89 research outputs found

    Involvement of (pro)renin receptor in the glomerular filtration barrier

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    (Pro)renin receptor-bound prorenin not only causes the generation of angiotensin II via the nonproteolytic activation of prorenin, it also activates the receptor’s own intracellular signaling pathways independent of the generated angiotensin II. Within the kidneys, the (pro)renin receptor is not only present in the glomerular mesangium, it is also abundant in podocytes, which play an important role in the maintenance of the glomerular filtration barrier. Recent in vivo studies have demonstrated that the overexpression of the (pro)renin receptor to a degree similar to that observed in hypertensive rat kidneys leads to slowly progressive nephropathy with proteinuria. In addition, the handle region peptide, which acts as a decoy peptide and competitively inhibits the binding of prorenin to the receptor, is more beneficial than an angiotensin-converting enzyme inhibitor with regard to alleviating proteinuria and glomerulosclerosis in experimental animal models of diabetes and essential hypertension. Thus, the (pro)renin receptor may be upregulated in podocytes under hypertensive conditions and may contribute to the breakdown of the glomerular filtration barrier

    Failure mechanisms in alloy of polyamide 6,6/polyphenylene oxide under severe conditions

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    Toughening mechanisms of a polyamide 6,6/polyphenylene oxide alloy containing an elastomer tested under a slow rate, an impact rate, and a low temperature have been investigated using various microscopy techniques. It is found that the toughening mechanisms of the alloy may change from crazing/shear yielding, to crack bridging/crazing, and to transparticle failure, depending on the testing conditions. Except for the low temperature high strain rate testing condition and in the plane stress region of the crack, the crazing mechanism has been observed in all the conditions we studied. When the testing rate is high, the shear yielding mechanism is suppressed; multiple crazing and particle bridging mechanisms appear to dominate.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44700/1/10853_2004_Article_BF00557130.pd

    Network Capacity Reliability Analysis Considering Traffic Regulation after a Major Disaster

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    The focuses of this paper are optimal traffic regulation after a major disaster and evaluation of capacity reliability of a network. The paper firstly discusses the context of traffic regulation and its importance after a major disaster. Then, this problem is formulated as an optimisation program in which the traffic regulator attempts to regulate the amount of traffic movements or access to some areas so as to maximise the traffic volumes in the network while (a) link flows must be less than link capacities and (b) re-routing effect due to changes of traffic condition in the network is allowed. The re-routing behaviour is assumed to follow Probit Stochastic User's Equilibrium (SUE). The paper explains an optimisation algorithm based on an implicit programming approach for solving this problem with the SUE condition. With this optimisation problem, the randomness of the link capacities (to represent random effects of the disaster) is introduced and the paper describes an approach to approximate the capacity reliability of the network using Monte-Carlo simulation. The paper then adopts this approach to evaluate the performances of different traffic regulation policies with a small network and a test network of Kobe city in Japan. Copyright Springer Science + Business Media, LLC 2006Network capacity reliability, Traffic regulation, MPEC and Probit Stochastic User Equilibrium,

    neuronal damage in cultured rat cortical neurons

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    Amyloid beta protein (A beta) is the major component of senile plaques, the pathological hallmark of the neurodegeneration associated with Alzheimer's disease (AD). This study investigated the effect of Toki-shakuyaku-san (TSS), a traditional medicine, on A beta(25-35)-induced neuronal death and lipid peroxidation assessed by measuring lactate dehydrogenase (LDH) and malondialdehyde (NIDA), respectively. A beta(25-35) at 10 mu M induced neuronall damage and increased the LDH and NIDA. TSS at concentrations of 100 and 300 mu g/mL significantly reduced the AP(25-35)-induced neuronal death and the lipid peroxidation. These results suggest that TSS has a protective effect against A beta(25-35)-induced neuronall damage. TSS may be beneficial for the treatment of AD. Copyright (c) 2005 John Wiley & Sons, Ltd
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