THE DYNAMICAL ANALYSIS OF TABLE TENNIS FOREHAND AND BACKHAND DRIVES

[[abstract]]The purpose of this study was to analyze the dynamics parameters of table tennis drives by Taiwan collegiate first class table tennis players when they were performing straight and cross court forehand and backhand drives from receiving topspin and backspin serves. Ten Vicon MX-13+ high-speed cameras (250Hz) and two Kistler force plates (1500 Hz) were used to collect the kinematics and kinetics data. The Wilcoxon matched-pairs signed-rank nonparametric statistical test was to compare the differences between forehand and backhand drives. The results showed that there were significant differences between forehand and backhand drives were in the ball initial velocity and the kinetics variables. The GRF data of the players were different between forehand and backhand drives when they performed four different paths of drive.[[conferencetype]]國際[[conferencedate]]20130707~20130711[[booktype]]紙本[[booktype]]電子版[[iscallforpapers]]Y[[iscallforpapers]]Y[[conferencelocation]]Taipei, Taiwa

THE DYNAMICAL ANALYSIS OF TABLE TENNIS FOREHAND AND BACKHAND DRIVES

The purpose of this study was to analyze the dynamics parameters of table tennis drives by Taiwan collegiate first class table tennis players when they were performing straight and cross court forehand and backhand drives from receiving topspin and backspin serves. Ten Vicon MX-13+ high-speed cameras (250Hz) and two Kistler force plates (1500 Hz) were used to collect the kinematics and kinetics data. The Wilcoxon matched-pairs signed-rank nonparametric statistical test was to compare the differences between forehand and backhand drives. The results showed that there were significant differences between forehand and backhand drives were in the ball initial velocity and the kinetics variables. The GRF data of the players were different between forehand and backhand drives when they performed four different paths of drive

Src-homology 2 domain-containing tyrosine phosphatase 2 promotes oral cancer invasion and metastasis

BACKGROUND: Tumor invasion and metastasis represent a major unsolved problem in cancer pathogenesis. Recent studies have indicated the involvement of Src-homology 2 domain-containing tyrosine phosphatase 2 (SHP2) in multiple malignancies; however, the role of SHP2 in oral cancer progression has yet to be elucidated. We propose that SHP2 is involved in the progression of oral cancer toward metastasis. METHODS: SHP2 expression was evaluated in paired oral cancer tissues by using immunohistochemical staining and real-time reverse transcription polymerase chain reaction. Isogenic highly invasive oral cancer cell lines from their respective low invasive parental lines were established using a Boyden chamber assay, and changes in the hallmarks of the epithelial-mesenchymal transition (EMT) were assessed to evaluate SHP2 function. SHP2 activity in oral cancer cells was reduced using si-RNA knockdown or enforced expression of a catalytically deficient mutant to analyze migratory and invasive ability in vitro and metastasis toward the lung in mice in vivo. RESULTS: We observed the significant upregulation of SHP2 in oral cancer tissues and cell lines. Following SHP2 knockdown, the oral cancer cells markedly attenuated migratory and invasion ability. We observed similar results in phosphatase-dead SHP2 C459S mutant expressing cells. Enhanced invasiveness was associated with significant upregulation of E-cadherin, vimentin, Snail/Twist1, and matrix metalloproteinase-2 in the highly invasive clones. In addition, we determined that SHP2 activity is required for the downregulation of phosphorylated ERK1/2, which modulates the downstream effectors, Snail and Twist1 at a transcript level. In lung tissue sections of mice, we observed that HSC3 tumors with SHP2 deletion exhibited significantly reduced metastatic capacity, compared with tumors administered control si-RNA. CONCLUSIONS: Our data suggest that SHP2 promotes the invasion and metastasis of oral cancer cells. These results provide a rationale for further investigating the effects of small-molecule SHP2 inhibitors on the progression of oral cancer, and indicate a previously unrecognized SHP2-ERK1/2-Snail/Twist1 pathway that is likely to play a crucial role in oral cancer invasion and metastasis

RINGdb: An integrated database for G protein-coupled receptors and regulators of G protein signaling

BACKGROUND: Many marketed therapeutic agents have been developed to modulate the function of G protein-coupled receptors (GPCRs). The regulators of G-protein signaling (RGS proteins) are also being examined as potential drug targets. To facilitate clinical and pharmacological research, we have developed a novel integrated biological database called RINGdb to provide comprehensive and organized RGS protein and GPCR information. RESULTS: RINGdb contains information on mutations, tissue distributions, protein-protein interactions, diseases/disorders and other features, which has been automatically collected from the Internet and manually extracted from the literature. In addition, RINGdb offers various user-friendly query functions to answer different questions about RGS proteins and GPCRs such as their possible contribution to disease processes, the putative direct or indirect relationship between RGS proteins and GPCRs. RINGdb also integrates organized database cross-references to allow users direct access to detailed information. The database is now available at . CONCLUSION: RINGdb is the only integrated database on the Internet to provide comprehensive RGS protein and GPCR information. This knowledgebase will be useful for clinical research, drug discovery and GPCR signaling pathway research

Magnesium-enriched deep-sea water inhibits NLRP3 inflammasome activation and dampens inflammation.

The NLRP3 inflammasome is an essential component of the innate immune system, but excessive activation can lead to inflammatory diseases. Ion fluxes across the plasma membrane or from intracellular stores are known to regulate NLRP3 inflammasome activation. Deep-sea water (DSW) contains high concentrations of many mineral ions, which could potentially influence NLRP3 inflammasome activation. However, the impact of DSW on NLRP3 inflammasome activation has not been investigated. Here, we demonstrated that DSW with water hardness levels up to 500 mg/L did not affect cell viability or the expression of NLRP3 inflammasome components in macrophages derived from THP-1 cells. However, the DSW significantly inhibited IL-1β secretion and caspase-1 activation in response to NLRP3 activators such as nigericin, ATP, or monosodium urate (MSU) crystals. Mechanically, it was discovered that the presence of 5 mM magnesium ions (Mg2+), equivalent to the Mg2+ concentration found in the DSW with a water hardness of 500 mg/L, inhibits NLRP3 inflammasome activation. This indicates that Mg2+ contributes to the mechanism by which DSW mitigates NLRP3 inflammasome activation. Moreover, DSW administration effectively lessens MSU-triggered peritonitis in mice, a commonly used model for examining the impacts of NLRP3 inflammasome activation. These results show that DSW enriched with Mg2+ could potentially be beneficial in modulating NLRP3 inflammasome-associated diseases

Randomized Comparative Study of the Effects of Treatment with Once-Daily, Niacin Extended-Release/Lovastatin and with Simvastatin on Lipid Profile and Fibrinolytic Parameters in Taiwan

Hyperlipidemia can be effectively treated either with niacin or HMG-CoA reductase inhibitor (statin), or a combination of both. Few reports showed the effects of the combination regimen with niacin and statin on hemostatic functions. We conducted a single-center, double-blind, double-dummy, randomized, two-arm study to assess the effects of the niacin extended-release/lovastatin therapy in a fixed-dose formulation and of simvastatin on lipid lowering and two fibrinolytic parameters, fibrinogen and d-dimer. All patients were enrolled according to NCEP-ATP III guidelines and underwent a placebo run-in period of 4 weeks before being randomized to either niacin extended-release/lovastatin tablets (500/20 mg) once daily (n = 36) or simvastatin capsule (20 mg) once daily (n = 34). After 16 weeks of treatment, both groups of patients showed significantly reduced low-density lipoprotein cholesterol and total cholesterol (LDL-C, p < 0.001 and < 0.001, respectively, p = 0.159 between the groups; TC, p < 0.001 and < 0.001, respectively, p = 0.018 between the groups). Both drugs were well tolerated. Only in the group treated with niacin extended-release/lovastatin was fibrinogen concentration significantly reduced after treatment (2.48 ± 0.65 to 1.99 ± 0.62 g/L, p = 0.008). No difference was found with d-dimer in either group. This study shows that both niacin extended-release/ lovastatin and simvastatin are effective and well-tolerated lipid-lowering drugs in Taiwanese patients with dyslipidemia. A combinational treatment with niacin extended-release/lovastatin may provide additional benefit in fibrinolysis

Identification of critical virulence factors of fusobacterium nucleatum in promoting colorectal carcinoma

Background: The presence of an oral commensal, Fusobacterium nucleatum, in colorectal cancer(CRC) has been identified as an indicator of poor prognosis and has also been shown to increase gradually from stage I to IV. Several adhesion molecules in F. nucleatum, including RadD, FadA and Fap2, have been identified as virulence factors in CRC. However, given that F. nucleatum contains over 2,000 genes, it is possible that additional undiscovered pathogenic factors are contributing to F. nucleatum induced CRC stimulation.Aims: (1) Identification of potential pathogenic genes involved in CRC progression; (2) Evaluation of biofilm properties of clinical F. nucleatum isolates and their carcinogenicity in CRC cell line.Methods: (1) A F. nucleatum transposon library was created through EZ-Tn5 transposon mutagenesis. The catP transposon DNA fragment contains a chloramphenicol/thiamphenicol resistant cassette that can be used as a selection marker for the insertion. F. nucleatum mutant colonies were inoculated into 96-well plates and stored at -80°C in 100% glycerol. (2) Clinical F. nucleatum isolates were successfully identified from saliva samples of 101 oral squamous cell carcinoma (OSCC) patients and 158 non-OSCC patients at a positive rate of 10%. The overnight bacterial culture was adjusted to OD 0.1 and anaerobically incubated at 37°C in 24-well plates for 96 hours. Bacterial biofilm stability was determined by comparing the density of attached biomass before and after washing with 500µl of 1X PBS twice. 1x106 of HCT116, a CRC cell line, were seeded in 6-well plates for 24 hours and a “+” mark was scratched with 200µl pipette tips. Overnight bacterial culture was resuspended in McCoy’s 5a medium (no supplements or antibiotics). HCT116 cells were then infected with MOI 10 of various clinical F. nucleatum isolates. Cell migration rates were calculated based on the distance traveled in 24 and 48 hours.Results and conclusions: A transposon mutant library of 9,600 mutant colonies of F. nucleatum was established, with a minimum genome coverage of 99% achieved. This robust genetic tool will be used to identify novel virulence genes. Clinical isolates from both OSCC and non-OSCC patients demonstrated varying levels of biofilm stability and CRC cell migration. Further experiments, such as bacterial cell adhesion and invasion, as well as RNA sequencing, will be performed to expand the knowledge towards the development of novel OSCC prevention and treatment strategies

Distinct Tumor Microenvironment at Tumor Edge as a Result of Astrocyte Activation Is Associated With Therapeutic Resistance for Brain Tumor

Tumor vasculatures and hypoxia are critical tumor micro-environmental factors associated with tumor response to the therapy and heterogeneous in both time- and location-dependent manner. Using a murine orthotopic anaplastic astrocytoma model, ALTS1C1, this study showed that brain tumor edge had a very unique microenvironment, having higher microvascular density (MVD) and better vessel function than the tumor core, but on the other hand was also positive for hypoxia markers, such as pimonidazole (PIMO), hypoxia inducible factor-1α (HIF-1α), and carbonic anhydrase IV (CAIX). The hypoxia at tumor edge was transient, named as peripheral hypoxia, and caused by different mechanisms from the chronic hypoxia in tumor core. The correlation of CAIX staining with astrocyte activation marker, glial fibrillary acid protein (GFAP), at the tumor edge indicated the involvement of astrocyte activation on the development of peripheral hypoxia. Peripheral hypoxia was a specific trait of orthotopic brain tumors at tumor edge, regardless of tumor origin. The hypoxic cells were resistant to the therapy, regardless of their location. Surviving cells, particularly those at the hypoxic region of tumor edge, are likely the cause of tumor recurrence after the therapy. New therapeutic platform that targets cells in tumor edge is likely to achieve better treatment outcomes

Modified Weekly Cisplatin-Based Chemotherapy Is Acceptable in Postoperative Concurrent Chemoradiotherapy for Locally Advanced Head and Neck Cancer

Background. Triweekly cisplatin-based postoperative concurrent chemoradiotherapy (CCRT) has high intolerance and toxicities in locally advanced head and neck cancer (LAHNC). We evaluated the effect of a modified weekly cisplatin-based chemotherapy in postoperative CCRT. Methods. A total of 117 patients with LAHNC were enrolled between December 2007 and December 2012. Survival, compliance/adverse events, and independent prognostic factors were analyzed. Results. Median follow-up time was 30.0 (3.1–73.0) months. Most patients completed the entire course of postoperative CCRT (radiotherapy ≥ 60 Gy, 94.9%; ≥6 times weekly chemotherapy, 75.2%). Only 17.1% patients required hospital admission. The most common adverse effect was grade 3/4 mucositis (28.2%). No patient died due to protocol-related adverse effects. Multivariate analysis revealed the following independent prognostic factors: oropharyngeal cancer, extracapsular spread, and total radiation dose. Two-year progression-free survival and overall survival rates were 70.9% and 79.5%, respectively. Conclusion. Modified weekly cisplatin-based chemotherapy is an acceptable regimen in postoperative CCRT for LAHNC