涂层粉末形成的固结材料及其生产方法

本发明涉及由几种涂层粉末形成的固结材料，在通过互相结合具有一定性能的粉末颗粒，形成一种模制品时，可以使粉末颗粒具有要求的排列方向，或可以以这样的预定的距离排列，以使固结材料达到所要求的性能。在粉末颗粒上有厚度0.01～20μm均匀涂膜，或者粘附各含有基体颗粒的粉末，在粉末颗粒上有多层涂膜，每层厚度均匀，为0.01～5μm，其中至少任何相邻的涂膜是不同类的，该粉末颗粒在涂膜处或通过粘合剂固结在一起，固结材料的特性归因于在其上有涂膜的粉末颗粒的特性，本发明也公开了一种由涂层粉末颗粒形成固结材料的方法。(专利申请号：97199239.8；公开号：CN1235567A；发明人：中∴胜人等；申请人：日铁矿业株式会社等；地址：日本东京都)。     

高能球磨（B4C）p／6061Al复合粉末特征

研究了高能球磨法制备的（Ｂ４Ｃ）ｐ／６０６１Ａｌ复合粉末中Ｂ４Ｃ颗粒的形貌，粒度以及在铝基体中的分布情况等，试验结果表明，高能球磨法是集改变增强颗粒形貌，控制增强体颗粒粒度，改善增强体颗粒分布均匀性和增强体与基体之间界面结合的有效方法，复合粉末Ｂ４Ｃ颗粒近似呈球形，弥散均匀分布于铝基体中，多数颗粒的粒度在亚微米范围内，并且颗粒粒度越小，分布越均匀。     

高能球磨(B_4C)_p/6061A1复合粉末特征

研究了高能球磨法制备的（Ｂ４Ｃ）ｐ／６０６１Ａｌ复合粉末中Ｂ４Ｃ颗粒的形貌、粒度以及在铝基体中的分布情况等。试验结果表明，高能球磨法是集改变增强体颗粒形貌、控制增强体颗粒粒度、改善增强体颗粒分布均匀性和增强体与基体之间界面结合的有效方法。复合粉末中Ｂ４Ｃ颗粒近似呈球形，弥散均匀分布于铝基体中，多数颗粒的粒度在亚微米范围内，并且颗粒粒度越小，分布越均匀。     

用喷雾干燥法制备PSZ-3Y粉末颗粒的形貌研究

用激光衍射法和SEM（Scanning Electron Microscope)法研究了喷雾干燥法制备PSZ-3Y粉末的粒度分布和形貌特征，表明用传统法制备的PSZ-3Y虽然可以获得细颗粒粉末，但是团聚非常严重，分散性能和流动性都很差，而用喷雾干燥法制备的PSZ-3Y粉末和造粒可以获得粒度分布均匀，流动性和分散性好的不团聚的球状颗粒。粉末的形貌与其采用的制粉原料的组成形态和工艺关系不大，但从原粉中喷雾制粒获得粉末的颗粒表面较粗糙和有小裂纹，其分布性能比直接喷雾粉末颗粒性能好。     

粘结剂和分散剂对喷雾干燥PSZ-3Y粉末性能的影响

用激光衍射法(Laser Diffractometry)、SEM(Scanning Electron Microscope)和BET(Brunner-Emmett-Feller method)法研究了．喷雾干燥法制备PSZ-3Y粉末的过程中添加粘结剂和分散剂对粉末颗粒的分布和形貌的影响。结果表明：在喷雾干燥中，通过高速高压的离心作用，可以改变粉末的形貌，获得球状的颗粒；而添加粘结剂和分散剂起着粘合和隔离的作用，使粉末颗粒分散。因此，采用喷雾干燥技术，添加合适的粘结剂和一定量的分散剂，就能制备粒度分布均匀、不团聚、分散性能好的球状颗粒。颗粒表面布满了许多细小的空洞，似棉花状的聚合物，晶粒很细小。     

电弧等离子法球化镍粉的研究

粉末颗粒的形状是粉末性质的一项重要指标。粉末制品的强度、透过性以及性能的均匀性都与粉末颗粒形状有关。球形粉末流动性好、松装密度大,广泛用于核燃料、多孔材料、研磨材料以及喷涂材料等方面。球     

热等静压制备粉末高温合金原始颗粒边界研究现状

粉末高温合金作为先进高温材料被广泛应用于航空航天领域。热等静压（hot isostatic pressing,HIP）是粉末高温合金构件的制备方法之一，但是原始颗粒边界（prior particle boundaries,PPBs）的存在会极大的影响构件的性能。本文综述了热等静压制备粉末高温合金原始颗粒边界的研究现状，概述了原始颗粒边界的形成机理及其影响，总结了粉末高温合金中原始颗粒边界的消除方法，并对这些方法应用的可行性及有效性进行了分析和展望。原始颗粒边界的消除方法主要包括向粉末添加Hf、Nb等强碳化物形成元素，对粉末进行预热处理，真空动态脱气处理或等离子体滴凝处理；优化粉末制备工艺，选用纯度更高、尺寸分布更均匀的粉末；选用合适的热等静压工艺参数和工艺方式；对制件采取热挤压、退火、固溶处理和热等静压后处理等。     

过程控制剂对Al2O3/Mo复合粉末细化的影响

采用溶胶一凝胶技术制备Al2O3/Mo复合粉末,研究了过程控制剂(PCA)——硬脂酸和无水乙醇对Al2O3/Mo复合粉末细化的影响.利用X射线衍射仪和扫描电镜对复合粉末进行物相和形貌分析,利用激光粒度分布测试仪测试了粉末的粒度分布.结果表明:添加过程控制剂可以有效降低粉末粘球和结块的现象,提高出粉率;不添加过程控制剂时,粉末颗粒大小极不均匀;以硬脂酸和无水乙醇作PCA时,随着球磨时间的延长,Al2O3/Mo复合粉末逐渐被细化,颗粒大小相对均匀,颗粒形态经历了从球状向片状再到球形的转化,其中以无水乙醇作PCA时,粉末被细化的速率较高.以硬脂酸作PCA最终制得的粉末较以无水乙醇作PCA最终得到的粉末,粒度分布较为均匀,且细小颗粒的粒径分布较多.     

用活性氧化钨制取中细W和WC工艺研究

利用活性氧化钨粉末细、表面能发达、活性高、相成分单一等特点，经过工艺试验和优化，生产出粒度分布较用蓝色氧化钨生产的中细钨、碳化钨粉末均匀，同时也减少了中细钨、碳化钨粉末中的粗大晶粒和聚集颗粒，从而提高了中细钨、碳化钨粉末的质量，并且利用此碳化钨粉末还可以生产出高质量的合金产品。     

粉体粒径级配比对粉末冶金SiC_p/6061Al复合材料组织与性能的影响

选择不同粒径的6061Al粉末和SiC颗粒,采用真空热压法制备含35%SiC体积分数的SiCp/6061Al复合材料,研究不同级配比对复合材料显微组织和抗拉强度的影响。结果表明:复合粉末的粒径级配比可影响复合材料的微观组织和力学性能;当增强体颗粒粒径为15μm时,随基体6061粉末与SiC颗粒粒径比降低,SiC颗粒在复合材料中的分布越来越均匀,抗拉强度提高;当基体6061Al粒径为10μm时,随SiC颗粒粒径减小,复合材料微观组织的均匀性降低,但抗拉强度提高。并建立了理想的复合粉末颗粒分布模型,模型的理论计算结果与Slipenyuk公式计算结果接近。     

Genotoxic activity of 1-chloromethylpyrene in stomach epithelium in vivo: insensitivity of the stomach scintillation UDS assay

An acknowledged weakness of current testing programmes for genotoxic hazard has been the potential insensitivity of the established mouse bone marrow micronucleus test and rat liver unscheduled DNA synthesis (UDS) assays to direct-acting or short-lived mutagens, which may be consumed at the site of initial contact. In such cases, in vivo test systems sampling tissues such as the skin or the stomach would provide valuable data. To test these principles a stomach UDS assay was evaluated using the potent locally active mutagen 1-chloromethylpyrene (1-CMP). Contrary to expectations, no UDS response was observed 16 h following 1-CMP dosage by oral gavage. To confirm the integrity of the 1-CMP used for the stomach UDS assay, a sample of the stored chemical was re-evaluated in vitro and shown to be still strongly positive in the Ames assay and to have alkylating activity at least 15 min after incubation at stomach acid pH. No UDS response was observed when test dose levels were reduced or when earlier sampling times were used. Other genotoxic endpoints were examined in stomach. 32P-Postlabelling analysis revealed high levels of adduct formation in gastric DNA. An assay utilizing electrophoresis of DNA (the comet assay) showed the occurrence of DNA damage following dosing with 1-CMP in vivo. These positive results confirmed that 1-CMP should be regarded as a potential in vivo genotoxin. The failure to detect a UDS response to 1-CMP in stomach was investigated; a strong UDS response was observed in an in vitro hepatocyte UDS assay of 1-CMP indicating that the rat was capable of repairing 1-CMP-derived DNA adducts. Pretreatment of rats with hydroxyurea depressed the level of incorporation of thymidine into DNA both in negative and positive [methyl-N-nitrosoguanidine (MNNG)] controls. The results of these studies indicated that the protease digestion method employed did not selectively or efficiently sample those cells with any UDS response to 1-CMP or MNNG, and the activity seen for the latter was most likely due to the presence of S phase cells within the digests. As a result of the finding that UDS responses were not demonstrated for the potent direct-acting mutagens 1-CMP and MNNG, the protease digestion/scintillation method for stomach UDS does not appear to have general value in a screening programme for locally active genotoxic agents.     

Prevalence of upper abdominal complaints and their effect on the quality of life and utilization of medical resources. Swiss Primary Care Group

The authors present the results obtained in Switzerland, as part of an international survey (DIGEST), on 3 months' prevalence of upper digestive symptoms (UDS) and their influence on quality of life and consumption of medical services. 514 randomized adults from the general population in 8 different cities were interviewed. In these interviews data were recorded concerning demographic and socio economic aspects, quality of life, severity and frequency of UDS, consultations and medication. The sub-population with relevant UDS (i.e. UDS at least once a week and/or of moderate to severe degree) was compared with the rest of the population interviewed. 19% of the interviewees reported relevant UDS; of these, two thirds were women. No differences were found between people with and without UDS as far as education, professional activities, consumption of alcohol or smoking are concerned. The most frequent symptoms reported were fullness, bloating and nausea. However, daily activities were most impaired by nausea, epigastric pain and heartburn. Interviewees with UDS more frequently reported "life events" in the preceding year (48% vs 33%). Interviewees with UDS also more frequently reported back pain (7% vs 2%) and migraine (10% vs 6%). Furthermore, more interviewees with UDS reported sick leave (11% vs 3%); they also had a poorer life quality score (74 vs 89, PGWBI), reported more medical visits (50% vs 19%) and consumed more medication, both prescribed (65% vs 25%) and non-prescribed (OTC: 70% vs 31%).     

Contribution of serum protein association to discrepancy between the in vivo and in vitro UDS results for 6,7-dimethyl-2,4-di-1-pyrrolidinyl-7H-pyrrolo[2,3-d]pyrimidine (U-89843)

U-89843 has been shown to undergo biotransformation, both in vitro and in vivo, to form U-97924 as a major primary metabolite. U-89843 was found to be positive in an in vitro UDS mutagenesis screen conducted with primary rat hepatocytes in serum-free media. In contrast to in vitro results, no evidence of genetic toxicity of U-89843 was observed in rats in the in vivo/in vitro version of the UDS test with single oral doses up to 1400 mg/kg. The negative results may be related to more robust in vivo detoxification mechanisms or relatively lower exposure to reactive metabolites formed by bioactivation of U-89843 as compared to that observed in the serum-free in vitro hepatocyte test system. Further studies showed rat serum suppressed the in vitro metabolism of U-89843 as well as the formation of the corresponding hydroxylated metabolite, U-97924, the putative precursor of proposed reactive electrophilic metabolite. The measured in vivo systemic clearance of U-89843 (0.53 l/h/kg) in rats was about 1000-fold slower than the in vitro intrinsic clearance (606 l/h/kg) estimated by measuring the formation of U-97924 in rat liver microsomal incubations. Since U-89843 is extensively associated with serum proteins a poor extraction ratio into the liver may account for the slower biotransformation of U-89843 in vivo as compared to that exhibited in in vitro serum-free hepatocyte incubations. Addition of bovine serum albumin (1-40 mg/ml) to the in vitro UDS assay medium decreased the UDS mean net grains per nucleus response of U-89843. These results suggest that the effect of serum protein should be considered when comparing serum-free in vitro UDS and in vivo UDS results for highly serum protein bound compounds.     

Modulation of DNA repair by various inhibitors of DNA synthesis following 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induced DNA damage

The tobacco specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is present in tobacco smoke and is hepatocarcinogenic in rats. Its bioactivation in rat hepatocytes leads to methylation and pyridyloxobutylation of DNA. Rat hepatocytes were cultured in serum-free William medium E on collagen-coated dishes. We demonstrated that some enzymes of the base and/or excision-repair pathways were involved in repair of NNK-induced DNA damage, measured by [methyl-3H] thymidine incorporation. Unscheduled DNA synthesis (UDS) induced by N-methyl-N-nitrosourea (MNU), NNK, N'-nitrosonornicotine (NNN) and 4-(acetoxymethylnitrosamino)-1-(3-pyridyl)-1-butanone (NNKOAc) increased 2.9-, 2.8-, 1.5- and 3.5-fold, respectively, suggesting that methylated and/or pyridyloxobutylated-DNA by these four nitroso compounds is repaired by the excision pathway. Moreover, levels of NNK-induced UDS were dose (1-3 mM) and time (1-18 h) dependent. Enzymes involved in the excision repair pathways were selectively inhibited. Inhibitors of DNA topoisomerase I (camptothecin) and topoisomerase II (etoposide, nalidixic acid) did not decrease the induction of UDS, suggesting that topoisomerases are not involved in the repair of NNK-induced damage. While aphidicolin and arabinocytidine (DNA polymerase alpha, delta, epsilon inhibitors) totally inhibited NNK- and NNKOAc-induced UDS, dideoxythymidine (DNA polymerase beta inhibitor) inhibited NNK- and NNKOAc-induced UDS by 40 and 33%, respectively. We conclude that DNA polymerase alpha, delta or epsilon and to a lesser degree polymerase beta are involved in the repair of pyridyloxobutylated DNA. Previous studies showed that inhibition of poly(ADP-ribosyl) polymerase (PARP) by 3-aminobenzamide (3-ab) facilitated DNA ligation. Our results demonstrate that 3-ab increased NNK-induced UDS, but does not affect NNKOAc-induced UDS. These observations suggest that the ligation step is rate limiting in the repair of methylated DNA but not of pyridyloxobutylated DNA.     

Lack of effect of piperonyl butoxide on unscheduled DNA synthesis in precision-cut human liver slices

In this study the effect of piperonyl butoxide (PBO) on unscheduled DNA synthesis in precision-cut human liver slices has been examined. Liver slices prepared from tissue samples from five human donors were cultured in medium containing [3H]thymidine and 0-2.5 mM PBO using a dynamic organ culture system. After 24 h the liver slices were processed for autoradiographic examination of UDS. As positive controls, liver slices were also cultured with three known genotoxic agents, namely 2-acetylaminofluorene (2-AAF), aflatoxin B1 (AFB1) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). UDS was quantified as the net grain count in centrilobular hepatocytes and as the percentage of centrilobular hepatocyte nuclei with > 5 and > 10 net grains. Compared to control liver slice cultures PBO had no effect on UDS. In contrast, treatment with 0.02 and 0.05 mM 2-AAF, 0.002 and 0.02 mM AFB1 and 0.005 and 0.05 mM PhIP produced significant increases in net grain counts of centrilobular hepatocytes. The greatest induction of UDS was observed in liver slices treated with 0.05 mM PhIP. Treatment with 2-AAF, AFB1 and PhIP also produced increases in the number of centrilobular hepatocyte nuclei with > 5 and > 10 net grains. At the concentrations examined neither PBO, 2-AAF nor PhIP had any significant effect on replicative DNA synthesis in 24 h cultured human liver slices. In cultured liver slices treated with 0.02, but not 0.002, mM AFB1 a significant reduction in the rate of replicative DNA synthesis was observed. These results demonstrate that PBO does not induce UDS in cultured human liver slices. However, all three positive control compounds produced marked significant increases in UDS, thus confirming the functional viability of the human liver slice preparations used in this study. In conclusion, these results provide further evidence that PBO is a non-genotoxic agent which does not damage DNA in human liver.     

Features of DNA repair during chronic exposure to mutagenic factors

Long-time in vivo influence of chemical mutagens in low doses can decrease the level of unscheduled DNA synthesis (UDS) induced in human as well as in laboratory mammals. The phenomenon under investigation is not specific neither for chronically acting mutagens nor for challenging agent. A decrease in UV- and gamma-ray-induced UDS was registered after chronic irradiation in plant populations and also in Chernobyl ameliorators and inhabitants of radioactively contaminated regions. The observed effect seems to have general biological character.     

Contingency management for accurate predictions of urinalysis test results and lack of correspondence with self-reported drug use among polydrug abusers.

Contingency management procedures have proven effective in the treatment of drug-dependent patients. These procedures, however, often require frequent urine testing, which is too costly for community treatment programs. To make urine testing procedures more cost effective, the feasibility of reinforcing accurate predictions of urine drug screen (UDS) results was evaluated. Participants made extremely accurate UDS predictions, particularly when they made drug-positive predictions, regardless of whether predictions were reinforced. However, self reports of recent drug use had poor correspondence with predictions of UDS results. Results suggested that if programs only tested samples predicted to be drug free, considerable cost savings could be incurred. Further research is needed to determine if validity would be enhanced by using a proportion of costs saved to provide nominal reinforcement when samples were verified to be drug free. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of areca nut, inflorescence piper betle extracts and arecoline on cytotoxicity, total and unscheduled DNA synthesis in cultured gingival keratinocytes

Betel quid (BQ) chewing has a strong correlation with oral leukoplakia, submucous fibrosis and oral cancer. For elucidation of its pathogenesis, we investigated the effects of areca nut (AN) and inflorescence piper betle (IPB) extracts and arecoline on the growth, total DNA synthesis (TDS) and unscheduled DNA synthesis (UDS) of cultured human gingival keratinocytes (GK). Arecoline and AN extract suppressed the growth of GK over 5 days of incubation in a dose-dependent fashion. At concentrations of 100, 200 and 400 microg/ml, AN extract suppressed the growth of GK by 31%, 46% and 90%, respectively. The IPB extracts exerted less inhibitory effect on the growth of GK. IPB extract (200-400 microg/ml) decreased cell numbers by 20-40% over 5 days of incubation. Moreover, at a concentration of 0.1, 0.2 and 0.4 mM, arecoline suppressed cell growth by 44%, 77% and 96%, respectively. However, only AN extract induced TDS and UDS in cultured GK within 6 h of exposure. Induction of UDS by AN extract was concomitant with the presence of apparent intracellular vacuolization. Arecoline was also toxic to GK, but did not induce intracellular vacuolization. At a concentration range of 200-1600 microg/ml, AN extract induced TDS by 2.1- to 6.5-fold. Furthermore, at a concentration of 400-1600 microg/ml, AN extract elevated the UDS by 2.4- to 5.5-fold more than that of untreated control. On the contrary, IPB extract (200-1600 microg/ml) and arecoline (0.2-1.6 mM) inhibited the TDS and UDS of GK to a different extent. Simultaneous exposure of confluent GK to AN extract, IPB extract and arecoline for 1 to 5 days led to different degrees of cytotoxicity that was dose- and time-dependent. These results indicate that AN, IPB and arecoline take part in the pathogenesis of BQ chewing-related oral mucosal lesions, possibly through both genotoxic and non-genotoxic mechanisms.     

Unscheduled DNA synthesis and mitochondrial DNA synthetic rate following injury of the facial nerve

Unscheduled DNA synthesis (UDS) of nuclear DNA and mitochondrial (mt) DNA synthetic rates were determined autoradiographically in different cell types of the rodent brain 14 days after unilateral facial nerve transection. In addition to an increased synthetic rate of mtDNA in facial motoneurons 12 h after axotomy, a significant increase of UDS, i.e., DNA repair, and mtDNA synthesis were found in the regenerating facial nucleus 4 days after axotomy. Specificity of the observed labeling was confirmed by injection of 3H2O instead of [3H]thymidine. Using electron microscopic autoradiography, it was further shown that cytoplasmic labeling of neurons was mainly due to incorporation of radioactive label into mitochondria, indicating their subsequent multiplication by division. The observation that Northern blot signals for O6-alkylguanine-DNA-alkyltransferase mRNA from homogenized facial nuclei of both the axotomized and normal side remained unchanged over 14 days after axotomy indicated that the observed DNA-repair activity was not caused by endogenously produced alkylating agents. The combined presence of transiently increased UDS, enhanced mtDNA synthesis and elevated protein synthetic rates of regenerating motoneurons (as shown in the literature) suggests that free radicals produced by mitochondria in injured nerve cells could cause unspecific DNA damage followed by immediate repair.     

Carbamazepine in the treatment of cocaine dependence: Subtyping by affective disorder.

Studies investigating carbamazepine (CBZ) in the treatment of cocaine dependence have been inconsistent. In this study, cocaine-dependent individuals with (n=57) and without (n=82) affective disorder were compared in a 12-week, double-blind, placebo-controlled trial. Urine drug screens (UDS) and self-report of drug use were collected weekly. Affective symptoms were measured monthly. Subjects receiving CBZ attended more medication sessions (p=.03). The CBZ-treated affective group had a trend toward fewer cocaine-positive UDS (p=.08) and a significantly longer time to first cocaine use (p=.06). CBZ treatment did not have any impact on cocaine use in individuals without affective disorders. (PsycINFO Database Record (c) 2010 APA, all rights reserved)