浅谈“问题解决“教学

问题解决自提出以来就受到数学教育界的普遍关注。本文简述了“问题解决“教学的意义,着重从问题解决的影响因素出发阐述如何进行有效的“问题解决“教学,并指出了“问题提出“的重要性。     

A flower image retrieval method based on ROI feature

Flower image retrieval is a very important step for computer-aided plant species recognition. In this paper, we propose an efficient segmentation method based on color clustering and domain knowledge to extract flower regions from flower images. For flower retrieval, we use the color histogram of a flower region to characterize the color features of flower and two shape-based features sets, Centroid-Contour Distance (CCD) and Angle Code Histogram (ACH), to characterize the shape features of a flower contour. Experimental results showed that our flower region extraction method based on color clustering and domain knowledge can produce accurate flower regions. Flower retrieval results on a database of 885 flower images collected from 14 plant species showed that our Region-of-Interest (ROI) based retrieval approach using both color and shape features can perform better than a method based on the global color histogram proposed by Swain and Ballard (1991) and a method based on domain knowledge-driven segmentation and color names proposed by Das et al.(1999).     

Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms

Subcellular localization of nitric oxide (NO) synthases with effector molecules is an important regulatory mechanism for NO signalling. In the heart, NO inhibits L-type Ca2+ channels but stimulates sarcoplasmic reticulum (SR) Ca2+ release, leading to variable effects on myocardial contractility. Here we show that spatial confinement of specific NO synthase isoforms regulates this process. Endothelial NO synthase (NOS3) localizes to caveolae, where compartmentalization with beta-adrenergic receptors and L-type Ca2+ channels allows NO to inhibit beta-adrenergic-induced inotropy. Neuronal NO synthase (NOS1), however, is targeted to cardiac SR. NO stimulation of SR Ca2+ release via the ryanodine receptor (RyR) in vitro, suggests that NOS1 has an opposite, facilitative effect on contractility. We demonstrate that NOS1-deficient mice have suppressed inotropic response, whereas NOS3-deficient mice have enhanced contractility, owing to corresponding changes in SR Ca2+ release. Both NOS1-/- and NOS3-/- mice develop age-related hypertrophy, although only NOS3-/- mice are hypertensive. NOS1/3-/- double knockout mice have suppressed beta-adrenergic responses and an additive phenotype of marked ventricular remodelling. Thus, NOS1 and NOS3 mediate independent, and in some cases opposite, effects on cardiac structure and function.     

禀经酌伟 弥纶一代－《中国现代寓言史纲》读后

《中国现代寓言史纲》是陈蒲清先生《中国古代寓言史》的续篇,是又一部填补空白 的著作。他的问世,不仅完成了他中国寓言史的宏大建构,而且,通过对我国现代寓言史的全面、深入地探究、总结,将会极大地推动我国当代的寓言研究与寓言创作向前发展。     

“雅”译观的历史与现实

本文探讨了严氏“雅”译观产生的历史、社会、教育背景和哲学基础。从辩证历史观的角度看 ,“雅”译观作为译事中宏观的指导理论和译文评鉴标准 ,与西学的“等值论”相得益彰 ,仍不失具有重要的现实意义和指导作用     

A natural allele of Nxf1 suppresses retrovirus insertional mutations

Endogenous retroviruses have shaped the evolution of mammalian genomes. Host genes that control the effects of retrovirus insertions are therefore of great interest. The modifier-of-vibrator-1 locus (Mvb1) controls levels of correctly processed mRNA from genes mutated by endogenous retrovirus insertions into introns, including the Pitpn(vb) tremor mutation and the Eya1(BOR) model of human branchiootorenal syndrome. Positional complementation cloning identifies Mvb1 as the nuclear export factor Nxf1, providing an unexpected link between the mRNA export receptor and pre-mRNA processing. Population structure of the suppressive allele in wild Mus musculus castaneus suggests selective advantage. A congenic Mvb1(CAST) allele is a useful tool for modifying gene expression from existing mutations and could be used to manipulate engineered mutations containing retroviral elements.     

Dysregulation of TGF-beta activation contributes to pathogenesis in Marfan syndrome

Marfan syndrome is an autosomal dominant disorder of connective tissue caused by mutations in fibrillin-1 (encoded by FBN1 in humans and Fbn1 in mice), a matrix component of extracellular microfibrils. A distinct subgroup of individuals with Marfan syndrome have distal airspace enlargement, historically described as emphysema, which frequently results in spontaneous lung rupture (pneumothorax; refs. 1-3). To investigate the pathogenesis of genetically imposed emphysema, we analyzed the lung phenotype of mice deficient in fibrillin-1, an accepted model of Marfan syndrome. Lung abnormalities are evident in the immediate postnatal period and manifest as a developmental impairment of distal alveolar septation. Aged mice deficient in fibrillin-1 develop destructive emphysema consistent with the view that early developmental perturbations can predispose to late-onset, seemingly acquired phenotypes. We show that mice deficient in fibrillin-1 have marked dysregulation of transforming growth factor-beta (TGF-beta) activation and signaling, resulting in apoptosis in the developing lung. Perinatal antagonism of TGF-beta attenuates apoptosis and rescues alveolar septation in vivo. These data indicate that matrix sequestration of cytokines is crucial to their regulated activation and signaling and that perturbation of this function can contribute to the pathogenesis of disease.