Turbulent flow structures induced by an engine intake port

Magdeburg, Univ., Fak. für Verfahrens- und Systemtechnik, Diss., 2009

Management of XML data by means of schema matching

Magdeburg, Univ., Fak. für Informatik, Diss., 2010

Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure

Abstract Background: Tobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti‑inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties. Objective: The present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking. Methods: Wistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%. Results: TS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables. Conclusion: TS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis.

Fractal Dimension in Quantifying Experimental-Pulmonary-Hypertension-Induced Cardiac Dysfunction in Rats

Abstract Background: Right-sided heart failure has high morbidity and mortality, and may be caused by pulmonary arterial hypertension. Fractal dimension is a differentiated and innovative method used in histological evaluations that allows the characterization of irregular and complex structures and the quantification of structural tissue changes. Objective: To assess the use of fractal dimension in cardiomyocytes of rats with monocrotaline-induced pulmonary arterial hypertension, in addition to providing histological and functional analysis. Methods: Male Wistar rats were divided into 2 groups: control (C; n = 8) and monocrotaline-induced pulmonary arterial hypertension (M; n = 8). Five weeks after pulmonary arterial hypertension induction with monocrotaline, echocardiography was performed and the animals were euthanized. The heart was dissected, the ventricles weighed to assess anatomical parameters, and histological slides were prepared and stained with hematoxylin/eosin for fractal dimension analysis, performed using box-counting method. Data normality was tested (Shapiro-Wilk test), and the groups were compared with non-paired Student t test or Mann Whitney test (p < 0.05). Results: Higher fractal dimension values were observed in group M as compared to group C (1.39 ± 0.05 vs. 1.37 ± 0.04; p < 0.05). Echocardiography showed lower pulmonary artery flow velocity, pulmonary acceleration time and ejection time values in group M, suggesting function worsening in those animals. Conclusion: The changes observed confirm pulmonary-arterial-hypertension-induced cardiac dysfunction, and point to fractal dimension as an effective method to evaluate cardiac morphological changes induced by ventricular dysfunction.

Molecular mechanisms of Campylobacter jejuni induced transmigration and invasion of host target cells

Magdeburg, Univ., Fak. für Naturwiss., Diss., 2012

CD95-induced apoptosis in health and disease dimers at the DISC and the effect of c-FLIP R on L. Monocytogenes infection

Magdeburg, Univ., Fak. für Naturwiss., Diss., 2013

Early life stress-induced histone acetylations correlate with activation of the synaptic plasticity genes Arc and Egr1 in the mouse brain

Magdeburg, Univ., Fak. für Naturwiss., Diss., 2013

Genetic influences on long-term memory control : COMT and retrieval-induced forgetting

Magdeburg, Univ., Med. Fak., Diss., 2014

The influence of specific mitochondrial polymorphisms on the α-synuclein-induced pathology in a mouse model of Parkinson's disease

Magdeburg, Univ., Fak. für Naturwiss., Diss., 2015

Dynamic matching and bargaining: the role of deadlines

We consider a dynamic model where traders in each period are matched randomly into pairs who then bargain about the division of a fixed surplus. When agreement is reached the traders leave the market. Traders who do not come to an agreement return next period in which they will be matched again, as long as their deadline has not expired yet. New traders enter exogenously in each period. We assume that traders within a pair know each other's deadline. We define and characterize the stationary equilibrium configurations. Traders with longer deadlines fare better than traders with short deadlines. It is shown that the heterogeneity of deadlines may cause delay. It is then shown that a centralized mechanism that controls the matching protocol, but does not interfere with the bargaining, eliminates all delay. Even though this efficient centralized mechanism is not as good for traders with long deadlines, it is shown that in a model where all traders can choose which mechanism to

Median stable matching for college admission

We give a simple and concise proof that so-called generalized median stable matchings are well-defined stable matchings for college admissions problems. Furthermore, we discuss the fairness properties of median stable matchings and conclude with two illustrative examples of college admissions markets, the lattices of stable matchings, and the corresponding generalized median stable matchings.

Corrigendum to "On randomized matching mechanisms" [Economic Theory 8(1996)377-381]

Ma (1996) studied the random order mechanism, a matching mechanism suggested by Roth and Vande Vate (1990) for marriage markets. By means of an example he showed that the random order mechanism does not always reach all stable matchings. Although Ma's (1996) result is true, we show that the probability distribution he presented - and therefore the proof of his Claim 2 - is not correct. The mistake in the calculations by Ma (1996) is due to the fact that even though the example looks very symmetric, some of the calculations are not as ''symmetric.''

Paths to stability for matching markets with couples

We study two-sided matching markets with couples and show that for a natural preference domain for couples, the domain of weakly responsive preferences, stable outcomes can always be reached by means of decentralized decision making. Starting from an arbitrary matching, we construct a path of matchings obtained from `satisfying' blocking coalitions that yields a stable matching. Hence, we establish a generalization of Roth and Vande Vate's (1990) result on path convergence to stability for decentralized singles markets. Furthermore, we show that when stable matchings exist, but preferences are not weakly responsive, for some initial matchings there may not exist any path obtained from `satisfying' blocking coalitions that yields a stable matching.