Abstract Die Komplexe (I) wurden durch Umsetzung des entsprechenden Dichloro‐Pt‐ Komplexes mit n‐Alkyl‐Li‐Verbindungen dargestellt.
Research at the interface between nanoscience and biology could yield breakthroughs in fundamental science and lead to revolutionary technologies. In this review, we focus on the interfaces between nanoelectronics and biology. First, we discuss nanoscale field effect transistors (nanoFETs) as probes to study cellular systems; specifically, we describe the development of nanoFETs that are comparable in size to biological nanostructures involved in communication through synthesized nanowires. Second, we review current progress in multiplexed extracellular sensing using planar nanoFET arrays. Third, we describe the designs and implementation of three distinct nanoFETs used to perform the first intracellular electrical recording from single cells. Fourth, we present recent progress in merging electronic and biological systems at the three-dimensional tissue level by use of macro-porous nanoelectronic scaffolds. Finally, we discuss future developments in this research area, unique challenges and opportunities, and the tremendous impact these nanoFET-based technologies might have on biological and medical sciences.
Abstract : A technique is described for attaching thin, conformal, pin-hole free electrically insulating polyethylene films to flat gold surfaces (previously modified by adsorption of a monolayer of an organic disulfide) by plasma polymerization. These polyethylene films are tough enough to support the attachment of gold electrodes. The adhesion of plasma polymerized polyethylene (PPE) thin films to a gold surface can be dramatically improved by coupling the synthesis of the PPE thin film with the prior assembly of an organic monolayer chemisorbed to the metal surface. These thin film assemblies have good physical characteristics and are stable to the ambient environment for long intervals. This method should be applicable to other systems with appropriate modifications.
Type 2 diabetes is one of the fastest growing public health problems worldwide. Both environmental (e.g. physical activity, obesity, and diet) and genetic factors are involved in the development of type 2 diabetes. The associations between physical activity and diabetes risk have been assessed by a number of prospective studies and clinical trials. The results from these studies consistently indicate that the regular physical activity during occupation, commuting, leisure time or daily life reduces the risk of type 2 diabetes by 15-60%; and lifestyle intervention, including counselling for physical activity, nutrition, and body weight, can reduce the risk of type 2 diabetes by 40-60% among adults with impaired glucose tolerance and by about 20% among general individuals. In the past decade, studies using traditional linkage analysis and candidate-gene association approach have found dozens of genes harboring common variants that were related to the common-form type 2 diabetes. However, most reported associations are lack of reproducibility, except TCF7L2, PPARG, CAPN10, and KCNJ11. Since 2007, seven genome-wide association (GWA) studies emerged to generate a list of new diabetes genes. The genetic effects are largely of moderate size. These findings provide novel insight into the diabetes etiology and pave new avenue for predicting the disease risk using genetic information. In addition, data especially those from intervention trials display preliminary but promising evidence that the genetic variants might interact with physical activity in predisposing to type 2 diabetes. The gene-environment interactions merit extensive exploration in large, prospective studies.
<p>Supplementary methods and tables 1-7. Supplementary Methods: Covariate assessment and statistical analysis Supplementary Table 1. Relative risk of colorectal cancer by body mass index according to weight change from age 18 (women) or 21 (men) years to baseline Supplementary Table 2. Relative risk of colorectal cancer by baseline age according to weight change from age 18 (women) or 21 (men) years to baseline Supplementary Table 3. Subsite-specific relative risk of colorectal cancer according to weight change from age 18 (women) or 21 (men) years to baseline Supplementary Table 4. Relative risk of colorectal cancer by baseline use of aspirin according to weight change from age 18 (women) or 21 (men) years to baseline Supplementary Table 5. Relative risk of colorectal cancer by current age according to weight change from baseline to present Supplementary Table 6. Relative risk of colorectal cancer by current age according to 4-year weight change during follow-up Supplementary Table 7. Relative risk of colorectal cancer by postmenopausal hormone use according to postmenopausal weight change</p>