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Authors: Su, Hao | Chen, Ming

Article Type: Research Article

Abstract: Through the analysis of the J-A model, the metal magnetic memory signal of Δ B (the distance between Br and -Br ) can reflect the fatigue degree, and can be verified by bending fatigue test of 45# steel. The test results show that Δ B has three stages in the fatigue process, which correspond to the entire crack propagation process. By measuring the Δ B values, the fatigue state of the specimen can be evaluated.

Keywords: Metal magnetic memory, J-A model, rotating bending fatigue

DOI: 10.3233/JAE-162082

Citation: International Journal of Applied Electromagnetics and Mechanics, vol. 52, no. 3-4, pp. 1623-1628, 2016

Authors: Chen, Ming | Hofestädt, Ralf

Article Type: Research Article

Abstract: A method to exploit hybrid Petri nets (HPN) for quantitatively modeling and simulating gene regulated metabolic networks is demonstrated. A global kinetic modeling strategy and Petri net modeling algorithm are applied to perform the bioprocess functioning and model analysis. With the model, the interrelations between pathway analysis and metabolic control mechanism are outlined. Diagrammatical results of the dynamics of metabolites are simulated and observed by implementing a HPN tool, Visual Object Net ++. An explanation of the observed behavior of the urea cycle is proposed to indicate possibilities for metabolic engineering and medical care. Finally, the perspective of Petri nets …on modeling and simulation of metabolic networks is discussed. Show more

Keywords: metabolic network, gene regulation, Petri nets, quantitative model, urea cycle, modeling and simulation

Citation: In Silico Biology, vol. 3, no. 3, pp. 347-365, 2003

Authors: Su, Hao | Chen, Ming

Article Type: Research Article

Abstract: Tension tests were conducted on 45# steel to investigate metal magnetic memory in stress concentration areas. The normal and tangential components of metal magnetic memory signals at seven test points in each specimen were simultaneously measured with probe lift-off values of 1 mm, 3 mm, and 5 mm. Axial tensile load was applied until visible necking occurred, and magnetic flux density was compared with the fracture location predicted according to Doubov's theory. Experimental results showed that the final fracture locations were inconsistent with the locations predicted by metal magnetic memory testing theory. A theoretical analysis of the determination criterion in …Doubov's theory also revealed that no perfect correlation between the two areas existed. Show more

Keywords: Metal, magnetic, memory, stress, concentration, tension, test

DOI: 10.3233/JAE-141777

Citation: International Journal of Applied Electromagnetics and Mechanics, vol. 46, no. 1, pp. 271-280, 2014

Authors: Chen, Ming | Hofestädt, Ralf

Article Type: Research Article

Abstract: Metabolic pathway alignment represents one of the most powerful tools for comparative analysis of metabolism. It involves recognition of metabolites common to a set of functionally-related metabolic pathways, interpretation of biological evolution processes and determination of alternative metabolic pathways. Moreover, it is of assistance in function prediction and metabolism modeling. Although research on genomic sequence alignment is extensive, the problem of aligning metabolic pathways has received less attention. We are motivated to develop an algorithm of metabolic pathway alignment to reveal the similarities between metabolic pathways. A new definition of the metabolic pathway is introduced. The algorithm has been implemented …into the PathAligner system; its web-based interface is available at http://bibiserv.techfak.uni-bielefeld.de/pathaligner/. Show more

Keywords: metabolic pathways, alignment, algorithm, PathAligner

Citation: In Silico Biology, vol. 5, no. 2, pp. 111-128, 2005

Authors: Chen, Ming | Fernandez, Hugo L.

Article Type: Article Commentary

DOI: 10.3233/JAD-2000-2211

Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 119-121, 2000

Authors: Chen, Ming | Fernandez, Hugo L.

Article Type: Research Article

Abstract: Alzheimer's disease (AD) has been intensively studied for decades, but why has its common pathological cause remained so enigmatic? Our studies have suggested that plaques and tangles occur spontaneously during aging as a result of a natural decline of energy metabolism and Ca2+ signaling, but not necessarily due to conventional pathogens. This view would lead to an unexpected outcome; that is, natural aging plays a more important role in neurodegeneration than is currently recognized. Does this model over-simplify the disease origin? We know that AD-type neurodegeneration typically occurs at the end stages of life when not only do plaques and …tangles appear, but also many other bodily changes as well (bone loss and skin wrinkling, etc). Neurodegeneration differs from the latter changes mainly by “social” consequences, not by “physiological” origin. If neurodegeneration is a natural event, then why do only some people, but not others, develop AD? Obviously, additional factors are required for neurodegeneration to develop into AD. By comparing current models and ruling out other possibilities, we think that several known “risk factors” most likely play a critical role in the late-onset sporadic AD. These risk factors can exert their effects either by providing the conditions for ailing neurons to die (extended longevity and sedentary lifestyle), or by enhancing the individual's “vulnerability” to natural neurodegeneration (low synapse reserve). In this context, late-onset sporadic AD would be similar to many other age-related conditions where perhaps no single pathogen can be held exclusively responsible for most cases; rather, many risk factors are important to allow the initial defect to turn into clinical diseases. Accordingly, these factors should be the primary targets for AD prevention. Yet, some other AD cases, especially the early-onset ones, may be complicated by the concomitant involvement of other diseases in the brain. Show more

Keywords: Alzheimer, aging, calcium, amyloid, presenilin, osteoporosis, atherosclerosis, Parkinson's

DOI: 10.3233/JAD-2000-2206

Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 97-108, 2000

Authors: Xu, Meng | Chen, Ming | Pan, Fangyuan

Article Type: Research Article

Abstract: The energy factor is the foundation of economic and social development, and it is also an important prerequisite for the effective operation of the elderly care industry. Based on the perspective of energy factor input, this paper constructs the DPSR mechanism model of the energy-elderly care industry system. Taking Shanghai as an example, through its 2010–2019 15 index data such as energy factors and industrial economy, the Entropy-TOPSIS method is comprehensively used to evaluate the energy-elderly care industry system. Finally, the following conclusions are drawn: (1) The energy factor has an important impact on the operation of the elderly care …industry through its effect on the driving force module, the pressure module and the state module; (2) The elderly care industry has an important impact on the energy factor through the conduction of the response module; (3) The evaluation results of the Shanghai energy-elderly care industry system showed a continuous improvement trend from 2010 to 2019. Show more

Keywords: Energy elements, DPSR model, TOPSIS method, systematic evaluation

DOI: 10.3233/JCM-247317

Citation: Journal of Computational Methods in Sciences and Engineering, vol. 24, no. 2, pp. 1119-1130, 2024

Authors: Chen, Ming | Nguyen, Huey T. | Sawmiller, Darrell R.

Article Type: Research Article

Abstract: We have contended that senile conditions—illnesses after age 60 and fully age-penetrating, such as tooth, hearing or memory loss—are not distinct “diseases” in medical nature, because they are caused by aging. Since the pace of aging varies among individuals and is much influenced by risk factors, senile conditions will only affect some but not all elderly. However, perhaps due to its unusually heavy burdens and tremendous social pressures, senile dementia (SD) has been singled out from other senile conditions and redefined as a curable “disease” (Alzheimer's). This highly popular definition has thus opened a Pandora's box that has been confusing …us up until now and warrants further scrutiny. In this article we discuss: a) what should we logically look for in SD beyond “pathogenic” factors?; b) why Ca2+ , a central regulator in neurotransmission, should be the primary player in SD; c) why the functionality of Ca2+ signaling, or its vibrant wave frequency and amplitude, must undergo down-regulation during aging, though this is intriguingly accompanied by an increase of Ca2+ “levels”; d) why intervention for SD should target Ca2+ function by promoting energy metabolisms and by Ca2+ agonists such as caffeine and nicotine, but not by “antagonists” as widely believed; and e) why our study should focus on aging, not “cell death”, a seemingly attractive paradigm but perhaps too late for intervention. We also seek answers for why unproven hypotheses can become dogmas and inhibit self-correcting mechanisms of science. Show more

Keywords: Alzheimer's disease, amyloid, calcium, review

DOI: 10.3233/JAD-2011-111142

Citation: Journal of Alzheimer's Disease, vol. 27, no. 4, pp. 679-689, 2011

Authors: Nguyen, Huey T. | Sawmiller, Darrell R. | Markov, Olga | Chen, Ming

Article Type: Research Article

Abstract: Elevated intracellular Ca2+ levels in the aging brain are widely thought to hyperactivate Ca2+ signaling and Ca2+ -dependent enzymes, leading to neuronal death through an excitatory mechanism in Alzheimer's disease (AD). This “Ca2+ overload” hypothesis has been questioned by our theoretical analyses. To better understand the relationship between the “level” and functionality of Ca2+ in aging, in this study we simultaneously measured intracellular Ca2+ transients and calpain activity in cultured human fibroblasts. We found that Ca2+ transitions elicited by bradykinin were indeed overstayed or elevated in levels in old cells but, remarkably, calpain activity was decreased compared to young cells. …Also, treating young cells with the energy inhibitor rotenone or with H2 O2 recapitulated the Ca2+ overstay and calpain inactivation found in old cells. More importantly, treating old cells with high-energy compounds such as phosphoenol pyruvate or phosphocreatine, which boosted cellular ATP content, reduced the Ca2+ overstay and re-activated calpain. Moreover, Ca2+ levels and calpain activity were dramatically raised in the dying cells killed by detergent. Finally, Ca2+ oscillations induced by low dose of bradykinin in old cells exhibited lower spike frequency, but higher overall levels. Collectively, these results suggest that (a) Ca2+ overload in old cells arises from an inefficient Ca2+ handling system compromised by age-related energy depletion and oxidative stress; and (b) despite elevated levels, the functionality of Ca2+ signaling has diminished in old cells. Thus, the study reinforces the concept that tonic promotion of bioenergetics and Ca2+ signaling function is a reasonable and new paradigm to protect the aging brain cells to prevent AD. Show more

Keywords: Alzheimer's disease, calcium, calpain, energy

DOI: 10.3233/JAD-131001

Citation: Journal of Alzheimer's Disease, vol. 37, no. 4, pp. 835-848, 2013

Authors: Chen, Ming | Maleski, Jerome J. | Sawmiller, Darrell R.

Article Type: Research Article

Abstract: In this paper, we argue that the current official definition for Alzheimer's disease is misleading, since it defines senile dementia (SD), a long-known incurable senile/geriatric condition, as a discrete/curable disease. This overly optimistic definition was incepted in the 1970s amid the public's fear of the upcoming SD crisis and desperate hope for a cure. Scientifically, however, it has overturned Alois Alzheimer's age-based concept for disease classification—the essence of modern Geriatric Medicine and the National Institute of Aging. Thus, the current definition for SD, though socially and politically appealing, would be scientifically flawed. As an authoritative study guideline, it has caused …profound and far-reaching confusions in research by misleading attention to the presumptive pathogenic/erroneous factors as drug targets for “silver bullets”. Such well-intentioned studies would generate numerous data, but render SD a scientific and logical enigma. In this context we discuss: 1) why and how senile conditions including SD differ from discrete diseases by origin, thus also by study paradigm and intervention strategy; 2) why senile conditions may not be explained by abnormal/pathogenic factors, but logically should be explained by “normal” elements in life, perhaps advanced aging plus risk factors; and 3) why the “amyloid-β toxicity” controversy, a simple scientific issue, has lasted for so long. Finally, we ask: can scientific inquiry preserve its integrity and objectivity under social pressure? It appears that these fundamental questions warrant serious attention if the scientific nature of SD is to be eventually understood. Corresponding author: Ming Chen. E-mail: [email protected] Show more

Keywords: Alzheimer's disease, amyloid, aging, tau

DOI: 10.3233/JAD-2010-101638

Citation: Journal of Alzheimer's Disease, vol. 24, no. 1, pp. 3-10, 2011