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1.
Active production of anti-human T-lymphotropic virus type I (HTLV-I) IgM antibody in HTLV-I-associated myelopathy 总被引:2,自引:0,他引:2
Kunihiko Nagasato Tatsufumi Nakamura Ohishi Kiyosumi Kohji Shibayama Masakatsu Motomura Ichinose Katsuhiro Mitsuhiro Tsujihata Shigenobu Nagataki 《Journal of neuroimmunology》1991,32(2):105-109
We investigated the presence of anti-human T-lymphotropic virus type I (HTLV-I) IgM in sera and cerebrospinal fluid from patients with HTLV-I-associated myelopathy (HAM) by Western blot analysis. Analyses of 36 serum samples revealed that most patients (31/36; 86.1%) had anti-HTLV-I IgM, whereas only four of 23 (17.4%) HTLV-I carriers had it. In studies of cerebrospinal fluid, anti-HTLV-I IgM was detected in 24 of 36 (66.7%) HAM patients, whereas none was detected in nine HTLV-I carriers. The differences were statistically significant (p less than 0.01). These results suggest that persistent active replication of HTLV-I occurs in the central nervous system as well as in the peripheral blood of HAM patients, and may contribute to the development of HAM. 相似文献
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Yoshiharu Kikawa Akio Nakai Yosuke Shigematsu Masakatsu Sudo Kimitaka Kato Shinichi Haruki 《Pediatric nephrology (Berlin, Germany)》1990,4(4):343-344
Leukotriene B4 (LTB4) production in polymorphonuclear leucocytes (PMN) was examined in ten children with steroid-responsive nephrotic syndrome (SRNS) before, during, and after steroid administration. Comparison of LTB4 production was made in 14 children with non-inflammatory disease who were not receiving steroid therapy. No significant change was noted in PMN LTB4 biosynthesis in children with SRNS throughout any phase of the disease. Furthermore, there was no significant difference in LTB4 biosynthesis in PMN between SRNS patients before steroid therapy and patients with non-inflammatory disease. These findings suggest that inhibition of LTB4 production is not involved in the mechanism underlying steroid action in SRNS. 相似文献
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应用Y型迷宫研究了急性与慢性东莨菪碱和吗啡对小鼠记忆能力的影响。单剂量东莨菪碱(1mg/kgip)和吗啡(10mg/kgip)均能显著损害小鼠的短时记忆(workingmemory)。重复给药后东莨菪碱的这种作用很快消失。但吗啡每天一次,连续3次给药这种作用加强,连续5次给药这种作用反而减弱。东莨菪碱不能损害小鼠长时记忆(referencememory),而吗啡对长时记忆有损害作用。结果还提示小鼠短时记忆不受自发活动能力的影响。 相似文献
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Gou Takeo Masakatsu Motomura Hidenori Matsuo Kiyosumi Ohishi Toshiro Yoshimura Shigenobu Nagataki Mitsuhiro Tsujihata 《Muscle & nerve》1993,16(8):840-848
We investigated the effect of the lgG from patients with myasthenia gravis (MG) on the degradation of normal rat junctional acetylcholine receptor (AChR) labeled with 125l-α-bungarotoxin (BuTx) and calculated the degradation rate (DR). The DR for the lgG from these patients was significantly higher than that from healthy volunteers and patients with other autoimmune diseases. For MG, DR was significantly correlated with the severity of the disease but not with anti-AChR antibody titer. DR was accelerated by lgG from patients with generalized MG whose antibody titers were in the normal range and by lgG from patients with ocular MG. These results indicate that measurement of the DR of junctional AChR in normal rats is more closely correlated with the severity of the disease than is measurement of anti-AChR antibody and that the former is a sensitive and confirmatory method for evaluating MG. © 1993 John Wiley & Sons, Inc. 相似文献
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Murata K Inami M Hasegawa A Kubo S Kimura M Yamashita M Hosokawa H Nagao T Suzuki K Hashimoto K Shinkai H Koseki H Taniguchi M Ziegler SF Nakayama T 《International immunology》2003,15(8):987-992
CD69, known as an early activation marker antigen on T and B cells, is also expressed on platelets and activated neutrophils, suggesting certain roles in inflammatory diseases. In order to address the role of CD69 in the pathogenesis of arthritis, we established CD69-null mice. CD69-null mice displayed a markedly attenuated arthritic inflammatory response when injected with anti-type II collagen antibodies. Cell transfer experiments with neutrophils, but not T cells or spleen cells, from wild-type mice into CD69-null mice restored the induction of arthritis. These results indicate a critical role for CD69 in neutrophil function in arthritis induction during the effector phase. Thus, CD69 would be a possible therapeutic target for arthritis in human patients. 相似文献
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