Variants in KCNQ1 are associated with susceptibility to type 2 diabetes mellitus

We carried out a multistage genome-wide association study of type 2 diabetes mellitus in Japanese individuals, with a total of 1,612 cases and 1,424 controls and 100,000 SNPs. The most significant association was obtained with SNPs in KCNQ1, and dense mapping within the gene revealed that rs2237892 in intron 15 showed the lowest Pvalue (6.7 x 10(-13), odds ratio (OR) = 1.49). The association of KCNQ1 with type 2 diabetes was replicated in populations of Korean, Chinese and European ancestry as well as in two independent Japanese populations, and meta-analysis with a total of 19,930 individuals (9,569 cases and 10,361 controls) yielded a P value of 1.7 x 10(-42) (OR = 1.40; 95% CI = 1.34-1.47) for rs2237892. Among control subjects, the risk allele of this polymorphism was associated with impairment of insulin secretion according to the homeostasis model assessment of beta-cell function or the corrected insulin response. Our data thus implicate KCNQ1 as a diabetes susceptibility gene in groups of different ancestries.     

A 160-kilobit molecular electronic memory patterned at 10(11) bits per square centimetre

The primary metric for gauging progress in the various semiconductor integrated circuit technologies is the spacing, or pitch, between the most closely spaced wires within a dynamic random access memory (DRAM) circuit. Modern DRAM circuits have 140 nm pitch wires and a memory cell size of 0.0408 mum(2). Improving integrated circuit technology will require that these dimensions decrease over time. However, at present a large fraction of the patterning and materials requirements that we expect to need for the construction of new integrated circuit technologies in 2013 have 'no known solution'. Promising ingredients for advances in integrated circuit technology are nanowires, molecular electronics and defect-tolerant architectures, as demonstrated by reports of single devices and small circuits. Methods of extending these approaches to large-scale, high-density circuitry are largely undeveloped. Here we describe a 160,000-bit molecular electronic memory circuit, fabricated at a density of 10(11) bits cm(-2) (pitch 33 nm; memory cell size 0.0011 microm2), that is, roughly analogous to the dimensions of a DRAM circuit projected to be available by 2020. A monolayer of bistable, [2]rotaxane molecules served as the data storage elements. Although the circuit has large numbers of defects, those defects could be readily identified through electronic testing and isolated using software coding. The working bits were then configured to form a fully functional random access memory circuit for storing and retrieving information.     

Assessment of superoxide-mediated release of vascular-inhibitory factor(s) from endothelial cells by using a two-bath system

Release of a vascular-inhibitory factor from endothelial cells (EC), different from endothelium-derived relaxant factor (EDRF), was identified through use of a two-bath system. This two-bath system precluded the effects of oxygen-free radicals that appear when electrical field stimulation (EFS) is directly imposed on detector muscle.     

天然树脂紫胶的热裂解-气相色谱特性

研究了有机碱试剂,氢氧化四甲铵(tetramethylammonium hydroxide TMAH)共存下的反应热裂解气相色谱(Py-GC)应用于天然树脂紫胶的化学组成分析.并在反应Py-GC测得的化学组成的基础上,应用主成分分析(principal component analysis,PCA)对印度和泰国产紫胶进行产地识别分析.     

热解析GC用的大容量固相萃取器的开发及其基本特性的探讨

开发了一种用于液体和气体样品中微量组分富集的大容量固相萃取装置.在小金属钛管(内径1.2mm外径1.6mm长6～30mm)的外壁键合上一层聚二甲基硅氧烷(厚0.32mm),就能有效地萃取多种有机物,结果可用热解吸-气相色谱-质谱联检.     

韩国松萎蔫病的研究及防控现状

自从松萎蔫病于1988年首次报道以来,该病已经扩散到韩国大部分地区并引起未能预见的危害。从2000年该病危害急剧增加,到2006年危害面积已达7 871 hm2。2000—2008年伐除的病树已达1 851 225株,年经济损失达1 000万美元。2006年后危害面积下降,2008年下降到6 015 hm2。但至2008年该病已经扩散至韩国54个地区、县和11省。调查发现松材线虫可以被云杉花墨天牛(Monochamus saltuarius)所携带。防治的策略为：(1)连续地监测;(2)病株的早期检测;(3)伐除病株;(4)焚烧和熏蒸伐除的病木。对人文和旅游景点及成熟林可以采取注射法防治,也可采取飞防的方法防治天牛。韩国已经通过了法律,禁止病木的运输。在首次发现该病后连续3 a未发生重复感染的地区,建立无病区和优选系统。     

IkappaB kinase-alpha acts in the epidermis to control skeletal and craniofacial morphogenesis

IkappaB kinase-alpha (IKK-alpha) exhibits protein-kinase-dependent and -independent functions. Its kinase activity is required for lymphoid organogenesis and mammary gland development, whereas a kinase-independent activity is required for epidermal keratinocyte differentiation. In addition to failed epidermal differentiation, IKK-alpha-deficient mice exhibit abnormal skeletal and craniofacial morphogenesis. As similar defects are not exhibited by mice that experience systemic inhibition of NF-kappaB, we postulated that the morphogenetic defects in IKK-alpha-deficient mice are not caused by reduced NF-kappaB activity but instead are due to failed epidermal differentiation that disrupts proper epidermal-mesodermal interactions. We tested this hypothesis by introducing an epidermal-specific Ikka (also known as Chuk) transgene into IKK-alpha-deficient mice. Mice lacking IKK-alpha in all cell types including bone and cartilage, but not in basal epidermal keratinocytes, exhibit normal epidermal differentiation and skeletal morphology. Thus, epidermal differentiation is required for proper morphogenesis of mesodermally derived skeletal elements. One way by which IKK-alpha controls skeletal and craniofacial morphogenesis is by repressing expression of fibroblast growth factor (FGF) family members, such as FGF8, whose expression is specifically elevated in the limb bud ectoderm of IKK-alpha-deficient mice.