Facing a Break Point in Global Inflation Transmission?

2009 ◽  
Author(s):  
Georg Erber ◽  
Alexandra Rudolph ◽  
Sebastian Weber
Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 321-342
Author(s):  
Eugene M Rinchik ◽  
Liane B Russell ◽  
Neal G Copeland ◽  
Nancy A Jenkins

ABSTRACT Genes of the dilute-short ear (d-se) region of mouse chromosome 9 comprise an array of loci important to the normal development of the animal. Over 200 spontaneous, chemically induced and radiation-induced mutations at these loci have been identified, making it one of the most genetically well-characterized regions of the mouse. Molecular analysis of this region has recently become feasible by the identification of a dilute mutation that was induced by integration of an ecotropic murine leukemia virus genome. Several unique sequence cellular DNA probes flanking this provirus have now been identified and used to investigate the organization of wild-type chromosomes and chromosomes with radiation-induced d-se region mutations. As expected, several of these mutations are associated with deletions, and, in general, the molecular and genetic complementation maps of these mutants are concordant. Furthermore, a deletion break-point fusion fragment has been identified and has been used to orient the physical map of the d-se region with respect to the genetic complementation map. These experiments provide important initial steps for analyzing this developmentally important region at the molecular level, as well as for studying in detail how a diverse group of mutagens acts on the mammalian germline.


Sensors ◽  
2021 ◽  
Vol 21 (3) ◽  
pp. 824
Author(s):  
Wenting Qiao ◽  
Biao Ma ◽  
Qiangwei Liu ◽  
Xiaoguang Wu ◽  
Gang Li

Cracks and exposed steel bars are the main factors that affect the service life of bridges. It is necessary to detect the surface damage during regular bridge inspections. Due to the complex structure of bridges, automatically detecting bridge damage is a challenging task. In the field of crack classification and segmentation, convolutional neural networks have offer advantages, but ordinary networks cannot completely solve the environmental impact problems in reality. To further overcome these problems, in this paper a new algorithm to detect surface damage called EMA-DenseNet is proposed. The main contribution of this article is to redesign the structure of the densely connected convolutional networks (DenseNet) and add the expected maximum attention (EMA) module after the last pooling layer. The EMA module is obviously helpful to the bridge damage feature extraction. Besides, we use a new loss function which considers the connectivity of pixels, it has been proved to be effective in reducing the break point of fracture prediction and improving the accuracy. To train and test the model, we captured many images from multiple bridges located in Zhejiang (China), and then built a dataset of bridge damage images. First, experiments were carried out on an open concrete crack dataset. The mean pixel accuracy (MPA), mean intersection over union (MIoU), precision and frames per second (FPS) of the EMA-DenseNet are 87.42%, 92.59%, 81.97% and 25.4, respectively. Then we also conducted experiments on a more challenging bridge damage dataset, the MIoU, where MPA, precision and FPS were 79.87%, 86.35%, 74.70% and 14.6, respectively. Compared with the current state-of-the-art algorithms, the proposed algorithm is more accurate and robust in bridge damage detection.


Author(s):  
M. Mongiardini ◽  
J. D. Reid

Numerical simulations allow engineers in roadside safety to investigate the safety of retrofit designs minimizing or, in some cases, avoiding the high costs related to the execution of full-scale experimental tests. This paper describes the numerical investigation made to assess the performance of a roadside safety barrier when relocated behind the break point of a 3H:1V slope, found on a Mechanically Stabilized Earth (MSE) system. A safe barrier relocation in the slope would allow reducing the installation width of the MSE system by an equivalent amount, thus decreasing the overall construction costs. The dynamics of a pick-up truck impacting the relocated barrier and the system deformation were simulated in detail using the explicit non-linear dynamic finite element code LS-DYNA. The model was initially calibrated and subsequently validated against results from a previous full-scale crash test with the barrier placed at the slope break point. After a sensitivity analysis regarding the role of suspension failure and tire deflation on the vehicle stability, the system performance was assessed when it was relocated into the slope. Two different configurations were considered, differing for the height of the rail respect to the road surface and the corresponding post embedment into the soil. Conclusions and recommendations were drawn based on the results obtained from the numerical analysis.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Sonoda ◽  
S Ohno ◽  
M Horie

Abstract Background Genome structural variants (SVs) have larger effect on human genome functions than single nucleotide variants (SNVs). Although short-read sequencing (SRS) is current major next generation sequencing method and has given us a great benefit to elucidate the genetic background of inherited diseases, it does not detect SVs accurately. Long-read sequencing (LRS) produces tens to thousands of kilobases reads and detects the breakpoints of complex SVs. This study aimed to confirm a large deletion, which was suspected by SRS, using LRS by Oxford Nanopore technology (ONT). Methods Genomic libraries for SRS was prepared with HaloPlex. Targeted SRS was performed for 58 genes with MiSeq. Genomic libraries for LRS were prepared using the Ligation sequencing 1D kit SQK-LSK109 (ONT). Whole genome LRS was performed with GridION X5 and R9.4 flow cells (ONT). Results The patient was a five-month-old boy with atrial septal defect (ASD) and atrial tachycardia. Though SRS failed to identify any causative SNVs, the results with SureCall software (Agilent) suspected a deletion between exon 3 to exon 26 in MYH6 encoding α heavy chains of cardiac myosin. The variants in MYH6 are known to be associated with ASD. Because a deletion between MYH6 exon 26 and MYH7 exon 27 was reported as esv2748480 on the Database of Genomic Variants, we performed long-range PCR from MYH6 intron26 to MYH7 exon26 and found an abnormal 1.5K bases PCR product only in the case. Due to high homology of MYH6 and MYH7, Sanger sequencing failed to detect the break point. In LRS, 3 flow cells generated 3.8M base-called reads containing 42G bases with N50 of 13K bases. We used NGMLR, which is a long-read mapper, to align the reads to the human reference genome (hg38). SVs were called by Sniffles detecting all types of SVs. The deletion was found to range from chr14: 23390037 to 23419824 (see figure) and did not contain other SVs. There was no pathogenic SV on ACTC1, GATA4, TBX20 and TLL1 which are genes related to ASD on Genetic Testing Registry. His mother had also ASD and harbored the same deletion. Conclusions This is the first report to identify a large deletion between MYH6 and MYH7 in the family with ASD. The combination of SRS and LRS is useful to detect SVs in patients with suspected inherited diseases but carried no causative SNVs. Funding Acknowledgement Type of funding source: None


1986 ◽  
Vol 6 (7) ◽  
pp. 2752-2755
Author(s):  
M Schwab ◽  
K H Klempnauer ◽  
K Alitalo ◽  
H Varmus ◽  
M Bishop

The proto-oncogene c-myc is amplified in sublines of human COLO 320 cells carrying either homogeneously staining chromosomal regions or double minutes. COLO 320 cells carrying homogeneously staining chromosomal regions have 15 to 20 copies of an apparently normal c-myc allele and 1 to 2 copies of an abnormal c-myc allele lacking exon 1 and express high levels of a normal c-myc mRNA 2.5 kilobases in size. COLO 320 cells carrying double minutes have about 25 copies each of the normal allele and the abnormal allele but express preferentially an abnormal c-myc mRNA 2.2 kilobases in size. Nucleotide sequence analyses revealed that the break point of rearrangement resulting in the loss of exon 1 in the abnormal allele lies within a region frequently rearranged in human and murine B-cell tumors.


2018 ◽  
Vol 2 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Dwight J Shawk ◽  
Robert D Goodband ◽  
Mike D Tokach ◽  
Steve S Dritz ◽  
Joel M DeRouchey ◽  
...  

Abstract Three studies evaluated the effects of added dietary salt on growth performance of pigs weighing 7 to 10, 11 to 30, and 27 to 65 kg. In experiment 1, 325 pigs were used with 5 pigs per pen and 13 pens per treatment. Pigs were fed a diet (0.39% Na and 0.78% Cl) for 7 d after weaning, then randomly assigned to diets with either 0, 0.20, 0.40, 0.60, or 0.80% added salt for 14 d. All diets were corn-soybean meal-based with 10% dried whey. Calculated Na concentrations were 0.11, 0.19, 0.27, 0.35, and 0.43% and calculated Cl concentrations were 0.23, 0.35, 0.47, 0.59, and 0.70%, respectively. Increasing salt increased (linear, P < 0.05) average daily gain (ADG) and gain to feed ratio (G:F). For ADG, the linear, quadratic polynomial (QP), and broken-line linear (BLL) models were competing with the breakpoint for the BLL at 0.59% salt. For G:F, the BLL reported a breakpoint at 0.33% while the QP indicated maximum G:F at 0.67% added salt. In experiment 2, 300 pigs were used in a 34-d trial with 5 pigs per pen and 12 pens per treatment. Pigs were weaned at 21 d of age and fed a phase 1 diet (0.50% Na and 0.67% Cl) for 11 d and then a phase 2 diet (0.35% Na and 0.59% Cl) for 14 d. Then pens of pigs were randomly assigned to corn-soybean meal-based diets containing 0.20, 0.35, 0.50, 0.65, or 0.80% added salt. Calculated dietary Na concentration were 0.10, 0.16, 0.22, 0.28, and 0.34% and calculated Cl concentrations were 0.23, 0.32, 0.41, 0.50, and 0.59%, respectively. Overall, ADG and G:F increased (quadratic, P < 0.07) with increasing added salt. For ADG, the QP and BLL had similar fit with the breakpoint for BLL at 0.51% added salt. For G:F, the BLL model predicted a break point at 0.35% added salt. In experiment 3, 1,188 pigs were used in a 44-d study with 27 pigs per pen and 11 pens per treatment. Pens of pigs were randomly assigned to corn-soybean meal-based diets containing 0.10, 0.33, 0.55, or 0.75% added salt. Calculated dietary Na concentrations were 0.10, 0.19, 0.28, and 0.36% and calculated Cl concentrations were 0.23, 0.36, 0.49, and 0.61%, respectively. Overall, there was no evidence to indicate that added salt above 0.10% of the diet affected growth. In conclusion, the BLL models suggested to maximize ADG for 7 to 10 and 11 to 30 kg pigs was 0.59% (0.34% Na and 0.58% Cl) and 0.51% added salt (0.22% Na and 0.42% Cl), respectively. There was no evidence that growth of 27 to 65 kg pigs was improved beyond 0.10% added salt (0.11% Na and 0.26% Cl).


1989 ◽  
Vol 67 (5) ◽  
pp. 1754-1758 ◽  
Author(s):  
H. Kimura ◽  
M. Mikami ◽  
T. Kuriyama ◽  
Y. Fukuda

Effects on ventilatory responses to progressive isocapnic hypoxia of a synthetic potent progestin, chlormadinone acetate (CMA), were determined in the halothane-anesthetized male rat. Ventilation during the breathing of hyperoxic gas was largely unaffected by treatment with CMA when carotid chemoreceptor afferents were kept intact. The sensitivity to hypoxia evaluated by hyperbolic regression analysis of the response curve did not differ between the control and CMA groups. The reduction of ventilation after bilateral section of the carotid sinus nerve (CSN) in hyperoxia was less severe in CMA-treated than in untreated animals. Furthermore, the CMA-treated rats showed a larger increase in ventilation during the hypoxia test and a lower PO2 break point for ventilatory depression. Inhibition of hypoxic ventilatory depression by CMA persisted even after the denervation of CSN. We conclude that exogenous progestin likely protects regulatory mechanism(s) for respiration against hypoxic depression through a stimulating action independent of carotid chemoreceptor afferents and without a change in the sensitivity of the ventilatory response to hypoxia.


1993 ◽  
Vol 74 (1) ◽  
pp. 159-165 ◽  
Author(s):  
CHI-KIN LEUNG ◽  
FUET-KIT LAM

Sign in / Sign up

Export Citation Format

Share Document