坏死原的

基本解释 (translations)

necrogenous

与坏死原的相关的网络例句 [注：此内容来源于网络，仅供参考]

Methods Mimicry and speculation on possible displaced amino acids in proper positions of peptide increased the biological effects of TNFR blocking peptide by compote modeling. The original peptide and its mutant were synthesized. The competitively inhibitory effects on green fluorescence protein-tumor necrosis factor fusion protein with TNFR were compared between original peptide and its mutant (receptor competitively inhibitory binding assays). The inhibitory effects on cytotoxicity were compared between original peptide and its mutant.

通过计算机模建，模拟并推测提高TNFR封闭肽生物学效应需置换的位点和氨基酸；合成原封闭肽和突变肽；受体竞争抑制结合实验比较原肽与突变肽对绿色荧光蛋白－肿瘤坏死因子融合蛋白结合TNFR的竞争抑制效应；细胞毒作用抑制实验比较原肽与突变肽对TNFR的封闭效应。

In treatment group, there was no progressive necrosis in stasis zone, and at 24 h post injury, capillary dilation, cell edema and inflammatory infiltration were lessened significantly. In control group, 2 wounds had progressive necrosis (accounted for 10% of the total). Cell edema, inflammatory infiltration and capillary thrombosis were serious, Until 72 hr post injury, cell edema did not subside and necrosis of the dermis worsened. 2. Pathological assessment of the stasis zone tissue: As compared with that in control group, in treatment group the dermis structure in stasis zone was intact and the collagenous fiber bundle was normal.

结果：①创面细胞形态学改变：伤后8h毛细血管扩张、细胞水肿，炎性浸润最明显；治疗组中央淤滞区无进行性坏死，伤后24h后毛细血管扩张、细胞水肿、炎性浸润减轻；对照组2个创面呈进行性坏死（占10%），中央淤滞区细胞水肿、炎性浸润明显，毛细血管血栓形成，伤后72h水肿仍明显，真皮坏死加重；②淤滞区组织病理学评分：治疗组与对照组相比，治疗侧淤滞区的表皮结构相对完整、胶原纤维束相对正常，粒细胞浸润小于5个/400倍视野。

Treatment temperatures are representative of those required for thermal necrosis of ingrowing nociceptor nerve fibers and disc cellularity alone, or with coagulation and restructuring of anular collagen in the high temperature case.

治疗温度代表那些需要热坏死处理的内生的伤害感受器神经纤维以及间盘细胞构成，或者在高温下造成胶原环的凝固和重构。

Treatment temperatures are representatie of those required for thermal necrosis of ingrowing nociceptor nere fibers and disc cellularity alone, or with coagulation and restructuring of anular collagen in the high temperature case.

治疗温度代表那些需要热坏死处理的内生的伤害感受器神经纤维以及间盘细胞构成，或者在高温下造成胶原环的凝固和重构。

Results:(1) In clinical pathology, swelling, denatured, even necrosis and putrescence could be picked out; Collagen fibers in tendon remarkedly swelled, and tissue structure disarranged, and collagen even ruptured, broken and dissolved; Obvious denature, apoptosis and necrosis could be found in tendon cells. There appeared to be a big accumulation of inflammatory cells.

结果 （1）临床病理组织学观察发现：肌腱组织肿胀、变性、甚者坏死、腐败；肌腱内胶原纤维肿胀明显、组织结构紊乱，失去正常排列，甚者出现胶原断裂、破碎、溶解等现象；腱细胞可见明显的变性、凋亡和坏死；病变部位可见大量炎性细胞聚集。

Methods: The mice for experiment were immunizied with subcutaneous injection of type Ⅱ collagen to induce arthritis after ovariectomy. Severity of joint swelling, radioimmunoassay of serum estradiol (E2),osteocalcin and tumor necrosis factor, and pathological changes of joint, including changes on synovia, articular cartilage and bone, were observed once weekly.

切除小鼠卵巢后，Ⅱ型胶原皮下注射以诱导关节炎；每周1次观察小鼠的关节肿胀程度；组织切片光镜下观察小鼠滑膜、关节软骨及骨的改变；放射免疫法检测小鼠血清雌二醇、骨钙素、肿瘤坏死因子的变化。

The findings of the newly identified goose paramyxovirus strain GPMV/HBexperimental infection were as follows: The challenge caused high morbidity and highmortality.The clinical signs included severe depression, decreased appetite or anorexia,white,yellow and green diarrhea, with neural symptoms;pathological changes showed thathaemorrhage and ulceration of intestine mucosa, necrosis of spleen and pancreas,andedema of liver and kidney, uratic deposition in kidney.Eosinophilic inclusion bodies werefound in the cytoplasm of pancreas and a large quantities of fiber protein were found inintestine. Lots of hemosidefin was found in some area of liver and kidney. A number ofT、B lymphocytes reduced sharply in spleen,lymph nodes in dead geese. Transmissionalelectron microscope showed that some cells had the morphological characteristics ofmitochondria swelling, morphological changes were condensation of nuclear chromatininto dense masses,followed by its marginating against the nuclear envelope, andespecially concentration of cytoplasm association with lots of lipid droplet.

人工感染雏鹅实验中，雏鹅临床表现为高发病率和高死亡率，食欲和饮水减少，拉白色、黄绿色稀粪，伴有神经症状；常规组织学观察，脾脏和胰腺肿大，有白色坏死斑点，肠道出血和坏死，肝脏肿大变性，肾脏肿大变性有尿酸盐沉着等；用特殊染色和组织化学方法首次对人工感染鹅副粘病毒的雏鹅的重要脏器进行研究，结果表明：胰腺中发现病毒包涵体，肠道中大量纤维素以及胶原纤维增生，肾脏、肺脏大量含铁血黄素沉着，免疫器官如脾脏和淋巴结中T、B淋巴细胞大量减少；电镜下多种细胞呈现线粒体水肿，多种实质细胞的染色质固缩，染色质边集，特别是细胞内容物如脂肪滴增多的病理变化特征。

Results T-2 toxin could cause rat articular chondroncytes degeneration, necrosis, and appeared many blank areas free cells. Weigert/Van Gieson staining showed obvious collagen fasciculi emergence could be seen. Scanning electronic microscope showed the surface of articular cartilage was wave and rough. Collagen fasciculi ruptured and stack up, and presented a typical 揳rticular dryness?phenomenon. ELISA results indicated, at the stage of 3 month, the level of rat serum CTX-II in T-2 toxin group was higher than that in control group, and the difference had a markedly significance.

结果 T－2毒素可致大鼠关节软骨细胞变性、坏死，出现大面积无细胞区，胶原染色可见明显的&胶原显现&；扫描电镜显示，关节面起伏不平，表面粗糙，胶原纤维断裂、剥脱，关节表面布满裂片状凸起，呈典型的关节&干燥&现象；ELISA检测结果表明， T-2毒素组大鼠血清CTX-II水平在3个月时较对照组明显增加，差异具有统计学意义。

The pathogen of gas gangrene mainly exist and live in local place, and seldom enter blood system to cause blood poisoning, but than can form lots of toxins, this toxins can harm blood system, kidney system, and also the tissue can putrescence and the wound will enlarge step by step, all tissue putrescence and toxin can make these bacteria easier to live and reproduce, all these situation if not being control in time will lead a serious situation that multiple organs dysfunction and then died

气性坏疽的病原菌主要在伤口内生长繁殖很少侵入血液循环引起败血症。产气夹膜杆菌产生α毒素、胶原酶透明质酸酶、溶纤维酶和脱氧核糖核酸酶等，红细胞破坏引起溶血血红蛋白尿、尿少、肾组织坏死水肿、液化，肌肉大片坏死使病变迅速扩散、恶化。糖类分解产生大量气体使组织膨胀；蛋白质的分解和明胶的液化，产生硫化氢，使伤口发生恶臭由于局部缺血，血浆渗出，及各种毒素的作用伤口内的组织和肌肉，进一步坏死和腐化，更利于细菌的繁殖使病变更为恶化。

To study the effects of leptin on tumor necrosis factor α secretion in murine peritoneal macrophages and the role of mitogen activated protein kinases in this process.

研究瘦素诱导小鼠腹腔巨噬细胞分泌肿瘤坏死因子α的影响，以及丝裂原活化蛋白激酶信号通路在这一过程中的作用。

与坏死原的相关的网络解释 [注：此内容来源于网络，仅供参考]

Pulmonary anthrax：肺炭疽

肺炭疽(pulmonary anthrax)是炭疽杆菌所致的急性传染病. 原系食草动物传染病,人因接触病畜及其产品或食用病畜的肉类而被感染. 最常见为皮肤炭疽,表现为皮肤坏死和黑痂,亦可吸入感染引起肺炭疽,误食感染可致肠炭疽,可以继发炭疽杆菌败血症.

fibrinoid degeneration：纤维素样变性

(2)纤维素样变性(fibrinoid degeneration)又称纤维蛋白样变性,为间质胶原纤维及小血管壁的一种变性,病变部位的组织结构逐渐消失,变为境界不清晰的颗粒状或块状无结构强嗜酸性红染物质,状似纤维素,故称之为纤维素样变性,由于其实为一种组织坏死,

euglobulin：优球蛋白

血小板减少,凝血酶原时间延长、纤维蛋白原减少,FDP增加的血液学变化未见改善作用,但病理组织学所见,对肝出血性坏死病灶有显着抑制作用. 应用优球蛋白(Euglobulin)溶解时间法对纤溶系的作用进行试验,甲醇提取物对纤溶系具有活化作用.

secretin：肠促胰液素

(2)胰液分泌亢进 暴饮暴食、酒精的刺激使胃酸及十二指肠促胰液素(secretin)分泌增多,进而促进胰液分泌增多,造成胰管内压增高. 重者可导致胰腺小导管及腺泡破裂,放出溶酶体内的蛋白水解酶激活胰蛋白酶原等,从而引起胰腺组织的出血坏死.

aminocaproic acid：氨基己酸

所以应该比较容易记忆. 这两种药都是纤溶酶原的药物. 溶栓药一定要早期使用,一般在心梗或脑血栓后6个小时内用,否则造成细胞缺血坏死再用就没有效果了. 所以6个小时后就不要再用了. 溶栓药的拮抗剂是氨基己酸(Aminocaproic acid).

Arteriolosclerosis：细动脉硬化

血浆蛋白的渗入连同由未坏死SMC产生的修复性胶原纤维及蛋白多糖使细动脉壁细胞愈来愈减少而陷于玻璃样变,形成细动脉硬化(arteriolosclerosis). 镜检下,细动脉内皮与中膜SMC之间有玻璃样物质沉积,其内的胶原纤维亦陷于均质化. 随着疾病的发展,

fibrinous inflammation：纤维素性炎

2.纤维素性炎(fibrinous inflammation) 是以渗出物中含有大量纤维素为特征的渗出性炎症. 纤维素的大量渗出,提示毛细血管和小静脉损伤较重,通透性明显升高,大量纤维蛋白原渗出到血管外,在坏死组织释出的组织因子作用下,转化为纤维素,故有纤维素性炎之称.

fibrinous inflammation：纤维素性炎症

2.纤维素性炎症 纤维素性炎症(fibrinous inflammation)时以纤维蛋白原渗出并在炎症灶内形成纤维素为主. 光镜下,苏木素伊红染色可见大量红染的纤维素交织呈网状,间隙中有中性粒细胞及坏死细胞的碎屑. 大片纤维素在镜下表现为片状、红染、质地均匀的物质.

necrogenic：坏死原的

necrocytosis 细胞坏死 | necrogenic 坏死原的 | necrolysis 坏死溶解

pancreatogenic,pancreatogenous：胰(原)性的

\\"坏死性胰炎\\",\\"pancreatitis,necrotizing\\" | \\"胰(原)性的\\",\\"pancreatogenic,pancreatogenous\\" | \\"胰激<>\\",\\"pancreatokinase\\"