Fu Jen Catholic University

About: Fu Jen Catholic University is a education organization based out in Taipei, Taiwan. It is known for research contribution in the topics: Population & Medicine. The organization has 6842 authors who have published 9512 publications receiving 171005 citations. The organization is also known as: FJU & Fu Jen.

Associations between accurate prognostic understanding and end‐of‐life care preferences and its correlates among Taiwanese terminally ill cancer patients surveyed in 2011–2012

Abstract: Objective Adequate knowledge of prognosis is a prerequisite for planning appropriate end-of-life (EOL) care. However, questions remain about whether the association between prognostic understanding and EOL-care intensity reflects terminally ill cancer patients' preferences for EOL care. This study investigated the associations between accurate prognostic understanding and EOL-care preferences, and identified correlates of accurate prognostic understanding. Methods A cross-sectional survey of 2452 terminally ill cancer patients from 23 hospitals throughout Taiwan. Results Nearly half the participants (49.80%) accurately understood their prognosis. These patients were significantly more likely to prefer comfort-oriented care as their goal for EOL care, but less likely to prefer life-prolonging treatments. Accurately understanding prognosis decreased the likelihood of preferring intensive care unit care, cardiac pulmonary resuscitation, cardiac massage, intubation, and mechanical ventilation support, but increased preference for hospice care. Participants were significantly more likely to accurately understand their prognosis if they were male, younger, better educated, with a stronger preference for physicians to disclose their prognosis to them, and receiving care at a hospital accredited as a medical center and in northwest Taiwan. The likelihood of accurate prognostic understanding was lower for patients recently (≤12 months) diagnosed with cancers with better prognosis and hematologic malignancies than for lung cancer patients. Conclusions Accurately understanding prognosis is associated with fewer preferences for life-sustaining treatments and is correlated with both patient and institutional characteristics. Interventions should be developed to improve accurate prognostic understanding, thus facilitating informed EOL-care decisions that may limit the use of aggressive interventions. Copyright © 2014 John Wiley & Sons, Ltd.

Cycling hypoxia induces chemoresistance through the activation of reactive oxygen species-mediated B-cell lymphoma extra-long pathway in glioblastoma multiforme

Abstract: Cycling hypoxia is a well-recognized phenomenon within animal and human solid tumors. It contributes to the resistance to cytotoxic therapies through anti-apoptotic effects. However, the mechanism underlying cycling hypoxia-mediated anti-apoptosis remains unclear. Reactive oxygen species (ROS) production, activation of the hypoxia-inducible factor-1 alpha (HIF-1α) and nuclear factor-κB (NF-κB) signaling pathways, B-cell lymphoma extra-long (Bcl-xL) expression, caspase activation, and apoptosis in in vitro hypoxic stress-treated glioblastoma cells or tumor hypoxic cells derived from human glioblastoma xenografts were determined by in vitro ROS analysis, reporter assay, western blotting analysis, quantitative real-time PCR, caspase-3 activity assay, and annexin V staining assay, respectively. Tempol, a membrane-permeable radical scavenger, Bcl-xL knockdown, and specific inhibitors of HIF-1α and NF-κB were utilized to explore the mechanisms of cycling hypoxia-mediated resistance to temozolomide (TMZ) in vitro and in vivo and to identify potential therapeutic targets. Bcl-xL expression and anti-apoptotic effects were upregulated under cycling hypoxia in glioblastoma cells concomitantly with decreased responses to TMZ through ROS-mediated HIF-1α and NF-κB activation. Tempol, YC-1 (HIF-1 inhibitor), and Bay 11-7082 (NF-κB inhibitor) suppressed the cycling hypoxia-mediated Bcl-xL induction in vitro and in vivo. Bcl-xL knockdown and Tempol treatment inhibited cycling hypoxia-induced chemoresistance. Moreover, Tempol treatment of intracerebral glioblastoma-bearing mice combined with TMZ chemotherapy synergistically suppressed tumor growth and increased survival rate. Cycling hypoxia-induced Bcl-xL expression via ROS-mediated HIF-1α and NF-κB activation plays an important role in the tumor microenvironment-promoted anti-apoptosis and chemoresistance in glioblastoma. Thus, ROS blockage may be an attractive therapeutic strategy for tumor microenvironment-induced chemoresistance.

Impact of excellence programs on Taiwan higher education in terms of quality assurance and academic excellence, examining the conflicting role of Taiwan’s accrediting agencies

Abstract: Higher Education Evaluation & Accreditation Council of Taiwan (HEEACT) was established in 2005 and began to accredit 76 four-year comprehensive universities and colleges in Taiwan in 2006. Commissioned officially with a dual mission, HEEACT has been encouraged to conduct various ranking research projects, including global and national ones starting in 2007. One of the HEEACT’s most influential rankings is “Performance Ranking of Scientific Papers for World Universities.” Given the fact that more and more national accrediting bodies are developing ranking systems, these dual roles like in the HEEACT case have led to many discussions and raised severe criticism in the quality assurance community due to their different aims and approaches. Therefore, the purposes of the paper are to provide an understanding of the functions of varying quality assessment tools in higher education, to analyze their impact on Taiwan higher education and to examine the conflicting roles of HEEACT while conducting both accreditation and rankings over the institutions that have been granted the two major national Research and Teaching Excellence Programs.

Folate deprivation promotes mitochondrial oxidative decay: DNA large deletions, cytochrome c oxidase dysfunction, membrane depolarization and superoxide overproduction in rat liver.

Abstract: Little is known about the biological effect of folate in the protection against mitochondrial (mt) oxidative decay. The objective of the present study was to examine the consequence of folate deprivation on mt oxidative degeneration, and the mechanistic link underlying the relationship. Male Wistar rats were fed with an amino acid-defined diet containing either 8 (control) or 0 (folate-deficient, FD) mg folic acid/kg diet. After a 4-week FD feeding period, significant elevation in oxidative stress was observed inside the liver mitochondria with a 77% decrease in mt folate level (P<0.001), a 28 % reduction in glutathione peroxidase activity (P= 0.0333), a 1.2-fold increase of mt protein carbonyls (P=0.0278) and an accumulated 4834 bp large-scale deletion in mtDNA. The elicited oxidative injuries in FD liver mitochondria were associated with 30 % reduction of cytochrome c oxidase (CcOX) activity (P=0.0264). The defective CcOX activity in FD hepatocytes coincided with mt membrane potential dissipation and intracellular superoxide elevation. Exposure of FD hepatocytes to pro-oxidant challenge (32 microM-copper sulphate for 48 h) led to a further loss in CcOX activity and mt membrane potential with a simultaneous increase in superoxide production. Preincubation of pro-oxidant-treated FD hepatocytes with supplemental folic acid (10-1000 microM) reversed the mt oxidative defects described earlier and diminished superoxide overproduction. Increased supplemented levels of folic acid strongly correlated with decreased lipid peroxidation (gamma - 0.824, P=0.0001) and protein oxidative injuries (gamma -0.865, P=0.0001) in pro-oxidant-challenged FD liver mitochondria. Taken together, the results demonstrated that folate deprivation induces oxidative stress in liver mitochondria, which is associated with CcOX dysfunction, membrane depolarization and superoxide overproduction. The antioxidant activity of supplemental folic acid may partially, if not fully, contribute to the amelioration of pro-oxidant-elicited mt oxidative decay.