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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TAMIYA Taiwan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.

社區原住民老人自我效能、社會支持、社會參與及遵醫囑行為之相關研究-以桃園市復興區長興里、奎輝里為例

為了解決TAMIYA Taiwan的問題，作者顏孟葶 這樣論述：

目的:隨著醫療技術不斷進步及大眾日漸重視健康的觀念，高齡人口比例隨之上升。臺灣原住民與非原住民在健康上有懸殊差異，城市與偏鄉生活及就醫形態相差甚遠，偏鄉老人遵醫囑行為的相關因素是相當值得探討的議題。故本研究目的希望透過問卷調查探究社區原住民老人之遵醫囑行為，分析研究對象背景變項與自我效能、社會支持、社會參與及遵醫囑行為的分布及現況，並探討其彼此間之關係以及其對遵醫囑行為之預測力，期望未來可以作為發展研究偏鄉社區原住民老人遵醫囑行為的相關策略參考。方法:本研究屬橫斷性研究，研究對象為桃園市復興區長興里與奎輝里55歲以上之原住民老人，排除未作答完者、無法以國語溝通者、無效問卷，採立意取樣方式一對

一面訪進行收案，研究工具包含個人背景變項及健康屬性資料、自我效能量表、社會支持量表、社會參與量表、遵醫囑行為量表。以描述性統計以及推論性統計包含單因子變異數分析、克-瓦單因子等級變異數分析、斯皮爾曼等級相關係數及多元迴歸分析。結果:以桃園市復興區社區原住民之55歲以上老人作為本研究之對象，一共發出180份問卷，最後收集有效問卷為128份，回收率為71%。影響遵醫囑行為的預測因子有自我效能及社會參與，其對遵醫囑行為的解釋力達28.8%。而遵醫囑行為與自我效能、社會支持及社會參與及皆呈顯著正相關，其中社會參與和遵醫囑行為關聯性最高，社會支持次之，表示當社區原住民老人社會參與程度及社會支持和自我效能

程度越高時，其遵醫囑行為就越佳，此結果與本研究假設相呼應。結論:研究結果發現重視老人自我效能及社會參與程度，其遵醫囑行為越好，建議未來可以多辦理相關社區活動，以提升老人之遵醫囑行為。