Towards Structured Deep Neural Network for Automatic Speech Recognition

In this paper we propose the Structured Deep Neural Network (Structured DNN) as a structured and deep learning algorithm, learning to find the best structured object (such as a label sequence) given a structured input (such as a vector sequence) by globally considering the mapping relationships between the structure rather than item by item. When automatic speech recognition is viewed as a special case of such a structured learning problem, where we have the acoustic vector sequence as the input and the phoneme label sequence as the output, it becomes possible to comprehensively learned utterance by utterance as a whole, rather than frame by frame. Structured Support Vector Machine (structured SVM) was proposed to perform ASR with structured learning previously, but limited by the linear nature of SVM. Here we propose structured DNN to use nonlinear transformations in multi-layers as a structured and deep learning algorithm. It was shown to beat structured SVM in preliminary experiments on TIMIT

The role of macroeconomic policy in export-led growth

노트 : - This PDF is a selection from an out-of-print volume from the National Bureau of Economic Research -Volume Title: Financial Deregulation and Integration in East Asia, NBER-EASE Volume

Slipped Capital Femoral Epiphysis as a Complication of Growth Hormone Therapy

Slipped capital femoral epiphysis (SCFE) is a rare complication of growth hormone (GH) therapy. Here, we report three patients who developed SCFE during GH therapy. The first two patients had hypopituitarism and had started GH therapy at the age of 15 years 6 months and 13 years 9 months, respectively. SCFE developed 4 years and 1 year after GH therapy, respectively. The third patient had Prader-Willi syndrome with obesity and hypogonadism and began GH therapy at the age of 12 years and 11 months. SCFE developed 2 months after starting GH therapy. Pain over the hip joints or over the knees is an early sign of SCFE. Despite recommendation, none of the three patients continued GH therapy. A high index of suspicion during GH therapy in patients at high risk of SCFE is important for early diagnosis and appropriate management. [J Formos Med Assoc 2007;106(2 Suppl):S46-S50

VI-Band Follow-Up Observations of Ultra-Long-Period Cepheid Candidates in M31

The ultra-long period Cepheids (ULPCs) are classical Cepheids with pulsation periods exceeding $\approx 80$ days. The intrinsic brightness of ULPCs are ~1 to ~3 mag brighter than their shorter period counterparts. This makes them attractive in future distance scale work to derive distances beyond the limit set by the shorter period Cepheids. We have initiated a program to search for ULPCs in M31, using the single-band data taken from the Palomar Transient Factory, and identified eight possible candidates. In this work, we presented the VI-band follow-up observations of these eight candidates. Based on our VI-band light curves of these candidates and their locations in the color-magnitude diagram and the Period-Wesenheit diagram, we verify two candidates as being truly ULPCs. The six other candidates are most likely other kinds of long-period variables. With the two confirmed M31 ULPCs, we tested the applicability of ULPCs in distance scale work by deriving the distance modulus of M31. It was found to be $\mu_{M31,ULPC}=24.30\pm0.76$ mag. The large error in the derived distance modulus, together with the large intrinsic dispersion of the Period-Wesenheit (PW) relation and the small number of ULPCs in a given host galaxy, means that the question of the suitability of ULPCs as standard candles is still open. Further work is needed to enlarge the sample of calibrating ULPCs and reduce the intrinsic dispersion of the PW relation before re-considering ULPCs as suitable distance indicators.Comment: 13 pages, with 14 Figures and 4 Tables (one online table). AJ accepte

台南縣新營地區高中職學生蔬果攝取行為及相關因素研究

[[volume]]36

Sox2, a stemness gene, regulates tumor-initiating and drug-resistant properties in CD133-positive glioblastoma stem cells

AbstractBackgroundGlioblastoma multiforme (GBM) is the most lethal type of adult brain cancer and performs outrageous growth and resistance regardless of adjuvant chemotherapies, eventually contributing to tumor recurrence and poor outcomes. Considering the common heterogeneity of cancer cells, the imbalanced regulatory mechanism could be switched on/off and contribute to drug resistance. Moreover, the subpopulation of GBM cells was recently discovered to share similar phenotypes with neural stem cells. These cancer stem cells (CSCs) promote the potency of tumor initiation. As a result, targeting of glioma stem cells has become the dominant way of improving the therapeutic outcome against GBM and extending the life span of patients. Among the biomarkers of CSCs, CD-133 (prominin-1) has been known to effectively isolate CSCs from cancer population, including GBM; however, the underlying mechanism of how stemness genes manipulate CSC-associated phenotypes, such as tumor initiation and relapse, is still unclear.MethodsTumorigenicity, drug resistance and embryonic stem cell markers were examined in primary CD133-positive (CD133+) GBM cells and CD133+ subpopulation. Stemness signature of CD133+ GBM cells was identified using microarray analysis. Stem cell potency, tumorigenicity and drug resistance were also tested in differential expression of SOX2 in GBM cells.ResultsIn this study, high tumorigenic and drug resistance was noticed in primary CD-133+ GBM cells; meanwhile, plenty of embryonic stem cell markers were also elevated in the CD-133+ subpopulation. Using microarray analysis, we identified SOX2 as the most enriched gene among the stemness signature in CD133+ GBM cells. Overexpression of SOX2 consistently enhanced the stem cell potency in the GBM cell lines, whereas knockdown of SOX2 dramatically withdrew CD133 expression in CD133+ GBM cells. Additionally, we silenced SOX2 expression using RNAi system, which abrogated the ability of tumor initiation as well as drug resistance of CD133+ GBM cells, suggesting that SOX2 plays a crucial role in regulating tumorigenicity in CD133+ GBM cells.ConclusionSOX2 plays a crucial role in regulating tumorigenicity in CD133+ GBM cells. Our results not only revealed the genetic plasticity contributing to drug resistance and stemness but also demonstrated the dominant role of SOX2 in maintenance of GBM CSCs, which may provide a novel therapeutic target to overcome the conundrum of poor survival of brain cancers

A novel deep intronic variant strongly associates with Alkaptonuria.

Alkaptonuria is a rare autosomal recessive inherited disorder of tyrosine metabolism, which causes ochronosis, arthropathy, cardiac valvular calcification, and urolithiasis. The epidemiology of alkaptonuria in East Asia is not clear. In this study, patients diagnosed with alkaptonuria from January 2010 to June 2020 were reviewed. Their clinical and molecular features were further compared with those of patients from other countries. Three patients were found to have alkaptonuria. Mutation analyses of the homogentisate 1,2-dioxygenase gene (HGD) showed four novel variants c.16-2063 A > C, p.(Thr196Ile), p.(Gly344AspfsTer25), and p.(Gly362Arg) in six mutated alleles (83.3%). RNA sequencing revealed that c.16-2063 A > C activates a cryptic exon, causing protein truncation p.(Tyr5_Ile6insValTer17). A literature search identified another 6 patients with alkaptonuria in East Asia; including our cases, 13 of the 18 mutated alleles have not been reported elsewhere in the world. Alkaptonuria is rare in Taiwan and East Asia, with HGD variants being mostly novel and private