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101.
Modulation of B-cell abnormalities in lupus-prone (NZB x NZW)F1 mice by normal bone marrow-derived B-lineage cells.
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(NZB x NZW)F1(NZB/WF1) mice spontaneously develop an autoimmune disease characterized by abnormality of haemopoietic stem cells. The present study examined a possible regulatory cell interaction between NZB/WF1 and normal bone marrow cells using radiation-induced chimeras. We demonstrated that the ability of NZB/WF1 bone marrow cells to transfer the typical disease with hypergammaglobulinemia including autoantibodies into lethally irradiated normal recipients was prevented by cotransfer of bone marrow from normal CBA/J mice but not from xid CBA/N mice carrying a selective defect in B-cell function. Flow cytometric analysis revealed that the generation of NZB/WF1 cells was reduced in the mixed chimeras given CBA/J but not CBA/N bone marrow cells. Interestingly, radiation chimeras reconstituted with a mixture of NZB/WF1 bone marrow and CBA/J splenic B cells did not show elevation of serum immunoglobulin levels, although most of the spleen cells were dominated by NZB/WF1 cells. On the other hand, NZB/WF1 B cells maturated in vivo in the presence of CBA/J bone marrow or splenic B cells lost the hyper-responsiveness to lipopolysaccharide (LPS) in the autoantibody production in vitro. These results suggest that radiosensitive normal B-lineage cells have the regulatory activity to ameliorate the hypergammaglobulinemia of NZB/WF1 mice by reducing the generation of NZB/WF1 B cells and/or by correcting their hyper-responsiveness, and that NZB/WF1 mice may have a defect(s) in the regulatory cell function. In addition, CBA/J splenic B cells were shown to modulate the B-cell abnormality even when injected into non-irradiated NZB/WF1 mice manifesting autoimmunity. 相似文献
102.
Leukotriene B4 Receptor (BLT-1) Modulates Neutrophil Influx into the Peritoneum but Not the Lung and Liver during Surgically Induced Bacterial Peritonitis in Mice
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Melanie J. Scott William G. Cheadle J. Jason Hoth James C. Peyton Krishnaprasad Subbarao Wen-Hai Shao Bodduluri Haribabu 《Clinical and Vaccine Immunology : CVI》2004,11(5):936-941
Leukotriene B4 (LTB4) is a rapidly synthesized, early neutrophil chemoattractant that signals via its cell surface receptor, BLT-1, to attract and activate neutrophils during peritonitis. BLT-1-deficient (BLT-1−/−) mice were used to determine the effects of LTB4 on neutrophil migration and activation, bacterial levels, and survival after cecal ligation and puncture (CLP). Male BLT-1−/− or wild-type (WT) BALB/c mice underwent CLP. Tissues were harvested for determination of levels of bacteria, myeloperoxidase (MPO), LTB4, macrophage inflammatory protein 2 (MIP-2), and neutrophil (polymorphonuclear leukocyte [PMN]) numbers at 4 and 18 h after CLP. PMN activation was determined by an assessment of phagocytosis ability and CD11b expression. Survival was also determined. BLT-1−/− mice had decreased numbers of PMNs in the peritoneum at both 4 and 18 h after CLP but increased numbers of PMNs in the blood at 18 h compared with WT mice. Liver and lung MPO levels were significantly higher in BLT-1−/− mice at both 4 and 18 h after CLP, with increased bacterial levels in the blood, the liver, and peritoneal fluid at 4 h. Bacterial levels remained higher in peritoneal fluid at 18 h, but blood and liver bacterial levels at 18 h were not different from levels at 4 h. PMN phagocytosis and CD11b levels were decreased in BLT-1−/− mice. LTB4 levels were similar between the groups before and after CLP, but MIP-2 levels were decreased both locally and systemically in BLT-1−/− mice. Survival was significantly improved in BLT-1−/− mice (71%) compared with WT mice (14%) at 48 h post-CLP. Thus, LTB4 modulates neutrophil migration into the mouse peritoneum, but not the lung or liver, after CLP. Despite higher bacterial and PMN levels at remote sites, there was increased survival in BLT-1−/− mice compared to WT mice. Decreased PMN activation may result in less remote organ dysfunction and improved survival. 相似文献
103.
以~3H地塞米松(Dex)为特异性配基,以一点分析法测得大白鼠腹腔中性粒细胞(PMNs)的糖皮质激素受体(GCR)位点数为5270±216/个PMN(n=18,X±SE下同);体外实验,PMNs直接与山莨菪碱(654-23×10~(-5)M)温育,对GCR无明显影响,测得位点数为4896±360/个PMNs(n=20,P>0.4);体内实验表明,给大鼠肌肉注射654-2(10mg/kg)每日两次共二天,则GCR位点数降至2740±101/个PMNs(n=18,P<0.001)。此时还测得血浆皮质酮含量明显增高(P<0.01)。提示654-2对GCR的影响可能与增加皮质激素所致的“降调节”有关。 相似文献
104.
Tong Chen Hao Bai Ying Shao Melanie Arzigian Viktor Janzen Eyal Attar Yi Xie David T Scadden Zack Z Wang 《Stem cells (Dayton, Ohio)》2007,25(2):392-401
The molecular mechanisms that regulate human blood vessel formation during early development are largely unknown. Here we used human ESCs (hESCs) as an in vitro model to explore early human vasculogenesis. We demonstrated that stromal cell-derived factor-1 (SDF-1) and CXCR4 were expressed concurrently with hESC-derived embryonic endothelial differentiation. Human ESC-derived embryonic endothelial cells underwent dose-dependent chemotaxis to SDF-1, which enhanced vascular network formation in Matrigel. Blocking of CXCR4 signaling abolished capillary-like structures induced by SDF-1. Inhibition of the SDF-1/CXCR4 signaling pathway by AMD3100, a CXCR4 antagonist, disrupted the endothelial sprouting outgrowth from human embryoid bodies, suggesting that the SDF-1/CXCR4 axis plays a critical role in regulating initial vessel formation, and may function as a morphogen during human embryonic vascular development. 相似文献
105.
Jiang X Gao X Zheng H Yan M Liang W Shao Z Li W Zhang E Hu Y Hai R Yu D Kan B Xu J 《Clinical and diagnostic laboratory immunology》2004,11(6):1182-1184
Specific immunoglobulin G antibody for severe acute respiratory syndrome (SARS) coronavirus was detected in maternal blood, umbilical blood, and amniotic fluid from a pregnant SARS patient. Potential protection of fetus from infection was suggested. 相似文献
106.
Cholinergic neurotransmission plays a role in regulation of respiratory pattern. Nicotine from cigarette smoke affects respiration and is a risk factor for sudden infant death syndrome (SIDS) and sleep-disordered breathing. The cellular and synaptic mechanisms underlying this regulation are not understood. Using a medullary slice preparation from neonatal rat that contains the preB?tzinger Complex (preB?tC), the hypothesized site for respiratory rhythm generation, and generates respiratory-related rhythm in vitro, we examined the effects of nicotine on excitatory neurotransmission affecting inspiratory neurons in preB?tC and on the respiratory-related motor activity from hypoglossal nerve (XIIn). Microinjection of nicotine into preB?tC increased respiratory frequency and decreased the amplitude of inspiratory bursts, whereas when injected into XII nucleus induced a tonic activity and an increase in amplitude but not in frequency of inspiratory bursts from XIIn. Bath application of nicotine (0.2--0.5 microM, approximately the arterial blood nicotine concentration immediately after smoking a cigarette) increased respiratory frequency up to 280% of control in a concentration-dependent manner. Nicotine decreased the amplitude to 82% and increased the duration to 124% of XIIn inspiratory bursts. In voltage-clamped preB?tC inspiratory neurons (including neurons with pacemaker properties), nicotine induced a tonic inward current of -19.4 +/- 13.4 pA associated with an increase in baseline noise. Spontaneous excitatory postsynaptic currents (sEPSCs) present during the expiratory period increased in frequency to 176% and in amplitude to 117% of control values; the phasic inspiratory drive inward currents decreased in amplitude to 66% and in duration to 89% of control values. The effects of nicotine were blocked by mecamylamine (Meca). The inspiratory drive current and sEPSCs were completely eliminated by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) in the presence or absence of nicotine. In the presence of tetrodotoxin (TTX), low concentrations of nicotine did not induce any tonic current or any increase in baseline noise, nor affect the input resistance in inspiratory neurons. In this study, we demonstrated that nicotine increased respiratory frequency and regulated respiratory pattern by modulating the excitatory neurotransmission in preB?tC. Activation of nicotinic acetylcholine receptors (nAChRs) enhanced the tonic excitatory synaptic input to inspiratory neurons including pacemaker neurons and at the same time, inhibited the phasic excitatory coupling between these neurons. These mechanisms may account for the cholinergic regulation of respiratory frequency and pattern. 相似文献
107.
作者自1994年始采用自行设计L形钢板内固定治疗不稳定股骨粗隆间骨折60例,平均随访25个月,X线片显示骨折愈合时间6~13周,平均8.9周,伤肢功能在3个月内基本恢复正常,无骨折延迟愈合及髋内翻现象。为论证改良L形钢板的优点,本文采用8具新鲜尸股骨沿着它的外侧、内侧骨皮质粘贴6个应变片,观察股骨近端应变和位移分布,以检验改良L形钢板固定粗隆间骨折的效果。在实验前后将股骨粗隆造成二部分或四部分骨折。利用实验结果给制成应变和位移图,并与鹅头打固定组相比较。在载荷加至1800N时比较两种内固定器械的生物力学性能。结果表明,在治疗不稳定粗隆间骨折中,L形钢板比鹅头钉更具有生物力学的优势。 相似文献
108.
109.
血浆ET-1和CGRP含量测定对脑出血病人的应用价值 总被引:5,自引:0,他引:5
目的 :探讨血浆内皮素 (ET)和降钙素基因相关肽 (CGRP)在脑出血病人急性期与恢复期中的变化。方法 :采用放射免疫分析技术 ,对 4 2例脑出血病人的急性期与恢复期 ,分别测定血浆ET和CGRP含量 ,并用 35例健康对照人员作比较。结果 :脑出血病人血浆ET含量明显高于对照组 (p <0 0 1) ,治疗后有所下降 ;而血浆CGRP含量 ,在脑出血的急性期 ,显著高于对照组 (p <0 0 1) ,恢复期降为正常。结论 :血浆ET和CGRP在脑出血的急性期显著升高 ,并与脑损伤程度有关 ,提示神经肽参与出血性脑损伤的发生发展过程 相似文献
110.
目的 研究病毒载量检测和CD4^ 计数在评价人类免疫缺陷病毒(HIV)感染者疗效中的应用效果。方法 对HIV感染者临床病例73例进行了实验室和临床观察,其中包括6例鸡尾酒治疗病例、36例中药试验性治疗病例及31例未进行治疗的感染者。主要实验室指标包括血浆病毒载量及T淋巴细胞亚群计数。结果 在进行治疗后3个月时联合治疗组的病毒载量明显低于其他两组,并且在其后保持在很低的水平,CD4^ 计数水平明显高于其他两组并在其后持续升高。在整个观察期间,中药治疗组的病毒载量检测和CD4^ 计数水平与未治疗组差异无显著性,但在临床症状观察中中药治疗组较未治疗组有明显改善。结论 病毒载量检测和CD4^ 计数试验是评价抗HIV治疗疗效的有效方法。 相似文献