In order to determine the prevalence of antibody against 2009 H1N1 influenza in Beijing, we conducted a serological survey in 710 subjects, 1 month after the epidemic peak. We found that 13·8% of our cohort was seropositive. Subjects aged ≥60 years recorded the lowest seroprevalence (4·5%). The age-weighted seroprevalence of 14·0% was far lower than the supposed infection rate at the epidemic peak, derived from the basic reproduction number for 2009 H1N1 virus. For subjects who had received the pandemic vaccine seroprevalence was 51·4%. In subjects aged ≥60 years the seasonal influenza vaccination was not significantly associated with being seropositive. Our study suggests that many factors, and not just the immunological level against 2009 H1N1 influenza in the community, affected the spread of the virus within the population of Beijing.

s: Objective To observe the effects of cryptotanshinone (CTS) on cytochrome P450 (CYP) isoforms in the rat liver microsomes. Method The rats were randomized into six groups according to the body weight, 3 rats in each group. CTS groups were treated with CTS at the doses of 20～ 540 mg/kg per day for 10 days, and the negative control group was treated with 10 mL/kg hydroxylpropyl-β -cyclodextrin solution. The positive group was injected with β -NF(80 mg/kg) intraperitoneally on the 7th day, and all the animals were sacrificed by decapitation on the 10th day after last dose. The liver was got out for the preparation of liver microsomes. The activities of six kinds of CYP isoforms were detected by cocktail in-vitro incubation method. Besides, the expression level of CYP isoforms mRNA and protein in rat liver was analyzed by reverse transcription polymerase chain reaction (RT-PCR) and western-blotting assay, respectively. Results CTS significantly increased the activity of CYP1A2 in a dose-dependent manner. In CTS groups at the dosages of 20～ 540 mg/kg, the activity of CYP1A2 was 60 % ～ 430 % higher, CYP1A2 protein expression level was 130 % ～ 320 % higher, and CYP1A2 mRNA expression level was 10 % ～ 150 % higher than that of the negative control group. CTS had no effect on other kinds of CYP isoforms. Conclusion CTS can induce hepatic microsome CYP1A2 expression significantly, which indicates potential drug-drug interaction might occured when CTS is co-administrated with those drugs metabolized by CYP1A2.

With the development of information technology, quality education are putting forward new requirements on teaching of the curriculums. Traditional teaching methods and learning environment show some obvious deficiencies in teaching certain courses because of the restrictions on the nature of their content. The emergence of interactive whiteboard is a revolutionary breakthrough in traditional mode in response to the information technology trends. This paper mainly focuses on the exploration of the way to improve the existing teaching of curriculums through constructing a model of collaborative visual learning environment based on interactive whiteboard.

Ginkgo biloba is one of the most popular herbal medicines in the world, due to its purported pharmacological effects, including memory-enhancing, cognition-improving, and antiplatelet effects. The study aimed to investigate the activity and expression of cytochrome P450 (CYP) 3A in human and rat primary hepatocytes treated with standardized G. biloba extract (100, 500, and 2500 ng/ml) for 72 hr, and to measure the protein expression of CYP3A in human and rat primary hepatocytes treated with bilobalide (2, 10, and 50 ng/ml) and ginkgolides B (2, 10, and 50 ng/ml). The activity of CYP3A was measured by the quantification of dehydronifedipine formation using a validated tandem liquid chromatography mass spectrometry (LC/MS/MS) method. The levels of mRNA and protein of CYP3A were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western-blotting analysis, respectively. The G. biloba extract at 100-2,500 ng/ml significantly induced the activity, protein and mRNA expression of CYP3A in a dose-dependent manner in human and rat primary hepatocytes. Bilobalide at 2-50 ng/ml significantly increased CYP3A protein expression in a dose-dependent manner in human and rat primary hepatocytes. However, ginkgolide B did not affect CYP3A protein expression in vitro. The results indicate that G. biloba extract pretreatment significantly induced the expression of CYP3A protein and mRNA and increased CYP3A activity, and there was no significant species difference between human and rat. G. biloba may cause potential interactions with substrate drugs of CYP3A. Bilobalide might play a key role in the enzyme-inducing effects of G. biloba extract. Further study is needed to identify the substances in GBE that induce CYPs in vivo, and elucidate the molecular mechanism of CYP3A induction by GBE and bilobalides.

Background The Alternative Splicing Mutation Database (ASMD) presents a collection of all known mutations inside human exons which affect splicing enhancers and silencers and cause changes in the alternative splicing pattern of the corresponding genes. Findings An algorithm was developed to derive a Splicing Potential (SP) table from the ASMD information. This table characterizes the influence of each oligonucleotide on the splicing effectiveness of the exon containing it. If the SP value for an oligonucleotide is positive, it promotes exon retention, while negative SP values mean the sequence favors exon skipping. The merit of the SP approach is the ability to separate splicing signals from a wide range of sequence motifs enriched in exonic sequences that are attributed to protein-coding properties and/or translation efficiency. Due to its direct derivation from observed splice site selection, SP has an advantage over other computational approaches for predicting alternative splicing. Conclusion We show that a vast majority of known exonic splicing enhancers have highly positive cumulative SP values, while known splicing silencers have core motifs with strongly negative cumulative SP values. Our approach allows for computation of the cumulative SP value of any sequence segment and, thus, gives researchers the ability to measure the possible contribution of any sequence to the pattern of splicing.

In the dinuclear centrosymmetric copper(II) title compound, [Cu(2)(C(11)H(11)N(2)O(2))(2)Cl(2)(H(2)O)(2)], each Cu(II) ion has a slightly distorted trigonal-bipyramidal geometry and is coordinated by one N and one O atom from one 3-(2-hydroxy-ethyl)-2-methyl-4-oxopyrido[1,2-a]pyrimidin-9-olate ligand, another O atom from the second ligand, one water mol-ecule and one Cl atom. The crystal structure involves inter-molecular C-H⋯Cl, O-H⋯Cl and O-H⋯O hydrogen bonds.

BACKGROUND:Some mutations in the internal regions of exons occur within splicing enhancers and silencers, influencing the pattern of alternative splicing in the corresponding genes. To understand how these sequence changes affect splicing, we created a database of these mutations.FINDINGS:The Alternative Splicing Mutation Database (ASMD) serves as a repository for all exonic mutations not associated with splicing junctions that measurably change the pattern of alternative splicing. In this initial published release (version 1.2), only human sequences are present, but the ASMD will grow to include other organisms, (see Availability and requirements section for the ASMD web address).This relational database allows users to investigate connections between mutations and features of the surrounding sequences, including flanking sequences, RNA secondary structures and strengths of splice junctions. Splicing effects of the mutations are quantified by the relative presence of alternative mRNA isoforms with and without a given mutation. This measure is further categorized by the accuracy of the experimental methods employed. The database currently contains 170 mutations in 66 exons, yet these numbers increase regularly.We developed an algorithm to derive a table of oligonucleotide Splicing Potential (SP) values from the ASMD dataset. We present the SP concept and tools in detail in our corresponding article.CONCLUSION:The current data set demonstrates that mutations affecting splicing are located throughout exons and might be enriched within local RNA secondary structures. Exons from the ASMD have below average splicing junction strength scores, but the difference is small and is judged not to be significant.

We assessed the temporal and spatial characteristics of PN-induced oxidative damage and its relationship to calpain-mediated cytoskeletal degradation and neurodegeneration in a severe unilateral controlled cortical impact (CCI) traumatic brain injury (TBI) model. Quantitative temporal time course studies were performed to measure two oxidative damage markers: 3-nitrotyrosine (3NT) and 4-hydroxynonenal (4HNE) at 30 min, 1, 3, 6, 12, 24, 48, 72 h and 7 days after injury in ipsilateral cortex of young adult male CF- I mice. Secondly, the time course of Ca++-activated, calpain-mediated proteolysis was also analyzed using quantitative western-blot measurement of breakdown products of the cytoskeletal protein alpha-spectrin. Finally, the time course of neurodegeneration was examined using de Olmos silver staining. Both oxidative damage markers increased in cortical tissue immediately after injury (30 min) and elevated for the first 3-6 h before returning to baseline. In the immunostaining study, the PN-selective marker, 3NT, and the lipid peroxidation marker, 4HNE, were intense and overlapping in the injured cortical tissue. alpha-Spectrin breakdown products, which were used as biomarker for calpain-mediated cytoskeletal degradation, were also increased after injury, but the time course lagged behind the peak of oxidative damage and did not reach its maximum until 24 h post-injury. In turn, cytoskeletal degradation preceded the peak of neurodegeneration which occurred at 48 h post-injury. These studies have led us to the hypothesis that PN-mediated oxidative damage is an early event that contributes to a compromise of Ca++ homeostatic mechanisms which causes a massive Ca++ overload and calpain activation which is a final common pathway that results in post-traumatic neurodegeneration. (C) 2007 Elsevier Inc. All rights reserved.

This paper presents a method for designing low-delay nonuniform pseudo quadrature mirror filter (QMF) banks. This method is motivated by the work of Li, Nguyen, and Tantaratana, in which the nonuniform filter bank is realized by combining an appropriate number of adjacent sub-bands of a uniform pseudo-QMF bank. In prior work, the prototype filter of the uniform pseudo-QMF bank was constrained to have linear phase and the overall delay associated with the filter bank was often unacceptably large for filter banks with a large number of sub-bands. This paper proposes a pseudo-QMF filter bank design technique that significantly reduces the delay by relaxing the linear phase constraints. An example in which an oversampled critical-band nonuniform filter bank is designed and applied to a two-state modeling speech enhancement system is presented in this paper. Comparison of the performance of this system to competing methods employing tree-structured, linear phase multiresolution analysis indicates that the approach described in this paper strikes a good balance between system performance and low delay

Objective. To develop a process that yields tissue-engineered articular cartilage constructs from skin-derived cells.Methods. Dermis-isolated, aggrecan-sensitive (DIAS) cells were isolated using a modified rapid adherence process. The chondrogenic potential was measured by quantitative reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent. assay, and immunohistochemistry. Filamentous actin (F-actin) and vinculin organization was detected using fluorescence microscopy.Results. The rapid adherence process led to a selection of DIAS cells, < 10% of the entire population. DIAS cells displayed greater chondroinduction potential, as evidenced by the formation of large numbers of chondrocytic nodules on aggrecan-coated surfaces. In addition, these cells showed higher gene expression and protein production in terms of chondrocytic markers when compared with unpurified dermis cells. Similar patterns of F-actin and vinculin organization were observed between DIAS cells and chondrocytes. Three-dimensional constructs from chondroinduced DIAS cells produced greater amounts of cartilage matrix than constructs from the rest of the dermis populations.Conclusion. These findings show a series of steps that work together to form tissue-engineered articular cartilage constructs using DIAS cells. Since skin presents a minimally invasive, relatively abundant cell source for tissue engineering, this study offers evidence of an efficient and stable technique to form cartilage constructs for future cartilage regeneration with autologous cells from skin.