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151.
目的 :研究不同剂量加味保元汤对束缚应激小鼠非特异性免疫功能的影响。方法 :80只小鼠随机等分为加味保元汤 5g/kg体重、 10g/kg体重、15g/kg体重和应激组 ,用巨噬细胞体内吞噬法 ,测其吞噬率及吞噬指数。结果 :吞噬指数 :10g/kg体重组明显高于 15g/kg体重组 (P <0 0 5 ) ,10g/kg体重组与 5g/kg体重组比较虽P >0 0 5 ,但均值高于 5g/kg体重组 ;吞噬率 :10g/kg体重组最高。结论 :10g/kg体重剂量加味保元汤对束缚应激小鼠非特异性免疫功能保护作用效果最佳。  相似文献   
152.
153.
Pregnancy is known to influence the course of rheumatoid arthritis (RA) in women, as well as type II collagen-induced arthritis (CIA) in DBA/1 mice. A characteristic feature is the remission during gestation and the exacerbation of the diseases during the post-partum period. In the case of CIA in DBA 1 mice, two hormonal changes have been assumed to be critical for the induction of the post-partum flare: (i) the fall in steroid hormone levels from those present during pregnancy; and (ii) surges of prolactin (PRL) release at and after delivery. Our results show that treatment with oestradiol during a short period immediately after parturition protects the mouse from a post-partum flare of the disease, and that treatment with bromocriptine, a drug known to inhibit the endogenous PRL release, has a significant though less marked effect. Studies of lactating (i.e. animals with physiological stimulation of endogenous PRL release) and non-lactating arthritic mice revealed no clear-cut differences, indicating that PRL is of minor importance for the induction of the post-partum flare. Some steroids other than oestradiol, which may be implicated in the exacerbation of arthritis, namely progesterone and hydrocortisone, had no clinical effect. Analyses of agalactosyl IgG levels in mice with CIA, and anti-collagen II antibodies in sera collected at the end of the experiments revealed no significant differences between the oestradiol and the control groups. The successful oestradiol treatment of the mice indicates that the drop in endogenous oestradiol levels prior to delivery ends the oestrogen-mediated protection against arthritis during pregnancy.  相似文献   
154.
This study presents a comparative analysis of gangliosides from lymphoid (spleen and thymus) and other (brain, liver, lungs and muscle) tissues of C57BL/6 mice lacking the gene for beta2-microglobulin (beta2M), a constitutive component of the MHC class I molecule. Ganglioside fractions in the tissues of mice homozygous (beta2M-/-) and heterozygous (beta2M-/+) for the gene deletion were determined by high performance thin-layer chromatography (HPTLC), followed by immunostaining with specific polyclonal antibodies. Ubiquitous gangliosides GM3(Neu5Ac) and GM3(Neu5Gc) were the dominant gangliosides in the lungs of the control beta2M-/+ mice, whereas the homozygous knockout mice had substantially decreased expression of these structures. The lungs of the beta2M-/- mice also had reduced expression of T-lymphocyte-specific GM1b-type gangliosides (GM1b and GalNAc-GM1b). beta2M-deficient mice also had more GM1a and GD1a gangliosides in the liver, and several neolacto-series gangliosides were increased in the brain and lungs. This study provides in vivo evidence that the beta2M molecule can influence the acquisition of a distinct ganglioside assembly in different mouse organs, implicating its non-immunological functions.  相似文献   
155.
低浓度芦笋原汁(0.1~1.0%)可明显促进正常小鼠胸腺细胞的增殖,也可刺激正常小鼠脾脏细胞的增殖,但对裸鼠脾脏细胞没有任何作用。由此提示,芦笋具有促T淋巴细胞有丝分裂的活性,而对B淋巴细胞没有作用。与常用的T细胞促有丝分裂素植物血凝素(PHA)及刀豆蛋白A(ConA)不同,芦笋原汁对人、绵羊、豚鼠和鸡的红细胞均无凝集作用。  相似文献   
156.
The development of tolerance to the protective effects of diazepam (4 mg/kg) against seizures induced by pentylenetetrazole (PTZ) were studied in 3 strains of mice. Significant tolerance developed to protection against myoclonic jerks induced by PTZ (90-100 mg/kg) by day 5 in Tuck No. 1 and by day 10 in C3H/HE and CD-1 mice. Tolerance developed to protection against tonic-clonic convulsions by day 10 in Tuck No. 1 mice and by day 30 in the other strains. Diazepam remained protective against tonic-clonic convulsions (but not against myoclonus) induced by threshold doses of PTZ for 30 days in all 3 strains.  相似文献   
157.
Summary CD8+ T cells from C57BL/6(B6) mice show cytotoxicity to B cell blasts prepared from syngeneic transgenic mice expressing HLA-DQ6 molecules in a mouse MHC class I H-2Db restricted manner. Although these results suggest that CD8+ T cells recognize peptides derived from DQ6 molecule bound to H-2Db on target cells, no direct evidence so far has been obtained. To clarify this, we synthesized 23 peptides corresponding to DQ6α orβ chain and carrying the motifs of Db-binding peptides, and examined their capacity to induce cytotoxicity in the CD8+ T cell line. We show here that DQA1-2, one of these peptides, induced cytotoxicity of the CD8+ T cells when this peptide was pulsed to H-2Db expressing target cells, as efficiently as HLA-DQ6 expressing target cells did. Thus, our results suggest that DQA1-2 can be naturally processed from DQ6 molecules and recognized by the CD8+ T cells in the context of H-2Db molecules. These results suggest that allogeneic HLA class II molecules are involved in the rejection not only as the ligand for T cell receptor of alloreactive CD4+ T cells but also as self-peptides bound to HLA class I molecules recognized by CD8+ T cells.  相似文献   
158.
Berta  Joseph  Wilson  James R. 《Behavior genetics》1992,22(3):345-359
An animal model of alcohol dependence is being produced by selecting mice for differences in severity of ethanol withdrawal seizures. Replicate lines of high-dependence (HA), low-dependence (LA), and control (CA) mice are being developed by within-family selection. After seven generations both (replicate) HA and LA lines have separated significantly. Some of the difference between the replicate pairs of HA and LA in the early generations was due to differences in ethanol consumption. This difference in consumption may be attributable to a difference in metabolic rate or activity level rather than to a difference in ethanol preference. Females are more susceptible to seizures than males; this appears to be due partly to their higher consumption of ethanol during treatment.This research was supported in part by Grant AA-03527 from the National Institute of Alcohol Abuse and Alcoholism to the University of Colorado Alcohol Research Center.  相似文献   
159.
杜仲对D-半乳糖所致衰老小鼠睾丸的形态学研究   总被引:3,自引:0,他引:3  
目的 本实验以D-半乳糖所致衰老小鼠为研究对象,研究了杜仲的抗衰老作用。方法 应用光镜电镜技术观察小鼠睾丸的重量、生精小管直径、生精上皮细胞数、间质细胞数的随龄变化,同时观察了杜仲对上述指标的影响。结果 1、随增龄,睾丸重量减轻,生精小管直径缩小。衰老时生精细胞缺如,仅剩支持细胞或见散在分布,间质细胞随龄递减。2、杜仲具有一定的抗衰老作用,使生精过程活跃,生精细胞增多,间质细胞增多不明显,生精小管直径改变不显著。结论 杜仲具有一定的抗衰老作用。  相似文献   
160.
Heavy-ion radiation accounts for the major component of absorbed cosmic radiation and is thus regarded as a significant risk during long-term manned space missions. To evaluate the genetic damage induced by heavy particle radiation, gpt delta transgenic mice were exposed to carbon particle irradiation and the induced mutations were compared with those induced by reference radiations, i.e., X-rays and gamma-rays. In the transgenic mouse model, deletions and point mutations were individually identified as Spi(-) and gpt mutations, respectively. Two days after 10 Gy of whole-body irradiation, the mutant frequencies (MFs) of Spi(-) and gpt were determined. Carbon particle irradiation significantly increased Spi(-) MF in the liver, spleen, and kidney but not in the testis, suggesting an organ-specific induction of mutations by heavy-ion irradiation. In the liver, the potency of inducing Spi(-) mutation was highest for carbon particles (3.3-fold increase) followed by X-rays (2.1-fold increase) and gamma-rays (1.3-fold increase), while the potency of inducing gpt mutations was highest for gamma-rays (3.3-fold increase) followed by X-rays (2.1-fold increase) and carbon particles (1.6-fold increase). DNA sequence analysis revealed that carbon particles induced deletions that were mainly more than 1,000 base pairs in size, whereas gamma-rays induced deletions of less than 100 base pairs and base substitutions. X-rays induced various-sized deletions and base substitutions. These results suggest that heavy-ion beam irradiation is effective at inducing deletions via DNA double-strand breaks but less effective than X-ray and gamma-ray irradiation at producing oxidative DNA damage by free radicals.  相似文献   
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