A Probabilistic Risk Analysis for Taipei Seismic Hazards: An Application of HAZ-Taiwan with its Pre-processor and Post-processor

This paper employs probabilistic risk analysis to estimate exceedance probability curves, average annual loss (AAL) and probable maximum loss (PML) for seismic hazards. It utilizes and event-driven loss estimation model, HAZ-Taiwan, and develops its pre-processing and post-processing software modules. First, the pre-processingmodule establishes a set of hazard-consistent scenarios. Then, the HAZ-Taiwan modelextimates hazards, vulnerabilities and economic losses for each scenario. Finally, the aggregate and occurrence exceedance probability curves for losses and theirconfidence intervals are simulated using the Monte Carlo simulation in thepost-processing module. The methodology is then applied to analyze seismic risks in Taipei. It is found that the exceedance probability of an aggregate loss of NT$40.398 billion is 0.001. This amount of loss is approximately 2.78$37.41-43.12 billion. The average annual loss of buildings in Taipei is NT$1.06 billion r approximately 0.07% of the total stock.probabilistic risk analysis, Hazard analysis, vulnerability analysis, exceedance probability curve, HAZ-Taiwan

ICPR2017 – The Fourth International Conference on Practice Research: overview

This paper reports issues arising from the Fourth International Conference on Practice Research, held in Hong Kong in May 2017. The issues were identified by specially convened group of conference participants, and include the need to develop a better language to describe practice research in terms that make sense to practitioners, improved support for practitioners to conduct research, recognising the different drivers for practice research in different countries, and enhancing practitioners' coordinating and leadership roles

Mitochondrial Function and Nuclear Factor-KB–Mediated Signaling in Radiation-Induced Bystander Effects

Although radiation-induced bystander effects have been well described over the past decade, the mechanisms of the signaling processes involved in the bystander phenomenon remain unclear. In the present study, using the Columbia University charged particle microbeam, we found that mitochondrial DNA–depleted human skin fibroblasts (ρo) showed a higher bystander mutagenic response in confluent monolayers when a fraction of the same population were irradiated with lethal doses compared with their parental mitochondrial–functional cells (ρ+). However, using mixed cultures of ρo and ρ+ cells and targeting only one population of cells with a lethal dose of α-particles, a decreased bystander mutagenesis was uniformly found in nonirradiated bystander cells of both cell types, indicating that signals from one cell type can modulate expression of bystander response in another cell type. In addition, we found that Bay 11-7082, a pharmacologic inhibitor of nuclear factor-κB (NF-κB) activation, and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a scavenger of nitric oxide (NO), significantly decreased the mutation frequency in both bystander ρo and ρ+ cells. Furthermore, we found that NF-κB activity and its dependent proteins, cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS), were lower in bystander ρo cells when compared with their ρ+ counterparts. Our results indicated that mitochondria play an important role in the regulation of radiation-induced bystander effects and that mitochondria-dependent NF-κB/iNOS/NO and NF-κB/COX-2/prostaglandin E2 signaling pathways are important to the process

Causal Evidence for the Role of Specific GABAergic Interneuron Types in Entorhinal Recruitment of Dentate Granule Cells

The dentate gyrus (DG) is the primary gate of the hippocampus and controls information flow from the cortex to the hippocampus proper. To maintain normal function, granule cells (GCs), the principal neurons in the DG, receive fine- tuned inhibition from local-circuit GABAergic inhibitory interneurons (INs). Abnormalities of GABAergic circuits in the DG are associated with several brain disorders, including epilepsy, autism, schizophrenia, and Alzheimer disease. Therefore, understanding the network mechanisms of inhibitory control of GCs is of functional and pathophysiological importance. GABAergic inhibitory INs are heterogeneous, but it is unclear how individual subtypes contribute to GC activity. Using cell-type-specific optogenetic perturbation, we investigated whether and how two major IN populations defined by parvalbumin (PV) and somatostatin (SST) expression, regulate GC input transformations. We showed that PV-expressing (PV+) INs, and not SST- expressing (SST+) INs, primarily suppress GC responses to single cortical stimulation. In addition, these two IN classes differentially regulate GC responses to θ and γ frequency inputs from the cortex. Notably, PV+ INs specifically control the onset of the spike series, whereas SST+ INs preferentially regulate the later spikes in the series. Together, PV+ and SST+ GABAergic INs engage differentially in GC input-output transformations in response to various activity patterns

Association between genetic variant on chromosome 12p13 and stroke survival and recurrence: a one year prospective study in Taiwan

<p>Abstract</p> <p>Background</p> <p>The association between ischemic stroke and 2 single nucleotide polymorphisms (SNPs) on chromosome 12p13, rs12425791 and rs11833579 appears inconsistent across different samples. These SNPs are close to the ninjurin2 gene which may alter the risk of stroke by affecting brain response to ischemic injury. The purpose of this study was to investigate the association between these two SNPs and ischemic stroke risk, as well as prognostic outcomes in a Taiwanese sample.</p> <p>Methods</p> <p>We examined the relations of these two SNPs to the odds of new-onset ischemic stroke, ischemic stroke subtypes, and to the one year risk of stroke-related death or recurrent stroke following initial stroke in a case-control study. A total of 765 consecutive patients who had first-ever ischemic stroke were compared to 977 stroke-free, age-matched controls. SNPs were genotyped by Taqman fluorescent allelic discrimination assay. The association between ischemic stroke and SNPs were analyzed by multivariate logistic regression. Cox proportional hazard model was used to assess the effect of individual SNPs on stroke-related mortality or recurrent stroke.</p> <p>Results</p> <p>There was no significant association between SNP rs12425791 and rs11833579 and ischemic stroke after multiple testing corrections. However, the marginal significant association was observed between SNP rs12425791 and large artery atherosclerosis under recessive model (OR, 2.30; 95%CI, 1.22-4.34; q-value = 0.062). Among the 765 ischemic stroke patients, 59 died or developed a recurrent stroke. After adjustment for age, sex, vascular risk factors and baseline stroke severity, Cox proportional hazard analysis indicated that the hazard ratios were 2.76 (95%CI, 1.34-5.68; q-value, 0.02) and 2.15 (95%CI, 1.15-4.02; q-value, 0.03) for individuals with homozygous variant allele of rs12425791 and rs11833579, respectively.</p> <p>Conclusions</p> <p>This is a precedent study that found genetic variants of rs12425791 and rs11833579 on chromosome 12p13 are independent predictors of stroke-related mortality or stroke recurrence in patients with incident ischemic stroke in Taiwan. Further study is needed to explore the details of the physiological function and the molecular mechanisms underlying the association of this genetic locus with ischemic stroke.</p

Observations of a freshwater pulse induced by Typhoon Morakot off the northern coast of Taiwan in August 2009

Author Posting. © Sears Foundation for Marine Research, 2013. This article is posted here by permission of Sears Foundation for Marine Research for personal use, not for redistribution. The definitive version was published in Journal of Marine Research 71 (2013): 19-46, doi:10.1357/002224013807343452.In this paper we describe large-scale impacts from a typhoon on the circulation over the continental shelf and slope north of Taiwan. Typhoon Morakot was a category 2 tropical storm that landed in central Taiwan, but caused destruction primarily in southern Taiwan from Aug. 8–10, 2009. The typhoon brought record-breaking rainfall; approximately 3 m accumulated over four days in southern Taiwan. River discharge on the west coast of Taiwan increased rapidly from Aug. 6–7 and peaked on Aug. 8, yielding a total volume 27.2 km3 of freshwater discharged off the west coast of Taiwan over five days (Aug. 6–10). The freshwater mixed with ambient seawater, and was carried primarily by the northeastward-flowing Taiwan Strait current to the sea off the northern coast of Taiwan. Two joint surveys each measured the hydrography and current velocity in the Taiwan Strait and off the northeastern coast of Taiwan roughly one week and two and a half weeks after Morakot. The first survey observed an Ω-shaped freshwater pulse off the northern tip of Taiwan, in which the salinity was ∼1 lower than the climatological mean salinity. The freshwater pulse met the Kuroshio and formed a density front off the northeastern coast of Taiwan. The hydrographic data obtained in the second survey suggested that the major freshwater pulse left the sea off the northern and northeastern coasts of Taiwan, which may have been carried by the Kuroshio to the northeast. Biogeochemical sampling conducted after Morakot suggested that the concentrations of nutrients in the upper ocean off the northern coast of Taiwan increased remarkably compared with their normal values. A typhoon-induced biological bloom is attributed to the inputs both from the nutrient-rich river runoff and upwelling of the subsurface Kuroshio water.This study is supported by the National Science Council (NSC) of Taiwan under grant NSC98-2611-M-002-019-MY3. C.-C. Hung is supported by NSC under grant NSC100-2119-M- 110-003. LC was supported by ONR grant N00014-08-1-0557 and NOAA grant NA10OAR4320156

Solanum lyratum

We investigated the molecular mechanisms of cell cycle arrest and apoptotic death induced by Solanum lyratum extracts (SLE) or diosgenin in WEHI-3 murine leukemia cells in vitro and antitumor activity in vivo. Diosgenin is one of the components of SLE. Our study showed that SLE and diosgenin decreased the viable WEHI-3 cells and induced G0/G1 phase arrest and apoptosis in concentration- or time-dependent manners. Both reagents increased the levels of ROS production and decreased the mitochondrial membrane potential (ΔΨm). SLE- and diosgenin-triggered apoptosis is mediated through modulating the extrinsic and intrinsic signaling pathways. Intriguingly, the p53 inhibitor (pifithrin-α), anti-Fas ligand (FasL) mAb, and specific inhibitors of caspase-8 (z-IETD-fmk), caspase-9 (z-LEHD-fmk), and caspase-3 (z-DEVD-fmk) blocked SLE- and diosgenin-reduced cell viability of WEHI-3 cells. The in vivo study demonstrated that SLE has marked antitumor efficacy against tumors in the WEHI-3 cell allograft model. In conclusion, SLE- and diosgenin-induced G0/G1 phase arrest and triggered extrinsic and intrinsic apoptotic pathways via p53 activation in WEHI-3 cells. SLE also exhibited antitumor activity in vivo. Our findings showed that SLE may be potentially efficacious in the treatment of leukemia in the future

The Yuan-Tseh Lee Array for Microwave Background Anisotropy

The Yuan-Tseh Lee Array for Microwave Background Anisotropy (AMiBA) is the first interferometer dedicated to studying the cosmic microwave background (CMB) radiation at 3mm wavelength. The choice of 3mm was made to minimize the contributions from foreground synchrotron radiation and Galactic dust emission. The initial configuration of seven 0.6m telescopes mounted on a 6-m hexapod platform was dedicated in October 2006 on Mauna Loa, Hawaii. Scientific operations began with the detection of a number of clusters of galaxies via the thermal Sunyaev-Zel'dovich effect. We compare our data with Subaru weak lensing data in order to study the structure of dark matter. We also compare our data with X-ray data in order to derive the Hubble constant.Comment: accepted for publication in ApJ (13 pages, 7 figures); a version with high resolution figures available at http://www.asiaa.sinica.edu.tw/~keiichi/upfiles/AMiBA7/pho_highreso.pd

Prevalence of PIK3CA mutations in Taiwanese patients with breast cancer: a retrospective next-generation sequencing database analysis

BackgroundBreast cancer is the most common cancer type that affects women. In hormone receptor–positive (HR+), human epidermal growth factor receptor 2−negative (HER2–) advanced breast cancer (ABC), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) is the most frequently mutated gene associated with poor prognosis. This study evaluated the frequency of PIK3CA mutations in the Taiwanese breast cancer population.MethodologyThis is a retrospective study; patient data were collected for 2 years from a next-generation sequencing database linked to electronic health records (EHRs). The primary endpoint was the regional prevalence of PIK3CA mutation. The secondary endpoints were to decipher the mutation types across breast cancer subtype, menopausal status, and time to treatment failure after everolimus (an mTOR inhibitor) or cyclin-dependent kinase 4/6 (CDK4/6) inhibitor treatment.ResultsPIK3CA mutations were identified in 278 of 728 patients (38%). PIK3CA mutations were reported in 43% of patients with HR−/HER2+ subtype and 42% of patients with HR+/HER2– postmenopausal status. A lower prevalence of PIK3CA mutations was observed in triple-negative (27%) and HR+/HER2– premenopausal patients (29%). The most common mutation was at exon 20 (H1047R mutation, 41.6%), followed by exon 9 (E545K mutation, 18.9% and E542K mutation, 10.3%). Among patients treated with CDK4/6 inhibitors, the median time to treatment failure was 12 months (95% CI: 7-21 months) in the PIK3CA mutation cohort and 16 months (95% CI: 11-23 months) in the PIK3CA wild-type cohort, whereas patients receiving an mTOR inhibitor reported a median time to treatment failure of 20.5 months (95% CI: 8-33 months) in the PIK3CA mutation cohort and 6 months (95% CI: 2-9 months) in the PIK3CA wild-type cohort.ConclusionA high frequency of PIK3CA mutations was detected in Taiwanese patients with breast cancer, which was consistent with previous studies. Early detection of PIK3CA mutations might influence therapeutic decisions, leading to better treatment outcomes

Quantum metric nonlinear Hall effect in a topological antiferromagnetic heterostructure

Quantum geometry - the geometry of electron Bloch wavefunctions - is central to modern condensed matter physics. Due to the quantum nature, quantum geometry has two parts, the real part quantum metric and the imaginary part Berry curvature. The studies of Berry curvature have led to countless breakthroughs, ranging from the quantum Hall effect in 2DEGs to the anomalous Hall effect (AHE) in ferromagnets. However, in contrast to Berry curvature, the quantum metric has rarely been explored. Here, we report a new nonlinear Hall effect induced by quantum metric by interfacing even-layered MnBi2Te4 (a PT-symmetric antiferromagnet (AFM)) with black phosphorus. This novel nonlinear Hall effect switches direction upon reversing the AFM spins and exhibits distinct scaling that suggests a non-dissipative nature. Like the AHE brought Berry curvature under the spotlight, our results open the door to discovering quantum metric responses. Moreover, we demonstrate that the AFM can harvest wireless electromagnetic energy via the new nonlinear Hall effect, therefore enabling intriguing applications that bridges nonlinear electronics with AFM spintronics.Comment: 19 pages, 4 figures and a Supplementary Materials with 66 pages, 4 figures and 3 tables. Originally submitted to Science on Oct. 5, 202