THE EFFECT OF CHANGING-SPEED ON THE TOE HEIGHT ON TREADMILL RUNNING

The purpose of this investigation is to observe the differences of foot trajectory when having changing-speed running in treadmill. Subjects running on a treadmill at three different speeds and performing a dynamic data from the mark in toe box and heel counter. The result shows that with increased speed the first peak toe height just after toe-off and toe clearance (TC) increased significantly, and decreased significantly with decreased speed. The result has significant different from walking. In addition, one of four subjects has more obvious foot flat than other subjects. The reason of this phenomenon is still unclear, and we still expect that there will be more studies to establish the treadmill exercise model

Paxillin facilitates timely neurite initiation on soft-substrate environments by interacting with the endocytic machinery.

Neurite initiation is the first step in neuronal development and occurs spontaneously in soft tissue environments. Although the mechanisms regulating the morphology of migratory cells on rigid substrates in cell culture are widely known, how soft environments modulate neurite initiation remains elusive. Using hydrogel cultures, pharmacologic inhibition, and genetic approaches, we reveal that paxillin-linked endocytosis and adhesion are components of a bistable switch controlling neurite initiation in a substrate modulus-dependent manner. On soft substrates, most paxillin binds to endocytic factors and facilitates vesicle invagination, elevating neuritogenic Rac1 activity and expression of genes encoding the endocytic machinery. By contrast, on rigid substrates, cells develop extensive adhesions, increase RhoA activity and sequester paxillin from the endocytic machinery, thereby delaying neurite initiation. Our results highlight paxillin as a core molecule in substrate modulus-controlled morphogenesis and define a mechanism whereby neuronal cells respond to environments exhibiting varying mechanical properties

HPV infection and p53 inactivation in pterygium

PurposeOur recent report indicated that tumor suppressor gene (p53) mutations and protein aberrant expression were detected in pterygium. Inactivation of p53 by Human papillomavirus (HPV) 16/18 E6 plays a crucial role in cervical tumorigenesis. In this study, we further speculate that p53 inactivation may be linked with HPV infection in pterygium pathogenesis. To investigate the involvement of HPV 16/18 E6 in p53 inactivation in pterygium, the association between HPV 16 or HPV 18 infection, the HPV E6 oncoprotein, and p53 protein expression was analyzed in this study.MethodsHPV 16/18 infection was detected by nested-polymerase chain reaction (nested-PCR), the p53 mutation was detected by direct sequencing, and the p53 and the HPV 16/18 E6 proteins were studied using immunohistochemistry on 129 pterygial specimens and 20 normal conjunctivas.ResultsThe HPV 16/18 was detected in 24% of the pterygium tissues (31 of 129) but not in the normal conjunctiva, and the HPV16/18 E6 oncoprotein was detected in 48.3% of HPV 16/18 DNA-positive pterygium tissues (15 of 31). In addition, p53 protein negative expression in pterygium was correlated with HPV16/18 E6 oncoprotein expression but not with a p53 mutation.ConclusionsHPV 16/18 E6 contributes to HPV-mediated pterygium pathogenesis as it is partly involved in p53 inactivation and is expressed in HPV DNA-positive pterygium

State Transportation Improvement Program for Federal Fiscal Years 2011-2014

OBJECTIVES:To develop and validate a Taiwanese version of the Health Enhancement Lifestyle Profile (HELP-T) for community-dwelling older Taiwanese adults (≥ 55 years). METHODS:The original Health Enhancement Lifestyle Profile (HELP) is a 56-item self-report questionnaire measuring various aspects of health-related lifestyles in older adults. The standard cultural-adaptation procedure was used for questionnaire translation and modification. A field test was conducted for culturally specific item selection, rating-scale analysis, and psychometric validation of the HELP-T in a sample of 274 community-dwelling older adults via classical test theory. RESULTS:The 59-item HELP-T is culturally adapted from the original 56-item HELP. The original 6-point rating scale was modified to a 3-point scale for easy use by Taiwanese older adults. The HELP-T had good internal consistency (Cronbach's alpha = 0.82). The test-retest reliability for the total score was high (0.92), and moderate to high (range: 0.57-0.92) for subscales. The construct validity was supported by the significant correlations between each subscale and the total score (Spearman's rho = 0.41-0.67, p < 0.0001) and by the ability of the scores to significantly discriminate between participants with different levels of self-rated health (p = 0.0001). CONCLUSIONS:The HELP-T is a suitable clinical tool for assessing and monitoring lifestyle risk factors, establishing client-centered lifestyle intervention goals, and determining the outcomes of lifestyle interventions

Understanding Multidecadal Climate Changes

The 2012 National Taiwan University International Science Conference on Climate Change focused on two of the most difficult challenges in the study of climate change. The 23 invited reviews at the conference were presented in hour-long segments, each beginning with a lecture and followed by discussion. These reviews were augmented by 20 contributed oral and poster papers. The AMOC fingerprints described at the meeting may be used for reconstructing AMOC variations in the past and monitoring AMOC variations in the future. Modeling studies indicate that the AMOC weakens most at northern high latitudes in response to increasing greenhouse gas concentrations. The number, intensity, tracks, and landfall locations of WNP TCs also exhibit strong decadal or multidecadal variations. When adjusted for likely missed TCs, the observational record does not show evidence of a significant secular trend in North Atlantic hurricane activity

The nucleolar protein NIFK promotes cancer progression via CK1α/β-catenin in metastasis and Ki-67-dependent cell proliferation.

Nucleolar protein interacting with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein. However, its precise function in cancer remains largely uninvestigated. Here we show the clinical significance and metastatic mechanism of NIFK in lung cancer. NIFK expression is clinically associated with poor prognosis and metastasis. Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, invasion in vitro and metastasis in vivo via downregulation of casein kinase 1α (CK1α), a suppressor of pro-metastatic TCF4/β-catenin signaling. Inversely, CK1α is upregulated upon NIFK knockdown. The silencing of CK1α expression in NIFK-silenced cells restores TCF4/β-catenin transcriptional activity, cell migration, and metastasis. Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1 (CK1α) that is negatively regulated by NIFK. Our results demonstrate the prognostic value of NIFK, and suggest that NIFK is required for lung cancer progression via the RUNX1-dependent CK1α repression, which activates TCF4/β-catenin signaling in metastasis and the Ki-67-dependent regulation in cell proliferation