Poverty work program: poverty reduction in Nigeria in the last decade

The report consists of four chapters. Chapter one profiles the trends in growth, household consumption, and poverty rates at the national level between 2004 and 2013. Descriptive statistics of consumption and selected poverty indexes are presented and a profile of the characteristics of the poor is given. The chapter concludes with an analysis of nonmonetary indicators. Chapter two unpackages the national level data into subnational results (six zones) and shows the high and increasing divide of socioeconomic indicators. Chapter three uses descriptive and econometric technics to identify the drivers of this divide. Chapter four concludes and provides a road map for policy action to effectively address this divide

Japanese Lung Cancer Society Guidelines for Stage IV NSCLC With EGFR Mutations

Patients with NSCLC in East Asia, including Japan, frequently contain EGFR mutations. In 2018, we published the latest full clinical practice guidelines on the basis of those provided by the Japanese Lung Cancer Society Guidelines Committee. The purpose of this study was to update those recommendations, especially for the treatment of metastatic or recurrent EGFR-mutated NSCLC. We conducted a literature search of systematic reviews of randomized controlled and nonrandomized trials published between 2018 and 2019 that multiple physicians had reviewed independently. On the basis of those studies and the advice from the Japanese Society of Lung Cancer Expert Panel, we developed updated guidelines according to the Grading of Recommendations, Assessment, Development, and Evaluation system. We also evaluated the benefits of overall and progression-free survival, end points, toxicities, and patients’ reported outcomes. For patients with NSCLC harboring EGFR-activating mutations, the use of EGFR tyrosine kinase inhibitors (EGFR TKIs), especially osimertinib, had the best recommendation as to first-line treatment. We also recommended the combination of EGFR TKI with other agents (platinum-based chemotherapy or antiangiogenic agents); however, it can lead to toxicity. In the presence of EGFR uncommon mutations, except for an exon 20 insertion, we also recommended the EGFR TKI treatment. However, we could not provide recommendations for the treatment of EGFR mutations with immune checkpoint inhibitors, including monotherapy, and its combination with cytotoxic chemotherapy, because of the limited evidence present in the literature. The 2020 Japanese Lung Cancer Society Guidelines can help community-based physicians to determine the most appropriate treatments and adequately provide medical care to their patients

The E693Δ Mutation in Amyloid Precursor Protein Increases Intracellular Accumulation of Amyloid β Oligomers and Causes Endoplasmic Reticulum Stress-Induced Apoptosis in Cultured Cells

The E693Δ mutation within the amyloid precursor protein (APP) has been suggested to cause dementia via the enhanced formation of synaptotoxic amyloid β (Aβ) oligomers. However, this mutation markedly decreases Aβ secretion, implying the existence of an additional mechanism of neuronal dysfunction that is independent of extracellular Aβ. We therefore examined the effects of this mutation on both APP processing to produce Aβ as well as subcellular localization and accumulation of Aβ in transfected HEK293 and COS-7 cells. Both β- and γ-cleavage of mutant APP increased, indicating a lack of inhibition in Aβ production. Instead, this mutation promoted Aβ accumulation within cells, including the endoplasmic reticulum (ER), Golgi apparatus, early and late endosomes, lysosomes, and autophagosomes, all of which have been proposed as intracellular sites of Aβ generation and/or degradation, suggesting impairment of APP/Aβ trafficking. Notably, the intracellular mutant Aβ was found to predominantly form oligomers. Concomitant with this accumulation, the ER stress markers Grp78 and phosphorylated eIF2α were both strongly induced. Furthermore, the activation of caspase-4 and -3 as well as DNA fragmentation were detected in these cells. These results suggest that mutant Aβ induces alteration of Aβ trafficking and subsequent ER stress-induced apoptosis via enhancement of its intracellular oligomerization. Our findings suggest that Aβ oligomers exhibit toxicity in the extracellular space and within the cells themselves