Kinetics of 2-Methyl-6-acetyl-naphthalene Liquid Phase Catalytic Oxidation

In this paper, a kinetics model for the liquid-phase oxidation of 2-methyl-6-acetyl-naphthalene to 2,6-naphthalene dicarboxylic acid catalyzed by cobalt-manganese-bromide is proposed. The effects of the reaction temperature, catalyst concentration and ratio of catalyst on the lime evolution of the experimental concentration for the constituents including raw material, intermediates and product are investigated. The model parameters are determined in a nonlinear optimization, minimizing the difference between the simulated and experimental time evolution of the product composition obtained in a semi-batch oxidation reactor where the gas and liquid phase were well nuxed. The kinetics data demonstrate that the model is suitable to the liquid-phase oxidation of 2-methyl-6-acetyl-naphthalene to 2,6-naphthalene dicarboxylic acid.

Enhanced autophagic clearance of amyloid-βvia histone deacetylase 6-mediated V-ATPase assembly and lysosomal acidification protects against Alzheimer's disease in vitro and in vivo

Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.

Measurement and Correlation for Solubility of Dimethyl-2,6-naphthalene Dicarboxylate in Organic Solvents

Solubility of dimethyl-2,6-naphthalene dicarboxylate in acetic acid, N,N-dimethylfonnamide, N,N-dimethyl acetamide, dimethyl sulphoxide, and N-methyl-2-ketopyrrolidine were determined using a dynamic method. The measured systems were correlated by UNIFAC group contribution method. A new main group （aromatic ester, ACCOO） was defined to express the activity coefficients of the aromatic ester. New interaction parameters of the ACCOO group were expressed as the first-order function of temperature and were determined from the experimental data. The calculated results for the new interaction parameters were satisfactory. The measured systems were also correlated with the Wilson and 2-h models, and the results were compared with those of the UNIFAC model.

Synthesis of Dimethyl-2,6-Naphthalene Dicarboxylate by Esterification Catalyzed by Sodium Tungstate

The process of synthesis of dimethyl-2,6-naphthalene dicaboxylate from esterification of 2,6-naphthalene dicarboxylic acid (2,6-NDCA) by methanol using sodium tungstate as catalyst was investigated. The orthogonal tests method was used for optimizing the process factors. The effects of reaction temperature, mass percentage of catalyst, reaction time and mass ratio of methanol to 2,6-NDCA on the 2,6-NDCA conversion were investigated. It was found that all the four factors had significant effect on the conversion. The optimum reaction conditions were reaction temperature 215 ℃,mass percentage of catalyst 3%, reaction time 3 h, mass ratio of methanol to 2,6-NDCA 6∶1. The 2,6-NDCA conversion at above condition was 92.80%.

Hepatic steatosis is associated with dysregulated cholesterol metabolism and altered protein acetylation dynamics in chickens

Background Hepatic steatosis is a prevalent manifestation of fatty liver, that has detrimental effect on the health and productivity of laying hens, resulting in economic losses to the poultry industry. Here, we aimed to systematically investigate the genetic regulatory mechanisms of hepatic steatosis in laying hens.Methods Ninety individuals with the most prominent characteristics were selected from 686 laying hens according to the accumulation of lipid droplets in the liver, and were graded into three groups, including the control, mild hepatic steatosis and severe hepatic steatosis groups. A combination of transcriptome, proteome, acetylome and lipidome analyses, along with bioinformatics analysis were used to screen the key biological processes, modifications and lipids associated with hepatic steatosis.Results The rationality of the hepatic steatosis grouping was verified through liver biochemical assays and RNA-seq. Hepatic steatosis was characterized by increased lipid deposition and multiple metabolic abnormalities. Integration of proteome and acetylome revealed that differentially expressed proteins(DEPs) interacted with differentially acetylated proteins(DAPs) and were involved in maintaining the metabolic balance in the liver. Acetylation alterations mainly occurred in the progression from mild to severe hepatic steatosis, i.e., the enzymes in the fatty acid oxidation and bile acid synthesis pathways were significantly less acetylated in severe hepatic steatosis group than that in mild group(P < 0.05). Lipidomics detected a variety of sphingolipids(SPs) and glycerophospholipids(GPs) were negatively correlated with hepatic steatosis(r ≤-0.5, P < 0.05). Furthermore, the severity of hepatic steatosis was associated with a decrease in cholesterol and bile acid synthesis and an increase in exogenous cholesterol transport.Conclusions In addition to acquiring a global and thorough picture of hepatic steatosis in laying hens, we were able to reveal the role of acetylation in hepatic steatosis and depict the changes in hepatic cholesterol metabolism. The findings provides a wealth of information to facilitate a deeper understanding of the pathophysiology of fatty liver and contributes to the development of therapeutic strategies.

IL-17 induces NSCLC cell migration and invasion by elevating MMP19 gene transcription and expression through the interaction of p300-dependent STAT3-K631 acetylation and its Y705-phosphorylation

The cancer cell metastasis is a major death reason for patients with non-small cell lung cancer(NSCLC).Although researchers have disclosed that interleukin 17(IL-17)can increase matrix metalloproteinases(MMPs)induction causing NSCLC cell metastasis,the underlying mechanism remains unclear.In the study,we found that IL-17 receptor A(IL-17RA),p300,p-STAT3,Ack-STAT3,and MMP19 were up-regulated both in NSCLC tissues and NSCLC cells stimulated with IL-17.p300,STAT3 and MMP19 overexpression or knockdown could raise or reduce IL-17-induced p-STAT3,Ack-STAT3 and MMP19 level as well as the cell migration and invasion.Mechanism investigation revealed that STAT3 and p300 bound to the same region(−544 to−389 nt)of MMP19 promoter,and p300 could acetylate STAT3-K631 elevating STAT3 transcriptional activity,p-STAT3 or MMP19 expression and the cell mobility exposed to IL-17.Meanwhile,p300-mediated STAT3-K631 acetylation and its Y705-phosphorylation could interact,synergistically facilitating MMP19 gene transcription and enhancing cell migration and invasion.Besides,the animal experiments exhibited that the nude mice inoculated with NSCLC cells by silencing p300,STAT3 or MMP19 gene plus IL-17 treatment,the nodule number,and MMP19,Ack-STAT3,or p-STAT3 production in the lung metastatic nodules were all alleviated.Collectively,these outcomes uncover that IL-17-triggered NSCLC metastasis involves up-regulating MMP19 expression via the interaction of STAT3-K631 acetylation by p300 and its Y705-phosphorylation,which provides a new mechanistic insight and potential strategy for NSCLC metastasis and therapy.

组蛋白脱乙酰酶1基因抑制人脐静脉内皮细胞焦亡并减轻动脉粥样硬化及炎性反应

背景:细胞焦亡作为炎症细胞死亡的一种独特形式,在动脉粥样硬化病变的不稳定性中发挥重要作用。目的:探究重组B细胞淋巴瘤2相关蛋白A1(B-cell lymphoma 2-related protein A1,BCL2A1)在动脉粥样硬化中的作用机制。方法:①使用200μg/mL氧化低密度脂蛋白处理人脐静脉内皮细胞24 h以诱导内皮损伤。随后,分别使用50 nmol/L BCL2A1干扰质粒(sh-BCL2A1)和1.5μg/mL组蛋白脱乙酰酶1基因(histone deacetylase 1 gene,HDAC1)过表达载体(pcDNA-HDAC1)转染人脐静脉内皮细胞,或同时转染pcDNA-HDAC1和BCL2A1过表达载体(pcDNA-BCL2A1)。转染后培养48 h检测BCL2A1和HDAC1的表达水平、细胞活力、细胞焦亡水平以及BCL2A1乙酰化水平。②通过高脂喂养APOE-/-小鼠构建动脉粥样硬化小鼠模型进行体内验证。将500μL BCL2A1和HDAC1慢病毒过表达载体分别或同时尾静脉注射到小鼠体内,检测BCL2A1和HDAC1的表达水平以及小鼠动脉组织损伤情况。结果与结论:氧化低密度脂蛋白诱导的人脐静脉内皮细胞中BCL2A1上调,干扰BCL2A1可改善细胞活力并抑制细胞焦亡和炎症反应。此外,氧化低密度脂蛋白诱导的人脐静脉内皮细胞中HDAC1下调,通过促进BCL2A1去乙酰化提高了细胞活力及抑制了细胞焦亡和炎症反应。体内实验表明,BCL2A1在高脂喂养的小鼠动脉组织中高表达,而HDAC1低表达。此外,HDAC1通过促进BCL2A1去乙酰化减轻了高脂喂养诱导的ApoE-/-小鼠动脉组织病变。结果表明,HDAC1可能通过BCL2A1去乙酰化来抑制人脐静脉内皮细胞焦亡进而减轻动脉粥样硬化和炎症反应。

基于海马区乙酰化蛋白组学探讨原络通经针法对AD模型小鼠记忆损伤的影响

目的:基于海马区乙酰化蛋白组学探讨原络通经针法对阿尔茨海默病(AD)模型小鼠记忆损伤的影响。方法:按照随机数字表法将30只健康雄性昆明种小鼠分为空白组、模型组和针刺组各10只,模型组和针刺组小鼠腹腔注射东莨菪碱溶液[100 mg/(kg·d)],空白组腹腔注射等量的生理盐水,持续注射7d造模。针刺组小鼠采用原络通经针法进行针刺(1次/d),空白组和模型组进行相同时间和程度的捉抓,连续干预30 d。采用Morris水迷宫行为学实验和新物体识别实验检测小鼠记忆能力,采用HE染色观察小鼠海马组织病理损伤情况,采用液相色谱-串联质谱法(LC MS/MS)检测小鼠海马组织中乙酰化修饰蛋白,并对其进行生物学信息分析。结果:与模型组比较,针刺组的逃避潜伏期、逃逸路径长度均明显缩短,第2象限停留时间明显增长,通过原平台位置次数明显增多,识别指数明显增高,差异有统计学意义(P<0.05)。与模型组比较,针刺组小鼠海马组织的病理损伤明显减轻,凋亡细胞明显减少。LC MS/MS分析显示,与空白组及模型组比较,针刺组乙酰化修饰整体水平增高。通过乙酰化蛋白相互作用网络分析筛选出5个关键枢纽蛋白为Hspa8、Rab7a、Nsf、Ezr、Cfl1,模型组中该5个关键枢纽蛋白无乙酰化修饰,而针刺组该5个关键枢纽蛋白发生乙酰化修饰。结论:原络通经针法能有效改善AD模型小鼠记忆损伤,减轻海马区病理损害,可能与海马区关键枢纽蛋白乙酰化修饰有关。

Acetylation of Chinese bamboo flour and thermoplasticity

Chinese bamboo flour was chemically modified by acetylation with acetic anhydride by using trichloroacetic acid as an activation agent and the optimized condition for acetylation of bamboo flour was determined as the trichloroacetic acid amount 6.0 g per 1.5-g bamboo flour, ultrasosonication duration 40 min and the reaction time 1 h at 65℃. The composition, microstructure and thermal behavior of acetylated bamboo flour were preliminarily characterized by FT-IR, DSC and SEM etc. The acetylated bamboo flour can be molded into sheets at 130℃ and 10 MPa, indicating the modified bamboo flour possesses thermalplastic performance.

c-Myc、SIRT1、acetyl-p53在乳腺癌中的表达及其对预后的影响

目的:探讨c-Myc、SIRT1及acetyl-p53蛋白在乳腺癌中的表达及其对预后的影响。方法:应用免疫组织化学方法检测90例乳腺癌和30例乳腺增生症中的c-Myc、SIRT1(Sirtuin type 1)、acetyl-p53蛋白表达,结合临床病理资料和随访资料,进行预后分析。结果:c-Myc阳性组乳腺癌患者的5年无瘤生存率和5年总生存率(分别为5 9.0%/6 7.2%)低于c-M y c阴性组(分别为8 6.2%/8 6.2%),S I RT 1阳性组乳腺癌患者的5年无瘤生存率和5年总生存率(分别为5 6.1%/6 4.9%)低于S I RT 1阴性组(87.9%/87.9%);acetyl-p53阳性组乳腺癌患者的5年无瘤生存率和5年总生存率(分别为86.7%/86.7%)高于acetyl-p53阴性组(分别为58.3%/66.7%),差异均有统计学意义(P<0.05)。结论:c-Myc及SIRT1蛋白高表达的乳腺癌患者预后差,而acetyl-p53蛋白高表达的乳腺癌患者预后好。

RP-HPLC法测定茜草中1,3,6-trihydroxy-2-methylanthraquinone-3-O-[3-O-acetyl-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranoside]的含量

首次采用反相高效液相色谱法测定茜草根中1,3,6-trihydroxy-2-methylanthraquinone-3-O-[3-O-acetyl-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranoside]的含量。色谱柱为Purospher star RP C18色谱柱(250mm×4.6mm,5μm),流动相为甲醇:水:四氢呋喃(65:34.7:0.3),流速为1.0mL/min,检测波长为276nm,柱温为25℃。该方法的线性范围为0.020~0.160μg,r=0.9998,平均回收率为101.5%,RSD为2.0%(n=6)。该方法测定1,3,6-trihydroxy-2-methylanthraquinone-3-O-[3-O-acetyl-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranoside]含量灵敏、准确、重现性好。

合成乙酰水杨酸(acetyl salicylic acid)实验教学研究

乙酰水杨酸的合成是大学生在生物与化工类有机合成中的一个经典性实验。目前各高校常采用王清廉的方法进行实验教学,笔者经多年的实验教学观察,发现学生按照该方法进行该实验时,常出现油状物而没有真正产物生成,或产物为假性产物(经性质检验为水杨酸本身)。另外,该实验即使在具有较好通风设备条件下进行,也会产生较大刺激气味且反应残余物对环境污染较大。为此,笔者从反应条件、器皿等方面着手进行该实验教学研究,并在保证教学双方的成功率、保护环境、节约药品和严格控制教学时间等方面已取得较理想的效果。

一种环烯醚萜甙(8-O-acetyl-shanzhiside methylester)的2D NMR

利用二维核磁共振（2DNMR）技术对从独一味植物中分离的环烯醚萜甙化合物进行1H和13CNMR的归属，并确定其糖与甙的接点。

一种DNA标记配体S-Acetyl-NHS-MAG3的合成研究

报导了S 乙酰基 巯基乙酸N 羟基丁二酰亚胺酯 (SATA) ,S 乙酰基 巯基乙酸三甘氨酸 (S Acetyl MAG3) ,S 乙酰基 巯基乙酸三甘氨酸N 羟基丁二酰亚胺酯 (S Acetyl NHS MAG3)的合成方法 ,用IR和1HNMR对其结构进行了表征 .室验表明 :S 乙酰基 巯基乙酸三甘氨酸与N 羟基丁二酰亚胺在二环己基碳二亚胺 (DCC)的二氯甲烷溶液中 ,在 40～ 5 0℃下反应 2 4h得到S 乙酰基 巯基乙酸三甘氨酸N 羟基丁二酰亚胺酯 (S Acetyl NHS MAG3)的产率较高 ,副产物较少 。

Acetyl-DL-leucine对猫单侧前庭神经切断后运动平衡能力和前庭外侧核神经元放电活动恢复的影响

本文观测了Ａｃｅｔｙｌ－ＤＬ－ｌｅｕｃｉｎｅ（ＡＬ、一种抗眩晕药）对猫单侧前庭神经切断后前庭代偿的影响。结果显示：ＡＬ加快术后猫在转动横梁测试中运动平衡能力的恢复，但抑制去传入前庭外侧核神经元（ｎ＝５０６）静息自发放电频率的恢复。ＡＬ促进放电活动与头部左右摆动体位相关的神经元数量和比例的恢复，从术后的第１周的１０％（ｎ＝４５４），逐渐提高到术后第３周的６０％，第５周的７５％

Removal of siloxanes from biogas using acetylated silica gel as adsorbent

Biogas can be used as an alternative energy source for producing heat and electricity;however, volatile methylsiloxanes(VOSiC) present in biogas can severely damage heat exchangers, turbines and gas engines. Consequently, e cient removal of VOSiC from biogas that is used as a biofuel is required. In this work, acetylated silica gel(Ac@SG) was synthesized,via treatment of microporous silica gel(SG) with acetic anhydride as an adsorbent, for removal of VOSiC from biogas,and characterized with XRD, SEM–EDS, N2-BET and FT-IR. This Ac@SG adsorbent exhibited a meso-/microporous structure and hydrophobic surface, indicating it was a more e cient adsorbent for removing hexamethyldisiloxane(L2) and octamethylcyclotetrasiloxane(D4) from biogas samples than conventional SG. It was found that the adsorption capacities of Ac@SG reached 304 mg L2/g for hexamethyldisiloxane and 916 mg D4/g for octamethylcyclotetrasiloxane at lower temperatures in the experimental range, and water had no significant e ect on its absorption e ciency. The used Ac@SG could be easily regenerated by heating it at 110 °C, and the adsorption capacity of recycled Ac@SG for hexamethyldisiloxane and octamethylcyclotetrasiloxane was kept constant in four recycle adsorption experiments.

p-Toluenesulfonyl chloride as a new and effective catalyst for acetylation and formylation of hydroxyl compounds under mild conditions

The catalytic application of p-toluenesulfonyl chloride for efficient acetylation of various types of alcohols and phenols with acetic anhydride in solvent-free conditions is reported.Also structurally diverse alcohols were formylated using formic acid based on the use of catalytic amount of p-toluenesulfonyl chloride under solvent-free condition.The reactions were carried out in short reaction time and in good to excellent yields at room temperature.

Two new acetylated ginsenosides from the roots of Panax quinquefolium

Two new acetylated ginsenosides, 20（S）-protopanaxatriol-6-O-α-L-rhamnopyranosyl （1 → 2）-β-D-6＇-O-acetylglucopyranoside （1） and 20（R）-protopanaxatrol-6-O-α-L-rhamnopyranosyl （1 → 2）-β-o-6＇-O-acetylglucopyranoside （2）, were isolated from the roots of Panax quinquefolium. The structures were elucidated on the basis of spectroscopic techniques and chemical means.

Combined Detection of Serum Matrix Metalloproteinase 9,Acetyl Heparinase and Cathepsin L in Diagnosis of Ovarian Cancer

Objective： To investigate the clinic values of combining test of serum matrix metalloproteinase 9 （MMP-9）, acetyl heparinase （Hpa） and Cathepsin L （CL） in diagnosis of ovarian cancer. Methods： Serum levels of MMP-9, Hpa and CL were detected in a total of 418 cases, including 217 cases with ovarian malignant tumor, 100 cases with ovarian benign tumor and 101 healthy controls, by using enzyme-linked immunosorbent assay （ELISA）. Their correlation with clinicopathologic feature of ovarian malignant tumor was analyzed and their diagnosis performance was evaluated by receiver operating characteristic （ROC）. The combined diagnosis model was established by logistic regression analysis. Results： The serum levels of MMP-9, Hpa and CL were significantly higher in patients with ovarian malignant tumor than in benign tumor and healthy control, the serum levels of CL and Hpa were higher in epithelial cancer than in non-epithelial tumor, and MMP-9, Hpa and CL were elevated in low grade and advanced stage compared to high grade and early stage. The sensitivity for diagnosis of ovarian malignant tumor from high to low was CL, Hpa and MMP-9, and the specificity was MMP-9, CL and Hpa. The united diagnosis model was established and showed the sensitivity and specificity of combined detection were 84.6% and 82.1%, respectively, which were significantly higher than a single tumor marker. Conclusion： Serum MMP-9, Hpa and CL were correlated with ovarian malignant tumor and the combined detection of which may be valuable for clinical diagnosis of ovarian malignant tumor.

Histone deacetylase inhibitor suberoylanilide hydroxamic acid alleviates liver fibrosis by suppressing the transforming growth factor-β1 signal pathway

Background: Histone deacetylases(HDACs) inhibitors are new anti-fibrotic drugs that inhibit the activity of hepatic stellate cells. The present study focused on the anti-fibrotic function of HDAC inhibitor suberoylanilide hydroxamic acid(SAHA) by suppressing transforming growth factor-β1(TGF-β1) signaling. Methods: Male Sprague-Dawley rats were used to induce liver fibrosis with carbon tetrachloride(CCl 4) and LX2 cell(human hepatic stellate cell line) was stimulated by TGF-β1. Both animals and cells were treated with SAHA. The Smad7 and connective tissue growth factor(CTGF) mRNA levels were detected by real-time polymerase chain reaction(PCR). Western blotting was used to examine the protein levels of CTGF, Histone H3(H3), Smad7, Smad2/3, Acetyl-Histone H3(AH3), HDAC2, α-smooth muscle actin( α-SMA), HDAC6, p-Smad2/3 and HDAC8. In addition, the TGF-β1 and liver enzyme levels from rat serum were detected. Histopathological changes were examined by hematoxylin and eosin(HE), Sirius red and Masson trichrome staining. The α-SMA expression was detected by immumohistochemical staining. Results: Compared with control group, the TGF-β1 and liver enzyme levels from rat serum, together with the mRNA levels of CTGF and protein levels of CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were elevated in fibrotic rats( P < 0.01). But the Smad7 mRNA and AH3 protein levels were notably suppressed in the fibrotic rats( P < 0.01). Pathological examination showed the typical changes of liver fibrosis in the fibrotic rats. After the treatment with SAHA, the levels of liver enzymes, TGF-β1, CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were reduced( P < 0.01) and Smad7 and AH3 protein contents were elevated in liver fibrotic rats( P < 0.01). Moreover, immumohistochemistry showed that SAHA significantly suppressed the α-SMA protein content in fibrotic liver( P < 0.01). Conclusion: The HDAC inhibitor SAHA alleviated liver fibrosis by suppressing the TGF-β1 signaling.