Branching fractions, polarisation and asymmetries of B -> VV decays

We calculate the hard-scattering kernels relevant to the negative-helicity decay amplitude in B decays to two vector mesons in the framework of QCD factorisation. We then perform a comprehensive analysis of the 34 B->VV decays, including B_s decays and the complete set of polarisation observables. We find considerable uncertainties from weak annihilation and the non-factorisation of spectator-scattering. Large longitudinal polarisation is expected with certainty only for a few tree-dominated colour-allowed modes, which receive small penguin and spectator-scattering contributions. This allows for an accurate determination of the CKM angle alpha (or gamma) from S_L(rhorho) resulting in alpha=(85.6^{+7.4}_{-7.3}) degrees. We also emphasize that the rho K* system is ideal for an investigation of electroweak penguin effects.Comment: 39 pages, v2: matches published versio

PCA-based lung motion model

Organ motion induced by respiration may cause clinically significant targeting errors and greatly degrade the effectiveness of conformal radiotherapy. It is therefore crucial to be able to model respiratory motion accurately. A recently proposed lung motion model based on principal component analysis (PCA) has been shown to be promising on a few patients. However, there is still a need to understand the underlying reason why it works. In this paper, we present a much deeper and detailed analysis of the PCA-based lung motion model. We provide the theoretical justification of the effectiveness of PCA in modeling lung motion. We also prove that under certain conditions, the PCA motion model is equivalent to 5D motion model, which is based on physiology and anatomy of the lung. The modeling power of PCA model was tested on clinical data and the average 3D error was found to be below 1 mm.Comment: 4 pages, 1 figure. submitted to International Conference on the use of Computers in Radiation Therapy 201

Method of Multiobject Detecting and Tracking Based on DM643

The technology of moving objects detection has become an important research subject for its extensive application prospect. In this paper, it is presented that interframe difference algorithm and background difference algorithm are combined to update the background. The algorithm can deal with the flaw of background difference algorithm. The mathematical morphology method is employed to denoise the image, which may be helpful to improve the accuracy of the detection. The Pyramid algorithm is used to compress each frame data of video sequence. Then, the detecting and tracking of moving objects are tested on the hardware platform (DM643) and the software frame (RF5). The running speed is about 3 times faster than before. The result shows that the accuracy demanded by the detection is met. This method can provide a useful reference for similar application.</jats:p

An outbreak of aseptic meningitis caused by coxsackievirus A9 in Gansu, the People's Republic of China

<p>Abstract</p> <p>Background</p> <p>An outbreak of aseptic meningitis occurred in Tianshui city of Gansu Province, the People's Republic of China, from March to June 2005. A total of 85 patients were clinical confirmed as aseptic meningitis in this outbreak.</p> <p>Results</p> <p>CVA9 was mainly responsible for this outbreak supported by the clinical manifestations of the patients, epidemiological data of the outbreak, the results of RT-PCR and complete VP1 sequence determination, conventional neutralization assays, IgM serological assays, viral isolation and phylogenetics analysis. Through phylogenetic analysis and homogeneity analysis for partial VP1 gene, the nucleotide and amino acid homologies between Gansu isolates and former Chinese CVA9 strains were 88.2%-96.1% and 97.2%-99.2%, respectively. Multiple transmission chains of CVA9 occurred in different provinces or years in China. Moreover, in order to clarify the genotype of CVA9, Gansu CVA9 strains isolated in this outbreak were compared with other CVA9 isolates based on VP1/2A junction regions (genotyping region) and they might belong to a new genotype of CVA9, which could be assigned for genotype XIII,</p> <p>Conclusions</p> <p>CVA9 was confirmed as the pathogen responsible for this outbreak. The phylogenetic analysis indicated that the CVA9 strains isolated in this outbreak might belong to a new genotype.</p

Fibroblast Growth Factor–21 ameliorates hepatic encephalopathy by activating the STAT3-SOCS3 pathway to inhibit activated hepatic stellate cells

Neurological dysfunction, one of the consequences of acute liver failure (ALF), and also referred to as hepatic encephalopathy (HE), contributes to mortality posing challenges for clinical management. FGF21 has been implicated in the inhibition of cognitive decline and fibrogenesis. However, the effects of FGF21 on the clinical and molecular presentations of HE has not been elucidated. HE was induced by fulminant hepatic failure using thioacetamide (TAA) in male C57BL/6J mice while controls were injected with saline. For two consecutive weeks, mice were treated intraperitoneally with FGF21 (3 mg/kg) while controls were treated with saline. Cognitive, neurological, and activity function scores were recorded. Serum, liver, and brain samples were taken for analysis of CCL5 and GABA by ELISA, and RT qPCR was used to measure the expressions of fibrotic and pro-inflammatory markers. We report significant improvement in both cognitive and neurological scores by FGF21 treatment after impairment by TAA. GABA and CCL5, key factors in the progression of HE were also significantly reduced in the treatment group. Furthermore, the expression of fibrotic markers such as TGFβ and Col1 were also significantly downregulated after FGF21 treatment. TNFα and IL-6 were significantly reduced in the liver while in the brain, TNFα and IL-1 were downregulated. However, both in the liver and the brain, IL-10 was significantly upregulated. FGF21 inhibits CXCR4/CCL5 activation and upregulates the production of IL-10 in the damaged liver stimulating the production pro-inflammatory cytokines and apoptosis of hepatic stellate cells through the STAT3-SOCS3 pathway terminating the underlying fibrosis in HE