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排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
Anderson IE Buxton D Campbell I Russell G Davis WC Hamilton MJ Haig DM 《Journal of comparative pathology》2007,136(2-3):156-166
Malignant catarrhal fever (MCF) is an often-fatal lymphoproliferative disease of a variety of ungulates that occurs worldwide. It is caused by either of the highly related but distinct gammaherpesviruses alcelaphine herpesvirus-1 (AlHV-1, wildebeest reservoir) or ovine herpesvirus-2 (OvHV-2, sheep reservoir). MCF in rabbits is an excellent model as it closely resembles the disease in susceptible ungulates that include cattle, deer and bison. In this study, newly available and previously characterized monoclonal antibodies specific for rabbit leucocyte differentiation molecules were used to perform a detailed immunohistochemical examination of both AlHV-1 MCF and OvHV-2 MCF in rabbits. Differences in the MCF caused by the two viruses included: less tissue necrosis and more lymphoid cell accumulations in AlHV-1 MCF compared with OvHV-2 MCF, and in particular marked tissue necrosis in the mesenteric lymph node, appendix and liver of OvHV-2-infected animals when compared with either other tissues in OvHV-2 MCF or AlHV-1 MCF lesions in any tissue. In both AlHV-1 MCF and OvHV-2 MCF, lymphoid cell accumulations in lymphoid and non-lymphoid tissues consisted mainly of T-cells with a corresponding absence of B-cells. CD8(+) T-cells accounted for a proportion of these in the non-lymphoid tissues, but there was evidence for the accumulation of an unidentified T-cell subset/subsets as well. This study extends our understanding of the mechanisms of immuno-pathogenesis of MCF. 相似文献
992.
993.
Tardito D Gennarelli M Musazzi L Gesuete R Chiarini S Barbiero VS Rydel RE Racagni G Popoli M 《Neurobiology of aging》2007,28(9):1388-1395
Recent findings suggested a role for soluble amyloid-beta (Abeta) peptides in Alzheimer's disease associated cognitive decline. We investigated the action of soluble, monomeric Abeta(1-40) on CaM kinase II, a kinase involved in neuroplasticity and cognition. We treated organotypic hippocampal cultures short-term (up to 4h) and long-term (5 days) with Abeta(1-40) (1nM-5microM). Abeta did not induce cell damage, apoptosis or synaptic loss. Short-term treatment down-regulated enzymatic activity of the kinase, by reducing its Thr(286) phosphorylation. In contrast, long-term treatment (1nM-microM) markedly and significantly up-regulated enzymatic activity, with peak stimulation at 10nM (three-fold). Up-regulation of activity was associated with increased expression of the alpha-isoform of CaM kinase II, increased phosphorylation at Thr(286) (activator residue) and decreased phosphorylation at Thr(305-306) (inhibitory residues). We investigated the effect of glutamate on CaM kinase II following exposure to 1 or 10nM Abeta(1-40). As previously reported, glutamate increased CaM kinase II activity. However, the glutamate effect was not altered by pretreatment of slices with Abeta. Short- and long-term Abeta treatment showed opposite effects on CaM kinase II, suggesting that long-term changes are an adaptation to the kinase early down-regulation. The marked effect of Abeta(1-40) on the kinase suggests that semi-physiological and slowly raising peptide concentrations may have a significant impact on synaptic plasticity in the absence of synaptic loss or neuronal cell death. 相似文献
994.
995.
Aarons CB Bajenova O Andrews C Heydrick S Bushell KN Reed KL Thomas P Becker JM Stucchi AF 《Clinical & experimental metastasis》2007,24(3):201-209
The liver is the most common site for metastasis by colorectal cancer, and numerous studies have shown a relationship between
serum carcinoembryonic antigen (CEA) levels and metastasis to this site. CEA activates hepatic macrophages or Kupffer cells
via binding to the CEA receptor (CEA-R), which results in the production of cytokines and the up-regulation of endothelial
adhesion molecules, both of which are implicated in hepatic metastasis. Since tissue macrophages implicated in the metastatic
process can often be difficult to isolate, the aim of this study was to develop an in vitro model system to study the complex
mechanisms of CEA-induced macrophage activation and metastasis. Undifferentiated, human monocytic THP-1 (U-THP) cells were
differentiated (D-THP) to macrophages by exposure to 200 ng/ml phorbol myristate acetate (PMA) for 18 h. Immunohistochemistry
showed two CEA-R isoforms present in both U- and D-THP cells. The receptors were localized primarily to the nucleus in U-THP
cells, while a significant cell-surface presence was observed following PMA-differentiation. Incubation of D-THP-1 cells with
CEA resulted in a significant increase in tumor necrosis factor-alpha (TNF-α) release over 24 h compared to untreated D-THP-1
or U-THP controls confirming the functionality of these cell surface receptors. U-THP cells were unresponsive to CEA. Attachment
of HT-29 cells to human umbilical vein endothelial cells significantly increased at 1 h after incubation with both recombinant
TNF-α and conditioned media from CEA stimulated D-THP cells by six and eightfold, respectively. This study establishes an
in vitro system utilizing a human macrophage cell line expressing functional CEA-Rs to study activation and signaling mechanisms
of CEA that facilitate tumor cell attachment to activated endothelial cells. Utilization of this in vitro system may lead
to a more complete understanding of the expression and function of CEA-R and facilitate the design of anti-CEA-R therapeutic
modalities that may significantly diminish the metastatic potential of CEA overexpressing colorectal tumors. 相似文献
996.
997.
Townley RG Hopp RJ Rosenthal RR 《The Journal of allergy and clinical immunology》2007,119(4):1026-7; author reply 1027-9
998.
999.
Tachykinins are present in lamprey spinal cord. The goal of this study was to investigate whether an endogenous release of tachykinins contributes to the activity of the spinal network generating locomotor activity. The locomotor network of the isolated lamprey spinal cord was activated by bath-applied N-methyl-D-aspartate (NMDA) and the efferent activity recorded from the ventral roots. When spantide II, a tachykinin receptor antagonist, was bath-applied after reaching a steady-state burst frequency (>2 h), it significantly lowered the burst rate compared with control pieces from the same animal. In addition, the time to reach the steady-state burst frequency (>2 h) was lengthened in spantide II. These data indicate that an endogenous tachykinin release contributes to the ongoing activity of the locomotor network by modulating the glutamate-glycine neuronal network responsible for the locomotor pattern. We also explored the effects of a 10-min exogenous application of substance P (1 microM), a tachykinin, and showed that its effect on the burst rate depended on the initial NMDA induced burst frequency. At low initial burst rates (approximately 0.5 Hz), tachykinins caused a marked further slowing to 0.1 Hz, whereas at higher initial burst rates, it instead caused an enhanced burst rate as previously reported, and in addition, a slower modulation (0.1 Hz) of the amplitude of the motor activity. These effects occurred during an initial period of approximately 1 h, whereas a modest long-lasting increase of the burst rate remained after >2 h. 相似文献
1000.