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Supplemental Material for Spectral Reflectance Reconstruction from Red-Green-Blue (RGB) Images for Chlorophyll Content Detection by Lianxiang Gong, Chenxi Zhu, Yifeng Luo, and Xiaping Fu in Applied Spectroscopy

This dissertation contributes to the ongoing debate on how educational inputs make a difference and how to allocate them efficiently. Educational inputs could be broadly defined as any personnel inputs such as teachers and career service staff, learning environment that includes peers and school facilities, and policies that facilitate learning. This dissertation explores three topics: peer effects in higher education, the consequences of college expansion, and the impacts of school closures. Chapter I estimates the peer effects of non-cognitive skills. I show how peers’ non-cognitive skills influence students' academic outcomes and own non-cognitive skills. I use a unique dataset that includes information on student non-cognitive skills, course grades, and friendship from a university in China that randomly assigns students to dormitories. My first main finding is that peers’ non-cognitive skills affect students’ academic outcomes positively but differentially. All students benefit from exposure to “persistent” peers, while students with low baseline academic ability also benefit from exposure to “motivated” peers. My second main finding is that peers also affect the development of students’ self-control and willingness to socialize. These findings have important implications in evaluating the social returns to interventions that improve non-cognitive skills and education policies that change peer group composition. Chapter II summarizes the current literature on college expansions, which change the education resource for many students. Studies have explored the impact of College Expansions that happened worldwide and this chapter summarizes literature in the field of economics of education. This chapter pays special attention to studies that explore the impact on wages and employment and how current studies identify causal relationships. Meanwhile, this chapter reviews how current studies examine the impacts of college expansion in China starting from 1999, which was unparalleled in magnitude. Finally, I discuss how future studies could improve to identify causal effects of the impact of the tremendous college expansion in China. Chapter III, a joint work with Ying Xu, estimates the effect of school closures causedby wildfires. School closures are a common and disruptive feature of education systems when sudden shocks from weather, natural disasters, or infectious disease require that students remain at home rather than in the classroom. Indeed, since January 2020, school closures have happened all around the world due to the COVID-19 pandemic. In the United States, more than 50 million students are currently out of school due to COVID-related closures. This raises an important question: How do sudden school closures affect student development in the short and medium term? In this chapter, we use administrative data to examine the causal effect of unexpected school closures, exploiting sudden variations in these closures due to wildfires in California. We show that unexpected closures have negative effects on student test scores, and the loss of school time is one of the most important mechanisms of decline in student achievement. Meanwhile, minority students and students from school districts with low socioeconomic status experience larger negative effects from such unexpected closures. We argue that these results can help inform policy to identify and address the negative impacts of such closures.

In this study, a total of 26 tests were conducted to investigate the post-fire mechanical and ductile fracture performances of high strength structural steel (HSSS) Q690. The purpose of this experimental research is to evaluate the residual strength and residual ductility of the HSSS Q690 after a fire. Tensile coupons obtained from the HSSS Q690 sheets were heated to various temperatures up to 900℃, and then were cooled down in air to ambient temperature. Tensile coupon tests were carried out to obtain their post-fire nominal stress-nominal strain curves, post-fire true stress-true strain curves, corresponding mechanical properties (including yield stress, ultimate strength, Poisson’s ratio, elastic modulus and elongation), and ductile fracture behaviors. Test results showed that the HSSS Q690 can keep the unchanged mechanical performances after it experiences temperatures up to 600℃. And then a set of prediction equations are obtained to evaluate the post-fire mechanical performances of such high strength steels. The results presented in this experimental study are expected to lead to accurate assessing the post-fire performances, including mechanical performances and ductility performances, of the HSSS Q690.

Ningyuan Chen,1,* Zhibing Zhou,2,* Ji Li,2,* Bocheng Li,2 Jihua Feng,2 Dan He,2 Yifeng Luo,2 Xiaowen Zheng,2 Jiefeng Luo,3 Jianfeng Zhang2 1Department of Pathophysiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, People’s Republic of China; 2Department of Emergency, The Second Affiliated Hospital of Guangxi Medical University, Nanning 530007, People’s Republic of China; 3Department of Neurology, The Second Affiliated Hospital of Guangxi Medical University, Nanning 530007, People’s Republic of China *These authors contributed equally to this work Purpose: This study examined whether the neuroprotective drug, 3-n-butylphthalide (NBP), which is used to treat ischemic stroke, prevents mitochondrial dysfunction. Materials and methods: PC12 neuronal cells were pretreated for 24 hours with NBP (10 µmol/L), then exposed to oxygen and glucose deprivation (OGD) for 8 hours as an invitro model of ischemic stroke. Indices of anti-oxidative response, mitochondrial function and mitochondrial dynamics were evaluated. Results: OGD suppressed cell viability, induced apoptosis and increased caspase-3 activity. NBP significantly reversed these effects. NBP prevented oxidative damage by increasing the activity of superoxide dismutase and lowering levels of malondialdehyde (MDA) and reactive oxygen species (ROS). At the same time, it increased expression of Nrf2, HO-1 and AMPK. NBP attenuated mitochondrial dysfunction by enhancing mitochondrial membrane potential and increasing the activity of mitochondrial respiratory chain complexes I–IV and ATPase. NBP altered the balance of proteins regulating mitochondrial fusion and division. Conclusion: NBP exerts neuroprotective actions by enhancing anti-oxidation and attenuating mitochondrial dysfunction. Our findings provide insight into how NBP may exert neuroprotective effects in ischemic stroke and raise the possibility that it may function similarly against other neurodegenerative diseases involving mitochondrial dysfunction. Keywords: ischemic stroke, mitochondrial dysfunction, mitochondrial dynamics, neuroprotective

The volumetry of the hippocampal subregion may provide additional information in the early investigation of amnestic mild cognitive impairment (aMCI) and the T2 signal intensity (T2-SI) of the hippocampal subregion has not been well studied quantitatively by magnetic resonance imaging (MRI) in aMCI.Using combined MRI-based hippocampal volumetry and T2-SI at the levels of the whole hippocampus and hippocampal subregion, 18 patients with aMCI and 18 age-matched controls were investigated.Significantly lower left whole hippocampal and hippocampal head volumes and higher T2-SI in the bilateral whole hippocampus and hippocampal head were shown, whereas atrophy of the right whole hippocampus and hippocampal subregion was not significant in aMCI. Additionally, correlations were found among the hippocampal volume, T2-SI and Mini-Mental State Examination (MMSE) scores for aMCI in the whole hippocampus and some hippocampal subregions and an almost perfect correlation was found between T2-SI of the left hippocampal head and MMSE scores regarding aMCI (r = -0.831, P = 0.000).Abnormalities of the hippocampal volume and T2-SI were documented in aMCI, whereas T2-SI was implied to be more susceptible than the volume in the pathohistological progression in aMCI. Additionally, T2-SI in the left hippocampal head may be a potential biomarker to facilitate the early diagnosis of aMCI.

Background Macrophage migration inhibitory factor (MIF) is important in regulating cell proliferation and apoptosis in both normal and cancerous cells, and may be important in cancer progression and metastasis. In human non-small cell lung cancer (NSCLC), the underlying mechanisms responsible for MIF-dependent regulation of cellular proliferation, and cell death remain poorly appreciated. Methods The human H460 lung cancer cell-line was treated with an optimally determined dose of 50 pmol/ml MIF siRNA, following which cell proliferation, cell cycle and apoptosis were analyzed. Additionally, known pathways of apoptosis including expression of Annexin-V, enhanced production of caspases-3 and −4 and expression of the Akt signaling protein were assessed in an attempt to provide insights into the signaling pathways involved in apoptosis following disruption of MIF expression. Results Specific siRNA sequences markedly decreased MIF expression in H460 cells by 2 to 5-fold as compared with the negative control. Moreover, MIF miRNA dampened not only cellular proliferation, but increased the frequency of apoptotic cells as assessed by cell-surface Annexin-V expression. Entry of cells into apoptosis was partly dependent on enhanced production of caspases −3 and −4 while not affecting the expression of either caspase-8 or the Akt signaling pathway. Conclusions In a model of NSCLC, knockdown of MIF mRNA expression dampened H460 proliferation by mechanisms partly dependent on entry of cells into apoptosis and enhanced production of caspase-3 and −4. MIF expression may thus be important in NSCLC progression. Targeting MIF may have clinical utility in the management of human lung cancer.