Effect of real-time visual feedback device 'Quality Cardiopulmonary Resuscitation (QCPR) Classroom' with a metronome sound on layperson CPR training in Japan: a cluster randomized control trial.

OBJECTIVES: 'Quality Cardiopulmonary Resuscitation (QCPR) Classroom' was recently introduced to provide higher-quality Cardiopulmonary Resuscitation (CPR) training. This study aimed to examine whether novel QCPR Classroom training can lead to higher chest-compression quality than standard CPR training. DESIGN: A cluster randomised controlled trial was conducted to compare standard CPR training (control) and QCPR Classroom (intervention). SETTING: Layperson CPR training in Japan. PARTICIPANTS: Six hundred forty-two people aged over 15 years were recruited from among CPR trainees. INTERVENTIONS: CPR performance data were registered without feedback on instrumented Little Anne prototypes for 1 min pretraining and post-training. A large classroom was used in which QCPR Classroom participants could see their CPR performance on a big screen at the front; the control group only received instructor's subjective feedback. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcomes were compression depth (mm), rate (compressions per minute (cpm)), percentage of adequate depth (%) and recoil (%). Survey scores were a secondary outcome. The survey included participants' confidence regarding CPR parameters and ease of understanding instructor feedback. RESULTS: In total, 259 and 238 people in the control and QCPR Classroom groups, respectively, were eligible for analysis. After training, the mean compression depth and rate were 56.1±9.8 mm and 119.2±7.3 cpm in the control group and 59.5±7.9 mm and 116.8±5.5 cpm in the QCPR Classroom group. The QCPR Classroom group showed significantly more adequate depth than the control group (p=0.001). There were 39.0% (95% CI 33.8 to 44.2; p<0.0001) and 20.0% improvements (95% CI 15.4 to 24.7; P<0.0001) in the QCPR Classroom and control groups, respectively. The difference in adequate recoil between pretraining and post-training was 2.7% (95% CI -1.7 to 7.1; pre 64.2±36.5% vs post 66.9%±34.6%; p=0.23) and 22.6% in the control and QCPR Classroom groups (95% CI 17.8 to 27.3; pre 64.8±37.5% vs post 87.4%±22.9%; p<0.0001), respectively. CONCLUSIONS: QCPR Classroom helped students achieve high-quality CPR training, especially for proper compression depth and full recoil. For good educational achievement, a novel QCPR Classroom with a metronome sound is recommended.

Novel VCP modulators mitigate major pathologies of rd10, a mouse model of retinitis pigmentosa.

Neuroprotection may prevent or forestall the progression of incurable eye diseases, such as retinitis pigmentosa, one of the major causes of adult blindness. Decreased cellular ATP levels may contribute to the pathology of this eye disease and other neurodegenerative diseases. Here we describe small compounds (Kyoto University Substances, KUSs) that were developed to inhibit the ATPase activity of VCP (valosin-containing protein), the most abundant soluble ATPase in the cell. Surprisingly, KUSs did not significantly impair reported cellular functions of VCP but nonetheless suppressed the VCP-dependent decrease of cellular ATP levels. Moreover, KUSs, as well as exogenous ATP or ATP-producing compounds, e.g. methylpyruvate, suppressed endoplasmic reticulum stress, and demonstrably protected various types of cultured cells from death, including several types of retinal neuronal cells. We then examined their in vivo efficacies in rd10, a mouse model of retinitis pigmentosa. KUSs prevented photoreceptor cell death and preserved visual function. These results reveal an unexpected, crucial role of ATP consumption by VCP in determining cell fate in this pathological context, and point to a promising new neuroprotective strategy for currently incurable retinitis pigmentosa.

Continuation of exercise is necessary to inhibit high fat diet-induced ß-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice.

High fat diet (HFD) is prevalent in many modern societies and HFD-induced metabolic condition is a growing concern worldwide. It has been previously reported that HFD clearly worsens cognitive function in amyloid precursor protein (APP) transgenic mice. On the other hand, we have demonstrated that voluntary exercise in an enriched environment is an effective intervention to rescue HFD-induced ß-amyloid (Aß) deposition and memory deficit. However, it had been unclear whether consumption of HFD after exercising abolished the beneficial effect of exercise on the inhibition of Alzheimer's disease (AD) pathology. To examine this question, we exposed wild type (WT) and APP mice fed with HFD to exercise conditions at different time periods. In our previous experiment, we gave HFD to mice for 20 weeks and subjected them to exercise during weeks 10-20. In the present study, mice were subjected to exercise conditions during weeks 0-10 or weeks 5-15 while being on HFD. Interestingly, we found that the effect of exercise during weeks 0-10 or weeks 5-15 on memory function was not abolished in WT mice even if they kept having HFD after finishing exercise. However, in APP transgenic mice, HFD clearly disrupted the effect of exercise during weeks 0-10 or weeks 5-15 on memory function. Importantly, we observed that the level of Aß oligomer was significantly elevated in the APP mice that exercised during weeks 0-10: this might have been caused by the up-regulation of Aß production. These results provide solid evidence that continuation of exercise is necessary to rescue HFD-induced aggravation of cognitive decline in the pathological setting of AD.