Unilateral nail dystrophy after C4 complete spinal cord injury

Unilateral nail dystrophy after C4 complete spinal cord injury
复制标题

C4完全性脊髓损伤后单侧指甲营养不良

DOI:
10.1111/j.1365-2133.1996.tb03904.x
复制
发表时间:
1996
影响因子:
10.3
通讯作者:
B. Gardener
B. Gardener
中科院分区:
医学1区
文献类型:
--
作者:
A. Harris;S. Burge;B. Gardener

文献摘要

被引文献

相似文献

1刘易斯RE.Buchsbaum M.Vhitaker D.Murphy(JF.进化过程中细胞间黏附分子的表达;人皮肤迟发型超敏反应。/Invest Dcnmitol 1989:9J:672-7.2加里奥赫I)。Mackie Rm。在进化性变态反应性接触性皮炎反应中,角质形成细胞表达细胞间黏附分子1(ICAM-1)与淋巴细胞功能相关抗原1(LFA-JL)阳性细胞的渗透相关。历史:我是S、L。珍妮·阿赫。卡兹西。早期分子事件处于接触敏感度的诱导期。美国::第1期J98-402.4考曼西南。干扰素-γHHN的调节--,!诱导的细胞间黏附分子-1(IICAM-I)在人角质形成细胞IHK1。临床研究1989:37:348A。T·达斯汀·ML。歌手KH,Tuck DT。斯普林格助教。T淋巴母细胞与表皮角质形成细胞的黏附受干扰素-甘尼玛调节,并由细胞间黏附分子(ICAM11./f:.v/j,VW 198S:167:1525-40)介导。6格里菲斯CEM。V‘oorheesJJ.尼克洛夫B|。干扰素诱导角质形成细胞表达不同的人类白细胞抗原-DRDQ和细胞内黏附分子Ik‘ami)。皮肤醇19H9:120:1-8。7巴克|西北地区。艾伦·马赫。麦克唐奈DM.干扰素-γ体内对正常人皮肤LFA-1和ICAM-1分布的影响/投资皮肤科:93:439-42。8Fong TATP Mosmann tr.干扰素-γ在Th1克隆介导的迟发型超敏反应中的作用/liunuiuol 1989:^4^^,2887-93。9 Hoefakkar S.Caubo M.van‘t Erve EHM el al.过敏性和刺激性接触性皮炎的体内细胞因子谱。接触性皮炎1995:33:258-66。访问数/每百万人:Reach for[Gneniche A.镍通过IL-1和ICAM-1表达对正常人角质形成细胞活化状态的影响BR I皮肤科,1994:131:250-6。
1 Lewis RE. Buchsbaum M. VVhitaker D. Murphy (JF. Intercellular adhesion molecule expression in evolvinf; human cutaneous delayed hypersensitivity reaction. / Invest Dcnmitol 1989: 9J: 672-7. 2 Garrioch I). MacKie RM. Campbell I. Forsyth A. Keratinocyte expression of intercellular adhesion molecule 1 (ICAM-1) correlated with infiltration of lymphocyte function associated antigen 1 (LFA-Jl positive cells in evolving allergic contact dermatitis reactions. HistoptUiwIoiltj 1991: 19: i S l 4 . J Enk AH. KatzSi. Farly molecular events in the induction phase of contact sensitivity. I'roc \fll/ Acad Sci USA 1992: 89: 1 J98-402. 4 Caughman SW. Regulation of interferon-gamma HhN--,! induced intercellular adhesion molecule-1 IICAM-I) in human keratinocyles iHKl. Clin Res 1989: 37: 348A. T Dustin ML. Singer KH, Tuck DT. Springer TA. Adhesion of T lymphoblasts to epidermal keratinocytes is regulated by interferon-ganima and is mediated by intercellular adhesion molecule (ICAMll./f:.v/j,VW 198S: 167: 1525-40. 6 Griffiths CEM. V'oorheesJJ. NickoloffB|. Gamma interferon induces different keratinocyte cellular patterns of expression of HLA-DRDQ and inlercellular adhesimi molecule IK'AMI) antigens. Br ] Dermatol 19H9: 120: 1-8. 7 Barker |NWN. Allen MH. MacDonaid DM. The effect of in vivo interferon-gamma on the distribution of LFA-1 and ICAM-1 in normal human skin. / Invest Dermatol 1989: 93: 439-42. 8 Fong TATp Mosmann TR. The role of IFN-gamtna in delayed-type hypersensitivily mediated by Th 1 clones. / liunuiuol 1989: ^4^^, 2887-93. 9 Hoefakkar S. Caubo M. van't Erve EHM el al. In vivo cytokine profiles in allergic and irritant contact dermatitis. Contact Dermatitis 1995: 33: 258-66. ] 0 Gneniche A. Viac J, Lizard G et al. Effect of nickel on the activation state of normal human keratinocytes through interleukin 1 and ICAM-1 expression. Br I Dermatol 1994: 131:250-6 .