Validation of learning style measures: implications for medical education practice

It is unclear which learners would most benefit from the more individualised, student-structured, interactive approaches characteristic of problem-based and computer-assisted learning. The validity of learning style measures is uncertain, and there is no unifying learning style construct identified to predict such learners. Objective  This study was conducted to validate learning style constructs and to identify the learners most likely to benefit from problem-based and computer-assisted curricula. Methods  Using a cross-sectional design, 3 established learning style inventories were administered to 97 post-Year 2 medical students. Cognitive personality was measured by the Group Embedded Figures Test, information processing by the Learning Styles Inventory, and instructional preference by the Learning Preference Inventory. The 11 subscales from the 3 inventories were factor-analysed to identify common learning constructs and to verify construct validity. Concurrent validity was determined by intercorrelations of the 11 subscales. Results  A total of 94 pre-clinical medical students completed all 3 inventories. Five meaningful learning style constructs were derived from the 11 subscales: student- versus teacher-structured learning; concrete versus abstract learning; passive versus active learning; individual versus group learning, and field-dependence versus field-independence. The concurrent validity of 10 of 11 subscales was supported by correlation analysis. Medical students most likely to thrive in a problem-based or computer-assisted learning environment would be expected to score highly on abstract, active and individual learning constructs and would be more field-independent. Conclusions  Learning style measures were validated in a medical student population and learning constructs were established for identifying learners who would most likely benefit from a problem-based or computer-assisted curriculum.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72443/1/j.1365-2929.2006.02476.x.pd

Streptococcus pneumoniae induced c-Jun-N-terminal kinase- and AP-1 -dependent IL-8 release by lung epithelial BEAS-2B cells

BACKGROUND: Although pneumococcal pneumonia is one of the most common causes of death due to infectious diseases, little is known about pneumococci-lung cell interaction. Herein we tested the hypothesis that pneumococci activated pulmonary epithelial cell cytokine release by c-Jun-NH(2)-terminal kinase (JNK) METHODS: Human bronchial epithelial cells (BEAS-2B) or epithelial HEK293 cells were infected with S. pneumoniae R6x and cytokine induction was measured by RT-PCR, ELISA and Bioplex assay. JNK-phosphorylation was detected by Western blot and nuclear signaling was assessed by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP). JNK was modulated by the small molecule inhibitor SP600125 and AP1 by transfection of a dominant negative mutant. RESULTS: S. pneumoniae induced the release of distinct CC and CXC, as well as Th1 and Th2 cytokines and growth factors by human lung epithelial cell line BEAS-2B. Furthermore, pneumococci infection resulted in JNK phosphorylation in BEAS-2B cells. Inhibition of JNK by small molecule inhibitor SP600125 reduced pneumococci-induced IL-8 mRNA expression and release of IL-8 and IL-6. One regulator of the il8 promoter is JNK-phosphorylated activator protein 1 (AP-1). We showed that S. pneumoniae time-dependently induced DNA binding of AP-1 and its phosphorylated subunit c-Jun with a maximum at 3 to 5 h after infection. Recruitment of Ser(63/73)-phosphorylated c-Jun and RNA polymerase II to the endogenous il8 promoter was found 2 h after S. pneumoniae infection by chromatin immunoprecipitation. AP-1 repressor A-Fos reduced IL-8 release by TLR2-overexpressing HEK293 cells induced by pneumococci but not by TNFα. Antisense-constructs targeting the AP-1 subunits Fra1 and Fra2 had no inhibitory effect on pneumococci-induced IL-8 release. CONCLUSION: S. pneumoniae-induced IL-8 expression by human epithelial BEAS-2B cells depended on activation of JNK and recruitment of phosphorylated c-Jun to the il8 promoter

Legionella pneumophila induces human beta Defensin-3 in pulmonary cells

<p>Abstract</p> <p>Background</p> <p><it>Legionella pneumophila </it>is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards <it>L. pneumophila</it>.</p> <p>Methods</p> <p>We investigated the effects of <it>L. pneumophila </it>and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis.</p> <p>Results</p> <p><it>L. pneumophila </it>induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-κB. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on <it>L. pneumophila </it>replication.</p> <p>Conclusions</p> <p>Taken together, human pulmonary cells produce hBD-3 upon <it>L. pneumophila </it>infection via a TLR-JNK-AP-1-dependent pathway which may contribute to an efficient innate immune defense.</p

Rac1 Regulates the NLRP3 Inflammasome Which Mediates IL-1beta Production in Chlamydophila pneumoniae Infected Human Mononuclear Cells

Chlamydophila pneumoniae causes acute respiratory tract infections and has been associated with development of asthma and atherosclerosis. The production of IL-1β, a key mediator of acute and chronic inflammation, is regulated on a transcriptional level and additionally on a posttranslational level by inflammasomes. In the present study we show that C. pneumoniae-infected human mononuclear cells produce IL-1β protein depending on an inflammasome consisting of NLRP3, the adapter protein ASC and caspase-1. We further found that the small GTPase Rac1 is activated in C. pneumoniae-infected cells. Importantly, studies with specific inhibitors as well as siRNA show that Rac1 regulates inflammasome activation in C. pneumoniae-infected cells. In conclusion, C. pneumoniae infection of mononuclear cells stimulates IL-1β production dependent on a NLRP3 inflammasome-mediated processing of proIL-1β which is controlled by Rac1

Determinants of quality of life in children with psychiatric disorders

Objective: To assess factors that, in addition to childhood psychopathology, are associated with Quality of Life (QoL) in children with psychiatric problems. Methods: In a referred sample of 252 8 to 18-year-olds, information concerning QoL, psychopathology and a broad range of child, parent, and family/ social network factors was obtained from children, parents, teachers and clinicians. Results: Poor child, parent, and clinician reported QoL was associated with child psychopathology, but given the presence of psychopathology, also with child factors, such as low self-esteem, and poor social skills, and family/social network factors, such as poor family functioning, and poor social support. In multiple linear regression analyses the importance of parent factors, such as parenting stress, was almost negligible. Conclusion: To increase QoL of children with psychiatric problems, treatment of symptoms is important, but outcome might improve if treatment is also focussed on other factors that may affect QoL. Results are discussed in relation to current treatment programs. © Springer 2005