58 resultados para cracking due to shrinkage


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Large-scale integration of non-inertial generators such as wind farms will create frequency stability issues due to reduced system inertia. Inertia based frequency stability study is important to predict the performance of power system with increased level of renewables. This paper focuses on the impact large-scale wind penetration on frequency stability of the Australian Power Network. MATLAB simulink is used to develop a frequency based dynamic model utilizing the network data from a simplified 14-generator Australian power system. The loss of generation is modeled as the active power disturbance and minimum inertia required to maintain the frequency stability is determined for five-area power system.

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This study examines the impact of incentives on commuters' travel behavior based upon a questionnaire survey conducted with respect to the Beijing Subway System. Overall, we find that offering incentives to commuters, particularly fast food restaurant-related services and reduced ticket fares, has a positive influence on avoiding the morning rush hour. Furthermore, by using an interaction analysis, we discover that a flexible work schedule has an impact on commuters' behavior and the efficiency of the subway system. Finally, we recommend two possible policies to maximize the utility of the subway system and to reduce congestion at the peak of morning service: (1) a set of incentives that includes free wireless internet service with a coupon for breakfast and a discount on ticket fares before the morning peak, and; (2) the introduction of a flexible work schedule.

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This article describes research conducted for the Japanese government in the wake of the magnitude 9.0 earthquake and tsunami that struck eastern Japan on March 11, 2011. In this study, material stock analysis (MSA) is used to examine the losses of building and infrastructure materials after this disaster. Estimates of the magnitude of material stock that has lost its social function as a result of a disaster can indicate the quantities required for reconstruction, help garner a better understanding of the volumes of waste flows generated by that disaster, and also help in the course of policy deliberations in the recovery of disaster-stricken areas. Calculations of the lost building and road materials in the five prefectures most affected were undertaken. Analysis in this study is based on the use of geographical information systems (GIS) databases and statistics; it aims to (1) describe in spatial terms what construction materials were lost, (2) estimate the amount of infrastructure material needed to rehabilitate disaster areas, and (3) indicate the amount of lost material stock that should be taken into consideration during government policy deliberations. Our analysis concludes that the material stock losses of buildings and road infrastructure are 31.8 and 2.1 million tonnes, respectively. This research approach and the use of spatial MSA can be useful for urban planners and may also convey more appropriate information about disposal based on the work of municipalities in disaster-afflicted areas.

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Injury as a result of road traffic crashes is one of the most significant public health problems in developing countries. It intersects with disability as a development issue because a substantial proportion of people injured in road traffic crashes experience disability, both short term and long term. While there have been significant steps towards better management of road safety globally, especially in developing countries, the implications for road safety policy and practice of disability due road traffic crashes is not fully appreciated. In particular, qualitative information on the lived experience people with a long term disability as a result of a road traffic crash can inform better road safety policy and practice, as demonstrated in a case study from Thailand. The benefits of better policies and practices are likely to accrue to a wide range of road users, and to contribute to the achievement of sustainable development.

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Pollution on electrical insulators is one of the greatest causes of failure of substations subjected to high levels of salinity and environmental pollution. Considering leakage current as the main indicator of pollution on insulators, this paper focus on establishing the effect of the environmental conditions on the risk of failure due to pollution on insulators and determining the significant change in the magnitude of the pollution on the insulators during dry and humid periods. Hierarchical segmentation analysis was used to establish the effect of environmental conditions on the risk of failure due to pollution on insulators. The Kruskal-Wallis test was utilized to determine the significant changes in the magnitude of the pollution due to climate periods. An important result was the discovery that leakage current was more common on insulators during dry periods than humid ones. There was also a higher risk of failure due to pollution during dry periods. During the humid period, various temperatures and wind directions produced a small change in the risk of failure. As a technical result, operators of electrical substations can now identify the cause of an increase in risk of failure due to pollution in the area. The research provides a contribution towards the behaviour of the leakage current under conditions similar to those of the Colombian Caribbean coast and how they affect the risk of failure of the substation due to pollution.

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A teaching laboratory experiment is described that uses Archimedes’ principle to precisely investigate the effect of global warming on the oceans. A large component of sea level rise is due to the increase in the volume of water due to the decrease in water density with increasing temperature. Water close to 0 °C is placed in a beaker and a glass marble hung from an electronic balance immersed in the water. As the water warms, the weight of the marble increases as the water is less buoyant due to the decrease in density. In the experiment performed in this paper a balance with a precision of 0.1 mg was used with a marble 40.0 cm3 and mass of 99.3 g, yielding water density measurements with an average error of -0.008 ± 0.011%.

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Chronic kidney disease (CKD) is characterized by renal fibrosis that can lead to end-stage renal failure, and studies have supported a strong genetic influence on the risk of developing CKD. However, investigations of the underlying molecular mechanisms are hampered by the lack of suitable hereditary models in animals. We therefore sought to establish hereditary mouse models for CKD and renal fibrosis by investigating mice treated with the chemical mutagen N-ethyl-N-nitrosourea, and identified a mouse with autosomal recessive renal failure, designated RENF. Three-week old RENF mice were smaller than their littermates, whereas at birth they had been of similar size. RENF mice, at 4-weeks of age, had elevated concentrations of plasma urea and creatinine, indicating renal failure, which was associated with small and irregularly shaped kidneys. Genetic studies using DNA from 10 affected mice and 91 single nucleotide polymorphisms mapped the Renf locus to a 5.8Mbp region on chromosome 17E1.3. DNA sequencing of the xanthine dehydrogenase (Xdh) gene revealed a nonsense mutation at codon 26 that co-segregated with affected RENF mice. The Xdh mutation resulted in loss of hepatic XDH and renal Cyclooxygenase-2 (COX-2) expression. XDH mutations in man cause xanthinuria with undetectable plasma uric acid levels and three RENF mice had plasma uric acid levels below the limit of detection. Histological analysis of RENF kidney sections revealed abnormal arrangement of glomeruli, intratubular casts, cellular infiltration in the interstitial space, and interstitial fibrosis. TUNEL analysis of RENF kidney sections showed extensive apoptosis predominantly affecting the tubules. Thus, we have established a mouse model for autosomal recessive early-onset renal failure due to a nonsense mutation in Xdh that is a model for xanthinuria in man. This mouse model could help to increase our understanding of the molecular mechanisms associated with renal fibrosis and the specific roles of XDH and uric acid. © 2012 Piret et al.

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Progeny of mice treated with the mutagen N-ethyl-N-nitrosourea (ENU) revealed a mouse, designated Longpockets (Lpk), with short humeri, abnormal vertebrae, and disorganized growth plates, features consistent with spondyloepiphyseal dysplasia congenita (SEDC). The Lpk phenotype was inherited as an autosomal dominant trait. Lpk/+ mice were viable and fertile and Lpk/Lpk mice died perinatally. Lpk was mapped to chromosome 15 and mutational analysis of likely candidates from the interval revealed a Col2a1 missense Ser1386Pro mutation. Transient transfection of wild-type and Ser1386Pro mutant Col2a1 c-Myc constructs in COS-7 cells and CH8 chondrocytes demonstrated abnormal processing and endoplasmic reticulum retention of the mutant protein. Histology revealed growth plate disorganization in 14-day-old Lpk/+ mice and embryonic cartilage from Lpk/+ and Lpk/Lpk mice had reduced safranin-O and type-II collagen staining in the extracellular matrix. The wild-type and Lpk/+ embryos had vertical columns of proliferating chondrocytes, whereas those in Lpk/Lpk mice were perpendicular to the direction of bone growth. Electron microscopy of cartilage from 18.5 dpc wild-type, Lpk/+, and Lpk/Lpk embryos revealed fewer and less elaborate collagen fibrils in the mutants, with enlarged vacuoles in the endoplasmic reticulum that contained amorphous inclusions. Micro-computed tomography (CT) scans of 12-week-old Lpk/+ mice revealed them to have decreased bone mineral density, and total bone volume, with erosions and osteophytes at the joints. Thus, an ENU mouse model with a Ser1386Pro mutation of the Col2a1 C-propeptide domain that results in abnormal collagen processing and phenotypic features consistent with SEDC and secondary osteoarthritis has been established.

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A 17-year-old white adolescent had a history of chronic diarrhea, delayed puberty, and growth failure. Investigations excluded cystic fibrosis, Shwachman syndrome, and endocrine causes of growth failure. Severe steatorrhea was diagnosed from fecal fat studies, and a jejunal suction biopsy showed total villus atrophy, consistent with a diagnosis of celiac diseases. Following introduction of a gluten-free diet, his appetite and growth improved, but he continued to have abdominal discomfort and loose offensive bowel motions. One year later, severe steatorrhea was present. A repeat jejunal biopsy showed partial recovery of villus architecture. Serum immunoreactive trypsinogen level was low, which was highly suggestive of exocrine pancreatic failure. Results of quantitative pancreatic stimulation test confirmed the presence of primary pancreatic insufficiency. After introduction of oral pancreatic enzyme supplements with meals, his gastrointestinal symptoms resolved and growth velocity accelerated. Previously, primary pancreatic insufficiency has only been described in elderly patients with long-standing untreated celiac disease. This case, however, emphasizes that pancreatic failure can occur with celiac disease at any age. Determination of a serum immunoreactive trypsinogen level should be considered a useful screening tool for pancreatic insufficiency in patients with celiac disease who have not responded to a gluten-free diet.

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The most common causes of urinary tract infections (UTIs) are Gram-negative pathogens such as Escherichia coli; however, Gram-positive organisms including Streptococcus agalactiae, or group B streptococcus (GBS), also cause UTI. In GBS infection, UTI progresses to cystitis once the bacteria colonize bladder, but the host responses triggered in the bladder immediately following infection are largely unknown. Here, we used genome-wide expression profiling to map the bladder transcriptome of GBS UTI in mice infected transurethrally with uropathogenic GBS that was cultured from a 35 year-old women with cystitis. RNA from bladders was applied to Affymetrix Gene-1.0ST microarrays; qRT-PCR was used to analyze selected gene responses identified in array datasets. A surprisingly small significant gene list of 172 genes was identified at 24h; this compared to 2507 genes identified in a side-by-side comparison with uropathogenic E. coli (UPEC). No genes exhibited significantly altered expression at 2h in GBS-infected mice according to arrays despite high bladder bacterial loads at this early time point. The absence of a marked early host response to GBS juxtaposed with broad-based bladder responses activated by UPEC at 2h. Bioinformatics analyses including integrative systems-level network mapping revealed multiple activated biological pathways in the GBS cystitis transcriptome that regulate leukocyte activation, inflammation, apoptosis, and cytokine-chemokine biosynthesis. These findings define a novel, minimalistic type of bladder host response triggered by GBS UTI, which comprises collective antimicrobial pathways that differ dramatically from those activated by UPEC. Overall, this study emphasizes the unique nature of bladder immune activation mechanisms triggered by distinct uropathogens.

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The impact of erroneous genotypes having passed standard quality control (QC) can be severe in genome-wide association studies, genotype imputation, and estimation of heritability and prediction of genetic risk based on single nucleotide polymorphisms (SNP). To detect such genotyping errors, a simple two-locus QC method, based on the difference in test statistic of association between single SNPs and pairs of SNPs, was developed and applied. The proposed approach could detect many problematic SNPs with statistical significance even when standard single SNP QC analyses fail to detect them in real data. Depending on the data set used, the number of erroneous SNPs that were not filtered out by standard single SNP QC but detected by the proposed approach varied from a few hundred to thousands. Using simulated data, it was shown that the proposed method was powerful and performed better than other tested existing methods. The power of the proposed approach to detect erroneous genotypes was approximately 80% for a 3% error rate per SNP. This novel QC approach is easy to implement and computationally efficient, and can lead to a better quality of genotypes for subsequent genotype-phenotype investigations.

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The amount of financial loss from online fraud suffered by people in Western Australia has almost halved, dropping from A$16.8 million in 2014 to A$9.8 million for 2015, according to a statement this January from the state’s Attorney General and Minister for Commerce, Michael Mischin. In addition, the minister noted that losses from relationship and dating fraud have fallen by 55%, to A$4.9 million lost last year. These are both impressive claims, and at face value, there is truth to the statistics. Both assertions are based on data received by WA’s Scamnet, which is the public interface between consumer protection and citizens. While it is good to see a reduction in the number of losses overall, particularly to relationship and dating fraud, it is highly unlikely that the statistics tell the full story.