Decision Support System For Safety Warning Of Bridge – A Case Study In Central Taiwan

This study aims at developing the decision support system (DSS) for safety warning of bridge. In the DSS, real-time and forecasted radar rainfalls are used to predict flood stage, velocity and scouring depth around bridge piers for one to three hours ahead. The techniques adopted in the DSS include (1) measurement and correction models of radar rainfall, (2) a grid-based distributed rainfall-runoff model for simulating reservoir inflows, (3) models for predicting flood stages, velocities and scouring depths around bridge piers, and (4) ultimate analysis approaches for evaluating safety of pier foundation. The DSS can support the management department to decide whether they should close bridges or not during floods. The proposed DSS gave a test-run during Typhoon Morakot in 2009 in Dajia River Basin, central Taiwan. The results show the DSS has reasonable performances during floods

Effects of Domain Selection on Singular-Value-Decomposition Based Statistical Downscaling of Monthly Rainfall Accumulation in Southern Taiwan

A singular-value-decomposition (SVD) statistical downscaling technique was developed for monthly rainfall over southern Taiwan. The statistical model was applied to seven different general circulation models. Seven different geographical domains for the large-scale atmospheric predictors were tested and their effects on rainfall projections were evaluated. Because different climate models indicate different future rainfall projections, a multi-model ensemble approach was applied to provide best guess estimates. Using the multi-model ensemble, and a range of metrics, it was found that the different predictor geographical domains had little influence on the projected monthly rainfalls. Two emission climate change scenarios (A1B and B1) were used to project the future rainfalls for the period from 2010 to 2045 across southern Taiwan. Overall, future rainfall shows an increasing trend during the May-to-October wet season and a decreasing trend during the November-to-April dry season

Sap Flow Sensors: Construction, Quality Control and Comparison

This work provides a design for two types of sensors, based on the thermal dissipation and heat ratio methods of sap flow calculation, for moderate to large scale deployments for the purpose of monitoring tree transpiration. These designs include a procedure for making these sensors, a quality control method for the final products, and a complete list of components with vendors and pricing information. Both sensor designs were field tested alongside a commercial sap flow sensor to assess their performance and show the importance for quality controlling the sensor outputs. Results show that for roughly 2% of the cost of commercial sensors, self-made sap flow sensors can provide acceptable estimates of the sap flow measurements compared to the commercial sensors

Rainfall Variation under Different Climate Change Scenarios Based on Cmip3 and Cmip5 Projections: a Case Study in Taiwan

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchive

Adiponectin gene (ADIPOQ) polymorphisms correlate with the progression of nephropathy in Taiwanese male patients with type 2 diabetes

Aims: Polymorphisms of the ADIPOQ gene were associated with diabetic nephropathy (DN) in case-control studies predominantly among European populations. Gender may modify the ADIPOQ associated risk for DN. We investigated the association of 18 ADIPOQ polymorphisms with DN in a prospective Taiwanese cohort of type 2 diabetes (T2D) and explored whether gender plays a role in this genetic association. Methods: Selected single nucleotide polymorphisms (SNPs) of ADIPOQ were genotyped in 566 T2D patients with normoalbuminuria at baseline. DN was defined based on urinary albumin-to-creatinine ratio (ACR). The Cox proportional hazard model was used to explore the association of individual SNP to DN events under different genetic models over a 6-year follow-up period. Analyses were further stratified by gender. Results: In male patients, the adjusted hazard ratios under the recessive models were 1.81 for rs2241766 TT (vs. GT+GG, 95% CI=1.10-2.96, p=0.019) and 1.89 for rs1063537 CC (vs. CT+TT, 95% CI=1.15-3.11, p=0.013). In the Kaplan-Meier survival curve, males carrying rs2241766 TT (vs. GT+GG, p=0.050) and rs1063537 CC (vs. CT+TT, p=0.037) recessive homozygotes also had a reduced nephropathy-free survival rate. SNPs rs2241767 and rs2082940, both in strong correlation with tag SNP rs1063537 (r≥0.96), were also associated with DN progression in males. In females, ADIPOQ polymorphisms were not associated with the progression of DN. Conclusions: ADIPOQ genetic polymorphisms rs2241766 (+45T>G), rs1063537, rs2241767 and rs2082940 were correlated with the progression of DN in Taiwanese male patients with T2D. The role of gender in this ADIPOQ genetic association needs to be further investigated in other populations

New provincial CO2 emission inventories in China based on apparent energy consumption data and updated emission factors

This study employs “apparent energy consumption” approach and updated emissions factors to re-calculate Chinese provincial CO2 emissions during 2000–2012 to reduce the uncertainty in Chinese CO2 emission estimates for the first time. The study presents the changing emission-socioeconomic features of each provinces as well. The results indicate that Chinese provincial aggregated CO2 emissions calculated by the apparent energy consumption and updated emissions factors are coincident with the national emissions estimated by the same approach, which are 12.69% smaller than the one calculated by the traditional approach and IPCC default emission factors. The provincial aggregated CO2 emissions increased from 3160 million tonnes in 2000 to 8583 million tonnes in 2012. During the period, Shandong province contributed most to national emissions accumulatively (with an average percentage of 10.35%), followed by Liaoning (6.69%), Hebei (6.69%) and Shanxi provinces (6.25%). Most of the CO2 emissions were from raw coal, which is primarily burned in the thermal power sector. The analyses of per capita emissions and emission intensity in 2012 indicates that provinces located in the northwest and north had higher per capita CO2 emissions and emission intensities than the central and southeast coastal regions. Understanding the emissions and emission-socioeconomic characteristics of different provinces is critical for developing mitigation strategies

Systems Biology Modeling Reveals a Possible Mechanism of the Tumor Cell Death upon Oncogene Inactivation in EGFR Addicted Cancers

Despite many evidences supporting the concept of “oncogene addiction” and many hypotheses rationalizing it, there is still a lack of detailed understanding to the precise molecular mechanism underlying oncogene addiction. In this account, we developed a mathematic model of epidermal growth factor receptor (EGFR) associated signaling network, which involves EGFR-driving proliferation/pro-survival signaling pathways Ras/extracellular-signal-regulated kinase (ERK) and phosphoinositol-3 kinase (PI3K)/AKT, and pro-apoptotic signaling pathway apoptosis signal-regulating kinase 1 (ASK1)/p38. In the setting of sustained EGFR activation, the simulation results show a persistent high level of proliferation/pro-survival effectors phospho-ERK and phospho-AKT, and a basal level of pro-apoptotic effector phospho-p38. The potential of p38 activation (apoptotic potential) due to the elevated level of reactive oxygen species (ROS) is largely suppressed by the negative crosstalk between PI3K/AKT and ASK1/p38 pathways. Upon acute EGFR inactivation, the survival signals decay rapidly, followed by a fast increase of the apoptotic signal due to the release of apoptotic potential. Overall, our systems biology modeling together with experimental validations reveals that inhibition of survival signals and concomitant release of apoptotic potential jointly contribute to the tumor cell death following the inhibition of addicted oncogene in EGFR addicted cancers

Hierarchical Modeling of Activation Mechanisms in the ABL and EGFR Kinase Domains: Thermodynamic and Mechanistic Catalysts of Kinase Activation by Cancer Mutations

Structural and functional studies of the ABL and EGFR kinase domains have recently suggested a common mechanism of activation by cancer-causing mutations. However, dynamics and mechanistic aspects of kinase activation by cancer mutations that stimulate conformational transitions and thermodynamic stabilization of the constitutively active kinase form remain elusive. We present a large-scale computational investigation of activation mechanisms in the ABL and EGFR kinase domains by a panel of clinically important cancer mutants ABL-T315I, ABL-L387M, EGFR-T790M, and EGFR-L858R. We have also simulated the activating effect of the gatekeeper mutation on conformational dynamics and allosteric interactions in functional states of the ABL-SH2-SH3 regulatory complexes. A comprehensive analysis was conducted using a hierarchy of computational approaches that included homology modeling, molecular dynamics simulations, protein stability analysis, targeted molecular dynamics, and molecular docking. Collectively, the results of this study have revealed thermodynamic and mechanistic catalysts of kinase activation by major cancer-causing mutations in the ABL and EGFR kinase domains. By using multiple crystallographic states of ABL and EGFR, computer simulations have allowed one to map dynamics of conformational fluctuations and transitions in the normal (wild-type) and oncogenic kinase forms. A proposed multi-stage mechanistic model of activation involves a series of cooperative transitions between different conformational states, including assembly of the hydrophobic spine, the formation of the Src-like intermediate structure, and a cooperative breakage and formation of characteristic salt bridges, which signify transition to the active kinase form. We suggest that molecular mechanisms of activation by cancer mutations could mimic the activation process of the normal kinase, yet exploiting conserved structural catalysts to accelerate a conformational transition and the enhanced stabilization of the active kinase form. The results of this study reconcile current experimental data with insights from theoretical approaches, pointing to general mechanistic aspects of activating transitions in protein kinases