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91.
观察了5种常用螯合剂对大鼠体内微量元素排出量、组织分布的变化。结果表明,5种螯合剂可不同程度地增加机体必需微量元素Zn、Cu、Mg和Ca经尿液排出量。EDTA和DTPA的影响尤为明显。EDTA和DTPA可使Zn经尿液的排出量增加16-52倍,DTPA使肝脏Zn含量减少15.9%(P〈0.05),肝脏Cu含量下降60%(P〈0.05)。EDTA和DTPA注射后,肾中Zn含量明显增高,相当对照大鼠3. 相似文献
92.
93.
由于人体组织的各向异性,超声成像中存在相位偏差。相差制约了超声成像分辨率的进一步提高。互相关及其类似相位估计技术可以用于相差校正,jitter是此类算法的基本限制。并行自适应接收补偿算法可以校正较小的相差,结合互相关技术能够得到比较理想的相差校正效果。 相似文献
94.
经丝裂霉素C体外处理后,将IL-6基因转染的、高分泌的IL-6的B16黑色素瘤细胞制成瘤苗。结果发现,体内注射IL-6基因转染的瘤苗后,小鼠脾脏CTL活性、NK活性及IL-2诱导的LAK活性显著升高。经IL-6基因转染瘤苗体内治疗后,荷瘤小鼠的皮下肿瘤生长显著减慢、肺转移结节数显著降低、存活期显著延长,若同时合用低剂量IL-2,则上述治疗效果更好。可见IL-6基因转染的瘤苗能有效地通过诱导机体抗肿瘤免疫功能而发挥抗肿瘤作用,与低剂量IL-2合用后,IL-6基因转染的瘤苗的抗肿瘤效果更佳。 相似文献
95.
Anca Ram Qiuhe Cao Paul E. Keck Harrison G. Pope Koichi Otani Gerard Addonizio Susan L. McElroy Sunao Kaneko Michaela Redlichova Elliot S. Gershon Pablo V. Gejman 《American journal of medical genetics. Part A》1995,60(3):228-230
Dysfunction of the dopaminergic system has been suggested as a pathogenic mechanism in neuroleptic malignant syndrome. Therefore, we examined the complete coding sequences of the dopamine D2 receptor (DRD2) gene for structural abnormalities in 12 patients with a history of NMS, including two cases of familial NMS. Mutational analysis was performed by denaturing gradient gel electrophoresis (DGGE), a highly sensitive technique for detecting sequence differences. We found in one patient with a history of NMS a nucleotide substitution at codon 310 (CCG→TCG) of exon 7 of the DRD2 gene which predicts the replacement of proline to serine in the third cytoplasmic loop of the receptor, a part of the receptor that interacts with G-proteins. A larger series of patients with NMS needs to be investigated to establish whether this allele is associated with an increased susceptibility to NMS. © 1995 Wiley-Liss, Inc. 相似文献
96.
97.
16通道人工耳蜗植入装置的原理和研制 总被引:3,自引:0,他引:3
人工耳蜗植入是利用电听觉原理恢复聋人听觉的一种有效方法,作者依据耳蜗在电刺激条件下的听觉生理学原理和心理声学参量,提出汉语主意编码方案的设想,研制出16通道耳蜗植入电极系统和语言处理装置,并进行初步动物实验研究。 相似文献
98.
Z. Gori W. Tangheroni A. Cao 《Virchows Archiv : an international journal of pathology》1971,354(3):223-238
Summary Muscles of three patients (2 years, 2 years and 7 months, and 11 years of age) affected by congenital hypothyroidism due to dysgenesis of the thyroid gland were studied by electron microscope. The biopsies were performed on the quadriceps muscle. Several alterations were found in the ultrastructure of the muscle fibers. The contractile material underwent atrophy by two recessive processes: by reduction and by degeneration. The former, which affected mainly the white fibers, led to the progressive detachment of myofilaments from the periphery of the myofibrils while they maintainad a normal arrangement in the center. Consequently, their diameter decreased and their interfibrillar spaces enlarged. The latter enlargment, involving the red fibers, caused areas of dedifferentiation involving either the contractile apparatus or the other cell organelles. Modifications of the sarcolemma and basement membrane were seen in the fibers affected by the atrophying processes of the contractile material. Changes of the ultrastructure of the sarcoplasmic reticulum and of the T system were observed with numerous morphological abnormalities of the mitochondria. In addition, accumulation of glycogen and striking changes of the satellite cells were found. The ultrastructural findings are reviewed and discussed in relation to the literature on hypothyroid myopathy. 相似文献
99.
Involvement of ERK, p38 and NF-kappaB signal transduction in regulation of TLR2, TLR4 and TLR9 gene expression induced by lipopolysaccharide in mouse dendritic cells 总被引:7,自引:0,他引:7 下载免费PDF全文
An H Yu Y Zhang M Xu H Qi R Yan X Liu S Wang W Guo Z Guo J Qin Z Cao X 《Immunology》2002,106(1):38-45
Toll-like receptors (TLR) are sentinel receptors capable of recognizing pathogen-associated molecule patterns (PAMP) such as lipopolysaccharide (LPS) and CpG-containing oligonucleotides (CpG ODN). TLR2 and TLR4 are major receptors for Gram-positive and Gram-negative bacterial cell wall components, respectively. TLR9 is necessary for CpG signalling. LPS or CpG ODN can activate immature dendritic cells (DC) and induce DC maturation characterized by production of cytokines, up-regulation of co-stimulatory molecules, and increased ability to activate T cells. However, little is known regarding the regulation of TLR gene expression in mouse DC. In this study, we investigated the regulation of TLR2, TLR4 and TLR9 gene expression by LPS in murine immature DC. TLR2, TLR4 and TLR9 mRNA were up-regulated following LPS stimulation. The up-regulation of TLR9 expression coincided with significantly increased production of tumour necrosis factor-alpha induced by LPS plus CpG ODN. While inhibition of extracellular signal-related kinase and NF-kappaB activation suppressed the up-regulation of the expression of TLR2, TLR4 and TLR9 mRNA, inhibition of p38 kinase prevented the up-regulation of TLR2 and TLR4 mRNA expression but enhanced the up-regulation of TLR9 expression. These results demonstrated that TLR2, TLR4 and TLR9 gene expression was differently regulated by LPS in mouse immature DC. Up-regulation of TLR2, TLR4 and TLR9 expression by LPS might promote the overall responses of DC to bacteria and help to explain the synergy between LPS and other bacterial products in the induction of cytokine production. 相似文献
100.
Infusion of genetically modified dendritic cells (DC) expressing immunosuppressive molecules is a potential therapy for organ rejection. IL-12p70, a cytokine produced mainly by DC and macrophages, consists of two subunits, p40 and p35. IL-12p70 is an activator of T cells, while the IL-12p40 subunit serves as a natural antagonist for IL-12p70 action. The primary aim of this study was to evaluate the effect of IL-12p40 gene-modification on both the T-cell stimulatory activity of immature DC (imDC) and their ability to prolong cardiac allograft survival. IL-12p40 gene-modified imDC (DC-p40) exhibited a phenotype characteristic of imDC and displayed impaired T-cell allostimulatory ability in vitro. However, to our surprise, for murine vascularized heterotopic heart transplantation (HHT), administration of donor-derived DC-p40 7 days prior to transplantation did not prolong allograft survival but instead significantly exacerbated cardiac allograft rejection. Further study showed that DC-p40 augmented NK cell activity both in vitro and in vivo and enhanced interferon-gamma (IFN-gamma) production in vivo, which might be due to the increased IL-23 production by DC-p40. Our data suggested that although IL-12p40 gene-modified immature DC can induce T cell hyporesponsiveness in vitro, their ability to activate NK cells and induce IFN-gamma production counterbalances this, exacerbating cardiac allograft rejection. The unexpected effects of DC-p40 limit their value in promoting allograft survival in vivo and likely reflect the complexity of IL-12p40 biology. 相似文献