漿細胞增多 的英文怎麼說
中文拼音 [jiāngxìbāozēngduō]
漿細胞增多
英文
plasmacytosis-
The steady dead generation and time that was caused by the isolated virus was certain by chicken embryo which was inoculated on seven or nine days. the histopathological changs of the infectious stunting syndrom were studied by the way of ordinary paraffin section and he dying. the experimental result were as follows : the test proved that the changes of the chicken embryo were different in different stage. the chicken embryo dead in a week after it inoculated. the body was dropsy and hemorrhage. dead before it hatched out, the embyo body were dropsy, pale and slime. the liver was yellow and swolled, gallbladder ( vesica fellea ) was filled with bile. bursa and glandula thymus analosis. the kindey dropsy. bowel lamina were humble, dilatation. gas and yellow foam were filled the bowel. histopathological changes were that, in early stage, obvious changes of liver and kindey were dropsy, hemorrhage and necrosis. two types eosinophilic intranuclear inclusion bodies including large round and little granular were present in cells of the above organs. the obvious changes of bursa were dropsy, adverse folliiculated growth and little lymphocytes proliferating, 19 - 21 days chicken embryo, one or two big empty vacuoles were prensent in cells of liver and kindey. the number of the folliculi was growing, the vacuoles between cells were larger
膽囊充盈、其內充滿稀薄的膽汁；法氏囊、胸腺萎縮，腸道擴張、腸壁菲薄、內充滿氣體及黃色泡沫狀物；腎臟腫大。病理組織學變化方面，早期肝臟、腎臟、腸主要以出血、水腫和壞死為主，且肝細胞核及腎小管的上皮細胞核內均發現有核內包涵體，包涵體呈嗜酸性，為大型圓形包涵體或不規則的顆粒狀；法氏囊則以水腫、濾泡發育不良、小型淋巴細胞數量增多為主。 19 21日齡雞胚肝細胞、腎小管上皮細胞的胞漿內出現1 2各大的空泡，法氏囊濾泡數目增多細胞間有較大空隙。The tumor cells hae abundant eosinophilic cytoplasm and enlarged hyperchromatic nuclei with prominent nucleoli. numerous mitotic figures were also present
腫瘤細胞富含嗜酸性細胞漿、增大深染的細胞核具有突出的核仁。也可以呈現出數目眾多的有絲分裂像。Here is a cervical pap smear in which dysplastic cells are present that have much larger and darker nuclei than the normal squamous cells with small nuclei and large amounts of cytoplasm
圖示是巴氏塗片后非典型增生的宮頸細胞的表現，細胞體積增大，胞核濃染，核體積縮小，細胞漿增多。Mechanism of glutamate - induced inhibition of pulmonary surfactant lipid synthesis ? mda receptor ( nmdar ) antagonist mk - 801 could reverse glutamate - induced inhibition of [ 3h ] - choline incorporation in lung explants ; ? he expression of nmdar1 subtype existed in alveolar type ii epithelial cells ; ? he effect of glu on pc synthesis required l - arginine in cultured lung explants, nos activity and no production were increased significantly in lung explants with glu treatment ; and mk - 801 and nos inhibitor l - nna could block the increase of nos activity and no production induced by glu ; l - nna also could reverse the inhibition of [ 3h ] - choline incorporation induced by glu ; ( 4 ) mda content increased and sod level decreased in cultured lung explants of glu treament groups, mk - 801 and l - nna could reverse these effects ; ( 3 ) mk - 801, l - nna could block the release of ldh induced by glu
谷氨酸對肺表面活性物質脂質合成抑制的機制研究nmda受體拮抗劑mk - 801能逆轉glu所致肺組織[ ~ 3h ] -膽堿摻入減少的效應；肺泡上皮細胞有nmda受體nmdar1亞單位的表達； glu對ps脂質合成的影響依賴l -精氨酸的存在， glu可使肺組織勻漿中nos活性、 no合成量升高； mk - 801 、 nos的抑制劑l - nna均可阻斷glu所致的這些效應； l - nna可逆轉glu所致肺組織[ ~ 3h ] -膽堿摻入減少的效應； glu可使肺組織勻漿中mda碩士學位論文中文摘要含量增高、 sod水平下降。 mk七0 、 l nna能阻斷q所致的這些效應； mk80 、 l nna還能阻斷gill誘導的ldh釋放增多的效應。3. calcitonin gene - related peptide attenuates glutamate - induced inhibition of pulmonary surfactant lipid synthesis ( d cgrp could reverse the decrease of [ 3h ] - choline incorporation induced by glu with dose - dependence ; ( 2 ) cgrp could block the decrease of the content of cct a mrna induced by glu in lung tissue ; ( 3 } cgrp could reduce the impairment of the ultrastructure of at ii cells induced by glu ; ( 4 ) cgrp could reverse the increase of mda content and decrease of sod level induced by glu in cultured lung explants, respectively ; ? grp had no significant effect on nos activity and increase of no production induced by glu
降鈣素基因相關肽減輕谷氨酸所致肺表面活性物質脂質合成抑制的保護作用降鈣素基因相關肽grp ）可顯著減輕0所致肺組織h一膽堿摻入pc量的降低，並且呈劑量依賴保護效應； cgrp可逆轉gill所致cctqinrna含量的降低； cgrp可減輕o所致肺11上皮細胞超微結構的損傷； cgrp可逆轉o所致肺組織勻漿中mda含量增多、 sod水平降低的效應，並可逆轉q所致肺組織ldh釋放增多的效應； cg販對gill引起的nos活性和no含量的升高均沒有顯著性影響。Our ultrastructural observations provided more convincing evidence that the hepatic phenotype was induced. before the sodium butyrate treatment, the cells contained few organelles except some mitochondria and ribosome
電鏡下觀察，胞漿中的細胞器較誘導前明顯增多，有線粒體、內質網和高爾基體以及大量的核糖體和糖原顆粒。分享友人