Differential effects of methamphetamine and haloperidol on the control of an internal clock.

Humans and animals process temporal information as if they were using an internal stopwatch that can be stopped and reset, and whose speed is adjustable. Previous data suggest that dopaminergic drugs affect the speed of this internal stopwatch. Using a paradigm in which rats have to filter out the gaps that (sometimes) interrupted timing, the authors found that methamphetamine and haloperidol also affect the stop and reset mechanism of the internal clock, possibly by modulating attentional components that are dependent on the content and salience of the timed events. This is the fist report of both clock and attentional effects of dopaminergic drugs on interval timing in the same experimental setting. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

对氯苯乙酮合成工艺的研究

本工作以新的方法合成了对氯苯乙酮 ,克服了传统合成法的缺点 ,并用重结晶法去除了邻位副产物 ,产品纯度可达 99.5 %以上。     

乙酰柠檬酸三丁酯的合成优化

以柠檬酸三丁酯、乙酸酐和正丁醇为原料,采用催化剂TS-121,以共乙酰化—酯化法合成出乙酰柠檬酸三丁酯,并联产乙酸正丁酯。考察了催化剂用量、原料配比、反应温度、反应时间等因素对反应过程的影响,确定了较佳的操作条件。     

分段醇解均相缩合生产聚乙烯醇缩丁醛

以聚醋酸乙烯(PVAc)和丁醛为原料,采用分段醇解-缩合均相法生产聚乙烯醇缩丁醛(PVB)。系统讨论了反应温度、催化剂用量和物料配比等因素对醇解反应和缩合反应的影响。结果表明:醇解反应较适宜的工艺条件为w(PVAc)=20%(相对于甲醇质量而言),n(NaOH)∶n(PVAc)=0.005∶1,反应温度40℃;缩醛化反应较适宜的工艺条件为m(HCl)∶m[聚乙烯醇(PVA)]=0.3∶1,n(丁醛)∶n(羟基)=1.1∶2,缩醛化反应温度50℃。各阶段最佳反应时间为第一阶段醇解15 min,缩合45 min;第二阶段醇解30 min,缩合60 min;第三阶段醇解50 min,缩合90 min。在最佳工艺条件下生产的PVB,其缩醛基分布均匀,并且其w(缩醛基)≈75%(相对于PVB质量而言)。     

乙酰丙酮比色法测定树脂类皮革化学品中游离甲醛的含量

本文论述了限制皮革化学品中游离甲醛含量的意义以及用乙酰丙酮比色法测定皮革化学品中游离甲醛含量的优越性和操作方法。     

Methane oxidation on alumina supported palladium catalysts: Effect of Pd precursor and solvent

Palladium precursors and solvents were studied for their effects on the activities of alumina-based palladium catalysts in methane combustion and the resistance of the catalysts to thermal aging. The properties of the catalysts were compared with those of a commercial reference. The palladium precursors were Pd(propionate)₂, Pd(acetate)₂ and Pd(acetyl acetonate)₂ and the solvents were acetone, acetic acid, propionic acid and toluene. Catalysts were prepared by the wet impregnation method.Catalysts were characterized by powder X-ray diffraction (XRD), field emission scanning electron microscopy (FE-SEM) and energy dispersive X-ray spectroscopy (EDS). The surface areas were measured by Brunauer–Emmett–Teller method (BET). Acidity of the alumina support was measured by NH₃ desorption. Activities of the catalysts in methane oxidation were screened under lean burn conditions.In methane oxidation with fresh catalyst, the best performance was obtained with a combination of Pd(acetate)₂ and acetic or propionic acid. The light-off temperatures of the fresh catalysts (562 K and 557 K, respectively) were slightly lower than the light-off temperature (567 K) of the commercial reference. Differences between the light-off temperatures of the aged and fresh catalysts were least when the catalysts were prepared with Pd(acetyl acetonate)₂ as Pd precursor and in acetic or propionic acid as solvent: +12 K and +18 K, respectively. The corresponding value for the reference was +64 K. For several of the fresh catalysts, conversion in methane oxidation at 623 K was over 90%. A comparison of methane combustion and NH₃ desorption results indicated that acidity of the support material affects catalysts activity.     

乙酰吗啉的合成

以吗啉和乙酰氯为原料合成农药中间体乙酰吗啉 ,反应条件温和 ,收率在 94 %以上 ,产品纯度 >95 %     

全基团保护法制备三氯蔗糖的研究

全基团保护法包括蔗糖 8个羟基团的完全保护、蔗糖 3个伯羟基的去保护作用、4 C位乙酰基向 6 C的迁移、对特定游离羟基团的氯化与脱除剩余保护基团等 5个步骤。其中 ,若采用碱性乙酰基迁移法 ,则乙酰基迁移与氯化反应 2步可合并为 1步。通过大量的试验 ,确定了具体的制备路线与各反应步骤之间的适宜组合方案 ,优化各种工艺参数 ,使三氯蔗糖终产品的得率达到 2 8 1 %。     

Norepinephrine Protects against Methamphetamine Toxicity through β2-Adrenergic Receptors Promoting LC3 Compartmentalization

Norepinephrine (NE) neurons and extracellular NE exert some protective effects against a variety of insults, including methamphetamine (Meth)-induced cell damage. The intimate mechanism of protection remains difficult to be analyzed in vivo. In fact, this may occur directly on target neurons or as the indirect consequence of NE-induced alterations in the activity of trans-synaptic loops. Therefore, to elude neuronal networks, which may contribute to these effects in vivo, the present study investigates whether NE still protects when directly applied to Meth-treated PC12 cells. Meth was selected based on its detrimental effects along various specific brain areas. The study shows that NE directly protects in vitro against Meth-induced cell damage. The present study indicates that such an effect fully depends on the activation of plasma membrane β2-adrenergic receptors (ARs). Evidence indicates that β2-ARs activation restores autophagy, which is impaired by Meth administration. This occurs via restoration of the autophagy flux and, as assessed by ultrastructural morphometry, by preventing the dissipation of microtubule-associated protein 1 light chain 3 (LC3) from autophagy vacuoles to the cytosol, which is produced instead during Meth toxicity. These findings may have an impact in a variety of degenerative conditions characterized by NE deficiency along with autophagy impairment.     

Deficient Strategic Control of Verbal Encoding and Retrieval in Individuals With Methamphetamine Dependence.

Methamphetamine (MA) dependence is associated with deficits in episodic verbal memory, but the cognitive mechanisms underlying such impairments are not known. The authors evaluated a component process model of episodic verbal memory in 87 persons with MA dependence (MA+) and 71 demographically similar non-MA-using controls (MA-). Compared with MA- controls, MA+ participants demonstrated deficient overall learning, free recall, and utilization of semantic clustering, as well as higher rates of repetitions and intrusions. No between-groups differences were evident on measures of serial clustering, retention, or recognition discrimination. Taken together, these findings indicate that MA dependence is associated with deficient strategic (i.e., executive) control of verbal encoding and retrieval, which is consistent with the sequelae of MA-related prefronto-striatal circuit neurotoxicity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)