AES-192的相关密钥飞去来器攻击和矩形攻击

相关密钥攻击是对AES十分有效的分析方法之一.在2022年亚密会上,Derbez等利用概率为2−108的10轮相关密钥飞去来器区分器给出了目前最好的AES-192的全轮攻击.本文改进了全轮AES-192的相关密钥飞去来器和矩形攻击.基于Wang等的9轮相关密钥飞去来器区分器的截断差分,本文利用飞去来器分布表(BDT)技术给出目前概率最高的10轮相关密钥飞去来器区分器,概率为2−105.92.基于该区分器,改进了全轮AES-192的相关密钥飞去来器攻击,时间、数据和存储复杂度分别为2^(121.92)、2^(121.92)和2^(90.92),与之前的结果相比时间复杂度改进了22.08.进一步,给出了全轮AES-192的相关密钥矩形攻击,时间、数据和存储复杂度分别为2^(127.9)、2^(119.5)和2^(131.5),这也是目前在选择明文模式下对全轮AES-192最好的攻击结果.

基于AES的车联网通信加密算法

随着V2X技术发展得越来越快,车辆与其他设备的通信量以及信息重要度都在急速增长,车载信息遭到攻击从而被截取或者发生泄漏的风险也相应地大大增加,因此信息交互安全性成为了一个不可避免的研究课题。本文针对车联网传输数据量大、数据加解密操作频繁等问题,通过分析经典加密算法,进而改进传统AES加密算法,使用RC4加密算法生成伪随机密钥代替AES加密算法的密钥生成模块,优化加密时间的同时提升安全性能,并开展实验验证了其加密效率以及安全性。

基于AES与ECC混合算法的计算机网络通信数据安全加密方法

为了提高通信数据在计算机网络中的安全性,提出一种基于AES与ECC混合算法的计算机网络通信数据安全加密方法。通过时域分析,得到通信数据在计算机网络边缘的频率分布情况,根据通信数据中冗余信息的密度,离散化处理通信数据内的噪声,提取出通信数据的特征向量。根据通信数据的明文空间进行加密处理,计算出待加密通信数据的密文值,将计算机网络通信数据的加密过程约束成加密函数的计算,设定通信数据安全加密的约束条件,采用AES算法加密通信数据的明文,利用ECC算法加密AES密钥,将AES与ECC结合,生成通信数据的密钥密文,实现通信数据的安全加密。实验结果表明,所提方法能够保证通信数据在计算机网络中的安全,可以将通信数据加密后的受攻击指数控制在0.1以内,提高通信数据的加密效果。

基于LSTM-AE的民机空调热交换器性能异常检测方法

空调热交换器性能异常检测技术是快速判断民机空调系统运行状态并合理安排维修任务的关键,传统的异常检测方法难以有效处理高维时序数据,无法实现系统早期故障预警。为此,本文提出了一种基于长短期记忆网络(LSTM,long-short term memory)与自编码器(AE,autoencoder)模型的无监督异常检测方法,用以识别民机空调系统异常运行状态。首先,基于民机空调系统原始传感器参数构建表征空调热交换器性能的特征监测参数;其次,构建LSTM-AE模型进行数据特征重构并计算重构误差;最后,使用孤立森林(iForest, isolation forest)进行无监督异常监测。将本文构建的无监督异常检测方法与传统方法对比,并建立模型评估指标,验证结果表明,所构建的模型方法可以对民机空调热交换器性能异常状态进行有效检测。

基于混沌序列和AES算法的数据库外层数据传输同步加密方法

为保障数据库外层数据的安全传输,提出一种基于混沌序列和AES算法的数据库外层数据传输同步加密方法。该方法结合AES算法的加密安全性和混沌序列的加密速度优势,通过加密代理服务器和应用服务器对数据库外层数据进行处理,利用混沌序列logistic映射参数初始化、混沌序列二进制量化、AES动态加密和尾端处理实现数据库外层数据传输同步加密。实验结果表明,该方法能够成功地对文本和图像数据进行加密和隐藏,同时提高加密效率,并兼顾了数据的安全性和传输效率。

基于AES算法的计算机数据库加密系统设计与实现

随着信息技术的迅猛发展,中等职业(中职)教育面临着教学资源更新和个性化教学需求的双重挑战。知识图谱是一种通过链接和整合广泛信息资源来创建、利用和分享知识的技术,能够在复杂的数据中寻找规律,为用户提供准确的信息推荐服务。研究通过分析数据库加密的常用方式和数据库透明加密(TDE)原理,设计了一套基于知识图谱的中职线上教学资源推荐系统的体系架构。系统采用高级加密标准(AES)算法加密设计保证数据安全,整合数据库提升系统效能,并详细说明了开发过程的实现。通过实验结果及分析,证明了系统的有效性和实用性,为中职教育提供了一种新的线上教学资源推荐解决方案。

Effects of endotoxin on expression of ras, p53 and bcl-2 oncoprotein in hepatocarcinogenesis induced by thioacetamide in rats

AIM To evaluate the relationship between expression of ras, p53, bcl 2 gene products, and hepatocarcinogenesis since endotoxemia produced from lipopolysaccharide admi nistration and/or the hypophagocytic state of splenectomy significantly accelerated hepatocarcinogenesis induced by thioacetamide. 〖WTH4〗METHODS〓〖WTXFZ〗The hepatocarcinoma model was induced by oral intake of 0 03% thioacetamide for six months. During the induction of hepatocarcinoma model, rats were additionally treated with splenectomy and/or lipopolysaccharide administration. The techniques of flow cytometry, immunohistochemistry and immunoelectronmicroscopy were applied to quantitative analysis of the expression of oncogene proteins. RESULTS In this model system, overexpression of ras p21 protein mainly occurred on precancerous cell population or in early stage of hepatocyte transformation. And the levels of ras p21 declined when nuclear DNA aneuploid increased. Expression of bcl 2 protein slowly and steadily rose with more hepatocytes staying in S+G2M phases as the hepatocarcinoma became more malignant. P53 was moderately expressed during the hepatocarcinogenesis. There was no statistical correlation between endotoxemia levels and the changes of ras, p53 and bcl 2 gene products. CONCLUSION Over expression of oncogene ras p21 was likely to be a precursor of the premalignant hepatocytes and it might be responsible for the initiation of hepatocarcinogenesis. Bcl 2 protein expression is proportional to the severity of the malignancies. P53 may be a key pathway on the transformation and development of hepatocarcinoma. This study confirmed the hypothesis that there are multiple genes and multiple steps involved in hepatocarcinogenesis. Expressions of oncogene proteins reflected the properties of the premalignant and malignant cells, but not directly related to endotoxemia statistically.[JP]

Protective effects of Phyllanthus acidus(L.) Skeels leaf extracts on acetaminophen and thioacetamide induced hepatic injuries in Wistar rats

Objective:To investigate and compare the hepatoprotective effects of crude ethanolic and aqueous extracts of Phyllanthus acidus（L.） Skeels（P.acidus） leaves on acetaminophen（APAP） and thioacetamide（TAA） induced liver toxicity in wistar rats.Silymarin was the reference hepatoprotective agent.Methods:In two different sets of experiments,the P.acidus extracts （200 and 400 mg/kg,body weight） and silymarin（100 mg/kg,body weight） were given orally for 7 days and a single dose of APAP（2 g/kg,per oral） or TAA（100 mg/kg,subcutaneous） were given to rats.The level of serum aspartate transaminase（AST）,alanine transaminase（ALT）,alkaline phosphatase（ALP）,total bilirubin and total protein were monitored to assess hepatotoxicity and hepatoprotection.Results:APAP or TAA administration caused severe hepatic damage in rats as evident from significant rise in serum AST,ALT,ALP,total bilirubin and concurrent depletion in total serum protein.The P.acidus extracts and silymarin prevented the toxic effects of APAP or TAA on the above serum parameters indicating the hepatoprotective action.The aqueous extract was found to be more potent than the corresponding ethanolic extract against both toxicants.The phenolic and flavonoid content（175.02±4.35 and 74.68±1.28,respectively） and 2,2-diphenyl-1- picrylhydrazil（DPPH）[IC50=（33.2±0.31）μg/mL]scavenging potential was found maximum with aqueous extract as compared to ethanolic extract.Conclusions:The results of present study suggests that the aqueous extract of P.acidus leaves has significant hepatoprotective activity on APAP and TAA induced hepatotoxicity,which might be associate with its high phenolic and flavonoid content and antioxidant properties.

Tetrandrine stimulates the apoptosis of hepatic stellate cells and ameliorates development of fibrosis in a thioacetamide rat model

AIM： To investigate the therapeutic effect of tetrandrine on liver fibrosis induced by thioacetamide in rats in vivo and in vitro. METHODS： In vitro study： we investigated the effect of tetrandrine on the apoptosis of rat hepatic stellate cells transformed by simian virus 40 （T-HSC/CI-6）, which retains the features of activated cells. In vivo study： hepatic fibrosis was induced in rats by thioacetamide. Tetrandrine was given orally to rats at doses of 5, 10 or 20 mg/kg for 4 wk compared with intraperitoneal injection of interferon-r. RESULTS： In vitro study： 5, 10 or 25 μg/mL of tetrandrine-induced activation of caspase-3 in t-HSC/CI-6 cells occurred dose-dependently. In vivo study： tetrandrine treatment as well as interferon-r significantly ameliorated the development of fibrosis as determined by lowered serum levels of aspartate aminotransferase （AST）, alanine aminotransferase （ALT）, total bilirubin （T-Bil） and the levels of liver hydroxyproline （Hyp）, hyaluronic acid （HA）, laminin （LN） and also improved histological findings. The effects of tetrandrine at the concentration of 20 mg/kg were better than the other concentration groups. CONCLUSION： Tetrandrine promotes the apoptosis of activated HSCs in vitro. Tetrandrine administration can prevent liver fibrosis and liver damage induced by thioacetamide in rats in vivo, indicating that it might exert a direct effect on rat HSCs.

Atorvastatin and rosuvastatin do not prevent thioacetamide induced liver cirrhosis in rats

AIM:To examine whether the administration of atorvastatin and rosuvastatin would prevent experimentallyinduced hepatic cirrhosis in rats.METHODS:Liver cirrhosis was induced by injections of thioacetamide(TAA).Rats were treated concurrently with TAA alone or TAA and either atorvastatin(1,10 and 20 mg/kg) or rosuvastatin(1,2.5,5,10 and 20 mg/kg) given daily by nasogastric gavage.RESULTS:Liver fibrosis and hepatic hydroxyproline content,in the TAA-treated group was significantly higher than those of the controls [11.5 ± 3.2 vs 2.6 ± 0.6 mg/g protein(P = 0.02)].There were no differences in serum aminotransferase levels in the TAA controls compared to all the groups treated concomitantly by statins.Both statins used in our study did not prevent liver fibrosis or reduce portal hypertension,and had no effect on hepatic oxidative stress.Accordingly,the hepatic level of malondialdehyde was not lower in those groups treated by TAA + statins compared to TAA only.In vitro studies,using the BrdU method have shown that atorvastatin had no effect of hepatic stellate cells proliferation.Nevertheless,statin treatment was not associated with worsening of liver damage,portal hypertension or survival rate.CONCLUSION:Atorvastatin or rosuvastatin did not inhibit TAA-induced liver cirrhosis or oxidative stress in rats.Whether statins may have therapeutic applications in hepatic fibrosis due to other etiologies deserve further investigation.

Protective effect of aqueous extract of Feronia elephantum correa leaves on thioacetamide induced liver necrosis in diabetic rats

Objective:To evalueate hepatoprotective effects Feronia elephantum(F.elephantum)correa against thioacctamide(TA)induced liver necrosis in diabetic rats.Methods:Male wistar rats were made diabetic with alloxan(160 mg/kg)on day 0 of the study.They were intoxicated with hepatotoxicant(thioacetamide,300 mg/kg,ip)on day 9 of study to produce liver necrosis.Effects of 7 day daily once administration(day 2 to day 9)of EF(400 and 800 mg/kg,po)were evaluated on necorosis of liver in terms of mortality,liver volume,liver weight,serum aspartate aminotransferase(AST)and serum alanine transaminase(ALT),and histopathology of liver sections(for signs of necorosis and inflammation)on day-9 of the study.Separate groups of rats with treated only with alloxan(DA control),thioacetamide(TA control)and both(TA+DA control)were maintained.Results:FE significantly lowered the mortality rate and showed improvement in liver function parameters in TA-induced diabetic rats without change in liver weight,volume and serum glucose levels.Conclusions:FE showed promising activity against TA-induced liver necorsis in diabetic rats and so might be useful for prevention of liver complications in DM.

Involvement of P53 and Bax/Bad triggering apoptosis in thioacetamide-induced hepatic epithelial cells

AIM： Thioacetamide （TAA） has been used in studying liver fibrosis and cirrhosis, however, the mechanisms of TAA-induced apoptosis in liver are still unclear. The hepatic epithelial cell line clone 9 was cultured and treated with TAA to investigate the causes of cell death. METHODS： The cell viability of TAA-induced clone 9 cells was determined using MTT assay. Total cellular GSH in TAA-induced clone 9 cells was measured using a slight modification of the Tietze assay. The activity of caspase 3 in TAA-induced clone 9 cells was monitored by the cleavage of DEVD-p-nitroanaline. TUNEL assay and flow cytometry were applied for the determination of DNA fragmentation and the proportion of apoptosis in TAA- induced clone 9 cells, respectively. The alterations of caspase 3, Bad, Bax and Phospho-P53 contents in TAA- induced clone 9 cells were measured by Western blot. RESULTS： The experimental data indicated that TAA caused rat hepatic epithelial cell line clone 9 cell death in a dose-and time-dependent manner; 60% of the cells died （MTT assay） within 24 h after 100 rag/1 TAA was applied. Apoptotic cell percentage （TUNE1 assay） and caspase 3 activities were highest after 100 rag/1 TAA was added for 8 h. The release of GSH and the elevation in caspase content after TAA treatment resulted in clone 9 cell apoptosis via oxidative stress and a caspasedependent mechanism. The phospho-p53, Bax and Bad protein expressions in clone 9 cells were increased after TAA treatment. CONCLUSION： These results reveal that TAA activates p53, increases caspase 3, Bax and Bad protein contents, perhaps causing the release of cytochrome c from mitochondria and the disintegration of membranes, leading to apoptosis of cells.

ICP-AES法测定电炉渣中二氧化硅

本文研究了采用酸溶的方式消解样品,ICP-AES光谱法测定电炉渣中二氧化硅的分析方法。采用浓盐酸和浓硝酸溶解电炉尾料样品,加入氢氟酸消解二氧化硅和硼酸络合氟离子,采用ICP-AES法测定电炉尾料样品中的二氧化硅含量。二氧化硅的相对标准偏差RSD为0.35%~0.58%,加标回收率为95.6%~102.3%。方法加标回收率好,满足分析方法要求。

Chrysanthemum indicum ethanol extract attenuates hepatic stellate cell activation in vitro and thioacetamide-induced hepatofibrosis in rats

Objective:To investigate the antifibrotic effects of Chrysanthemum indicum ethanol extract(CIEE)against activated hepatic stellate cells(HSC)and thioacetamide(TAA)-induced hepatofibrosis in rats.Methods:Cell viability and proliferation of HSC-T6 cells were measured using MTT assay.Primary HSCs were used to study morphology.TAA(200 mg/kg)was used to induced hepatic fibrosis in rats.CIEE(100 and 500 mg/kg)and silymarin(50 mg/kg)were administered orally.Liver functions including alanine transaminase,aspartate transaminase,glutathione,and hydroxyproline levels were measured using commercial kits.Liver sections and fibrotic biomarker expression were measured using hematoxylin and eosin staining and real-time polymerase chain reaction.Results:In vitro study revealed that CIEE(0.1,0.25,and 0.5 mg/mL)inhibited the proliferation of activated HSCs exposed to transforming growth factor(TGF)-β and restored the activated primary HSC morphology.In in vivo studies,TAA-induced increase in liver/body weight ratio(5.46±0.26)was significantly reduced(4.13±0.22)by CIEE(P<0.05 at 500 mg/kg).CIEE(100 and 500 mg/kg)improved the liver functions by significantly attenuating changes in alanine transaminase,aspartate transaminase,glutathione,and hydroxyproline levels(P<0.05).Further,CIEE(100 and 500 mg/kg)ameliorated the histological changes in liver tissue and TGF-β expression significantly(P<0.05)in TAA-induced rats.Conclusions:CIEE significantly protects against TAA-induced liver damage in rats and can be used in the treatment of liver fibrosis.

基于单通道AE盲源分离的结构损伤定位

声发射(acoustic emission,简称AE)能够实现复杂板状结构损伤定位,但多数AE检测定位方法仅针对单AE源的情况,而实际中复杂板状结构产生损伤时会伴随多个AE卷积混合信号。为了解决工程中多AE源定位的问题,提出一种单通道AE盲分离-模态提取定位方法。首先,对采集的AE信号进行信号降噪,使用单通道盲源分离算法分离出无回波成分的AE信号,将多源定位转为多个单源定位问题;其次,通过提取单频模态,求取声波传播速度,估计到达时间差来进行疲劳裂纹损伤定位;最后,经过计算机仿真实验和钢箱梁桥断铅半实物仿真实验,验证了方法的准确性和有效性,并通过载荷破坏AE检测实验验证了方法的实用性。结果表明,所提方法能够应用于复杂板状结构多AE源定位问题,为实际工程应用提供了可靠的依据及参考价值。

Protective effect of Amorphophallus campanulatus(Roxb.) Blunie.tuber against thioacetamide induced oxidative stress in rats

Objective:To identify the phytochemical constituents of Amorphopkallus campanulatus(A. campanulatus) tuber and to evaluate its antioxidant potential through in vitro and in vivo models. Methods:Phytochemical screening and in vitro antioxidant activities of A.campanulatus tuber n-hexane extract(ACHE) and methanolic extract(ACME) were evaluated using DPPH,hydroxyl radical,reducing power and total antioxidant capacity assays.The total phenolic and flavonoid contents were also investigated.The protective potential of two different doses of ACME(125 and 250 mg/kg) was also evaluated against thioaeetamide(TAA) induced oxidative stress in rats. Silymarin used as a standard drug control.Hepatotoxicitv was assessed by quantifying the serum levels of aspartate aminotransferase(AST),alanine aminotransferase(AIT),alkaline phosphatase (ALP) and lactate dehydrogenase(LDH).The antioxidant potential of ACME were also evaluated by the estimation of catalase(CAT),glutathione peroxidase(GPx),glutathione reductase (OR),glutathione-S-transferase(GST),reduced glutathione(GSH) and lipid peroxidation (Thiobarbituric acid reactive substances) in hepatic and renal tissues.Histopathologic changes of liver were also evaluated.Results:In vitro studies revealed that ACME has higher antioxidant and radical scavenging activity than ACHE,which may be attributed to its higher phenolic and flavonoid content.ACME significandy prevented the elevation of serum AST,ALT.ALP,LDH,and tissue malondialdehyde levels(P 【 0.05).Hepatic and renal GSH.GST.GR,GPx,and catalase levels were remarkably increased by the treatment with the extract.Quantification of histopathological changes also supported the dose dependent protective effects of ACME.Conclusions:The results do suggest that A.campanulatus tuber could be considered as a potential source of natural antioxidant.

Protective effect of Pisonia aculeata on thioacetamide induced hepatotoxicity in rats

Objective:To evaluate the protective effect of Pisonia aculeata(P.aculeata) on thioacetamide induced hepatotoxicity in rats.Methods:Male Wistar rats were administered 250 or 500 mg/kg p.o.of P.aculeata extract for 21 days and simultaneously administered thioacetamide(TAA) 50 mg/kg bw s.c.1 h alter the respective assigned treatments every 72 h.At the end of all experimental methods,all the animals were sacrificed by cervical decapitation.Blood samples were collected.Serum was separated and analyzed for various biochemical parameters.Results:TAA induced a significant rise in aspartate amino transferase(AST),alanine amino transferase(ALT),alkaline phosphatase(ALP),total bilirubin,gamma glutamate transpeptidase(GGTP),lipid peroxidase(LPO)with a reduction of total protein,superoxide dismutase(SOD),catalase,glutathione peroxidase(GPx) and glutathione S-transferase(GST).Treatment of rats with different does of plant extract(250 and 500 mg/kg) significantly(P<0.001) altered serum marker enzymes and antioxidant levels to near normal against TAA treated rats.The activity of the extract at a dose of 300 tug/kg was comparable to the standard drug,silymarin(50 mg/kg.p.o.).Conclusions:It can be concluded that P.aculeata extract possesses a remarkable hepaloprolective and antioxidant activity against TAA induced hepatotoxicitv.Wore research is required lo derive an optimal therapeutic dose.

Effect of dichloromethylene diphosphonate on liver regeneration following thioacetamide-induced necrosis in rats

AIM: To study the effect of dichloromethylene diphos-phonate (DMDP), a selective Kupffer cell toxicant in reference to liver damage and postnecrotic liver regeneration in rats induced by sublethal dose thioacetamide (TA). METHODS: Rats, intravenously (iv ) pre-treated with a single dose of DMDP (10 mg/kg), were intraperitoneally (ip ) injected with TA 6.6 mmol/kg (per 500 mg/kg body weight). Hepatocytes were isolated from rats at 0, 24, 48 and 72 h following TA intoxication and blood and liver samples were obtained. To evaluate the mecha-nisms involved in the postnecrotic regenerative state, DNA distribution and ploidy time course were assayed in isolated hepatocytes. Circulating cytokine tumor necrosis factor-alpha (TNF-α) was assayed in serum and determined by reverse transcriptase-polymerase chain reaction in liver extract. RESULTS: The effect of DMDP induced noticeable changes in postnecrotic regeneration, causing an increased percentage of hepatocytes in the cell cycle S phase. The increase at 24 h in S1 population in rats pretreated with DMDP + TA was significantly (P < 0.05) different compared with that of the TA group (18.07% vs 8.57%). Hepatocytes increased their proliferation as a result of these changes. Also, TNF-α expression and serum level were increased in rats pre-treated with DMDP. Thus, DMDP pre-treatment reduced TA-induced liver injury and accelerated postnecrotic liver regeneration. CONCLUSION: These results demonstrate that Kupffer cells are involved in TA-induced liver, as well as in post-necrotic proliferative liver states.

An unexpected reaction of cyanothioacetamide:Novel preparation of pyrazolo[3,4-b]-pyridine derivatives under MWI

An unexpected multi-component reaction of cyanothioacetarnide with aldehyde and aminopyrazole under MWI was reported. Through this reaction, a series of pyrazolo[3,4-b]-pyridine derivatives was prepared in high yields via simple operational procedure.

Endotoxins enhance hepatocarcinogenesis induced by oral intake of thioacetamide in rats

AIM To clarify whether endotoxin is of pathogenic importance for hepatocarcinogenesis, or the increased cancer risk results solely from the cirrhotic process. METHODS The rat model of hepatoma was treated by the intake of 0 03% thioacetamide in drinking water for six months. During induction of hepatoma, rats were additionally treated with splenectomy and/or lipopolysaccharide administration. The liver nuclear DNA index and proliferation index were quantitatively analyzed by flow cytometry. Hepatic histology was examined with light and electron microscopes. Plasmic endotoxin concentration and γ glutamyl transpeptidase activity were measured, and hepatoma incidence was recorded. RESULTS Thioacetamide induced cirrhosis and hepatoma in Wistar rats with histology or regenerative nodule, fibrosis and neoplastic foci were quite similar to the pathogenic process of human cirrhosis leading to hepatoma. In comparison with TAA controls (DNA index: 1 15±0 21), exo endotoxin increased the DNA index by 7 8% (1 24±0 25, P <0 02) and hepatoma rate by 16 7. Splenectomy induced enteric endotoxemia increased the DNA index by 25% (1 44±0 15, P <0 01) and hepatoma rate by 33%. A summation of the effects of these two factors increased the DNA index by 36% ( P <0 01)and hepatoma incidence by 50%, moreover, the level of endotoxemia showed a close relation with DNA index ( r =0 96, P <0 01), as well as with the occurrence rate of hepatoma ( r =0 00, P <0 01). Histological findings further verified such alterations. CONCLUSION Lipopolysaccharide administration and/or splenectomy induced enterogenic endotoxemia may enhance rat hepatocarcinogenesis induced by oral intake of thioacetamide.