TCP稳态流中慢启动序列对吞吐量性能的影响

在计算TCP稳态数据流吞吐量时一般都忽略了由于分组丢失而形成的各个慢启动阶段。在考虑TCP稳态数据流中慢启动序列的情况下,对Padhye的经典TCP稳态数据流模型进行了扩展。通过将Padhye的模型与扩展后的模型作比较,证明了在使用Padhye的模型作为多媒体流量控制模型时忽略超时后慢启动阶段的可行性和正确性。     

USERS’ TWO-DIMENSIONAL INTEREST AND ITS STORAGE METHOD

The users‘ interest can be mined from the web cache and can be used widely.The interest can be specialized by the two-tuple(term,weight) in the simple interest model,in which the association relations are not mined.and then interest cannot be associated in expressing the users‘interest.Based on analyzing the WWW cache model,this letter brings forward a twodimensional interest model and gives the interrelated methods on how to store the two-dimensional interest model effectively.     

Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat

Delayed neurological damage after CO hypoxia was studied in rats to determine whether programmed cell death (PCD), in addition to necrosis, is involved in neuronal death. In rats exposed to either air or CO (2500 ppm), microdialysis in brain cortex and hippocampus was performed to determine the extent of glutamate release and hydroxyl radical generation during the exposures. Groups of control and CO-exposed rats also were tested in a radial maze to assess the effects of the CO exposures on learning and memory. At 3, 7, and 21 days after CO exposure brains were perfusion-fixed and hematoxylin-eosin (H&E) was used to assess injury and to select regions for further examination. DNA fragmentation was sought by examining cryosections with the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) reaction. We found significant increases in glutamate release and .OH generation during and immediately after CO hypoxia. CO-exposed rats showed learning and memory deficits after exposure associated with heterogeneous cell loss in cortex, globus pallidus, and cerebellum. The frontal cortex was affected most seriously; the damage was slight at Day 3, increased at Day 7, and persistent at Day 21 after CO exposure. TUNEL staining was positive at all three time points, and TUNEL-labeled cells were distributed similarly to eosinophilic cells. The number of cells stained by TUNEL was less than by H&E and amounted to 2 to 5% of all cell nuclei in regions of injury. Ultrastructural features of both neuronal necrosis and apoptosis also were observed readily by electron microscopy. These findings indicate that both necrosis and apoptosis (PCD) contribute to CO poisoning-induced brain cell death.     

Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate

We observed that pretreatment of male F344 rats with benzyl selenocyanate, a versatile organoselenium chemopreventive agent in several animal model systems, decreases the levels of DNA and RNA modifications produced in the liver by the hepatocarcinogen 2-nitropropane. To clarify the mechanisms involved, we pretreated male F344 rats with either benzyl selenocyanate, its sulfur analog benzyl thiocyanate, phenobarbital or cobalt protoporphyrin IX; the latter is a depletor of P450. We then determined (1) the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on 2-nitropropane-induced liver DNA and RNA modifications and (3) amount of nitrate excreted in rat urine following administration of the carcinogen. Pretreatment with benzyl selenocyanate or phenobarbital increased the denitrification activity of liver microsomes by 217 and 765%, respectively, increased liver P4502B1 by 31- and 435-fold, respectively, decreased the levels of 2-nitropropane-induced modifications in liver DNA (29-70% and 17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and increased the 24-h urinary excretion of nitrate by 157 and 209%, respectively. Pretreatment with benzyl thiocyanate had no significant effect on any of these parameters. Pretreatment with cobalt protoporphyrin IX decreased liver P4502B 1 by 87%, decreased the denitrification activity of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic acid modifications by 17-67%. These results indicate that the metabolic sequence from 2-nitropropane to the reactive species causing DNA and RNA modifications does not involve the removal of the nitro group. Moreover, they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic acid modifications in part by increasing its detoxication through induction of denitrification, although it is evident that other mechanisms must also be involved.     

超高分子量聚乙烯的辐照效应

通过密度测定和ＤＳＣ热分析，观测了超高分子量聚乙烯的辐射效应。实验结果表明：在吸收剂量０—１．１３ＭＧｙ范围内，密度随吸收剂量的增加而增大，熔化热和熔点也有所增加，特别是在低剂量范围内增加十分明显。以上结果都说明，超高分子量聚乙烯在辐照过程中，结晶在完善或有新的结晶形成     

辊式拉拔模用于连续拉拔机组的新技术

针对进口连续拉拔机组，独创设计了可配套使用的二连式辊模，并首次很好地解决了惯用模在辊模后的安装问题，是一种很有前途的新技术。     

用轴向气胎式离合器,制动器改造旧飞剪

采用轴向式气胎离合、制动器，改造了旧飞剪，解决了原剪机电磁离合、制动器控制不准确的问题；该剪机改造后在成品轧机后使用，剪切用１２０ｍｍ×１２０ｍｍ坯生产的大规格产品（１８ｍｍ以上），增产、增效，年总经济效益为９７．８万元     

Σ-ΔA/D转换技术及仿真

Σ－ΔＡ／Ｄ转换技术近年来颇受重视，因为基于该技术的Ａ／Ｄ转换器能达到很高的分辨率（１６ｂｉｔ以上），并另具一系列优点。本文对Σ－ΔＡ／Ｄ转换器的基本原理，包括过采样（Ｏｖｅｒｓａｍｐｌｉｎｇ），噪声成形（ＮｏｉｓｅＳｈａｐｉｎｇ），以及数字抽取滤波（ＤｉｇｉｔａｌＤｅｃｉｍａｔｉｏｎＦｉｌｔｅｒｉｎｇ）等内容，均作了叙述。作者还对一个２０ｂｉｔΣ－Δ转换器的算法进行了计算机仿真。该转换器采用了高阶ＭＡＳＨ噪声成形技术，而其数字抽取滤波部分则由梳状滤波器与级联的半带滤波器构成。文章中给出了仿真结果。     

铌酸锂γ射线辐照色心缺陷的研究

对铌酸锂晶体进行γ射线辐照处理，吸收光谱显示基础吸收边紫移，４８０ｎｍ波长附近出现一明显吸收峰，这是由空位色心Ｖ０和Ｎｂ＾４＋缺陷引起的，Ｎｂ＾４＋的存在进一步被ＥＰＲ实验所证实。本文对上述辐照缺陷的产生机理进行了讨论。