Random Stress-Dependent Strength Models Through Bivariate Exponential Conditionals Distributions

2007 ◽  
pp. 327-339 ◽  
Author(s):  
Ashis SenGupta
Keyword(s):  
Bivariate Exponential ◽  
Strength Models ◽  
Stress Dependent

scholarly journals Reliability for some bivariate exponential distributions

2006 ◽  
Vol 2006 ◽  
pp. 1-14 ◽  
Author(s):  
Saralees Nadarajah ◽  
Samuel Kotz
Keyword(s):  
Joint Distribution ◽  
Special Functions ◽  
Random Variables ◽  
Independent Random Variables ◽  
Exponential Distributions ◽  
Bivariate Distributions ◽  
Algebraic Form ◽  
Bivariate Exponential ◽  
Strength Models ◽  
Explicit Expressions

In the area of stress-strength models, there has been a large amount of work as regards estimation of the reliabilityR=Pr⁡(X<Y). The algebraic form forR=Pr⁡(X<Y)has been worked out for the vast majority of the well-known distributions whenXandYare independent random variables belonging to the same univariate family. In this paper, forms ofRare considered when(X,Y)follow bivariate distributions with dependence betweenXandY. In particular, explicit expressions forRare derived when the joint distribution isbivariate exponential. The calculations involve the use of special functions. An application of the results is also provided.

On Modeling and Tracking Control for a Smart Structure with Stress-dependent Hysteresis Nonlinearity

2010 ◽  
Vol 36 (11) ◽  
pp. 1611-1619 ◽  
Author(s):  
Yan-Hua MA ◽  
Jian-Qin MAO
Keyword(s):  
Tracking Control ◽  
Smart Structure ◽  
Hysteresis Nonlinearity ◽  
Stress Dependent

Moving Average Models with Bivariate Exponential and Geometric Distributions.

1985 ◽  
Author(s):  
Naftali A. Langberg ◽  
David S. Stoffer
Keyword(s):  
Moving Average ◽  
Bivariate Exponential ◽  
Moving Average Models

L-carnosine and its Derivatives as New Therapeutic Agents for the Prevention and Treatment of Vascular Complications of Diabetes

2020 ◽  
Vol 27 (11) ◽  
pp. 1744-1763 ◽  
Author(s):  
Stefano Menini ◽  
Carla Iacobini ◽  
Claudia Blasetti Fantauzzi ◽  
Giuseppe Pugliese
Keyword(s):  
Diabetic Nephropathy ◽  
Life Quality ◽  
Vascular Complications ◽  
Carbonyl Stress ◽  
Complications Of Diabetes ◽  
Diabetic Vascular Complications ◽  
Reactive Carbonyl Species ◽  
Stage Renal Disease ◽  
Stress Dependent ◽  
End Stage

Vascular complications are among the most serious manifestations of diabetes. Atherosclerosis is the main cause of reduced life quality and expectancy in diabetics, whereas diabetic nephropathy and retinopathy are the most common causes of end-stage renal disease and blindness. An effective therapeutic approach to prevent vascular complications should counteract the mechanisms of injury. Among them, the toxic effects of Advanced Glycation (AGEs) and Lipoxidation (ALEs) end-products are well-recognized contributors to these sequelae. L-carnosine (β-alanyl-Lhistidine) acts as a quencher of the AGE/ALE precursors Reactive Carbonyl Species (RCS), which are highly reactive aldehydes derived from oxidative and non-oxidative modifications of sugars and lipids. Consistently, L-carnosine was found to be effective in several disease models in which glyco/lipoxidation plays a central pathogenic role. Unfortunately, in humans, L-carnosine is rapidly inactivated by serum carnosinase. Therefore, the search for carnosinase-resistant derivatives of Lcarnosine represents a suitable strategy against carbonyl stress-dependent disorders, particularly diabetic vascular complications. In this review, we present and discuss available data on the efficacy of L-carnosine and its derivatives in preventing vascular complications in rodent models of diabetes and metabolic syndrome. We also discuss genetic findings providing evidence for the involvement of the carnosinase/L-carnosine system in the risk of developing diabetic nephropathy and for preferring the use of carnosinase-resistant compounds in human disease. The availability of therapeutic strategies capable to prevent both long-term glucose toxicity, resulting from insufficient glucoselowering therapy, and lipotoxicity may help reduce the clinical and economic burden of vascular complications of diabetes and related metabolic disorders.

Mycoplasmas bovis P48 induces apoptosis in EBL cells via an endoplasmic reticulum stress-dependent signaling pathway

2021 ◽  
Vol 255 ◽  
pp. 109013
Author(s):  
Xiaochun Wu ◽  
Shengying Zhang ◽  
Cuiqin Long ◽  
Zhen An ◽  
Xiaoyong Xing ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathway ◽  
Stress Dependent ◽  
Dependent Signaling Pathway

scholarly journals Patients with Gaucher disease display systemic oxidative stress dependent on therapy status

2020 ◽  
Vol 25 ◽  
pp. 100667
Author(s):  
Reena V. Kartha ◽  
Marcia R. Terluk ◽  
Roland Brown ◽  
Abigail Travis ◽  
Usha R. Mishra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gaucher Disease ◽  
Systemic Oxidative Stress ◽  
Stress Dependent

scholarly journals SVIP is a molecular determinant of lysosomal dynamic stability, neurodegeneration and lifespan

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Alyssa E. Johnson ◽  
Brian O. Orr ◽  
Richard D. Fetter ◽  
Armen J. Moughamian ◽  
Logan A. Primeaux ◽  
...  
Keyword(s):  
Dynamic Stability ◽  
Muscle Wasting ◽  
Dependent Manner ◽  
Missense Mutations ◽  
Over Expression ◽  
System A ◽  
Molecular Determinant ◽  
Intracellular Organelles ◽  
Stress Dependent ◽  
Lateral Sclerosis

AbstractMissense mutations in Valosin-Containing Protein (VCP) are linked to diverse degenerative diseases including IBMPFD, amyotrophic lateral sclerosis (ALS), muscular dystrophy and Parkinson’s disease. Here, we characterize a VCP-binding co-factor (SVIP) that specifically recruits VCP to lysosomes. SVIP is essential for lysosomal dynamic stability and autophagosomal–lysosomal fusion. SVIP mutations cause muscle wasting and neuromuscular degeneration while muscle-specific SVIP over-expression increases lysosomal abundance and is sufficient to extend lifespan in a context, stress-dependent manner. We also establish multiple links between SVIP and VCP-dependent disease in our Drosophila model system. A biochemical screen identifies a disease-causing VCP mutation that prevents SVIP binding. Conversely, over-expression of an SVIP mutation that prevents VCP binding is deleterious. Finally, we identify a human SVIP mutation and confirm the pathogenicity of this mutation in our Drosophila model. We propose a model for VCP disease based on the differential, co-factor-dependent recruitment of VCP to intracellular organelles.

scholarly journals Stress-Dependent Deformation and Permeability of a Fractured Coal Subject to Excavation-Related Loading Paths

2021 ◽  
Author(s):  
Wenzhuo Cao ◽  
Qinghua Lei ◽  
Wu Cai
Keyword(s):  
Coal Mining ◽  
Coalbed Methane ◽  
Axial Stress ◽  
Equilibrium Phase ◽  
Natural Fracture ◽  
Equivalent Permeability ◽  
Coal Matrix ◽  
Bedding Planes ◽  
Fractured Coal ◽  
Stress Dependent

AbstractThe deformation and permeability of coal are largely affected by the presence and distribution of natural fractures such as cleats and bedding planes with orthogonal and abutting characteristics, resulting in distinct hydromechanical responses to stress loading during coal mining processes. In this research, a two-dimensional (2D) fracture network is constructed based on a real coal cleat trace data collected from the Fukang mine area, China. Realistic multi-stage stress loading is designed to sequentially mimic an initial equilibrium phase and a mining-induced perturbation phase involving an increase of axial stress and a decrease of confining stress. The geomechanical and hydrological behaviour of the fractured coal under various stress loading conditions is modelled using a finite element model, which can simulate the deformation of coal matrix, the shearing and dilatancy of coal cleats, the variation of cleat aperture induced by combined effects of closure/opening, and shear and tensile-induced damage. The influence of different excavation stress paths and directions of mining is further investigated. The simulation results illustrate correlated variations among the shear-induced cleat dilation, damage in coal matrix, and equivalent permeability of the fractured coal. Model results are compared with results of previous work based on conventional approaches in which natural fracture networks are not explicitly represented. In particular, the numerical model reproduces the evolution of equivalent permeability under the competing influence of the effective stress perpendicular to cleats and shear-induced cleat dilation and associated damage. Model results also indicate that coal mining at low stress rates is conducive to the stability of surrounding coal seams, and that coal mining in parallel to cleat directions is desirable. The research findings of this paper have important implications for efficient and safe exploitation of coal and coalbed methane resources.

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