Seasonality in human sleep.

The timing of sleep and sleep EEG parameters in 10 healthy male subjects were investigated in four seasons under controlled conditions. The phase of nocturnal sleep was delayed about one and a half hours in winter as compared to that in summer. The duration of stage 4 sleep decreased and REM sleep increased significantly in winter compared with summer. The seasonality in the timing of sleep can be explained by photoperiodic time cues, but the changes in sleep EEG parameters are difficult to explain in terms of photoperiod.     

Making light work with optical tweezers.

Microscopic objects, including biological material, can be remotely manipulated with tightly focused beams of infrared laser light. The use of optical traps, or 'optical tweezers', holds great promise for noninvasive micromanipulation and mechanical measurement in cell biology. Optical tweezers are the 'tractor beams' of today's technology.     

最优吸收截面的存在性

对被真空包围的无穷平行平板，运用勒贝格控制收敛定理和Ｃａｕｃｈｙ－Ｓｃｈｗａｒｔｙ不等式，给出稳态中子迁移系统最优吸收截面的存在性。     

Prediction of the structure of a receptor-protein complex using a binary docking method.

To validate procedures of rational drug design, it is important to develop computational methods that predict binding sites between a protein and a ligand molecule. Many small molecules have been tested using such programs, but examination of protein-protein and peptide-protein interactions has been sparse. We were able to test such applications once the structures of both the maltose-binding protein (MBP) and the ligand-binding domain of the aspartate receptor, which binds MBP, became available. Here we predict the binding site of MBP to its receptor using a 'binary docking' technique in which two MBP octapeptide sequences containing mutations that eliminate maltose chemotaxis are independently docked to the receptor. The peptides in the docked solutions superimpose on their original positions in the structure of MBP and allow the formation of an MBP-receptor complex. The consistency of the computational and biological results supports this approach for predicting protein-protein and peptide-protein interactions.     

Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.     

混合氯化稀土催化合成DOP,DOM和DOA

本文报道:价廉的混合氯化稀土,对合成DOP等增塑剂有明显的催化效果。产品精制简单,转化率高,有应用前景。     

Biotransformation, by Enterobacter agglomerans, of pyrimidine acyclonucleosides to acyclonucleotides.

The ability of Enterobacter agglomerans to transform naturally occurring nucleosides into nucleotides has been utilized to transform newly synthesized pyrimidine acyclonucleosides into the corresponding acyclonucleotides. Unselected bacteria were used as the source of nucleoside phosphotransferase, the phosphate group donor being 4-nitrophenyl phosphate in the presence of Zn2+ ions. Optimal reaction conditions are outlined.     

Short alanine-based peptides may form 3(10)-helices and not alpha-helices in aqueous solution.

Short alanine peptides, containing 16 or 17 residues, appear to form alpha-helices in aqueous solution. But the main spectroscopic analyses used on helical peptides (circular dichroism and nuclear magnetic resonance) cannot distinguish between an alpha-helix (in which the ith residue is hydrogen-bonded to residue i + 4; ref. 9) and the next most common peptide helix, the 3(10)-helix10 (i-->i + 3 hydrogen-bonding). To address this problem we have designed single and doubly spin-labelled analogues of alanine-based peptides in which the nitroxide spin label forms an unbranched side chain extending from the sulphur atom of a cysteine residue. Here we report the circular dichroism, Fourier-transform infrared and electron-spin resonance spectra of these peptides under helix-forming conditions. The infrared absorbance gives an amide I' band with a frequency that is substantially different from that observed for alpha-helices. The electron-spin resonance spectra of doubly labelled helices show that the ranking of distances between side chains, around a single turn (residues 4-8), is inconsistent with an alpha-helical structure. Our experiments suggest that the more likely peptide geometry is a 3(10)-helix.     

Simulation of Weld Depth in A-TIG Welding with Unified Arc-electrode model

Ｉｔｋｎｏｗｎｔｈａｔｓｍａｌｌａｍｏｕｎｔｓｏｆｆｌｕｘｏｎｔｈｅｓｕｒｆａｃｅｏｆｓｔａｉｎｌｅｓｓｓｔｅｅｌｃａｎｉｎｃｒｅａｓｅｔｈｅｄｅｐｔｈｏｆｗｅｌｄｐｅｎｅ ｔｒａｔｉｏｎｉｎＴＩＧｗｅｌｄｉｎｇｂｙａｆａｃｔｏｒｏｆｔｈｒｅｅ[1] .Ｔｈｉｓｐｒｏｃｅｓｓｉｓｒｅｆｅｒｒｅｄｔｏａｓ”ＡＴＩＧ”ｏｒＴＩＧｗｅｌｄｉｎｇａｃｔｉ ｖａｔｅｄｂｙｆｌｕｘ .Ｔｈｅｒｅｈａｖｅｂｅｅｎｔｈｒｅｅｐｕｂｌｉｓｈｅｄｐｈｙｓ ｉｃａｌｍｅｃｈａｎｉｓｍｓｔｈａｔａｒｅｐｏｓｓｉｂｌｅｃｏｎｔｒｉ…     

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1.