On the Margins of the "Economic Miracle" : Non English-Literate Chinese Factory Workers in Singapore, 1980-1990

この論文は国立情報学研究所の学術雑誌公開支援事業により電子化されました。While the writing of Singapore's "history from below" has begun to gain momentum inacademic circles, there is still a considerable lack of understanding about the contributionsand experiences of the ordinary person to the city-state's remarkable growth after 1965. InSingapore's broader historiography, the success of the nation's economy is commonlyattributed to the genius and foresight of key personalities, or in more recent times, thespirit of entrepreneurship by a select few. Thus, the non English-literate Chinese factoryworker in Singapore currently only exists in a marginalised space in Singaporean historicaldiscourse, in spite of their role in Singapore's transition "from Third World to First," touse the parlance of Lee Kuan Yew. Through the use of collective reminiscence andbiography, this paper seeks to present the lives of the workers in narrative. In doing so, itaims to solicit an alternative, Chinese working-class account of the "economic miracle"epoch

Multiancestry analysis of the HLA locus in Alzheimer’s and Parkinson’s diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes

Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson’s disease (PD) and Alzheimer’s disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues

Autonomous wearable sensor nodes with flexible energy harvesting

Distributed wearable wireless sensors are widely employed in wireless body sensor network for various physiological monitoring purposes like health or performance related monitoring applications. The real challenges in employing these wearable wireless sensors on human subjects include: 1) bulky and rigid system design thus, it is difficult to conform to human body contour and 2) limited operational lifespan of batteries with finite energy supply. In this paper, an autonomous body-worn wireless sensor node with flexible energy harvesting (FEH) mechanism, able to conform to body contour, is proposed for biometric monitoring. To be totally sustainable and compact, the FEH mechanism is equipped with an ultralow power management circuit (PMC) specially designed on a flexible PCB. The flexible PMC is able to transfer near maximum electrical power from the input solar energy source to store in the supercapacitor for powering the wireless sensor node. The power consumption of the flexible PMC is only 32.86 μW. Experimental results show that under indoor condition, typical average lighting intensity of 320 lux, the wearable sensor node is able to continuously monitor the temperature of the wearer, read, and transmit back to the base node in a wireless manner, without the need of any battery. In addition, the designed FEH sensor node flexed onto the wearer body contour at an angle of 30° generates 56 μW of electrical power, sufficient to sustain its operation for >15h

Core-binding factor fusion downregulation of ADAR2 RNA editing contributes to AML leukemogenesis

Adenosine-to-inosine RNA editing, which is catalyzed by adenosine deaminases acting on RNA (ADAR) family of enzymes, ADAR1 and ADAR2, has been shown to contribute to multiple cancers. However, other than the chronic myeloid leukemia blast crisis, relatively little is known about its role in other types of hematological malignancies. Here, we found that ADAR2, but not ADAR1 and ADAR3, was specifically downregulated in the core-binding factor (CBF) acute myeloid leukemia (AML) with t(8;21) or inv(16) translocations. In t(8;21) AML, RUNX1-driven transcription of ADAR2 was repressed by the RUNX1-ETO additional exon 9a fusion protein in a dominant-negative manner. Further functional studies confirmed that ADAR2 could suppress leukemogenesis specifically in t(8;21) and inv16 AML cells dependent on its RNA editing capability. Expression of 2 exemplary ADAR2-regulated RNA editing targets coatomer subunit α and component of oligomeric Golgi complex 3 inhibits the clonogenic growth of human t(8;21) AML cells. Our findings support a hitherto, unappreciated mechanism leading to ADAR2 dysregulation in CBF AML and highlight the functional relevance of loss of ADAR2-mediated RNA editing to CBF AML.Published versionThis work was supported by the Singapore Ministry of Health’s National Medical Research Council (NMRC), the Singapore National Research Foundation, the Singapore Ministry of Education (MOE) under its Research Centres of Excellence initiative, and the National Institutes of Health with following details: Singapore Translational Research Investigator Award, National Institutes of Health grant (P01 HL131477 (D.G.T.), MOE Tier 2 grants (MOE2019 T2-1-083 and MOE2019 T2-2-008), NMRC Clinician Scientist-Individual Research grants (project IDs: MOH 000214 and MOH-001092-00), and the Health and Biomedical Sciences Industry Alignment Fund Pre-Positioning (H20C6a0034) (L.C.), NMRC Open Fund Young Individual Research grant ( MOH OFYIRG20nov-0011) and MOE Research Scholarship Block grant (N 171 000 019 001) (Q.Z.), as well as MOE Tier 3 grant (MOE2014-T3-1-006) (D.G.T. and L.C.)