An aqueous extract of Liu Wei Di Huang Wan alters the labeling of blood constituents with Technetium-99m

The Liu Wei Di Huang Wan is a formula of a traditional Chinese medicine that is used to treat asthma patients and has been shown to have several important properties,such as antioxidant and free radical scavenging activities.The influence of an extract of Liu Wei Di Huang Wan on the labeling of blood constituents with technetium-99m was investigated.Anticoagulated blood(Wistar rats) was incubated with the extract,stannous chloride and technetium-99m,as sodium pertechnetate.Samples were centrifuged and aliquots of plasma and blood cells were separated and precipitated with trichloroacetic acid,to obtain soluble and insoluble fractions of the blood constituents.The percentage of radioactivity(%ATI) in all the fractions was determined.The analysis of the results shows that the extract at the highest concentration used(70 mg/mL) decreased significantly(P<0.05) the %ATI(from 96.48 ± 1.19 to 54.46 ± 7.38) on blood cells compartment,(from 81.11 ± 4.15 to 61.33 ± 4.74) on insoluble fractions of blood cells and(from 65.91 ± 2.44 to 13.15 ± 3.62) on insoluble fractions of plasma.In conclusion,the results suggest that the substances present on this extract can alter this labeling process,probably due to(i) redox properties(antioxidant and chelator activities) and/or(ii) specific actions in the binding sites where the 99mTc would be bound on the blood constituents.As a consequence,precaution is suggested on the interpretation of the nuclear medicine results from performed with blood constituents labeled with 99m Tc in patients that have undertaken LWDHW,although the current findings were obtained in experimental animal models.     

Evolution and maintenance of cooperation via inheritance of neighborhood relationship

Cooperative behaviors are ubiquitous in nature and human society. It is very important to understand the internal mechanism of emergence and maintenance of cooperation. As we know now, the offsprings inherit not only the phenotype but also the neighborhood relationship of their parents. Some recent research results show that the interactions among individuals facilitate survival of cooperation through network reciprocity of clustering cooperators. This paper aims at introducing an inheritance mechanism of neighborhood relationship to explore the evolution of cooperation. In detail, a mathematical model is proposed to characterize the evolutionary process with the above inheritance mechanism. Theoretical analysis and numerical simulations indicate that high-level cooperation can emerge and be maintained for a wide variety of cost-to-benefit ratios, even if mutation happens during the evolving process.     

High resolution imaging using scanning ion conductance microscopy with improved distance feedback control

Microscopy is an essential technique for observation on living cells. There is currently great interest in applying scanning probe microscopy to image-living biological cells in their natural environment at the nanometer scale. Scanning ion conductance microscopy is a new form of scanning probe microscopy, which enables non-contact high-resolution imaging of living biological cells. Based on a scanned nanopipette in physiological buffer, the distance feedback control uses the ion current to control the distance between the pipette tip and the sample surface. However, this feedback control has difficulties over slopes on convoluted cell surfaces, which limits its resolution. In this study, we present an improved form of feedback control that removes the contribution of up to the third-order slope from the ion current signal, hence providing a more accurate signal for controlling the distance. We show that this allows faster and lower noise topographic high-resolution imaging.     

卫星编队飞行的轨道和姿态GPS自主同步反馈控制

鉴于编队飞行之中卫星不但对轨道有要求,而且对姿态也有要求,例如有的编队飞行卫星在惯性空间中有指向控制的要求,或者相互之间有保持一定的姿态关系的要求,同时在轨道控制过程中也需要姿态信息,因此在编队飞行的建立过程中,需要考虑姿态和轨道的协调控制和同步控制问题.本文提出了用汗同步控制的相对轨道和相对姿态运动学和动力学模型、控制率的选择和设计以及用GPS的伪距和载波相位实现轨道和姿态同步实时反馈控制方法.其中包括用修改的Kodrigues参数实现无奇异的大姿态机动的非线性状态跟踪控制.对EO-1/Landsat 7编队飞行的同步控制进行了数字仿真,证实了设计的正确性和实现的可行性.     

Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1

Spinocerebellar ataxia type 1 (SCA1) is a dominantly inherited neurodegenerative disease caused by expansion of a glutamine-encoding repeat in ataxin 1 (ATXN1). In all known polyglutamine diseases, the glutamine expansion confers toxic functions onto the protein; however, the mechanism by which this occurs remains enigmatic, in light of the fact that the mutant protein apparently maintains interactions with its usual partners. Here we show that the expanded polyglutamine tract differentially affects the function of the host protein in the context of different endogenous protein complexes. Polyglutamine expansion in ATXN1 favours the formation of a particular protein complex containing RBM17, contributing to SCA1 neuropathology by means of a gain-of-function mechanism. Concomitantly, polyglutamine expansion attenuates the formation and function of another protein complex containing ATXN1 and capicua, contributing to SCA1 through a partial loss-of-function mechanism. This model provides mechanistic insight into the molecular pathogenesis of SCA1 as well as other polyglutamine diseases.     

Rapid appearance and local toxicity of amyloid-beta plaques in a mouse model of Alzheimer's disease

Senile plaques accumulate over the course of decades in the brains of patients with Alzheimer's disease. A fundamental tenet of the amyloid hypothesis of Alzheimer's disease is that the deposition of amyloid-beta precedes and induces the neuronal abnormalities that underlie dementia. This idea has been challenged, however, by the suggestion that alterations in axonal trafficking and morphological abnormalities precede and lead to senile plaques. The role of microglia in accelerating or retarding these processes has been uncertain. To investigate the temporal relation between plaque formation and the changes in local neuritic architecture, we used longitudinal in vivo multiphoton microscopy to sequentially image young APPswe/PS1d9xYFP (B6C3-YFP) transgenic mice. Here we show that plaques form extraordinarily quickly, over 24 h. Within 1-2 days of a new plaque's appearance, microglia are activated and recruited to the site. Progressive neuritic changes ensue, leading to increasingly dysmorphic neurites over the next days to weeks. These data establish plaques as a critical mediator of neuritic pathology.     

A role for VEGF as a negative regulator of pericyte function and vessel maturation

Angiogenesis does not only depend on endothelial cell invasion and proliferation: it also requires pericyte coverage of vascular sprouts for vessel stabilization. These processes are coordinated by vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) through their cognate receptors on endothelial cells and vascular smooth muscle cells (VSMCs), respectively. PDGF induces neovascularization by priming VSMCs/pericytes to release pro-angiogenic mediators. Although VEGF directly stimulates endothelial cell proliferation and migration, its role in pericyte biology is less clear. Here we define a role for VEGF as an inhibitor of neovascularization on the basis of its capacity to disrupt VSMC function. Specifically, under conditions of PDGF-mediated angiogenesis, VEGF ablates pericyte coverage of nascent vascular sprouts, leading to vessel destabilization. At the molecular level, VEGF-mediated activation of VEGF-R2 suppresses PDGF-Rbeta signalling in VSMCs through the assembly of a previously undescribed receptor complex consisting of PDGF-Rbeta and VEGF-R2. Inhibition of VEGF-R2 not only prevents assembly of this receptor complex but also restores angiogenesis in tissues exposed to both VEGF and PDGF. Finally, genetic deletion of tumour cell VEGF disrupts PDGF-Rbeta/VEGF-R2 complex formation and increases tumour vessel maturation. These findings underscore the importance of VSMCs/pericytes in neovascularization and reveal a dichotomous role for VEGF and VEGF-R2 signalling as both a promoter of endothelial cell function and a negative regulator of VSMCs and vessel maturation.     

Accurate whole human genome sequencing using reversible terminator chemistry

DNA sequence information underpins genetic research, enabling discoveries of important biological or medical benefit. Sequencing projects have traditionally used long (400-800 base pair) reads, but the existence of reference sequences for the human and many other genomes makes it possible to develop new, fast approaches to re-sequencing, whereby shorter reads are compared to a reference to identify intraspecies genetic variation. Here we report an approach that generates several billion bases of accurate nucleotide sequence per experiment at low cost. Single molecules of DNA are attached to a flat surface, amplified in situ and used as templates for synthetic sequencing with fluorescent reversible terminator deoxyribonucleotides. Images of the surface are analysed to generate high-quality sequence. We demonstrate application of this approach to human genome sequencing on flow-sorted X chromosomes and then scale the approach to determine the genome sequence of a male Yoruba from Ibadan, Nigeria. We build an accurate consensus sequence from >30x average depth of paired 35-base reads. We characterize four million single-nucleotide polymorphisms and four hundred thousand structural variants, many of which were previously unknown. Our approach is effective for accurate, rapid and economical whole-genome re-sequencing and many other biomedical applications.