东北朝鲜族村新农村建设中的问题与对策

东北朝鲜族村在新农村建设中取得了明显的成效,但是,也存在较大的问题。其问题不是新农村建设初级阶段的问题,是前进发展中的问题。东北朝鲜族村新农村建设中存在突出问题表现在发展不平衡问题、空巢化问题、民族自身发展问题、经济发展等问题。解决这些问题的对策是大力加强新集体经济体制的培育;以经济发展为首要任务,着力推进产业化发展;加快朝鲜族新聚居区的建设。     

Effects of a Solution-Focused Program on the Reduction of Aggressiveness and the Improvement of Social Readjustment for Korean Youth Probationers

ABSTRACT

The purpose of this investigation was to explore appropriate intervention methods for helping Korean youth probationers reduce their aggressiveness and increase their social adjustment. This study examined the effectiveness of solution-focused group treatment with Korean youth probationers using a pre- and post-test control group design. The researcher randomly assigned the consented 40 participants either to an experimental group that received the solution-focused session or to a control group that took individual supportive sessions on a needed basis. The pre- and post-test scores of each group were compared using the Aggressiveness and Social Readjustment Questionnaire to confirm the levels of statistical significance between the two groups. Results indicate that solution-focused group treatment was followed by positive changes with the participants' aggressiveness and social adjustment problems. This study also suggests that a solution-focused program is an appropriate short-term intervention for Korean probation youth.     

英汉互译中的韩国语专有名词音译问题

本文通过指出并纠正涉及韩国语专有名词的英汉互译中出现的误译现象 ,强调了在专有名词翻译中应遵循的“名从主人”原则 ,并且根据实例探讨了韩国语专有名词的英汉翻译问题     

万历朝鲜役及其对东亚政治格局的影响

万历朝鲜役是四百多年前发生在朝鲜半岛的一场国际战争,战争最终虽以正义的胜利而告终,却使明朝与朝鲜由盛转衰,并给女真以迅速崛起的机会.此后,后金取代明朝成为朝鲜的宗主国,形成了新的东亚政治格局.战争彻底改变了日本国内各派政治力量的对比,丰臣秀吉集团的势力彻底垮台,此后以史为鉴的德川幕府,再未动侵朝的念头,一直持续到明治维新以后.万历朝鲜之役对当时东亚的政治格局产生了深远的影响.     

关于朝鲜族女性涉外婚姻基本模式的探讨——以嫁到韩国的朝鲜族女性为个案研究

朝鲜族女性的涉外婚姻,从其婚姻动机、交往途径、婚姻现状看,都具有"交换"的性质,其基本模式为"交换婚姻".由于这种"交换"关系并非感情与感情的交换,故婚姻关系带有很多的不确定性.     

近代巴蜀诗人李士棻生卒年及别号考略

近代巴蜀诗人李士棻曾被曾国藩誉为“太白醉魂”,为曾府门下“四川三李”之一,其诗作有浓郁的巴蜀文化特色。然李氏仕宦不显,长期以来学界对其关注不足,学界近年不多的相关研究,多围绕国内所存的文献,对其诗歌创作进行艺术分析,对诗人的生平介绍多简单略过,没有严谨的考证,目前仍然很有争议。通过搜罗国内外现存典籍,综合目前所见李士棻本人著述,辅以晚清近代重要报刊《申报》和与李氏有交往的朝鲜文人文献,考证其生卒年及别号,冀为今后的相关研究解决基础问题。     

17世纪朝鲜人流入东北及其对后金(清)社会的影响

本文从中朝关系史的角度,对17世纪朝鲜人流入中国东北的主要渠道及其对后金(清)社会农业、手工业、军事、文化等诸方面的影响作了简要的论述。     

An Exposure‐Response Threshold for Lung Diseases and Lung Cancer Caused by Crystalline Silica

Whether crystalline silica (CS) exposure increases risk of lung cancer in humans without silicosis, and, if so, whether the exposure‐response relation has a threshold, have been much debated. Epidemiological evidence is ambiguous and conflicting. Experimental data show that high levels of CS cause lung cancer in rats, although not in other species, including mice, guinea pigs, or hamsters; but the relevance of such animal data to humans has been uncertain. This article applies recent insights into the toxicology of lung diseases caused by poorly soluble particles (PSPs), and by CS in particular, to model the exposure‐response relation between CS and risk of lung pathologies such as chronic inflammation, silicosis, fibrosis, and lung cancer. An inflammatory mode of action is described, having substantial empirical support, in which exposure increases alveolar macrophages and neutrophils in the alveolar epithelium, leading to increased reactive oxygen species (ROS) and nitrogen species (RNS), pro‐inflammatory mediators such as TNF‐alpha, and eventual damage to lung tissue and epithelial hyperplasia, resulting in fibrosis and increased lung cancer risk among silicotics. This mode of action involves several positive feedback loops. Exposures that increase the gain factors around such loops can create a disease state with elevated levels of ROS, TNF‐alpha, TGF‐beta, alveolar macrophages, and neutrophils. This mechanism implies a “tipping point” threshold for the exposure‐response relation. Applying this new model to epidemiological data, we conclude that current permissible exposure levels, on the order of 0.1 mg/m³, are probably below the threshold for triggering lung diseases in humans.     

Development of a Unit Risk Factor for 1,3-Butadiene Based on an Updated Carcinogenic Toxicity Assessment

The Texas Commission on Environmental Quality (TCEQ) has developed an inhalation unit risk factor (URF) for 1,3-butadiene based on leukemia mortality in an updated epidemiological study on styrene-butadiene rubber production workers conducted by researchers at the University of Alabama at Birmingham. Exposure estimates were updated and an exposure estimate validation study as well as dose-response modeling were conducted by these researchers. This information was not available to the U.S. Environmental Protection Agency when it prepared its health assessment of 1,3-butadiene in 2002. An extensive analysis conducted by TCEQ discusses dose-response modeling, estimating risk for the general population from occupational workers, estimating risk for potentially sensitive subpopulations, effect of occupational exposure estimation error, and use of mortality rates to predict incidence. The URF is 5.0 × 10⁻⁷ per μg/m³ or 1.1 × 10⁻⁶ per ppb and is based on a Cox regression dose-response model using restricted continuous data with age as a covariate, and a linear low-dose extrapolation default approach using the 95% lower confidence limit as the point of departure. Age-dependent adjustment factors were applied to account for possible increased susceptibility for early life exposure. The air concentration at 1 in 100,000 excess leukemia mortality, the no-significant-risk level, is 20 μg/m³ (9.1 ppb), which is slightly lower than the TCEQ chronic reference value of 33 μg/m³ (15 ppb) protective of ovarian atrophy. These values will be used to evaluate ambient air monitoring data so the general public is protected against adverse health effects from chronic exposure to 1,3-butadiene.     

Could Removing Arsenic from Tobacco Smoke Significantly Reduce Smoker Risks of Lung Cancer?

If a specific biological mechanism could be determined by which a carcinogen increases lung cancer risk, how might this knowledge be used to improve risk assessment? To explore this issue, we assume (perhaps incorrectly) that arsenic in cigarette smoke increases lung cancer risk by hypermethylating the promoter region of gene p16INK4a, leading to a more rapid entry of altered (initiated) cells into a clonal expansion phase. The potential impact on lung cancer of removing arsenic is then quantified using a three‐stage version of a multistage clonal expansion (MSCE) model. This refines the usual two‐stage clonal expansion (TSCE) model of carcinogenesis by resolving its intermediate or “initiated” cell compartment into two subcompartments, representing experimentally observed “patch” and “field” cells. This refinement allows p16 methylation effects to be represented as speeding transitions of cells from the patch state to the clonally expanding field state. Given these assumptions, removing arsenic might greatly reduce the number of nonsmall cell lung cancer cells (NSCLCs) produced in smokers, by up to two‐thirds, depending on the fraction (between 0 and 1) of the smoking‐induced increase in the patch‐to‐field transition rate prevented if arsenic were removed. At present, this fraction is unknown (and could be as low as zero), but the possibility that it could be high (close to 1) cannot be ruled out without further data.