In Respect to the Cognitive Load Theory: Adjusting Instructional Guidance with Student Expertise.

The amount of guidance supplied by educators to students in allied health programs is a factor in student learning. According to the cognitive load theory of learning, without adequate instructional support, novice learners will be overwhelmed and unable to store information, while unnecessary guidance supplied to advanced students will cause extraneous cognitive load on the working memory system. Adjusting instructional guidance for students according to their level of expertise to minimize extraneous cognitive load and optimize working memory storage capacity will enhance learning effectiveness. Novice students presented with complex subject matter require significant guidance during the initial stages, using strategies such as worked examples. As students comprehend information, instructional guidance needs to gradually fade to avoid elevated extraneous cognitive load from the expertise reversal effect. An instructional strategy that utilizes a systemic (fixed) or adjustable (adaptive) tapering of guidance to students in allied health programs depending on their expertise will optimize learning capability.

Effect of core strength and endurance training on performance in college students: randomized pilot study.

Core training continues to be emphasized with the proposed intent of improving athletic performance. The purpose of this investigation was to discover if core isometric endurance exercises were superior to core isotonic strengthening exercises and if either influenced specific endurance, strength, and performance measures. Ten untrained students were randomly assigned to core isometric endurance (n = 5) and core isotonic strength training (n = 5). Each performed three exercises, two times per week for six weeks. A repeated measures ANOVA was used to compare the measurements for the dependent variables and significance by bonferroni post-hoc testing. The training protocols were compared using a 2 × 3 mixed model ANOVA. Improvement in trunk flexor and extensor endurance (p < 0.05) along with squat and bench press strength (p < 0.05) occurred with the strength group. Improvement in trunk flexor and right lateral endurance (p < 0.05) along with strength in the squat (p < 0.05) were found with the endurance group. Neither training protocol claimed superiority and both were ineffective in improving performance.

"Toxic memory" via chaperone modification is a potential mechanism for rapid Mallory-Denk body reinduction.

UNLABELLED: The cytoplasmic hepatocyte inclusions, Mallory-Denk bodies (MDBs), are characteristic of several liver disorders, including alcoholic and nonalcoholic steatohepatitis. In mice, MDBs can be induced by long-term feeding with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) for 3 to 4 months or rapidly reformed in DDC-induced then recovered mice by DDC refeeding or exposure to a wide range of toxins for only 5 to 7 days. The molecular basis for such a rapid reinduction of MDBs is unknown. We hypothesized that protein changes retained after DDC priming contribute to the rapid MDB reappearance and associate with MDB formation in general terms. Two-dimensional differential-in-gel-electrophoresis coupled with mass spectrometry were used to characterize protein changes in livers from the various treatment groups. The alterations were assessed by real-time reverse-transcription polymerase chain reaction and confirmed by immunoblotting. DDC treatment led to pronounced charged isoform changes in several chaperone families, including Hsp25, 60, 70, GRP58, GRP75, and GRP78, which lasted at least for 1 month after discontinuation of DDC feeding, whereas changes in other proteins normalized during recovery. DDC feeding also resulted in altered expression of Hsp72, GRP75, and Hsp25 and in functional impairment of Hsp60 and Hsp70 as determined using a protein complex formation and release assay. The priming toward rapid MDB reinduction lasts for at least 3 months after DDC discontinuation, but becomes weaker after prolonged recovery. MDB reinduction parallels the rapid increase in p62 and Hsp25 levels as well as keratin 8 cross-linking that is normally associated with MDB formation. CONCLUSION: Persistent posttranslational modifications in chaperone proteins, coupled with protein cross-linking and altered chaperone expression and function likely contribute to the "toxic memory" of DDC-primed mice. We hypothesize that similar changes are important contributors to inclusion body formation in several diseases.