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It has been controversial whether the matching of learning styles with teaching environment has improved the teaching effects. This paper constructs matching modes by choosing Sternberg's three learning styles (liberal leaning, internal scope and global level) and adopts curriculum comprehensiveness and instructing modes. The research, based on data of off-line teaching collected from 456 college students in China, finds that (a) direct effect: three learning styles have significant effects on eight dimensions of learners' cognitive information processing (CIP); (b) matching effect: the alignment of learners' liberal leaning and instructing modes has a direct impact on the eight dimensions of learners' CIP; the alignment of learners' global level and curriculum characteristics has a direct impact on the 7 dimensions; the alignment of learners' internal scope and instructing modes have no significant direct impact on the 7 dimensions; (c) moderating effect of the mandatory use of IT (MUIT): MUIT may restrain or strengthen effects of some matching modes on some dimensions of CIP. The key conclusion is that whether personalized instructing based on learners' characteristics can improve teaching results requires the selection of appropriate matching modes. Not all matching modes have matching effects, and matching effect is influenced by MUIT. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF), the most common human cardiac arrhythmia, is associated with abnormal intracellular [Ca.sup.2+] handling. Diastolic [Ca.sup.2+] release from the sarcoplasmic reticulum via "leaky" ryanodine receptors (RyR2s) is hypothesized to contribute to arrhythmogenesis in AF, but the molecular mechanisms are incompletely understood. Here, we have shown that mice with a genetic gain-of-function defect in Ryr2 (which we termed [Ryr2.sup.R176Q/+] mice) did not exhibit spontaneous AF but that rapid atrial pacing unmasked an increased vulnerability to AF in these mice compared with wild-type mice. Rapid atrial pacing resulted in increased [Ca.sup.2+]/calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2, while both pharmacologic and genetic inhibition of CaMKII prevented AF inducibility in [Ryr2.sup.R176Q/+] mice. This result suggests that AF requires both an arrhythmogenic substrate (e.g., RyR2 mutation) and enhanced CaMKII activity. Increased CaMKII phosphorylation of RyR2 was observed in atrial biopsies from mice with atrial enlargement and spontaneous AF, goats with lone AF, and patients with chronic AF. Genetic inhibition of CaMKII phosphorylation of RyR2 in [Ryr2.sup.S2814A] knockin mice reduced AF inducibility in a vagotonic AF model. Together, these findings suggest that increased RyR2-dependent [Ca.sup.2+] leakage due to enhanced CaMKII activity is an important downstream effect of CaMKII in individuals susceptible to AF induction., Introduction Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is a significant contributor to cardiovascular morbidity and possibly mortality. Emerging evidence suggests an important role for abnormal [...]

[Ca.sup.2+] overload and reactive oxygen species can injure mitochondria during ischemia and reperfusion. We hypothesized that mitochondrial injury occurs during cardiac resuscitation, causing release of cytochrome c to the cytosol and bloodstream while activating apoptotic pathways. Plasma cytochrome c was measured using reverse-phase HPLC and Western immunoblotting in rats subjected to 4 or 8 min of untreated ventricular fibrillation and 8 min of closed-chest resuscitation followed by 240 min of postresuscitation hemodynamic observation. A sham group served as control. Plasma cytochrome c rose progressively to levels 10-fold higher than in sham rats 240 min after resuscitation (P < 0.01), despite reversal of whole body ischemia (decreases in arterial lactate). Cytochrome c levels were inversely correlated with left ventricular stroke work (r = -0.40, P = 0.02). Western immunoblotting of left ventricular tissue demonstrated increased levels of 17-kDa cleaved caspase-3 fragments in the cytosol. Plasma cytochrome c was then serially measured in 12 resuscitated rats until the rat died or cytochrome c returned to baseline. In three survivors, cytochrome c rose slightly to [less than or equal to] 2 [micro]g/ml and returned to baseline within 96 h. In nine nonsurvivors, cytochrome c rose progressively to significantly higher maximal levels [4.6 (SD 2.0) vs. 1.6 (SD 0.3) [micro]g/ml, P = 0.029] and at faster rates [0.7 (SD 0.5) vs. 0.1 (SD 0.1) [micro]g * [ml.sup.-1] * [h.sup.-1], P = 0.046] than in survivors. Plasma cytochrome c may represent a novel in vivo marker of mitochondrial injury after resuscitation from cardiac arrest that relates inversely with survival outcome. apoptosis; biological markers; cardiopulmonary resuscitation; myocardial ischemia; ventricular fibrillation