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Journal articles on the topic 'Overload model'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Tsay, Jaime, Zheiwei Yang, F. Patrick Ross, Susanna Cunningham-Rundles, Hong Lin, Rhima Coleman, Philipp Mayer-Kuckuk, et al. "Bone loss caused by iron overload in a murine model: importance of oxidative stress." Blood 116, no. 14 (October 7, 2010): 2582–89. http://dx.doi.org/10.1182/blood-2009-12-260083.

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AbstractOsteoporosis is a frequent problem in disorders characterized by iron overload, such as the thalassemias and hereditary hemochromatosis. The exact role of iron in the development of osteoporosis in these disorders is not established. To define the effect of iron excess in bone, we generated an iron-overloaded mouse by injecting iron dextran at 2 doses into C57/BL6 mice for 2 months. Compared with the placebo group, iron-overloaded mice exhibited dose-dependent increased tissue iron content, changes in bone composition, and trabecular and cortical thinning of bone accompanied by increased bone resorption. Iron-overloaded mice had increased reactive oxygen species and elevated serum tumor necrosis factor-α and interleukin-6 concentrations that correlated with severity of iron overload. Treatment of iron-overloaded mice with the antioxidant N-acetyl-L-cysteine prevented the development of trabecular but not cortical bone abnormalities. This is the first study to demonstrate that iron overload in mice results in increased bone resorption and oxidative stress, leading to changes in bone microarchitecture and material properties and thus bone loss.

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2

Stroebe, Margaret, and Henk Schut. "Overload." OMEGA - Journal of Death and Dying 74, no. 1 (September 21, 2016): 96–109. http://dx.doi.org/10.1177/0030222816666540.

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The Dual Process Model of Coping with Bereavement (DPM) was put forward as a framework to help understand reactions to the death of a loved person. Since its inception, there have been various developments and further specifications regarding the model’s parameters. A number of researchers have assessed the model’s contribution and put some of its parameters to empirical test. It has also been applied in clinical practice. Despite generally positive assessment among both scientific and applied communities, we recently discovered what we consider to be a major shortcoming. The concept of overload has been neglected. Incorporation of this feature helps explain the preponderance of mental and physical health problems beyond the previous DPM focus on complications of grief. In this article, we incorporate the phenomenon of overload within the original framework, illustrating its application, and we discuss broader implications for coping and adaptation to bereavement.

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3

Kidd, James M., Kamilia Abdelraouf, and David P. Nicolau. "1553. Human-Simulated Pharmacokinetic Profiles of Cefiderocol and Meropenem Are Conserved in Murine Models of Thigh Infection With or Without Iron Overload." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S567. http://dx.doi.org/10.1093/ofid/ofz360.1417.

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Abstract Background A translational murine model of thigh infection with comorbid iron overload was previously developed to study the efficacy of iron-dependent siderophore-antibiotic conjugates under conditions where the hypoferremic response of innate immunity may be compromised. Given the potential for functional organ damage from excessive tissue iron, which could alter the pharmacokinetic (PK) profiles of antibiotics being compared for efficacy using this model, the effects of iron overload on a siderophore-β-lactam conjugate, cefiderocol (CFDC), and a non-siderophore β-lactam, meropenem (MEM), were studied. Methods Female CD-1 mice received iron dextran (Fe-D) 100 mg/kg intraperitoneally for 14 days as previously shown to produce vastly supranormal iron concentrations in serum, liver, and spleen (ASM Microbe 2019 abstract HMB-373). Age-matched control mice were not dosed with Fe-D. Mice were rendered neutropenic. On day 15, both thighs of iron-overloaded and control mice were inoculated intramuscularly with Acinetobacter baumannii suspensions of 107 CFU/mL. Two hours after inoculation, mice in each model were dosed with previously developed human-simulated regimens (HSR) of CFDC or MEM simulating human PK profiles after doses of 2g q8h (3 hours infusion) for both drugs. At 4 time points per regimen, 6 mice per model were sacrificed for blood collection. Plasma total MEM and CFDC concentrations were measured with HPLC and LC-MS-MS, respectively. Free concentrations were calculated with murine protein binding. At each time point, mean free concentrations in both models were compared using Student’s t-test. Results Observed murine-free plasma concentrations ± 95% CI of CFDC and MEM are overlaid with simulated human and murine profiles in the figure. In both models, these regimens approximated human exposures after clinical doses. For all time points and both drugs, concentrations were not significantly different (P > 0.05) between models with or without iron overload. Conclusion Iron overload did not significantly alter PK profiles of a siderophore-β-lactam conjugate, CFDC, or a non-siderophore β-lactam, MEM. These data support the use of CFDC and MEM HSR for pharmacodynamic studies utilizing both iron-overloaded and standard murine thigh infection models. Disclosures All authors: No reported disclosures.

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4

Huang, Jiawei, Qingchun Meng, Zhixin Zhan, Weiping Hu, and Fei Shen. "Damage mechanics-based approach to studying effects of overload on fatigue life of notched specimens." International Journal of Damage Mechanics 28, no. 4 (May 9, 2018): 538–65. http://dx.doi.org/10.1177/1056789518775173.

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A continuum damage mechanics-based method is adopted to predict the fatigue life of notched specimens subjected to constant amplitude cyclic loading while containing single or multiple overloads. The residual stress and plastic damage induced by an overload are considered to be the main factors affecting the fatigue life of a specimen. The residual stress and plastic strain fields of a notched specimen are calculated using the elastic–plastic finite element method. The mean stress of the following cyclic loading is then varied by superimposing the residual stress. Meanwhile, the plastic damage is calculated based on the ductile damage model and accumulated into the total damage of the material. The quantitative effects of an overload on the damage evolution and the fatigue life are evaluated. Furthermore, the effects of the damage–overload ratio on the variation of the residual stress induced by an overload are investigated, and the effects of the occurrence time for a single overload and the occurrence frequency for multiple overloads are studied.

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5

Rushton, Philip A., Farid Taheri, and David C. Stredulinsky. "Fatigue Response and Characterization of 350WT Steel Under Semi-Random Loading." Journal of Pressure Vessel Technology 129, no. 3 (March 9, 2006): 525–34. http://dx.doi.org/10.1115/1.2748835.

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Novel data obtained through experimental investigation into the fatigue response of 350WT steel, subjected to semi-random loading, comprised of various combinations of intermittent tensile overloads and compressive underloads are presented. An effective model for predicting the fatigue response is also introduced. For that, the capabilities of some of the currently available models are investigated and then an exponential delay model, being capable of accounting for the effects of not only overload ratio, but also stress ratio and overload/underload ratio is introduced. Since most variable amplitude models are based on a constant amplitude model, efforts were also expended to identify a constant amplitude fatigue crack growth model that would be easy to use, requiring the calibration of few (if any) empirical curve-fitting parameters. The integrity of a selected model is examined and results are presented.

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6

Zou, Xiao Li, and Jian Hui Yang. "Simulation of Fatigue Crack Growth Under Random Overloads with Retardation." Key Engineering Materials 324-325 (November 2006): 923–26. http://dx.doi.org/10.4028/www.scientific.net/kem.324-325.923.

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In order to study the behavior of fatigue crack propagation under random overloads, a Monte Carlo simulation scheme is proposed. Overloads of Poisson flow with uniform distribution on base-line constant-amplitude cyclic loads are considered. The retardation effect of overload is taken into account using crack closure model and the crack opening stress level is assumed to vary linearly in the yield zone produced by the overload. The fatigue crack growth curve from initial crack size till fatigue failure is simulated step by step. Through the large number of the simulated samples, the average fatigue crack propagation life is calculated. Finally, the influence of overload intensity and magnitude on fatigue crack propagation life is studied.

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7

Pasipoularides, Ares, Ming Shu, Ashish Shah, Scott Silvestry, and Donald D. Glower. "Right ventricular diastolic function in canine models of pressure overload, volume overload, and ischemia." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 5 (November 1, 2002): H2140—H2150. http://dx.doi.org/10.1152/ajpheart.00462.2002.

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By limiting filling, abnormalities of right ventricular (RV) diastolic function may impair systolic function and affect adaptation to disease. To quantify diastolic RV pressure-volume relations and myocardial compliance (MC), a new sigmoidal model was developed. RV micromanometric and sonomicrometric data in alert dogs at control ( n = 16) and under surgically induced subacute (2–5 wk) RV pressure overload ( n = 6), volume overload ( n = 7), and ischemia ( n = 6) were analyzed. The conventional exponential model detected no changes from control in the passive filling pressure-volume (Ppf-V) relations. The new sigmoidal model revealed significant quantifiable changes in Ppf-V relations. Maximum RV MC (MCmax), attained during early filling, is reduced from control in pressure overload ( P = 0.0016), whereas filling pressure at maximum MC (PMCmax) is increased ( P = 0.0001). End-diastolic RV MC increases significantly in volume overload ( P = 0.0131), whereas end-diastolic pressure is unchanged. In ischemia, MCmax is decreased ( P = 0.0102), with no change in PMCmax. We conclude that the sigmoidal model quantifies important changes in RV diastolic function in alert dog models of pressure overload, volume overload, and ischemia.

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8

Alagna, Sheryle W. "An Overload(ed) Model of Stress Effects." Contemporary Psychology: A Journal of Reviews 30, no. 6 (June 1985): 499–500. http://dx.doi.org/10.1037/023876.

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9

Goel, H. S., and Satish Chand. "A Fatigue Crack Growth Model for Single Overload Tests." Journal of Engineering Materials and Technology 116, no. 2 (April 1, 1994): 168–72. http://dx.doi.org/10.1115/1.2904268.

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Crack growth rate experiments are conducted by applying an intermediate single overload cycle in constant amplitude load (CAL) tests. For a particular overload ratio, three to four tests are conducted by applying the overload cycle at different crack lengths. The loads are selected in such a way that for a given overload ratio, the size of the overload and CAL monotonic plastic zones are the same at each crack length. A functional form for the crack growth during the retardation was developed that accurately describes all the tests. For comparison, the corresponding CA-load tests are also conducted separately. Finally, a crack growth rate model is developed.

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10

Yoshihara, Fumiki, Toshio Nishikimi, Takeshi Horio, Chikao Yutani, Noritoshi Nagaya, Hisayuki Matsuo, Tohru Ohe, and Kenji Kangawa. "Ventricular adrenomedullin concentration is a sensitive biochemical marker for volume and pressure overload in rats." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (February 1, 2000): H633—H642. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h633.

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This study was designed to investigate the pathophysiological significance of adrenomedullin (AM) concentration in volume- and pressure-overloaded cardiac hypertrophy. We measured ventricular AM concentrations and compared them with changes of α-actin and myosin heavy chain (MHC) mRNA isoforms after the creation of an aortocaval (AC) shunt as a volume-overload model or the injection of monocrotaline (MCT) as a pressure-overload model, respectively. The left ventricular AM levels after the creation of AC shunt and the right ventricular AM levels after the injection of MCT were significantly increased and correlated with changes of the α-actin and MHC mRNA isoforms. However, the ventricular AM mRNA expressions were increased and correlated with ventricular AM concentrations only in the AC shunt model. These results suggest that the ventricular AM levels are upregulated in both the volume- and pressure-overloaded cardiac hypertrophy by differential transcriptional regulation and that the ventricular AM may be a biochemical marker for the volume and pressure overload to the ventricle.

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11

Anton, IVANOVICI, and PANAIT Marius Alexandru. "Overload prevention in model supports for wind tunnel model testing." INCAS BULLETIN 7, no. 3 (September 10, 2015): 173–80. http://dx.doi.org/10.13111/2066-8201.2015.7.3.16.

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12

Harper, J., E. Harper, and J. W. Covell. "Collagen characterization in volume-overload- and pressure-overload-induced cardiac hypertrophy in minipigs." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 2 (August 1, 1993): H434—H438. http://dx.doi.org/10.1152/ajpheart.1993.265.2.h434.

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Previous studies in several different species have shown reduced extractability of collagens in some types of cardiac hypertrophy (volume overload) but not others (pressure overload). The objective of the present study was to examine collagen proteins from the same species (minipigs) with both pressure-overload- and volume-overload-induced cardiac hypertrophy. Hypertrophy was induced by two methods: thoracic banding of the aorta to create pressure overload and arteriovenous shunt to cause volume overload in a porcine model. Collagen types I, III, IV, and V were isolated by pepsin digestion from normal and hypertrophied pig left ventricle tissues. Types I and III collagens from normal and hypertrophied samples, when separated from types IV and V, were digested with cyanogen bromide (CB), and the peptides were examined. Collagen concentration was increased in myocardium removed from hearts subjected to volume overload and unchanged in hearts subjected to pressure overload. The extractability of total collagen was unaffected in pressure-overloaded left ventricles but lower in samples from volume-overloaded hearts. CB digestion cleaved all of the types I and III collagens into similar smaller CB peptides with the exception of a 100-kDa peptide that was observed in both control and hypertrophied hearts. This peptide corresponds to one of the high-molecular-weight peptides found in canine heart tissue. The mature collagen cross-link hydroxylysylpyridinoline (HP) was identified in normal and hypertrophied types I and III collagen from porcine sources. Pressure-overload- and volume-overload-induced cardiac hypertrophy in the pig produced different alterations in the extracellular matrix.(ABSTRACT TRUNCATED AT 250 WORDS)

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13

Kłysz, Sylwester, and Paweł Szabracki. "Methodical Approach to the Analysis of Experimental Data Associated with the Fatigue Cracks Propagation Under Overload Conditions." Research Works of Air Force Institute of Technology 25, no. 1 (January 1, 2009): 171–83. http://dx.doi.org/10.2478/v10041-009-0015-9.

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Methodical Approach to the Analysis of Experimental Data Associated with the Fatigue Cracks Propagation Under Overload Conditions The paper presents an analysis how overloads affect of fatigue cracks propagation rate where the analysis is carried out with use of the retardation model. The completed analysis covered the results of experimental examination of RCT-type samples made of the WT3-1 titanium alloy and was intended to determine interrelationships between individual parameters of the applied model. Comparison between theoretical calculations and experimental data was carried out for two options: with the analysis of samples for the entire range of lifetime until the sample was destroyed, and with a separate analysis of data for time intervals between the overload moments, whereby the values of C, m and n coefficients were determined each time for the retardation model. Finally, the dependence of coefficient values on the stress intensity factor during overload cycles is developed.

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14

Marino, T. A., R. L. Kent, C. E. Uboh, E. Fernandez, E. W. Thompson, and G. Cooper. "Structural analysis of pressure versus volume overload hypertrophy of cat right ventricle." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 2 (August 1, 1985): H371—H379. http://dx.doi.org/10.1152/ajpheart.1985.249.2.h371.

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Pressure overload of cat right ventricle causes progressive abnormalities of in vitro contractile function at a time when in vivo contractile function is normal. In marked contrast, the same degree and duration of volume overload of cat right ventricle results in neither in vitro nor in vivo contractile dysfunction. The purpose of the present quantitative structural study was to determine whether there were any histological alterations in pressure-overloaded myocardium that might be causally related to the contractile dysfunction found only in this model. Four experimental groups of eight cats each were studied: a group with pulmonary arterial banding to create a pressure overload, sham-operated controls for this group, a group with atrial septal defects to create a volume overload, and sham-operated controls for this group. Seven to ten weeks after each operative procedure, right ventricular pressure was elevated only in the pressure-overloaded group, pulmonary-to-systemic blood flow ratio was increased only in the volume-overloaded group, and right ventricle-to-body weight ratio was significantly and comparably increased in both the pressure- and the volume-overloaded groups. There was a single striking histological distinction between myocardium hypertrophying in response to pressure as opposed to volume overload: the volume density of cardiocytes in papillary muscles from pressure-overloaded right ventricles was decreased significantly with a proportional increase in connective tissue. Given the critical importance of these two myocardial components to both systolic and diastolic cardiac function, these data provide a potential structural basis for at least some of the functional abnormalities observed in pressure but not in volume overload hypertrophy of the cat right ventricle.

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15

Bautista, Joaquín, and Jaime Cano. "Minimizing work overload in mixed-model assembly lines." International Journal of Production Economics 112, no. 1 (March 2008): 177–91. http://dx.doi.org/10.1016/j.ijpe.2006.08.019.

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16

Kaiser, Lana, John M. Davis, and Kenneth A. Schwartz. "Does the gerbil model mimic human iron overload?" Journal of Laboratory and Clinical Medicine 141, no. 6 (June 2003): 419–20. http://dx.doi.org/10.1016/s0022-2143(03)00038-6.

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17

Jackson, Thomas W., and Pourya Farzaneh. "Theory-based model of factors affecting information overload." International Journal of Information Management 32, no. 6 (December 2012): 523–32. http://dx.doi.org/10.1016/j.ijinfomgt.2012.04.006.

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18

Zhang, Yun Peng. "Research and Application of Importance Degree Evaluation Method of Complex Network Cascade Connection Node Based on Load Redistribution." Advanced Materials Research 998-999 (July 2014): 1174–77. http://dx.doi.org/10.4028/www.scientific.net/amr.998-999.1174.

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This paper presented a model with overload function for cascading failure. The main differences with respect to previous models are as follows: overload function is defined for each node, according to the value of overload function, one node has th ree states: success, overload, failure. After the load decreases, an overloaded node can be success again. The evolution of topology is replaced by the evolution of value of overload function during the process of cascading failure. It’s needless to delete the failure nodes and its edges, the load will avoid the failure nodes automat ically and the decrease of network performance will be reflected by network efficiency. An evaluation method of node importance considering cascading failure is proposed, and its algorithm is presented. A new definition of node importance is proposed. The most important node is the one who see failure results in the largest decrease of networks efficiency at the end of cascading. The evaluation method can help us to find some potential critical nodes which are sensitive to the efficiency of networks but not so important intuitively. Final example verifies its efficiency and feasibility.

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19

Kim, Kyung Su, Dong In Cho, Jae Wook Ahn, and Seung Bok Choi. "An Experimental Study on Fatigue Crack Propagation under Cyclic Loading with Multiple Overloads." Key Engineering Materials 297-300 (November 2005): 2495–500. http://dx.doi.org/10.4028/www.scientific.net/kem.297-300.2495.

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For many fatigue-critical parts of machines and structures, the load history under operating conditions generally involves variable amplitude loading rather than constant amplitude loading. An accurate prediction of fatigue crack propagation life under variable amplitude loading requires a thorough evaluation of the load interaction effects. In this study, fatigue tests under both constant and variable amplitude loading were carried out to investigate the overload effects on fatigue crack propagation of the notched specimens. Strain distributions around the crack tip before and after a tensile overloading were measured using the ESPI (Electronic Speckle Pattern Interferometry) system. The size of the plastic zone was determined from the measured strain distributions. The study proposes a crack propagation prediction model that incorporates the overload ratio effect. A comparative work for the overload ratio effect demonstrated that the prediction by the proposed model was in good agreement with the experimental results. The prediction of fatigue crack propagation including multiple overloads with the proposed model show also a good agreement with test results.

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20

Willett, Thomas L., Rosalind S. Labow, and J. Michael Lee. "Mechanical overload decreases the thermal stability of collagen in an in vitro tensile overload tendon model." Journal of Orthopaedic Research 26, no. 12 (June 3, 2008): 1605–10. http://dx.doi.org/10.1002/jor.20672.

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21

Jiang, Shan, Wei Zhang, Xiaoyang Li, and Fuqiang Sun. "An Analytical Model for Fatigue Crack Propagation Prediction with Overload Effect." Mathematical Problems in Engineering 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/713678.

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In this paper a theoretical model was developed to predict the fatigue crack growth behavior under the constant amplitude loading with single overload. In the proposed model, crack growth retardation was accounted for by using crack closure and plastic zone. The virtual crack annealing model modified by Bauschinger effect was used to calculate the crack closure level in the outside of retardation effect region. And the Dugdale plastic zone model was employed to estimate the size of retardation effect region. A sophisticated equation was developed to calculate the crack closure variation during the retardation area. Model validation was performed in D16 aluminum alloy and 350WT steel specimens subjected to constant amplitude load with single or multiple overloads. The predictions of the proposed model were contrasted with experimental data, and fairly good agreements were observed.

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22

Szada-Borzyszkowski, Wiesław, and Monika Szada-Borzyszkowska. "Influence of selected road parameters on overloads during a vehicle collision with a fixed obstacle." AUTOBUSY – Technika, Eksploatacja, Systemy Transportowe 19, no. 9 (September 30, 2018): 71–74. http://dx.doi.org/10.24136/atest.2018.286.

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The article presents general characteristics of road accidents. The influence of overload on the human body during impact was discussed. Authors created a mathematical model describing the impact of selected road parameters on overloads during a car collision with a fixed obstacle.

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23

Lin, Yi-Hsin, Suyu Gu, Wei-Sheng Wu, Rujun Wang, and Fan Wu. "Analysis and Prediction of Overloaded Extra-Heavy Vehicles for Highway Safety Using Machine Learning." Mobile Information Systems 2020 (December 30, 2020): 1–20. http://dx.doi.org/10.1155/2020/6667897.

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Along with the prosperity and rapid development of the national economy, the transportation industry has rapidly developed in China. However, overloaded vehicles have been causing frequent traffic accidents. Thus, to alleviate or resolve the corresponding problems associated with highway engineering safety and the market economy, an improved technique for overload management is urgently required. In this study, to analyze the overload data on expressways and highways in China, we developed a machine learning model by comparing the performances of cluster analysis, backpropagation neural network (BPNN), generalized regression neural network (GRNN), and wavelet neural network (WNN) in analyzing global and local time series overload data. In a case study, our results revealed the trends of overloading on highways in Jiangsu Province. Given sufficient data, BPNN performed better than GRNN and WNN. As the amount of training data increased, GRNN performed better, but the runtime increased. WNN had the shortest runtime among the three methods and could reflect the future trends of the overload rate in the monthly data prediction of overload. Our model provides information with potential value for expressway network management departments through data mining. This information could help management departments allocate resources reasonably and optimize the information utilization rate.

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24

Gao, Zhi, Roy S. Colby, Thomas G. Habetler, and Ronald G. Harley. "A Model Reduction Perspective on Thermal Models for Induction Machine Overload Relays." IEEE Transactions on Industrial Electronics 55, no. 10 (October 2008): 3525–34. http://dx.doi.org/10.1109/tie.2008.926772.

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25

Molina, Ezequiel J., Dipin Gupta, Jon Palma, Denise Torres, John P. Gaughan, Steven Houser, and Mahender Macha. "Novel Experimental Model of Pressure Overload Hypertrophy in Rats." Journal of Surgical Research 153, no. 2 (May 2009): 287–94. http://dx.doi.org/10.1016/j.jss.2008.03.043.

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26

Ransom, Daniel L., and Randy Hamilton. "Extending Motor Life With Updated Thermal Model Overload Protection." IEEE Transactions on Industry Applications 49, no. 6 (November 2013): 2471–77. http://dx.doi.org/10.1109/tia.2013.2265375.

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27

Honda, M., Y. Hori, Y. Shionoya, K. Yamamoto, F. Kojima, and T. Nakamura. "Fluid overload deteriorate chylothorax: evaluation in a canine model." Diseases of the Esophagus 25, no. 3 (August 24, 2011): 269–72. http://dx.doi.org/10.1111/j.1442-2050.2011.01237.x.

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28

Ballew, Mary A., David Kriebel, and Thomas J. Smith. "Epidemiologic Application of a Dosimetric Model of Dust Overload." American Journal of Epidemiology 141, no. 7 (April 1, 1995): 690–96. http://dx.doi.org/10.1093/oxfordjournals.aje.a117486.

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29

LAUD, ROBERT L., and DONALD H. SCHEPERS. "Beyond Transparency: Information Overload and a Model for Intelligibility." Business and Society Review 114, no. 3 (September 2009): 365–91. http://dx.doi.org/10.1111/j.1467-8594.2009.00347.x.

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30

MATANACHAI, SITTICHAI, and CANDACE ARAI YANO. "Balancing mixed-model assembly lines to reduce work overload." IIE Transactions 33, no. 1 (January 2001): 29–42. http://dx.doi.org/10.1080/07408170108936804.

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Cumbermack, Kristopher M., Jun Cheng, Yibing Nong, William T. Mahle, Ronald W. Joyner, William L. Border, Mary B. Wagner, Derek A. Fyfe, Traci Leong, and Yanggan Wang. "A Juvenile Murine Heart Failure Model of Pressure Overload." Pediatric Cardiology 32, no. 2 (November 21, 2010): 145–53. http://dx.doi.org/10.1007/s00246-010-9833-3.

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32

Brandão, A. F. "A model for substation reliability analysis including overload effects." International Journal of Electrical Power & Energy Systems 9, no. 4 (October 1987): 194–205. http://dx.doi.org/10.1016/0142-0615(87)90001-9.

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33

Sheu, B. C., P. S. Song, and S. Hwang. "Shaping exponent in wheeler model under a single overload." Engineering Fracture Mechanics 51, no. 1 (May 1995): 135–43. http://dx.doi.org/10.1016/0013-7944(94)00250-l.

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34

Nedopetalski, Felipe, and Joslaine Cristina Jeske de Freitas. "Overload Control in a Token Player for a Fuzzy Workflow Management System." Revista de Informática Teórica e Aplicada 28, no. 1 (January 19, 2021): 11–21. http://dx.doi.org/10.22456/2175-2745.105893.

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The underlying proposal of this work is to control overload of a Token Player in a Fuzzy Workflow Management System. In order to accomplish this, possibility theory is used to measure how much the Token Player can be overloaded. The model used in this work is built using Colored Petri net and the simulation is made using CPN Tools. Finally, is possible to control overload of the Token Player in a Fuzzy Workflow Management System, nevertheless more time is spent to achieve the end of activities.

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35

Molina-Sánchez, Pedro, and Amaia Lujambio. "Iron overload and liver cancer." Journal of Experimental Medicine 216, no. 4 (March 18, 2019): 723–24. http://dx.doi.org/10.1084/jem.20190257.

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In this issue of JEM, Muto et al. (https://doi.org/10.1084/jem.20180900) generate a novel mouse model of liver cancer induced by iron overload by deleting the iron-sensing ubiquitin ligase FBXL5 specifically in hepatocytes and exposure to a chemical carcinogen.

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Chai, Xiao, Deguan Li, Mingfeng Zhao, Wenyi Lu, Juan Mu, Xia Xiao, Yuchen Zhang, et al. "ROS-Mediated Iron Overload Injures The Hematopoiesis Of Bone Marrow By Damaging Hematopoietic Stem/Progenitor Cells In Mice." Blood 122, no. 21 (November 15, 2013): 962. http://dx.doi.org/10.1182/blood.v122.21.962.962.

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Abstract A substantial portion of patients with inherited blood disorders such as beta thalassemia, or bone marrow failure syndromes such as aplastic anemia(AA), myelodysplastic syndromes(MDS) require frequent transfusions of red blood cells. Frequent blood transfusions may lead to the excess of plasma non-transferrin -bound iron(NTBI) and iron overload occurs, which will significantly injure bone marrow (BM) function as well as induce organ dysfunctions such as liver cirrhosis, diabetes and cardiac diseases. However, the exact mechanism behind this effect remains elusive and ideal treatment needs to be explored. In our preliminary studies, we have demonstrated free iron catalyzes oxidative damage to hematopoietic cells/ mesenchymal stem cells in vitro and suppresses hematopoiesis in iron overload patients (Zhao et al.,blood, 2010 abstract; Lu et al.,blood,2012 abstract; Lu et al., Eur J Haematol, 2013). Here we observed the hematopoiesis inhibitory effects of iron overload on the basis of estabalished iron overload mice model and preliminarily disscussed the mechanism. In this study, we first established an iron overload mice model by administering different doses(12.5mg/ml,25mg/ml,50mg/ml) iron dextran by intraperitoneal injection every three days for four weeks. To confirm the efficacy of the mice model, the BM, hepatic and splenic iron deposits were observed by morphological study and the labile iron pool level (LIP) of bone marrow mononuclear cells(BMMNCs) was detected using the calcein-AM fluorescent dye. It was found that iron deposits in BM cells of iron overload mice, liver and spleen were markedly increased and the BMMNCs LIP level was much higher than that of normal control mice. The above results showed that the iron-overloaded mice model has been established successfully. Next we observed whether iron overload (25mg/ml) could affect the hematopoiesis of BM. The colony-forming cell assay was performed by culturing BMMNCs in MethoCult M3434 methylcellulose medium to evaluate hematopoietic progenitor cells(HPCs) proliferation function. The competitive repopulation assay and single-cell colony cultures of sorted hematopoietic stem cells (HSCs,CD34-Lin- sca1+c-kit+cells,LSK+)were used to validate HSCs function. The counts of BMMNCs have no significant difference. However, It was found that hematopoietic colony-forming unit (CFU-E, BFU-E, CFU-GM and CFU-mix) was much lower than that of normal control(P<0.05)(Fig.1). Notely, the number of LSK+ cells (*103/femur) was decreased significantly in iron overload mouse (26.43±3.28) compared with normal control(40.12±5.21) and the single-cell colony formation(/60wells) was reduced significantly in iron overload mouse(28.54±3.33) compared with normal control(47.93±4.82) (P<0.05). The long-term and multilineage engraftment capability of the iron-overloaded HSCs was weaken after transplantation. We then explored the possible mechanism of this inhibitory effects. Our previous studies have shown that iron overload could elevated reactive oxygen species (ROS) levels of mesenchymal stem cells and HSCs in vitro. Similarly, the intracellular ROS levels were analyzed by a flow cytometer. It was found that ROS level in iron overload BM was increased by 3.32 folds in erythroid cells, 1.51 folds in granulocytes and 4.80 folds in LSK+ cells,respectively. And also, the expression of p53, p38MAPK and p16Ink4a mRNA remained significantly elevated, which indicated that ROS related signal pathway was involved in the deficient hematopoiesis of iron overload BM. In addition, we also observed the effects of iron overload on the mice with deficient hematopoiesis exposed to 4Gy total body irradiation(TBI), which was more similar to clinical pathological conditions such as AA or MDS. It was found that BM damage caused by iron overload was aggravated in pathological conditions (primary findings were not shown). In conclusion, our study confirmed that iron overload injures the hematopoiesis of BM by enhancing oxidative stress in mice, which would be helpful to further study on the mechanism and would provide an experimental basis to find new therapeutic targets for the treatment of iron overload in patients with hematopoietic dysfunction.Figure 1Results of hematopoietic colony forming unit of different groups(*P<0.05)Figure 1. Results of hematopoietic colony forming unit of different groups(*P<0.05) Disclosures: No relevant conflicts of interest to declare.

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Chaillou, Thomas, Nathalie Koulmann, Nadine Simler, Adélie Meunier, Bernard Serrurier, Rachel Chapot, Andre Peinnequin, Michèle Beaudry, and Xavier Bigard. "Hypoxia transiently affects skeletal muscle hypertrophy in a functional overload model." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 5 (March 1, 2012): R643—R654. http://dx.doi.org/10.1152/ajpregu.00262.2011.

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Hypoxia induces a loss of skeletal muscle mass, but the signaling pathways and molecular mechanisms involved remain poorly understood. We hypothesized that hypoxia could impair skeletal muscle hypertrophy induced by functional overload (Ov). To test this hypothesis, plantaris muscles were overloaded during 5, 12, and 56 days in female rats exposed to hypobaric hypoxia (5,500 m), and then, we examined the responses of specific signaling pathways involved in protein synthesis (Akt/mTOR) and breakdown (atrogenes). Hypoxia minimized the Ov-induced hypertrophy at days 5 and 12 but did not affect the hypertrophic response measured at day 56. Hypoxia early reduced the phosphorylation levels of mTOR and its downstream targets P70S6K and rpS6, but it did not affect the phosphorylation levels of Akt and 4E-BP1, in Ov muscles. The role played by specific inhibitors of mTOR, such as AMPK and hypoxia-induced factors (i.e., REDD1 and BNIP-3) was studied. REDD1 protein levels were reduced by overload and were not affected by hypoxia in Ov muscles, whereas AMPK was not activated by hypoxia. Although hypoxia significantly increased BNIP-3 mRNA levels at day 5, protein levels remained unaffected. The mRNA levels of the two atrogenes MURF1 and MAFbx were early increased by hypoxia in Ov muscles. In conclusion, hypoxia induced a transient alteration of muscle growth in this hypertrophic model, at least partly due to a specific impairment of the mTOR/P70S6K pathway, independently of Akt, by an undefined mechanism, and increased transcript levels for MURF1 and MAFbx that could contribute to stimulate the proteasomal proteolysis.

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Chery, Josue, Shan Huang, Lianghui Gong, Shuyun Wang, Zhize Yuan, Joshua Wong, Jeffrey Lee, Sean Johnson, and Ming-Sing Si. "Human Neonatal Thymus Mesenchymal Stem/Stromal Cells and Chronic Right Ventricle Pressure Overload." Bioengineering 6, no. 1 (February 9, 2019): 15. http://dx.doi.org/10.3390/bioengineering6010015.

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Right ventricle (RV) failure secondary to pressure overload is associated with a loss of myocardial capillary density and an increase in oxidative stress. We have previously found that human neonatal thymus mesenchymal stem cells (ntMSCs) promote neovascularization, but the ability of ntMSCs to express the antioxidant extracellular superoxide dismutase (SOD3) is unknown. We hypothesized that ntMSCs express and secrete SOD3 as well as improve survival in the setting of chronic pressure overload. To evaluate this hypothesis, we compared SOD3 expression in ntMSCs to donor-matched bone-derived MSCs and evaluated the effect of ntMSCs in a rat RV pressure overload model induced by pulmonary artery banding (PAB). The primary outcome was survival, and secondary measures were an echocardiographic assessment of RV size and function as well as histological studies of the RV. We found that ntMSCs expressed SOD3 to a greater degree as compared to bone-derived MSCs. In the PAB model, all ntMSC-treated animals survived to the study endpoint whereas control animals had significantly decreased survival. Treatment animals had significantly less RV fibrosis and increased RV capillary density as compared to controls. We conclude that human ntMSCs demonstrate a therapeutic effect in a model of chronic RV pressure overload, which may in part be due to their antioxidative, antifibrotic, and proangiogenic effects. Given their readily available source, human ntMSCs may be a candidate cell therapy for individuals with congenital heart disease and a pressure-overloaded RV.

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Lattrich, Kai-Kristina, and Marion Büttgen. "Project leaders’ control resources and role overload as predictors of project success: developing the job demands–resources model." Business Research 13, no. 2 (May 22, 2020): 767–88. http://dx.doi.org/10.1007/s40685-020-00115-z.

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Abstract Drawing on the job demands–resources model (JD–R model), this article introduces information control and team control as project leader-specific job resources, as well as role overload as a demand, and then examines their influences on project experience appraisals and project success. With a sample of 185 project leaders, this study reveals that all three factors drive project success and project leader well-being. The moderating effects of role overload on the relationships between team control and negative experience and between team control and goal attainment are particularly remarkable; goal attainment is highest with high team control and high role overload. Similarly, the most positive experiences occur with high team control and high role overload. This further development of the JD–R model, thus, identifies information and team control as resources specific to project leaders and role overload as a predominant challenge stressor, with an ambivalent nature.

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Bartnikas, Thomas Benedict, Sheryl Wildt, Amy Wineinger, Klaus Schmitz-Abe, Kyriacos Markianos, Dale Cooper, and Mark D. Fleming. "A Novel Rat Model of Hereditary Hemochromatosis Due to a Mutation in Transferrin Receptor 2." Blood 120, no. 21 (November 16, 2012): 612. http://dx.doi.org/10.1182/blood.v120.21.612.612.

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Abstract Abstract 612 Sporadic iron overload has been reported previously in rats but the underlying cause has not been ascertained. In this study, phenotypic analysis of a subpopulation of Wistar rats designated Hsd:HHCL revealed a low incidence of histologically detected liver iron overload. One rat out of 132 screened animals exhibited liver iron accumulation in a predominantly periportal, hepatocellular distribution; this male rat expressed low RNA levels of the iron regulatory hormone hepcidin and low protein levels of transferrin receptor 2, a membrane protein essential for hepcidin expression in humans and mice and mutated in forms of hereditary hemochromatosis, a disease of excessive intestinal iron absorption and progressive tissue iron overload. Sequencing of the transferrin receptor 2 gene in the iron-overloaded rat revealed a novel Ala679Gly polymorphism affecting a highly conserved residue. Quantitative trait locus mapping revealed that a transferrin receptor 2 polymorphism correlated strongly with serum iron and transferrin saturations in male rats. Transfection of Tfr2 expression constructs into tissue culture cell lines revealed that the Gly679 Tfr2 variant is expressed at a lower level than the Ala679 variant. Selective breeding of rats carrying this polymorphism and characterization of iron metabolism in the resulting progeny indicated that homozygosity for the Ala679Gly allele leads to a hemochromatosis phenotype. The Hsd:HHCL rat is the first genetic rat model of hereditary hemochromatosis and may prove useful for understanding the molecular mechanisms underlying the regulation of iron metabolism and the pathogenesis of hereditary hemochromatosis. Disclosures: No relevant conflicts of interest to declare.

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Wu, Dijiong, Xiaowen Wen, Baodong Ye, Wenbin Liu, Yanting Gao, Yiping Shen, Yuhong Zhou, and Jie Jin. "Establishment of a Mouse Model of Aplastic Anemia Complicated By Iron Overload." Blood 126, no. 23 (December 3, 2015): 4555. http://dx.doi.org/10.1182/blood.v126.23.4555.4555.

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Abstract Aplastic anemia (AA) is a common hematologic disease characterized by hematopoietic failure of the bone marrow and pancytopenia of the peripheral blood. Some patients with AA suffer from transfusion-induced iron overload secondary to long-term blood transfusions due to moderate and severe anemia. Topics related to iron overload and chelation therapy have recently become important in hematologic diseases, especially in hematopoietic failure. However, no animal model of AA complicated by iron overload has been developed, which affects drug research and development. The purpose of our study is to establish a mouse model of aplastic anemia complicated by iron overload. We firstly controlled the total dose of iron supplements (2.0 *103 mg/kg) and compared how serum iron and ferritin levels varied among different dosage regimens to determine the best dosage and duration for the development of an iron overload model in mice (we finally chose the 200 mg/w/kg * 10 weeks). A composite model of AA was successfully established on the principle of immune-mediated bone marrow failure: DBA/2 mice were euthanized by cervical dislocation and the thymuses were taken out using aseptic techniques for the preparation of cell suspensions of 5 * 106/mL; Balb/c mouse were given whole-body irradiation with 60Co 6.0 Gy at 1 Gy/min, after which 0.2 mL of the prepared cell suspensions was injected into each mouse via the caudal vein within 4 h. We then compared the differences in liver volume, peripheral hemogram, bone marrow pathology, serum iron, serum ferritin, pathological iron deposition in multiple organs (liver, bone marrow, spleen), liver hepcidin, bone morphogenetic protein 6 (BMP6), SMAD family member 4 (SMAD4), transferrin receptor 2 (TfR2) protein, and mRNA expression levels among the Normal Control, AA, Iron Overload, and Composite Model groups to validate the composite model and to explore the pathogenesis and features of iron overload in the composite model. The results indicated significant abnormalities in iron metabolism parameters in mice with AA, which was reflected in the significant decrease of hepcidin expression in the liver (P < 0.01) that basically paralleled the changes in BMP6, SMAD4, and TfR2. Iron Overload Group had a suppressed hepcidin, BMP6, and SMAD4 mRNA expressions in liver, but these parameters were higher than in the AA group (P < 0.01). Association with iron overload would not further downregulate the negative parameters of iron deposition in mice with AA, and SMAD4 and TfR2 protein levels and hepcidin and SMAD4 mRNA expression levels were lower in the AA group than in the Composite Model group (P < 0.01 or P < 0.05). (see Fig.1 and Fig.2) The established model is basically consistent with the clinical manifestations and pathogenesis of AA complicated by transfusion-induced iron overload. This successful establishment will help in the screening of iron chelation drugs and studies on pharmacological mechanisms. Figure 1. Western-blot a nalysis of hepcidin, BMP6, SMAD4 and TfR2 expression among groups Figure 1. Western-blot a nalysis of hepcidin, BMP6, SMAD4 and TfR2 expression among groups Figure 2. Analysis of hepcidin, BMP6, SMAD4 and TfR2 mRNA expression levels among different groups Figure 2. Analysis of hepcidin, BMP6, SMAD4 and TfR2 mRNA expression levels among different groups Disclosures No relevant conflicts of interest to declare.

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Yin, Pengzhen, Carol X. J. Ou, Robert M. Davison, and Jie Wu. "Coping with mobile technology overload in the workplace." Internet Research 28, no. 5 (October 2, 2018): 1189–212. http://dx.doi.org/10.1108/intr-01-2017-0016.

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Purpose The overload effects associated with the use of mobile information and communication technologies (MICTs) in the workplace have become increasingly prevalent. The purpose of this paper is to examine the overload effects of using MICTs at work on employees’ job satisfaction, and explore the corresponding coping strategies. Design/methodology/approach The study is grounded on the cognitive load theory and the coping model of user adaptation. The overload antecedents and coping strategies are integrated into one model. Theoretical hypotheses are tested with survey data collected from a sample of 178 employees at work in China. Findings The results indicate that information overload significantly reduces job satisfaction, while the influence of interruption overload on job satisfaction is not significant. Two coping strategies (information processing timeliness and job control assistant support) can significantly improve job satisfaction. Information processing timeliness significantly moderates the relationships between two types of overload effects and job satisfaction. Job control assistant support also significantly moderates the relationship between interruption overload and job satisfaction. Practical implications This study suggests that information overload and interruption overload could constitute an important index to indicate employees’ overload level when using MICTs at work. The two coping strategies provide managers with effective ways to improve employees’ job satisfaction. By taking advantage of the moderation effects of coping strategies, managers could lower employees’ evaluation of overload to an appropriate level. Originality/value This study provides a comprehensive model to examine how the overload resulting from using MICTs in the workplace affects employees’ work status, and how to cope with it. Two types of overload are conceptualized and corresponding coping strategies are identified. The measurements of principal constructs are developed and empirically validated. The results provide theoretical and practical insights on human resource management and human–computer interaction.

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Chen, Xiaolong, Guozhong Huang, Xuehong Gao, Shengnan Ou, Yatao Li, and Ibrahim M. Hezam. "BN-RA: A Hybrid Model for Risk Analysis of Overload-Induced Early Cable Fires." Applied Sciences 11, no. 19 (September 24, 2021): 8922. http://dx.doi.org/10.3390/app11198922.

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Cable overload is one of the most critical contributors to early cable fires. This study proposes a hybrid Bayesian network (BN)-based fire risk analysis model, to investigate the evolution of overload-induced early cable fire risks. In particular, the fire risk transmission paths caused by cable overload are reported, considering the critical factors that likely lead to fires. A BN with a specific structure was considered using the fire risk transmission paths. Later, given the risk index system, a hybrid fire risk assessment model caused by cable overload was developed based on the entropy weight method. Subsequently, the corresponding risk levels were evaluated based on the evolution of the fire risk, using numerical simulations. Finally, a case study was conducted to validate the proposed methods, and the results indicated that the proposed methods can effectively evaluate the state of the cable and explain the causes of fire risk, which can be used for early fire warnings.

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Volani, Chiara, Giuseppe Paglia, Sigurdur Smarason, Peter Pramstaller, Egon Demetz, Christa Pfeifhofer-Obermair, and Guenter Weiss. "Metabolic Signature of Dietary Iron Overload in a Mouse Model." Cells 7, no. 12 (December 11, 2018): 264. http://dx.doi.org/10.3390/cells7120264.

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Iron is an essential co-factor for several metabolic processes, including the Krebs cycle and mitochondrial oxidative phosphorylation. Therefore, maintaining an appropriate iron balance is essential to ensure sufficient energy production and to avoid excessive reactive oxygen species formation. Iron overload impairs mitochondrial fitness; however, little is known about the associated metabolic changes. Here we aimed to characterize the metabolic signature triggered by dietary iron overload over time in a mouse model, where mice received either a standard or a high-iron diet. Metabolic profiling was assessed in blood, plasma and liver tissue. Peripheral blood was collected by means of volumetric absorptive microsampling (VAMS). Extracted blood and tissue metabolites were analyzed by liquid chromatography combined to high resolution mass spectrometry. Upon dietary iron loading we found increased glucose, aspartic acid and 2-/3-hydroxybutyric acid levels but low lactate and malate levels in peripheral blood and plasma, pointing to a re-programming of glucose homeostasis and the Krebs cycle. Further, iron loading resulted in the stimulation of the urea cycle in the liver. In addition, oxidative stress was enhanced in circulation and coincided with increased liver glutathione and systemic cysteine synthesis. Overall, iron supplementation affected several central metabolic circuits over time. Hence, in vivo investigation of metabolic signatures represents a novel and useful tool for getting deeper insights into iron-dependent regulatory circuits and for monitoring of patients with primary and secondary iron overload, and those ones receiving iron supplementation therapy.

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Karabeg, Reuf, Fikret Veljovic, Avdo Voloder, Semin Becirbegovic, Dzenan Jahic, Senad Burak, Edin Begic, and Izet Masic. "A Mathematical Model of Achilles Tendon Overload During Jump Shot." Medical Archives 73, no. 4 (2019): 228. http://dx.doi.org/10.5455/medarh.2019.73.228-233.

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Tapia Moore, Ernesto. "Information Overload and the Internationalization Process Model: An Implementation Attempt." Journal of Business 9, no. 1 (2017): 119–42. http://dx.doi.org/10.21678/jb.2017.827.

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DESJARDINS, S., R. W. MUELLER, and M. J. CAUCHY. "A pressure overload model of congestive heart failure in rats." Cardiovascular Research 22, no. 10 (October 1, 1988): 696–702. http://dx.doi.org/10.1093/cvr/22.10.696.

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Schwartz, Kenneth A., Jill Fisher, and E. Terence Adams. "Morphologic Investigations of the Guinea Pig Model of Iron Overload." Toxicologic Pathology 21, no. 3 (April 1993): 311–20. http://dx.doi.org/10.1177/019262339302100307.

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Norrdin, R. W., C. E. Kawcak, B. A. Capwell, and C. W. McIlwraith. "Subchondral Bone Failure in an Equine Model of Overload Arthrosis." Bone 22, no. 2 (February 1998): 133–39. http://dx.doi.org/10.1016/s8756-3282(97)00253-6.

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Yang, Tianen, Wei-Qiang Dong, Yuri A. Kuryshev, Carlos Obejero-Paz, Matthew N. Levy, Gary M. Brittenham, Songsak Kiatchoosakun, Darryl Kirkpatrick, Brian D. Hoit, and Arthur M. Brown. "Bimodal cardiac dysfunction in an animal model of iron overload." Journal of Laboratory and Clinical Medicine 140, no. 4 (October 2002): 263–71. http://dx.doi.org/10.1067/mlc.2002.127725.

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