133 research outputs found
Relationships Between Sensory Processing and Play Experiences Among Healthy Community-Dwelling Older Adults
Abstract
Date Presented 4/1/2017
This study aims to examine the relationships between sensory processing patterns and play experiences as well as to examine the feasibility of using the Adult Sensory Processing Scale and Daily Occupations Experience Survey with community-dwelling older adults.
Primary Author and Speaker: Megan Chang
Additional Authors and Speakers: Krista Yee, Nathan Nam, Naomi Starr, Larkin Petralli, Christine Huynh</jats:p
Pro-fibrotic effects of PFKFB4-mediated glycolytic reprogramming in fibrous dysplasia
Fibrous dysplasia (FD) caused by a mosaic somatic mutation of GNAS is characterized by replacement of the affected bone with abnormal fibrous tissue. Herein, we present novel disease models for FD developed with pairs of isogenic wild-type and GNASR201H-mutated induced pluripotent stem cells (iPSCs) and their derivative mesenchymal stem cells (MSCs). Both 2D and 3D MSC culture models for FD successfully reflect FD's typical molecular characteristics, such as enhanced cAMP level, PKA activity, CREB1 phosphorylation and the pathologic fibrotic phenotype. The fibrotic features of GNASR201H FD model cells were closely linked to augmented glycolysis and depended on glycolytic PFKFB4 and the activation of pro-fibrotic TGFβ signalling. Either depletion of PFKFB4 or inhibition of glycolysis or TGFβ signalling potentially blocked fibrosis progression in GNASR201H FD model cells. Our FD models could facilitate a better mechanistic understanding of FD and help develop effective therapeutics for FD and other fibrosis diseases.open
Generation and characterization of integration-free induced pluripotent stem cells from patients with autoimmune disease
Autoimmune diseases (AIDs), a heterogeneous group of immune-mediated disorders, are a major and growing health problem. Although AIDs are currently treated primarily with anti-inflammatory and immunosuppressive drugs, the use of stem cell transplantation in patients with AIDs is becoming increasingly common. However, stem cell transplantation therapy has limitations, including a shortage of available stem cells and immune rejection of cells from nonautologous sources. Induced pluripotent stem cell (iPSC) technology, which allows the generation of patient-specific pluripotent stem cells, could offer an alternative source for clinical applications of stem cell therapies in AID patients. We used nonintegrating oriP/EBNA-1-based episomal vectors to reprogram dermal fibroblasts from patients with AIDs such as ankylosing spondylitis (AS), Sjogren's syndrome (SS) and systemic lupus erythematosus (SLE). The pluripotency and multilineage differentiation capacity of each patient-specific iPSC line was validated. The safety of these iPSCs for use in stem cell transplantation is indicated by the fact that all AID-specific iPSCs are integrated transgene free. Finally, all AID-specific iPSCs derived in this study could be differentiated into cells of hematopoietic and mesenchymal lineages in vitro as shown by flow cytometric analysis and induction of terminal differentiation potential. Our results demonstrate the successful generation of integration-free iPSCs from patients with AS, SS and SLE. These findings support the possibility of using iPSC technology in autologous and allogeneic cell replacement therapy for various AIDs, including AS, SS and SLE.open
Biomarker discovery by modeling Behcet's disease with patient-specific human induced pluripotent stem cells
Behcet's disease (BD) is a chronic inflammatory and multisystemic autoimmune disease of unknown etiology. Due to the lack of a specific test for BD, its diagnosis is very difficult and therapeutic options are limited. Induced pluripotent stem cell (iPSC) technology, which provides inaccessible disease-relevant cell types, opens a new era for disease treatment. In this study, we generated BD iPSCs from patient somatic cells and differentiated them into hematopoietic precursor cells (BD iPSC-HPCs) as BD model cells. Based on comparative transcriptome analysis using our BD model cells, we identified eight novel BD-specific genes, AGTR2, CA9, CD44, CXCL1, HTN3, IL-2, PTGER4, and TSLP, which were differentially expressed in BD patients compared with healthy controls or patients with other immune diseases. The use of CXCL1 as a BD biomarker was further validated at the protein level using both a BD iPSC-HPC-based assay system and BD patient serum samples. Furthermore, we show that our BD iPSC-HPC-based drug screening system is highly effective for testing CXCL1 BD biomarkers, as determined by monitoring the efficacy of existing anti-inflammatory drugs. Our results shed new light on the usefulness of patient-specific iPSC technology in the development of a benchmarking platform for disease-specific biomarkers, phenotype- or target-driven drug discovery, and patient-tailored therapies.
Xiao shu hou chang chang shen jing xi tong de fa yu
Ph.D.The enteric nervous system (ENS) provides intrinsic innervation of the gastrointestinal tract, and regulates many gastrointestinal functions with minimal input from the central nervous system. This autonomous nature of the ENS is modulated by enteric neurons of the ENS in the myenteric and submucosal plexuses of the gastrointestinal tract. Enteric neurons are mainly derived from neural crest cells (NCCs) which migrated into the developing gut mesenchyme during the early embryonic development. NCCs colonise the entire length of the developing gut by embryonic day (E) 14 – E15 in the mouse. Although the colonisation of myenteric plexus by NCCs has been well studied, the subsequent neuronal differentiation in the myenteric plexus and the submucosal plexus is still not fully understood. To better understand the ENS development in mice, the current study examined these events in the hindgut (developing colon) between E14.5 and E17.5. By immunofluorescence staining, the spatiotemporal distribution of early differentiating myenteric neurons and neuronal subtypes containing neuronal nitric oxide synthase and calbindin in the myenteric plexus were revealed. It was found that while the calbindin neurons remained as a minority group between E14.5 and E17.5, the density of nitric oxide synthase-containing neuronal subtype was increased significantly during the same period of embryonic development. In the submucosa of the distal hindgut, NCCs were first identified at E15.5 and submucosal neurons were detected at E17.5. In addition, based on the previous observation that some NCCs in the distal hindgut originate from the pelvic ganglion, the origin of the NCCs observed in the distal hindgut was determined by performing a novel exo utero transplantation, where genetically labelled NCCs were allotransplanted into the pelvic ganglion of recipient embryos which then developed exo utero inside a pregnant mouse. Four days after transplantation, NCCs migrated into the distal hindgut mesenchyme by migrating on the projections from the pelvic plexus and differentiated into a small quantity of myenteric neurons in the region. Furthermore, cells within the pelvic plexus projected long nerve fibres into the myenteric and submucosal plexuses of the distal hindgut, and the projections in the myenteric plexus extended rostrally for about one-third of the length of the colon and caudally to the terminal end of the hindgut. Results of the current study provided information on the formation of neuronal subtypes in the myenteric plexus, the early appearance of NCCs and enteric neurons in the submucosa and also the contribution of NCCs from the pelvic ganglion to the hindgut ENS during the period of E14.5 to E17.5 of the mouse development.腸神經系統提供腸胃道內在的神經支配,並能以最小的中樞神經系統輸入調節許多腸胃功能。腸神經系統的這種自主性質是由其位於肌間神經叢和下層黏膜神經叢的腸神經元所調節。腸神經元主要源於早期胚胎發育期間遷移到腸間質中的神經脊細胞,而小鼠的神經脊細胞在胚胎日14–15定植整個發育中腸道。雖然神經脊細胞在肌神經叢的定植已經得到很好的研究,但其隨後於肌神經叢和下層黏膜神經叢的神經元分化並未完全清楚。為了更好地瞭解小鼠腸神經系統的發育,本研究查驗了在胚胎日14.5–17.5之間的後腸(發育中的結腸)發生的這些事件。免疫熒光染色確認了早期分化的肌間神經元以及含有神經型一氧化氮合酶或鈣結合蛋白的神經元在肌間神經叢的時空分佈,並發現了在胚胎日14.5–17.5之間含有神經型一氧化氮合酶的神經元的密度顯著增加但含有鈣結合蛋白的神經元仍然保持少數。而在末端後腸的下層粘膜,神經脊細胞和下層黏膜神經元分別在的胚胎日15.5和17.5被檢測到。此外,由於部分末端後腸的神經脊細胞在之前被觀察到是源於骨盆神經節,因此在本研究中也透過外子宮異體移植被標記的神經脊細胞進受體胚胎的骨盆神經節鑑定末端後腸的神經脊細胞來源。在移植後的四天,神經脊細胞透過骨盆神經叢伸延的神經纖維遷移到末端後腸的間質並在該區域分化為少量的肌間神經元。此外,骨盆神經叢內的細胞向末端後腸的肌間神經叢和下層黏膜神經叢伸延出長的神經纖維,而這些神經纖維在肌間神經叢中向口腔伸延大約三分之一的結腸長度並向尾端伸延到後腸的未端。本研究的結果提供了在胚胎日14.5–17.5之間的小鼠發育中關於肌間神經叢不同類型的神經元形成、下層粘膜神經脊細胞和腸神經元的出現、以及骨盆神經節中的神經脊細胞對後腸腸神經系統的貢獻的資訊。Ng, Tsz Chung.Thesis Ph.D. Chinese University of Hong Kong 2017.Includes bibliographical references (leaves 289-307).Abstracts also in Chinese.Title from PDF title page (viewed on 16, October, 2019).Ng, Tsz Chung
Cerebral AV Malformation in a Neonate Complicated by Intractable Congestive Heart Failure Treated with Balloon Embolization : A case Report
Cerebral arteriovenous malformation is a rare cause of congestive heart failure in neonates and is known to carry a very poor prognosis even wish prompt recognition and aggressive treatment. We recently encountered a 2-day-old male neonate with huge cerebral arteriovenous malformation who presented with intractable heart failure. Despite aggressive medical treatment and partial embolization with detachable balloon, baby died of severe hearts failure. Since there is no report of percutaneous balloon embolization in a neonate with this lesion in Korean literature, we wish to present our experience in one such neonate. Also we believe this is the first report of color Doppler findings in cerebral arteriovenous malformation in Korean literature.Cerebral arteriovenous malformation is a rare cause of congestive heart failure in neonates and is known to carry a very poor prognosis even wish prompt recognition and aggressive treatment. We recently encountered a 2-day-old male neonate with huge cerebral arteriovenous malformation who presented with intractable heart failure. Despite aggressive medical treatment and partial embolization with detachable balloon, baby died of severe hearts failure. Since there is no report of percutaneous balloon embolization in a neonate with this lesion in Korean literature, we wish to present our experience in one such neonate. Also we believe this is the first report of color Doppler findings in cerebral arteriovenous malformation in Korean literature
Ying xiang chang dao shen jing ji xi bao zheng chang qian yi de ji yin biao da de yan jiu
腸神經系統(enteric nervous system, ENS)是由大量神經元和神經膠質細胞聚集而成的最複雜的周圍神經系統。這些腸道的神經元和神經膠質細胞來源于迷走神經脊和骶神經脊細胞,在胚胎發育過程中,這些神經脊細胞沿著腸道移動最終占滿整個腸道。儘管神經脊細胞的遷移對於腸道神經系統的形成及功能的正常發揮起到很重要的作用,然而影響神經脊細胞遷移的分子機制的研究卻相對較少。因此找出參與調控神經脊細胞遷移的基因對於更好的瞭解腸道神經脊系統的發育起到非常重要的作用,並且為治療腸道神經系統紊亂所導致的相關疾病提供治療靶點。本研究論文是由兩部份實驗課題所組成來研究影響腸和調控道神經脊細胞遷移及腸道神經系統發育的相關基因。第一部份課題主要研究的是Semaphorin3A (Sema3A)對於骶神經脊細胞遷移的影響。本論文的研究發現Sema3A不僅被腸道內的上皮細胞所表達,腸道兩側的盆神經節周圍的間質細胞也表達Sema3A。同時Sema3A的受體neuropilin-1被骶神經脊細胞所表達。體外培養的實驗表明Sema3A能夠抑制骶神經脊細胞的遷移。另外,當表達Sema3A的腸道末端與骶神經脊細胞共同培養時,骶神經脊細胞的遷移同樣也受到抑制。這些研究結果表明由腸道末端的上皮細胞和腸道外圍的間質細胞所表達的Sema3A共同作用來調控骶神經脊細胞在停滯時期的遷移活動。第二部份的研究課題主要研究的是轉錄因子Sox10以及其靶基因對於迷走神經脊細胞遷移的影響。Dominant megacolon (Dom)是一種攜帶有Sox10突變的巨結腸癥小鼠模型。本研究利用這種小鼠模型來發現突變鼠中可能影響迷走神經脊細胞遷移的基因。從迷走神經脊細胞體外培養發現: 由於Sox10突變,迷走神經脊細胞在體外培養24小時后,細胞遷移延遲,細胞的分化能力被改變,並且細胞死亡增加。利用基因芯片的方法比較了純和變異鼠迷走神經脊細胞和正常鼠迷走神經脊細胞的基因表達的差異。螢光素酶報告基因分析顯示,Sox10可以結合Lama4, Itga4和Gfra2的啟動子并激活它們的表達。 Sox10能與Gfra2啟動子上-116bp到-58bp之間序列的結合誘導Gfra2的表達。在純和變異鼠迷走神經脊細胞中,通過上調Gfra2信使RNA的表達,細胞死亡的數目大大下降,表明Gfra2作為Sox10的靶基因,對迷走神經脊細胞的存亡有著重要作用。綜上所述,我們發現在骶神經脊細胞未進入腸道末端的這段停滯期內,Sema3A對於骶神經脊細胞的遷移起到抑制作用,Sema3A通過其表達在這段停滯期內的時空改變來調控骶神經脊細胞進入腸道。另外我們發現由於Sox10的突變,迷走神經脊細胞表現出非正常的遷移和基因表達的變化。作為Sox10的靶基因,Gfra2對於迷走神經脊細胞的死亡有重要的作用。The enteric nervous system (ENS) is the most complex part of the peripheral nervous system which is composed of a vast number of neurons and glial cells. The enteric neurons and glial cells arise from vagal and sacral neural crest cells (NCCs) which migrate along the gastrointestinal tract to colonize the whole gut during the embryonic development. The molecular mechanisms regulating the NCC migration are poorly characterized despite the importance of this migration process in the ENS formation. Therefore, identification and characterization of molecules involved in the modulation of NCC migration are essential to understand the ENS development and could provide potential therapeutic targets for the treatment of human ENS disorders.The present study was aimed to identify and characterize the molecules involved in modulating the NCC migration during the ENS development, and was divided into two parts. The first part focused on semaphorin3A (Sema3A) signaling, Sema3A was found to be expressed in the hindgut epithelium and also the adjacent regions of pelvic ganglia, while its receptor, neuropilin-1, was expressed by sacral NCCs before sacral NCCs entered the hindgut. Sacral NCC migration and neuronal fiber extension in vitro were retarded in the culture medium containing Sema3A. When a hindgut segment expressing Sema3A was co-cultured with sacral NCCs, sacral NCC migration and neuronal fiber extension were also suppressed by the hindgut segment. These findings provide evidence for the repulsive activity of Sema3A before the entry of sacral NCCs to the hindgut.The second part focused on the potential target genes of the transcription factor Sox10 which is expressed by migrating NCCs. A naturally occurring mouse mutant Dominant megacolon (Sox10Dom) which expresses a mutant Sox10 was used to identify candidate molecules which may possibly affect the NCC migration. After 24 hours in culture, vagal NCCs from Sox10Dom/Dom embryos showed retarded migration, abnormal cell differentiation and excessive cell death in vitro when compared to Sox10⁺/⁺ vagal NCCs. Results of microarray analyses revealed differentially expressed genes in Sox10Dom/Dom as compared to Sox10⁺/⁺ vagal NCCs after 24 hours in culture. Among these genes, Sox10 was able to bind to the promoter of Itga4, Lama4, and Gfra2 to induce their expression. Sox10 activated Gfra2 promoter by direct binding to the critical region located between -116bp and -58bp upstream of the Gfra2 transcription start site. Finally, re-expression of Gfra2 in Sox10Dom/Dom vagal NCCs resulted in decreased cell death, suggesting that down-regulation of Gfra2 in the mutant mice played an important role in early cell death of vagal NCCs.In conclusion, before sacral NCCs entered into the hindgut, Sema3A inhibited the sacral NCC migration, and the spatiotemporal change of the Sema3A distribution regulated the entry of sacral NCCs into hindgut. Furthermore, retarded cell migration, abnormal cell differentiation, increased cell death and differential gene expression were found in Sox10Dom/Dom vagal NCCs as compared with those from Sox10⁺/⁺ embryos in vitro. The expression of Gfra2, a potential target gene of Sox10, promoted the cell viability of vagal NCCs.Detailed summary in vernacular field only.Detailed summary in vernacular field only.Detailed summary in vernacular field only.Detailed summary in vernacular field only.Wang, Cuifang.Thesis (Ph.D.) Chinese University of Hong Kong, 2014.Includes bibliographical references (leaves 180-196).Abstracts also in Chinese.Wang, Cuifang
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The advertisements effects on festival and destination marketing: comparison study between old and new social media
The author has been teaching at Department of Leisure and Recreation Management since she graduated from Michigan State University in 2003. The author has three major research subjects: tourist wayfinding behavior in unfamiliar destinations, encounter experience among tourists, and Virtual Reality marketing effects on tourism destination.Innovations in Destination MarketingWith the development of modern technology, new types of media keep popping out one by one with different features. This study explored whether there would be significant differences in promotion benefits between the application of new media (YouTube, Facebook, Blog) and that of old media (Flyer, Magazine, Word of mouth in tourism festival (Tai Songkran Festival) and tourism destination marketing (Okinawan Island). The promotion benefits include three aspects: advertisement attitude; tourism images, and their future travel intentions. The 502 Study participants were randomly assigned in six different groups to watch different types of promotion advertisement. The result found that study participants who watched the promotion information through new media expressed higher level on its advertisement attitudes, tourism image and travel intentions. Two-Way ANOVA test revealed significant interaction between type of media and type of tourism products (festival and destination) with respect to advertisement contents, advertisement innovation, and negative tourism image
Chang fei bian ma RNA H19 zai shang pi jian chong zhi zhuan hua zhong de gong neng tan jiu
Colorectal cancer (CRC), with an estimated 1.2 million new cases annually, is the third leading cause of cancer incidence and death worldwide. Generally, the majority of CRC patients are diagnosed at the advanced stages with poor prognosis and unfavorable response to multiple therapeutic drugs. In spite of increasing knowledge of the molecular mechanism for the tumorigenesis in CRC patients, the translation from basic science into clinical therapy has been limited for quite a long time. In order to develop novel treatment strategies against CRC, intensive and extensive attempts have been made in the past decades.The epithelial to mesenchymal transition (EMT) is a multi-step process characterized by the loss of cell polarity, decreased cell-cell adhesion as well as enhanced migration and invasion capacity. It is well documented that EMT is essential for a variety of cellular biological events ranging from embryogenesis to tumor progression. The field of lncRNA is developing rapidly and currently it is one of the most intensively studied fields in the biomedical sciences. Emerging evidence indicates that the majority of human genome encodes thousands of non-protein-coding RNA transcripts, nevertheless, the function of long non-coding RNAs (lncRNAs) in orchestrating EMT progression remains elusive. Historically, the lncRNA H19 was the first identified imprinted non-coding RNA transcript in human, and the H19/IGF2 locus acted as an ideal paradigm for the investigation of genomic imprinting genes. In recent years, the expression profiling and functional characterization of the H19 gene in a variety of human diseases has been extensively studied.In our studies, H19 was characterized as a novel regulator of EMT in colon cancer. We first observed significant mesenchymal characteristics in the methotrexate-resistant HT-29 cells. Interestingly, significant upregulation of H19 was observed in mesenchymal-like MTX resistant HT-29 cells. We subsequently demonstrated that after treatment of TGF-β1, one of the most widely used EMT inducers, H19 presented dramatic increase during the EMT progression. To further investigate the functional role of H19 in EMT, we generated the stable cell lines overexpressing H19 in colon cancer cells using retroviral infection. Stable overexpression of H19 significantly promoted EMT progression in two epithelial colon cancer cell lines HT-29 and HCT-116. However, overexpression of H19 did not affect cell proliferation as well as cell cycle progression. Further proteomics studies screened out that ectopic expression of H19 upregulated the protein level of Vimentin, a vital biomarker for mesenchymal cells. By using the bioinformatics study in combination with luciferase reporter assays, we demonstrated that H19 potentiated the expression of several core marker genes essential for mesenchymal cells by serving as a competing endogenous RNA(ceRNA), which builds up the missing link between the regulatory miRNA network and EMT progression. According to the results from xenograft tumor model and soft agar assay, stable expression of H19 reinforced the in vitro and in vivo tumor growth. Moreover, the investigation of clinical specimens verified that H19 RNA level was significantly increased in colon cancer tissues compared with corresponding adjacent normal tissues. Taken together, the above observations imply that the lncRNA H19, by acting as a competing endogenous RNA, is an important regulator which tightly modulated the expression of multiple important genes involved in EMT and it could probably serve as a novel therapeutic target against colon cancer.大腸癌每年有一百二十萬新增個案,是世界第三大癌症殺手。通常情況下,大部分大腸癌病人發現時已經處於晚期,該時期的癌症病人對多種臨床治療藥物已無法治愈。盡管關於大腸癌發病的分子生物學機制已經不斷完善,但如何從基礎研究轉化為臨床治療手段在很長一段時間內不可實現。為了進一步研究新的抗擊大腸癌治療手段,廣泛且深入的研究已經不斷開展。上皮間充質轉化是一個多步驟的過程,該過程的典型特徵為失去細胞的極性,細胞間粘連減弱以及細胞爬行遷移能力的不斷加強。目前科學家已經知道上皮間充質轉化對於從胚胎發育到腫瘤發展都起著重要的作用。近年來,長非編碼RNA的研究不斷快速發展,已然成為醫學研究中最激烈的領域之一。眾多證據表明人體基因組編碼數以千計不編碼蛋白質的RNA轉錄體。然而,這些RNA轉錄體在上皮間充質轉化中的功能依然所知甚少。長非編碼RNA H19是人體內第一個被鑒別出來參與到基因印記的非編碼RNA。資料表明H19/IGF2位點是一個非常理想的研究基因印記的位點。近年來,H19在眾多癌症中的表達以及功能學研究已不斷湧現,同時也不斷取得令人鼓舞的研究成果。在我們的研究中,H19被鑒定為大腸癌裏上皮間充質轉化過程中一個重要的參與者。通過研究甲氨蝶呤耐藥大腸癌HT-29細胞株,我們發現該HT-29耐藥細胞株有著顯著的間充質細胞特性。有趣的是,H19在該細胞株中有著顯著升高。我們隨後用經典的上皮間充質轉化誘導劑TGF-β1處理兩株大腸癌細胞,處理後H19亦有著顯著升高。為了進一步研究H19在上皮間充質轉化,通過使用逆轉錄病毒,我們建立H19的穩定表達細胞株。穩定表達H19顯著地促進了HT-29以及SW620大腸癌細胞株的上皮間充質轉化。然後,高水平表達(過表達)H19並不影響細胞的生長以及細胞周期的進程。進一步的蛋白質組學研究表明,過表達H19能促進間充質細胞一個重要標記基因Vimentin的表達。通過生物信息學以及熒光素酶報告基因實驗,我們證明了H19通過其競爭內源性RNA的作用,能夠促進間充質細胞所需的幾個重要基因的表達。該發現建立起了miRNA網絡以及上皮間充質轉化進程的交流網絡。通過異位移植以及軟瓊脂實驗,我們發現過表達H19能夠促進腫瘤細胞的生長。而在臨床大腸癌病人組織中,我們更發現H19在大腸癌病人組織中高表達。綜上所述,我們的結果證明H19這一長非編碼RNA,能夠通過其競爭內源性RNA的作用機制,從而調控上皮間充質轉化過程中的關鍵基因。同時H19亦有可能成為治療大腸癌的臨床新靶點。Liang, Weicheng.Thesis (Ph.D.)--Chinese University of Hong Kong, 2014.Includes bibliographical references (leaves 95-124).Abstracts also in Chinese.Title from PDF title page (viewed on 24, October, 2016).Liang, Weicheng
Measuring the miracle: market imperfections and Asia's growth experience
The newly industrialized economies (NIEs) of Asia are the fastest-growing economies in the world since 1960. A clear understanding of their rapid development remains elusive, with continuing disputes over the roles of technology growth, capital accumulation, and international trade and investment. We reconcile seemingly contradictory explanations by accounting for imperfections in output and capital markets. For instance, in Singapore, growth-accounting studies using quantities (the primal approach) find rising capital-output ratios and a constant labor share; but studies using real factor prices (the dual approach) find a constant user cost. We provide evidence that "favored" firms reaped economic profits and received preferential tax treatment, subsidies, and access to capital-- market imperfections that are difficult to capture when implementing the dual approach. Further, declining pure profits can reconcile the constant or rising labor shares in revenue in the NIEs with theories of international trade that predict falling labor shares in cost. We provide empirical support for the quantitative importance of profits and heterogeneous user costs, describe the two-sector dynamics, and derive measures of technology growth, corrected for the imperfections that we quantify. We then discuss implications for broader disputes about Asian development.Asia ; Economic conditions ; Productivity
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