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931.
932.
通过密度、可见光光谱、红外吸收光谱、Co-60辐照损伤试验及荧光光谱的测试,研究了PbO-Bi2O3-B2O3-SiO2玻璃系的光学性能与结构.密度最高可达8.464g/cm3其紫外吸收达截止波长随Pb2+及Bi3+含量升高而红移.玻璃熔化温度低达850℃.在PbO-Bi2O3-B2O3系玻璃中加人SiO2可使玻璃结构更致密.室温下该系统玻璃在360nm有一个宽的激发峰,能产生418um及438um两个弱的发射峰.该系统玻璃的结构是由[SiO4]4-、[BO3]3-、[BO4]5-、[PbO4]6-及[BiO6]9-构成.其中部分Pb2+及Bi3+以网络外体进入玻璃. 相似文献
933.
934.
In this study, 16 cases of unilateral alveolar cleft with cleft lip and palate were repaired with autografts of cancellous bone (13 cases) or hydroxyapatite (3 cases). The grafts were covered by reflected mucoperiosteal flaps and a mucosal flap from the upper lip. Twelve of the thirteen cases were followed up for 1-5 years. Nine of whom using cancellous bone had bony continuity of the maxilla and 7 cases erupted permanent maxillary canines within the area of autografts. None of the 3 cases using hydroxyapatite erupted a canine tooth. The results showed that autograft was better than hydroxyapatite in terms of maxillary canine eruption. 相似文献
935.
We report the differences between using either EDTA plasma or serum in a turbidimetric assay for quantitation of C-reactive protein (CRP). A systematic discrepancy was found for these two sample materials. This was most pronounced in the low concentration range (below 20 mg1(-1)) at which lower values were found in serum than in EDTA plasma. Conversely, in the high concentration range, serum showed slightly higher values. Addition of K3-EDTA to the reaction buffer improved the kinetics for sera with low concentrations of CRP, thus increasing the sensitivity of the assay. We found an overall constant discrepancy of approximately 8% lower values in plasma than in serum (equally for low and high levels of CRP) after the addition of K3-EDTA. The most probable explanation for this effect seems to be the differing water content of serum and EDTA plasma. We discuss the role and function of EDTA in the CRP assay and suggest some hypothetical mechanisms. 相似文献
936.
Chua-Chin Wang Jyh-Ping Lee 《Neural Networks, IEEE Transactions on》1995,6(4):993-999
A method for modeling the learning of belief combination in evidential reasoning using a neural network is presented. A centralized network composed of multiple exponential bidirectional associative memories (eBAM's) sharing a single output array of neurons is proposed to process the uncertainty management of many pieces of evidence simultaneously. The stability of the proposed multiple eBAM network is proved. The sufficient condition to recall a stored pattern pair is discussed. Most important of all, a majority rule of decision making in presentation of multiple evidence is also found by the study of signal-noise-ratio of multiple eBAM network. A guaranteed stable state condition, i.e., the condition for the fastest recall of a pattern pair, is also studied. The result is coherent with the intuition of reasoning. 相似文献
937.
938.
设计一电路,将彩色图象信息编码到黑白CRT的亮度之中,并将其写入液晶光阀,用白光读出,当编码合适时,读出的象颜色可与原图像一致。本文讨论了这一技术原理并进行了单液晶光阀彩色大屏幕投影的实验验证。 相似文献
939.
BID: a novel BH3 domain-only death agonist 总被引:1,自引:0,他引:1
K Wang XM Yin DT Chao CL Milliman SJ Korsmeyer 《Canadian Metallurgical Quarterly》1996,10(22):2859-2869
The BCL-2 family of proteins consists of both antagonists (e.g., BCL-2) and agonists (e.g., BAX) that regulate apoptosis and compete through dimerization. The BH1 and BH2 domains of BCL-2 are required to heterodimerize with BAX and to repress cell death; conversely, the BH3 domain of BAX is required to heterodimerize with BCL-2 and to promote cell death. To extend this pathway, we used interactive cloning to identify Bid, which encodes a novel death agonist that heterodimerizes with either agonists (BAX) or antagonists (BCL-2). BID possesses only the BH3 domain, lacks a carboxy-terminal signal-anchor segment, and is found in both cytosolic and membrane locations. BID counters the protective effect of BCL-2. Moreover, expression of BID, without another death stimulus, induces ICE-like proteases and apoptosis. Mutagenesis revealed that an intact BH3 domain of BID was required to bind the BH1 domain of either BCL-2 or BAX. A BH3 mutant of BID that still heterodimerized with BCL-2 failed to promote apoptosis, dissociating these activities. In contrast, the only BID BH3 mutant that retained death promoting activity interacted with BAX, but not BCL-2. This BH3-only molecule supports BH3 as a death domain and favors a model in which BID represents a death ligand for the membrane-bound receptor BAX. 相似文献
940.