzed.3. The model of rabbit renal ischemia-reperfusion injury was set up and treated. Then BMSCs(5×105)were injected into 16 recipient rabbits(1abeled cells in 10,unlabeled cells in 6)from ear vein.MR images of kidneys were obtained respectively at the time points of 0,1,3,5, 8 days after transplantation and before transplantation. MR imaging findings were analyzed,which were correlated with histological findings.

实验方法1分离、纯化、培养、鉴定兔BMSCs并以SPIO以25μg Fe/ml培养液浓度标记,对标记后不同时间的细胞行普鲁士蓝染色和台盼蓝拒染后显微镜观察。2将不同细胞浓度标记细胞管(1×104/ml、5×104/ml、1×105/ml、5×105/ml、1×106/ml、5×106/ml),以不同扫描序列T1WI,T2WI,T2*WI(GRE进行MR成像,再选择相同细胞浓度组(5×104/ml、1×105/ml)进行不同时相MR成像,并测量信号强度,进行统计学分析。3缺血再灌注肾损伤模型建立和处理,然后将标记和未标记细胞(5×105个)经耳缘静脉移植入家兔体内(共16只:注入标记细胞者10只,注入未标记细胞者6只),两组均于注射前、注射后第0、1、3、5、8天应用MRI对移植细胞进行活体示踪并与肾脏组织切片对照,然后对收集的信号强度进行统计学分析。

Results By incubating cardiomyocytes with bFGF, ERKs was activated and the cellular viability 〔(70.0±4.6)%in bFGF 10 ng group vs.(53.0±4.5)%in H/R group, P<0.01) and the ATP content 〔(23.1±2.3) nmol/106 cells in bFGF 10 ng group vs.(12.3±2.1) nmol/106 cells in H/R group, P<0.01〕 were increased, also the LDH leakage 〔(257.3±51.0) U/L in bFGF 10 ng group vs.(372.5±69.2) U/L in H/R group, P<0.05〕, was decreased, then attenuation of H/R injury to cardiomyocytes was observed. PD098059, an inhibitor of upstream kinase of ERKs completely abolished the protective effects 〔viability (57.0±5.8)%,ATP content (15.1±2.6) nmol/106 cells,LDH activity in medium (325.5±59.0)U/L in PD098059 group vs. bFGF 10 ng group, P<0.01, respectively〕.

结果 bFGF激活ERKs,并呈剂量依赖性减轻H/R所致心肌细胞损伤,表现为细胞存活率〔bFGF 10 ng组(70.0±4.6)%,H/R组(53.0±4.5)%,P<0.01〕和细胞内ATP含量〔bFGF 10 ng组(23.1±2.3)nmol/106细胞,H/R组(12.3±2.1)nmol/106细胞,P<0.01〕升高,细胞浆酶LDH漏出〔bFGF 10 ng组(257.3±51.0)U/L,H/R组(372.5±69.2)U/L,P<0.05〕减少;ERKs上游激酶抑制剂PD098059完全消除上述保护作用〔PD098059组细胞存活率(57.0±5.8)%,ATP含量(15.1±2.6)nmol/106细胞,培养液中LDH活性(325.5±59.0)U/L,与bFGF 10 ng组比较均为P<0.01〕。

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