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學業自我概念之大魚小池效應與學業成就關係探究：以TIMSS 2019為例的跨國多層次分析

為了解決Marcus&Marcus ptt的問題，作者林青松 這樣論述：

本研究使用2019國際數學和科學研究趨勢（TIMSS 2019）的數據，以檢驗納入統計的44個國家或地區中，八年級學生的學業自我概念之大魚小池效應與學業成就關係。大魚小池效應(Big Fish-Little-Pond-Effect)，係指當所處群體的平均能力較高，學生會因為與同儕的社會比較而產生較低的學業自我概念；反之然當所處群體的平均能力較低，學生則產生較高的學業自我概念。主要研究目的歸納如下：(一)探討學生數學自我概念對於數學學業成就的影響。(二)探討個體與班級層面之數學學業成就對於學生的數學學業自我概念的影響。(三)探討個體層面之數學學業成就、知覺相對位階(perceived rela

tive standing對學生的學業自我概念中之BFLPE的影響。據此，本研究提出三個研究假設模型，第一個統計模型是數學自我概念的驗證性因素分析（Confirmatory Factor Analysis, CFA）模型。第二個統計模型是Lüdtke et al.(2008)提出的多層次潛在共變項模型(multilevel latent covariate model)的擴展。在第三個統計模型中，與先前的研究一致(Wang＆ Bergin,2017，Huguet et al.,2009，Wang, 2015)，加入知覺相對位階以作為組內層次數學自我概念的附加預測因子。研究結果顯示：(一)班級間

平均數學學業自我概念有顯著不同。(二)學生個人與班級之數學學業成就對學生的數學學業自我概念有顯著預測力。(三)學生個人之數學學業成就、知覺相對位階對學生的數學學業自我概念有顯著的預測力。本研究僅基於研究的相關發現與研究過程所遇挑戰提出後續研究的建議，依內容分為對教育實務方面與對後續欲進行類似取向的研究提出相關議題之建議，期能將研究結果提供教育行政主管機關、學校行政人員、教師及未來研究者作為參考。

Pharmacoinformatic analysis and preclinical evaluation of a novel first-in class onco-immunotherapeutic small molecule for the treatment of non-small-cell lung cancer (NSCLC)

為了解決Marcus&Marcus ptt的問題，作者Bashir Lawal 這樣論述：

Lung cancer poses a serious threat to human health and has recently been tagged the most common malignant disease with the highest incidence and mortality rate. Although epidermal growth factor (EGFR)-tyrosine kinase inhibitors (TKIs) have significantly improved the prognosis of advanced non-small

cell lung cancer (NSCLC) patients with EGFR mutations often develop resistance to these drugs. There is therefore a need to identify new drug candidates with multitarget potential for treating NSCLC. We hereby provide preclinical evidence of the therapeutic efficacy of NLOC-015A a multitarget first-

in class small-molecule inhibitor of EGFR/mitogen-activated protein (MAP) kinase kinase 1 (MAP2K1)/mammalian target of rapamycin (mTOR)/yes-associated protein 1 (YAP1) for the treatment NSCLC. Our multi-omics analysis of clinical data from cohorts of NSCLC revealed that dysregulation of EGFR/MEK1/mT

OR/YAP1 signaling pathways was associated with the progression, therapeutic resistance, immune-invasive phenotypes, and worse prognoses of NSCLC patients. Analysis of single-cell RNA sequencing datasets revealed that MAP2K1, mTOR, YAP1 and EGFR were predominantly located on monocytes/macrophages, Tr

eg and exhaustive CD8 T cell, and are involved in M2 polarization within the TME of patients with primary and metastatic NSCLC which further implied gene’s role in remodeling the tumor immune microenvironment. A molecular-docking analysis revealed that NLOC-015A bound to YAP1, EGFR, MEK1, and mTOR w

ith strong binding efficacies ranging –8.4 to –9.50 kcal/mol. Interestingly, compared to osimertinib, NLOC-015 bound with higher efficacy to the tyrosine kinase (TK) domains of both T790M and T790M/C797S mutant-bearing EGFR. Our in vitro studies revealed that NLOC-015A inhibited the proliferation an

d oncogenic properties of NSCLC with concomitant downregulation of EGFR/MAP2K1/mTOR/YAP1 signaling networks. In addition, the stemness inhibitory effect of NLOC0-15A was accompanied by decreased expression levels of aldehyde dehydrogenase (ALDH), c-Myc, and SOX2 in both H1975 and H1299 cell lines. F

urthermore, NLOC-015A suppressed the tumor burden and increased the body weight and survival of H1975 xenograft-bearing mice. Interestingly, NLOC-015A synergistically enhanced the anti-NSCLC activities of osimertinib both in vitro and in vivo models. We, therefore, suggest that NLOC-015A might repre

sent a new candidate for treating NSCLC via acting as a multitarget inhibitor of EGFR, mTOR/NF-κB, YAP1, MEK1 in NSCLC.