INTRODUCTIONProblem-based learning (PBL) embraces principles of good learning and teaching. It is student-directed, fosters intrinsic motivation, promotes active learning, encourages peer teaching, involves timely feedback, and can support student self and peer assessment. The most important function of the assessment process is to enhance student learning, to improve the curriculum and to improve teaching.

MATERIALS AND METHODSTo improve the PBL tutorial in Chung Shan Medical University, we developed an online evaluation system containing the evaluation forms for students, tutor, self and peer. The Cronbach alpha reliability coefficients were 0.9480, 0.9103, and 0.9198 for the Student, Tutor and Self and Peer Evaluation Form, respectively. The online evaluations were mandatory to both students and tutors, and the information was completely anonymous.

RESULTS AND CONCLUSIONSThe survey response rates of the online evaluations ranged from 95.6% to 100%. The online evaluations provided a documented feedback to the students on their knowledge, skills and attitudes. Correspondingly, tutors too received feedback from students in evaluating their performance on the appropriateness and effectiveness of tutoring the group. Although there was an initial lack of coordination regarding responsibilities and how to use the online system for both students and the Faculty, the system enabled us to look into how effective our PBL course had been, and it provided both process and outcome evaluations. Our strategy for evaluating the success of PBL is only at its initial stage; we are in an ongoing process of collecting outcome data for further analysis which will hopefully provide more constructive information to the PBL curricula.

Education, Medical ; standards ; Educational Measurement ; Humans ; Online Systems ; Pilot Projects ; Problem-Based Learning ; methods ; Taiwan ; Universities

The prevalence of asthma and allergic disease has increased worldwide over the last few decades. Many common environmental factors are associated with this increase. Several theories have been proposed to account for this trend, especially those concerning the impact of environmental toxicants. The development of the immune system, particularly in the prenatal period, has far-reaching consequences for health during early childhood, and throughout adult life. One underlying mechanism for the increased levels of allergic responses, secondary to exposure, appears to be an imbalance in the T-helper function caused by exposure to the toxicants. Exposure to environmental endocrine-disrupting chemicals can result in dramatic changes in cytokine production, the activity of the immune system, the overall Th1 and Th2 balance, and in mediators of type 1 hypersensitivity mediators, such as IgE. Passive exposure to tobacco smoke is a common risk factor for wheezing and asthma in children. People living in urban areas and close to roads with a high volume of traffic, and high levels of diesel exhaust fumes, have the highest exposure to environmental compounds, and these people are strongly linked with type 1 hypersensitivity disorders and enhanced Th2 responses. These data are consistent with epidemiological research that has consistently detected increased incidences of allergies and asthma in people living in these locations. During recent decades more than 100,000 new chemicals have been used in common consumer products and are released into the everyday environment. Therefore, in this review, we discuss the environmental effects on allergies of indoor and outside exposure.
Adult ; Asthma ; Child ; Humans ; Hypersensitivity ; Immune System ; Immunoglobulin E ; Incidence ; Inflammation* ; Prevalence ; Respiratory Sounds ; Risk Factors ; Smoke ; Smoking ; Tobacco ; Vehicle Emissions

Asthma, a chronic inflammatory disorder of the airway, has features of both heritability as well as environmental influences which can be introduced in utero exposures and modified through aging, and the features may attribute to epigenetic regulation. Epigenetic regulation explains the association between early prenatal maternal smoking and later asthma-related outcomes. Epigenetic marks (DNA methylation, modifications of histone tails or noncoding RNAs) work with other components of the cellular regulatory machinery to control the levels of expressed genes, and several allergy- and asthma-related genes have been found to be susceptible to epigenetic regulation, including genes important to T-effector pathways (IFN-γ, interleukin [IL] 4, IL-13, IL-17) and T-regulatory pathways (FoxP3). Therefore, the mechanism by which epigenetic regulation contributes to allergic diseases is a critical issue. In the past most published experimental work, with few exceptions, has only comprised small observational studies and models in cell systems and animals. However, very recently exciting and elegant experimental studies and novel translational research works were published with new and advanced technologies investigating epigenetic mark on a genomic scale and comprehensive approaches to data analysis. Interestingly, a potential link between exposure to environmental pollutants and the occurrence of allergic diseases is revealed recently, particular in developed and industrialized countries, and endocrine disrupting chemicals (EDCs) as environmental hormone may play a key role. This review addresses the important question of how EDCs (nonylphenol, 4 octylphenol, and phthalates) influences on asthma-related gene expression via epigenetic regulation in immune cells, and how anti-asthmatic agents prohibit expression of inflammatory genes via epigenetic modification. The discovery and validation of epigenetic biomarkers linking exposure to allergic diseases might lead to better epigenotyping of risk, prognosis, treatment prediction, and development of novel therapies.
Acetylation ; Aging ; Animals ; Anti-Asthmatic Agents ; Asthma ; Biomarkers ; Developed Countries ; Endocrine Disruptors ; Environmental Pollutants ; Epigenomics ; Gene Expression ; Histones ; Hypersensitivity ; Interleukin-13 ; Interleukins ; Methylation ; Prognosis ; Smoke ; Smoking ; Statistics as Topic ; Tail ; Translational Medical Research

Inflammation alters the neural stem cell (NSC) lineage from neuronal to astrogliogenesis. However, the underlying mechanism is elusive. Autophagy contributes to the decline in adult hippocampal neurogenesis under E. coli lipopolysaccharide (LPS) stimulation. SRY-box transcription Factor 2 (SOX2) is critical for NSC self-renewal and proliferation. In this study, we investigated the role of SOX2 in induced autophagy and hippocampal adult neurogenesis under LPS stimulation. LPS (5 ng•100 g -1 •hour -1 for 7 days) was intraperitoneally infused into male Sprague–Dawley rats (8 weeks old) to induce mild systemic inflammation. Beclin 1 and autophagy protein 12 (Atg12) were significantly upregulated concurrent with decreased numbers of Ki67- and doublecortin (DCX)-positive cells in the dentate gyrus. Synchronically, the levels of phospho(p)-mTOR, the p-mTOR/mTOR ratio, p-P85s6k, and the p-P85s6k/P85s6k ratio were suppressed. In contrast, SOX2 expression was increased. The fluorescence micrographs indicated that the colocalization of Beclin 1 and SOX2 was increased in the subgranular zone (SGZ) of the dentate gyrus. Moreover, increased S100β-positive astrocytes were colocalized with SOX2 in the SGZ. Intracerebroventricular infusion of 3-methyladenine (an autophagy inhibitor) effectively prevented the increases in Beclin 1, Atg12, and SOX2. The SOX2 + -Beclin 1 + and SOX2 + -S100β + cells were reduced. The levels of p-mTOR and p-P85s6k were enhanced. Most importantly, the number of DCX-positive cells was preserved. Altogether, these data suggest that LPS induced autophagy to inactivate the mTOR/P85s6k pathway, resulting in a decline in neural differentiation. SOX2 was upregulated to facilitate the NSC lineage, while the autophagy milieu could switch the SOX2-induced NSC lineage from neurogenesis to astrogliogenesis.

Objectives: Concerns about erythropoietin (EPO) therapy for anemia in patients with end-stage renal disease (ESRD) contributing to potential bone loss and increased fracture risks are growing. This study investigated the impact of EPO administration on the risk of common osteoporotic fractures in ESRD patients. Methods: This population-based retrospective cohort study compared EPO users and non-EPO users among ESRD patients undergoing hemodialysis, diagnosed with ESRD between 2000 and 2014 identified from the National Health Insurance Research Database of Taiwan. The cohorts were matched at a propensity score ratio of 1:1, resulting in equal sample sizes of 2839. Variables related to comorbidities were considered. Results: EPO users exhibited higher cumulative incidences of major osteoporotic fractures, hip fractures, spine fractures, and wrist fractures compared with the non-EPO user (all P < 0.001). In adjusted Cox regression models, higher adjusted subdistribution hazard ratios (aSHRs) were observed for major osteoporotic fractures (2.41, 95% confidence interval [CI] = 2.01–2.89), osteoporotic hip fractures (2.19, 95% CI = 1.69–2.85), spine fractures (2.50, 95% CI = 1.87–3.34), and wrist fractures (2.34, 95% CI = 1.44–3.78) in EPO users than in nonEPO users. The risk of major osteoporotic fractures significantly increased with increasing EPO doses (P for trend < 0.0001), and a similar trend was observed for the risks of osteoporotic spine and wrist fractures. Conclusions Our findings suggest that EPO treatment in patients with ESRD undergoing hemodialysis is associated with an increased risk of osteoporotic fractures.

Objectives: Concerns about erythropoietin (EPO) therapy for anemia in patients with end-stage renal disease (ESRD) contributing to potential bone loss and increased fracture risks are growing. This study investigated the impact of EPO administration on the risk of common osteoporotic fractures in ESRD patients. Methods: This population-based retrospective cohort study compared EPO users and non-EPO users among ESRD patients undergoing hemodialysis, diagnosed with ESRD between 2000 and 2014 identified from the National Health Insurance Research Database of Taiwan. The cohorts were matched at a propensity score ratio of 1:1, resulting in equal sample sizes of 2839. Variables related to comorbidities were considered. Results: EPO users exhibited higher cumulative incidences of major osteoporotic fractures, hip fractures, spine fractures, and wrist fractures compared with the non-EPO user (all P < 0.001). In adjusted Cox regression models, higher adjusted subdistribution hazard ratios (aSHRs) were observed for major osteoporotic fractures (2.41, 95% confidence interval [CI] = 2.01–2.89), osteoporotic hip fractures (2.19, 95% CI = 1.69–2.85), spine fractures (2.50, 95% CI = 1.87–3.34), and wrist fractures (2.34, 95% CI = 1.44–3.78) in EPO users than in nonEPO users. The risk of major osteoporotic fractures significantly increased with increasing EPO doses (P for trend < 0.0001), and a similar trend was observed for the risks of osteoporotic spine and wrist fractures. Conclusions Our findings suggest that EPO treatment in patients with ESRD undergoing hemodialysis is associated with an increased risk of osteoporotic fractures.

Objectives: Concerns about erythropoietin (EPO) therapy for anemia in patients with end-stage renal disease (ESRD) contributing to potential bone loss and increased fracture risks are growing. This study investigated the impact of EPO administration on the risk of common osteoporotic fractures in ESRD patients. Methods: This population-based retrospective cohort study compared EPO users and non-EPO users among ESRD patients undergoing hemodialysis, diagnosed with ESRD between 2000 and 2014 identified from the National Health Insurance Research Database of Taiwan. The cohorts were matched at a propensity score ratio of 1:1, resulting in equal sample sizes of 2839. Variables related to comorbidities were considered. Results: EPO users exhibited higher cumulative incidences of major osteoporotic fractures, hip fractures, spine fractures, and wrist fractures compared with the non-EPO user (all P < 0.001). In adjusted Cox regression models, higher adjusted subdistribution hazard ratios (aSHRs) were observed for major osteoporotic fractures (2.41, 95% confidence interval [CI] = 2.01–2.89), osteoporotic hip fractures (2.19, 95% CI = 1.69–2.85), spine fractures (2.50, 95% CI = 1.87–3.34), and wrist fractures (2.34, 95% CI = 1.44–3.78) in EPO users than in nonEPO users. The risk of major osteoporotic fractures significantly increased with increasing EPO doses (P for trend < 0.0001), and a similar trend was observed for the risks of osteoporotic spine and wrist fractures. Conclusions Our findings suggest that EPO treatment in patients with ESRD undergoing hemodialysis is associated with an increased risk of osteoporotic fractures.

Objectives: Concerns about erythropoietin (EPO) therapy for anemia in patients with end-stage renal disease (ESRD) contributing to potential bone loss and increased fracture risks are growing. This study investigated the impact of EPO administration on the risk of common osteoporotic fractures in ESRD patients. Methods: This population-based retrospective cohort study compared EPO users and non-EPO users among ESRD patients undergoing hemodialysis, diagnosed with ESRD between 2000 and 2014 identified from the National Health Insurance Research Database of Taiwan. The cohorts were matched at a propensity score ratio of 1:1, resulting in equal sample sizes of 2839. Variables related to comorbidities were considered. Results: EPO users exhibited higher cumulative incidences of major osteoporotic fractures, hip fractures, spine fractures, and wrist fractures compared with the non-EPO user (all P < 0.001). In adjusted Cox regression models, higher adjusted subdistribution hazard ratios (aSHRs) were observed for major osteoporotic fractures (2.41, 95% confidence interval [CI] = 2.01–2.89), osteoporotic hip fractures (2.19, 95% CI = 1.69–2.85), spine fractures (2.50, 95% CI = 1.87–3.34), and wrist fractures (2.34, 95% CI = 1.44–3.78) in EPO users than in nonEPO users. The risk of major osteoporotic fractures significantly increased with increasing EPO doses (P for trend < 0.0001), and a similar trend was observed for the risks of osteoporotic spine and wrist fractures. Conclusions Our findings suggest that EPO treatment in patients with ESRD undergoing hemodialysis is associated with an increased risk of osteoporotic fractures.

Objectives: Concerns about erythropoietin (EPO) therapy for anemia in patients with end-stage renal disease (ESRD) contributing to potential bone loss and increased fracture risks are growing. This study investigated the impact of EPO administration on the risk of common osteoporotic fractures in ESRD patients. Methods: This population-based retrospective cohort study compared EPO users and non-EPO users among ESRD patients undergoing hemodialysis, diagnosed with ESRD between 2000 and 2014 identified from the National Health Insurance Research Database of Taiwan. The cohorts were matched at a propensity score ratio of 1:1, resulting in equal sample sizes of 2839. Variables related to comorbidities were considered. Results: EPO users exhibited higher cumulative incidences of major osteoporotic fractures, hip fractures, spine fractures, and wrist fractures compared with the non-EPO user (all P < 0.001). In adjusted Cox regression models, higher adjusted subdistribution hazard ratios (aSHRs) were observed for major osteoporotic fractures (2.41, 95% confidence interval [CI] = 2.01–2.89), osteoporotic hip fractures (2.19, 95% CI = 1.69–2.85), spine fractures (2.50, 95% CI = 1.87–3.34), and wrist fractures (2.34, 95% CI = 1.44–3.78) in EPO users than in nonEPO users. The risk of major osteoporotic fractures significantly increased with increasing EPO doses (P for trend < 0.0001), and a similar trend was observed for the risks of osteoporotic spine and wrist fractures. Conclusions Our findings suggest that EPO treatment in patients with ESRD undergoing hemodialysis is associated with an increased risk of osteoporotic fractures.

Percutaneous transluminal coronary angioplasty with metal stent placement has become a well-developed treatment modality for coronary stenotic lesions. Although infection involving implanted stents is rare, it can, however, occur with high morbidity and mortality. We describe herein a case of an inserted coronary stent that was infected and complicated with recurrent stent thrombosis, pseudoaneurysm formation and severe sepsis. Despite repeated intervention and bypass surgery, the patient died from severe sepsis.
Aneurysm, False ; Angioplasty, Balloon, Coronary ; Humans ; Mortality ; Myocardial Infarction ; Sepsis ; Stents* ; Thrombosis*