Stress intensity factor for small embedded cracks in weldments

In the present work, the stress intensity factor (SIF) of embedded small cracks placed at the weld toe is calculated by means of two procedures based on the Oore-Burns integral. In the first approach, the defect is considered as a circular disk and the SIF is evaluated by means of the Oore- Burns weight function. By taking advantage of a suitable change of variable, the singularity of the weight function on the crack border can be removed. In this way, the numerical evaluation of the SIF is possible without the use of specific integration algorithms, although the nominal stress field becomes singular when the crack approaches a V-sharpe notch. As an example, the obtained equations are applied to a defect located in the neighbourhood of a weld toe with an opening angle of 135 degrees under mode I loading. Subsequently, for a crack similar to a star domain with a border expressed by means of the Fourier series, the SIF is given by means of an explicit equation based on the Oore-Burns weight function

Three-dimensional fatigue crack propagation by means of first order SIF approximation

In this paper we make use of a closed-form solution for mode I Stress Intensity Factors (SIF) in three-dimensional planar flaws based on homotopy transformations of a disc. The utilised equations are very accurate when the flaw is a small deviation from a circle. Under the hypothesis of an isolated crack, the SIF at each point of the crack border is calculated to assess the crack shape after propagation. The solution is proposed in terms of the Fourier series and the crack growth rate equation is taken according to Paris' low. Many examples are proposed with the aim of predicting the final shape of different types of embedded planar flaws in butt welded joints under fatigue tensile loading

Talking quiescence: a rigorous theory that supports parallel composition, action hiding and determinisation

The notion of quiescence - the absence of outputs - is vital in both behavioural modelling and testing theory. Although the need for quiescence was already recognised in the 90s, it has only been treated as a second-class citizen thus far. This paper moves quiescence into the foreground and introduces the notion of quiescent transition systems (QTSs): an extension of regular input-output transition systems (IOTSs) in which quiescence is represented explicitly, via quiescent transitions. Four carefully crafted rules on the use of quiescent transitions ensure that our QTSs naturally capture quiescent behaviour. We present the building blocks for a comprehensive theory on QTSs supporting parallel composition, action hiding and determinisation. In particular, we prove that these operations preserve all the aforementioned rules. Additionally, we provide a way to transform existing IOTSs into QTSs, allowing even IOTSs as input that already contain some quiescent transitions. As an important application, we show how our QTS framework simplifies the fundamental model-based testing theory formalised around ioco.Comment: In Proceedings MBT 2012, arXiv:1202.582

An Event Structure Model for Probabilistic Concurrent Kleene Algebra

We give a new true-concurrent model for probabilistic concurrent Kleene algebra. The model is based on probabilistic event structures, which combines ideas from Katoen's work on probabilistic concurrency and Varacca's probabilistic prime event structures. The event structures are compared with a true-concurrent version of Segala's probabilistic simulation. Finally, the algebraic properties of the model are summarised to the extent that they can be used to derive techniques such as probabilistic rely/guarantee inference rules.Comment: Submitted and accepted for LPAR19 (2013

Timed Parity Games: Complexity and Robustness

We consider two-player games played in real time on game structures with clocks where the objectives of players are described using parity conditions. The games are \emph{concurrent} in that at each turn, both players independently propose a time delay and an action, and the action with the shorter delay is chosen. To prevent a player from winning by blocking time, we restrict each player to play strategies that ensure that the player cannot be responsible for causing a zeno run. First, we present an efficient reduction of these games to \emph{turn-based} (i.e., not concurrent) \emph{finite-state} (i.e., untimed) parity games. Our reduction improves the best known complexity for solving timed parity games. Moreover, the rich class of algorithms for classical parity games can now be applied to timed parity games. The states of the resulting game are based on clock regions of the original game, and the state space of the finite game is linear in the size of the region graph. Second, we consider two restricted classes of strategies for the player that represents the controller in a real-time synthesis problem, namely, \emph{limit-robust} and \emph{bounded-robust} winning strategies. Using a limit-robust winning strategy, the controller cannot choose an exact real-valued time delay but must allow for some nonzero jitter in each of its actions. If there is a given lower bound on the jitter, then the strategy is bounded-robust winning. We show that exact strategies are more powerful than limit-robust strategies, which are more powerful than bounded-robust winning strategies for any bound. For both kinds of robust strategies, we present efficient reductions to standard timed automaton games. These reductions provide algorithms for the synthesis of robust real-time controllers

A balanced formula of essential amino acids promotes brain mitochondrial biogenesis and protects neurons from ischemic insult

Mitochondrial dysfunction plays a key role in the aging process, and aging is a strong risk factor for neurodegenerative diseases or brain injury characterized by impairment of mitochondrial function. Among these, ischemic stroke is one of the leading causes of death and permanent disability worldwide. Pharmacological approaches for its prevention and therapy are limited. Although non-pharmacological interventions such as physical exercise, which promotes brain mitochondrial biogenesis, have been shown to exert preventive effects against ischemic stroke, regular feasibility is complex in older people, and nutraceutical strategies could be valuable alternatives. We show here that dietary supplementation with a balanced essential amino acid mixture (BCAAem) increased mitochondrial biogenesis and the endogenous antioxidant response in the hippocampus of middle-aged mice to an extent comparable to those elicited by treadmill exercise training, suggesting BCAAem as an effective exercise mimetic on brain mitochondrial health and disease prevention. In vitro BCAAem treatment directly exerted mitochondrial biogenic effects and induced antioxidant enzyme expression in primary mouse cortical neurons. Further, exposure to BCAAem protected cortical neurons from the ischemic damage induced by an in vitro model of cerebral ischemia (oxygen-glucose deprivation, OGD). BCAAem-mediated protection against OGD was abolished in the presence of rapamycin, Torin-1, or L-NAME, indicating the requirement of both mTOR and eNOS signaling pathways in the BCAAem effects. We propose BCAAem supplementation as an alternative to physical exercise to prevent brain mitochondrial derangements leading to neurodegeneration and as a nutraceutical intervention aiding recovery after cerebral ischemia in conjunction with conventional drugs

Targeting Multiple Mitochondrial Processes by a Metabolic Modulator Prevents Sarcopenia and Cognitive Decline in SAMP8 Mice

The age-dependent declines of skeletal muscle and cognitive functions often coexist in elderly subjects. The underlying pathophysiological mechanisms share common features of mitochondrial dysfunction, which plays a central role in the development of overt sarcopenia and/or dementia. Dietary supplementation with formulations of essential and branched-chain amino acids (EAA-BCAA) is a promising preventive strategy because it can preserve mitochondrial biogenesis and function. The senescence-accelerated mouse prone 8 (SAMP8) is considered an accurate model of age-related muscular and cognitive alterations. Hence, we aimed to investigate the progression of mitochondrial dysfunctions during muscular and cognitive aging of SAMP8 mice and to study the effects of a novel EAA-BCAA-based metabolic modulator on these changes. We evaluated body condition, motor endurance, and working memory of SAMP8 mice at 5, 9, 12, and 15 months of age. Parallel changes in protein levels of mitochondrial respiratory chain subunits, regulators of mitochondrial biogenesis and dynamics, and the antioxidant response, as well as respiratory complex activities, were measured in the quadriceps femoris and the hippocampus. The same variables were assessed in 12-month-old SAMP8 mice that had received dietary supplementation with the novel EAA-BCAA formulation, containing tricarboxylic acid cycle intermediates and co-factors (PD-0E7, 1.5 mg/kg/body weight/day in drinking water) for 3 months. Contrary to untreated mice, which had a significant molecular and phenotypic impairment, PD-0E7-treated mice showed preserved healthy body condition, muscle weight to body weight ratio, motor endurance, and working memory at 12 months of age. The PD-0E7 mixture increased the protein levels and the enzymatic activities of mitochondrial complex I, II, and IV and the expression of proliferator-activated receptor \u3b3 coactivator-1\u3b1, optic atrophy protein 1, and nuclear factor, erythroid 2 like 2 in muscles and hippocampi. The mitochondrial amyloid-\u3b2-degrading pitrilysin metallopeptidase 1 was upregulated, while amyloid precursor protein was reduced in the hippocampi of PD-0E7 treated mice. In conclusion, we show that a dietary supplement tailored to boost mitochondrial respiration preserves skeletal muscle and hippocampal mitochondrial quality control and health. When administered at the early onset of age-related physical and cognitive decline, this novel metabolic inducer counteracts the deleterious effects of precocious aging in both domains

Probabilistic Mobility Models for Mobile and Wireless Networks

International audienceIn this paper we present a probabilistic broadcast calculus for mobile and wireless networks whose connections are unreliable. In our calculus, broadcasted messages can be lost with a certain probability, and due to mobility the connection probabilities may change. If a network broadcasts a message from a location, it will evolve to a network distribution depending on whether nodes at other locations receive the message or not. Mobility of nodes is not arbitrary but guarded by a probabilistic mobility function (PMF), and we also define the notion of a weak bisimulation given a PMF. It is possible to have weak bisimular networks which have different probabilistic connectivity information. We furthermore examine the relation between our weak bisimulation and a minor variant of PCTL* [1]. Finally, we apply our calculus on a small example called the Zeroconf protocol [2]