Improving middle school students' geometry problem solving ability through hands-on experience: An fNIRS study.

Hands-on learning is proposed as a prerequisite for mathematics learning in kindergarten and primary school. However, it remains unclear that whether hands-on experience aids understanding of geometry knowledge for middle school students. We also know little about the neural basis underlying the value of hands-on experience in math education. In this study, 40 right-handed Chinese students (20 boys and 20 girls) with different academic levels were selected from 126 seventh-grade students in the same school, who learnt "Axisymmetric of an Isosceles Triangle" in different learning style (hands-on operation vs. video observation). Half of them operated the concrete manipulatives while the other half watched the instructional videos. The learning-test paradigm and functional near-infrared spectroscopy (fNIRS) technique were used to compare the differences in geometry reasoning involved in solving well-structured problems and ill-structured problems. Behavioral results showed that hands-on experience promoted students' performances of geometry problem-solving. Students with lower academic level were more dependent on hands-on experience than those with higher academic level. The fNIRS results showed that meaningful hands-on experience with concrete manipulatives related to learning contents increased reactivation of the somatosensory association cortex during subsequent reasoning, which helped to improve the problem-solving performance. Hands-on experience also reduced students' cognitive load during the well-structured problem-solving process. These findings contribute to better understand the value of hands-on experience in geometry learning and the implications for future mathematics classroom practices.

Gfi1 and Zc3h12c orchestrate a negative feedback loop that inhibits NF-kB activation during inflammation in macrophages.

NF-κB activation is essential in mediating the induction of pro-inflammatory cytokines and also plays a key role in regulating the inflammatory response through intricate mechanisms. In this study, loss of Gfi1 was found to be associated with transcriptomic profiles related to NF-κB activation, including an increase in pro-inflammatory cytokines. Genetically inactivating the IKK/NF-κB signaling pathway in macrophages showed that Gfi1 deficiency led to pro-inflammatory cytokine production requiring NF-κB activation. More importantly, we revealed that one of the under-researched mechanisms, involving Gfi1 and Zc3h12c exerted negative regulation on NF-κB activation. Both Gfi1 and Zc3h12c were found to inhibit NF-κB activation, and double knockout exhibited additive roles of Gfi1 and Zc3h12c in preventing proinflammatory cytokine production. The loss of Gfi1 upregulated Zc3h12c which in turn inhibited NF-κB activation. Therefore, this study delineates the function of Zc3h12c in enhancing the negative regulation of Gfi1 through NF-κB activation during inflammation in macrophages.