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81.
刘尊年 《菏泽医学专科学校学报》2002,14(4):84-85
目的 探讨血细胞自动计数的方法。方法 采用微机彩色图像处理技术对血液细胞图像进行图像分割和细胞计数。结果 与人工计数相平行 ,相关系数r =0 .96 1~ 0 .997,P >0 .0 5。结论 该方法可行且计数相对精确、迅速、客观 相似文献
82.
n. holmén † s. isaksson † m. simrén h. sjövall & l. öhman † 《Neurogastroenterology and motility》2007,19(2):119-125
83.
Xinyu D. Li Esperanza Arias Ramamohana R. Jonnala Shyamala Mruthinti Jerry J. Buccafusco 《Journal of molecular neuroscience : MN》1996,27(3):325-336
The ability of nicotine to induce a cytoprotective or neuroprotective action occurs through several down-stream mechanisms.
One possibility is that the drug increases the expression of tyrosine kinase A (TrkA) nerve growth factor (NGF) receptors.
Certain β-amyloid peptides (e.g., Aβ1–42) have been shown to bind with high affinity to α7 nicotinic receptors and thus interfere
with a potentially neurotrophic influence. Treatment of differentiated PC-12 cells with nicotine produced a concentration-dependent
increase in cell-surface TrkA receptors that occurred concomitantly with cytoprotection. The effect of nicotine was blocked
by either of the α7 receptor antagonists α-bungarotoxin (α-BTX) or methyllycaconatine. The cytoprotective action of nicotine
also was inhibited by pretreatment with 10–100 nM Aβ1–42. Nicotine also was administered (four injections of 30 μg, spaced evenly over 24 h) to rats by direct injection into
a lateral cerebral ventricle. Brain TrkA expression was increased significantly in hippocampus and entorhinal cortex (up to
32% above control), with no changes found in cerebral cortex or hypothalamus. The nicotine-induced increases in TrKA expression
in hippocampus and entorhinal cortex were significantly inhibited by 10 μg α-BTX or by 10 nmol Aβ1–42. Therefore, physiologically
relevant concentrations of Aβ1–42 can prevent nicotine-induced TrkA receptor expression in brain regions containing cholinergic
neurons susceptible to the neurotoxicity associated with Alzheimer’s disease. 相似文献
84.
We have investigated Ca2+ mobilization in single T cells stimulated with their physiological ligand, i.e. antigenic peptide bound to major histocompatibility complex (MHC) molecules on antigen-presenting cells (APC). Fibroblasts expressing I-Ed class II molecules were pulsed with a peptide derived from the λ2315 immunoglobulin light chain. Onto such antigen-pulsed fibroblasts were sedimented cloned Th1 cells loaded with Fura-2. Changes in cytosolic Ca2+ concentration in single T cells were continually monitored by use of an imaging system based on fluorometry. Ca2+ mobilization was both peptide-specific and MHC-restricted. Within seconds of the initial APC-T cell contact, a Ca2+ spike could be observed. The Ca2+ response gradually declined over a 25-min period, during which oscillations were noted. Various parameters characterizing the magnitude of the Ca2+ response (latency, increase rate, max and mean Ca2+ increase, frequency and period of oscillations) all correlated with the amount of peptide used for pulsing the fibroblasts. Thus, Ca2+ mobilization in single T cells appears not to be an all or none phenomenon. Rather, activation is incremental (analog signaling), the degree of Ca2+ mobilization probably being related to the number of stimulatory peptide-MHC complexes on the surface of the APC. The extent of calcium mobilization and lymphokine production (interleukin (IL)-2, IL-3, interferon-γ) correlated, at least at the population level. 相似文献
85.
Margaret J. Tango Evelyn Safaris Margarita Romanella Atousa Aminian Marina Katerelos Christine Somerwille RIek G. Tearle Martin J. Pearse Anthony J.E d'Apice 《Xenotransplantation》1997,4(1):25-33
Abstract: Transgenic expression of the human complement regulatory molecule CD59 in mice and genetic deletion of the major xenoantigen galactose α 1,3 galactose (Gal KO) each resulted in partial protection of spleen cells from lysis by human serum. These protective effects were additive when the two genetic modifications were combined. However, when the effects of these genetic modifications were examined in an ex vivo model in which mouse hearts were perfused with human plasma, it was Gal KO which was the modification which determined protection. CD59 expression alone was not protective and CD59 expression in combination with Gal knockout did not result in a significant additional increase in protection over and above that provided by Gal knockout alone. The likely explanation for this discrepancy between the in vitro and ex vivo data is that the H2-Kb promoter used to drive CD59 expression results I in substantially less expression on endothelium than on spleen cells. 相似文献
86.
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89.
采用扫描电镜、透射电镜及光镜免疫金银法观察了31例慢性扁桃体炎患者和8例胎儿的扁桃体隐窝上皮结构及其中细胞的分布。电镜观察发现隐窝上皮表面存在三种类型微隐窝开口,其腔内有浸润细胞、异物及细菌。有三种特化上皮细胞(M细胞)覆盖于Ⅲ型微隐窝开口处,其结构与肠道M细胞相似,其数量随扁桃体炎的反复发作而减少。形态表明微隐窝是浸润细胞和外来抗原的出入口。M细胞与抗原的摄取及传递有关。光镜免疫金银法观察证明上皮浸润细胞中多数为OKT_s~+细胞,其中OKT_4~+者又占多数而OKT_s~+细胞较少,这些细胞是隐窝上皮参于免疫应答的结构基础。 相似文献
90.
This study sought to pharmacologically characterize bradykinin receptors on SV40-immortalized human trabecular meshwork (HTM3) cells. Phosphoinositide (PI) turnover studies were conducted using [3H]myo-inositol-labeled HTM3 cells and anion exchange chromatography to quantify [3H]inositol phosphates generated in response to bradykinin (BK) and various BK analogs. The blockade of these responses was studied using two potent and receptor-subtype selective antagonists. BK and T-kinin (Ile-Ser-BK; TK) induced a 4.2–4.4 fold stimulation of PI turnover above base levels at 1–10 μM. Several other peptides unrelated to BK, including angiotensin II, endothelin, cholecystokinin, bombesin and peptide YY tested at 1–10 μMwere essentially inactive. The molar potencies (EC50) of BK, TK and close analogs were: BK=4.5±0.5 nM(n=6), Lys-BK=6.5±0.7 nM(n=3), TK=38.8±6.6 nM(n=8), Met-Lys-BK=41.5±13.4 nM(n=4), Des-Arg9-BK=2093±626 nM(n=4). All the latter BK-related peptides>were full agonists. The actions of BK and TK were potently and competitively antagonized by Hoe-140 (molar potency=0.6–1 nM;pA2n=8.97–9.21,n=3–4) and byD-Arg0[Hyp3,-Thi5,8,-DPhe7]-BK (molar potency=251 nM;-log potency, pKb=6.6), two selective B2-type BK antagonists. In conclusion, rank order of potency of BK agonists and the blockade of BK- and TK-induced PI turnover by the selective antagonists are consistent with the classification of the BK receptors on HTM3 cells as the B2-receptor subtype. 相似文献