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In vitro Studies of Myofibers and Their Use in Analyzing the Differential Dynamics and Properties of α-Actinin IsoformsHsu, Cynthia Pu-Chun 04 June 2015 (has links)
Skeletal muscle is a highly organized tissue that requires cooperation of many different structures and components for proper function. We explored the use of a flexor digitorum brevis (FDB) myofiber culture system to better model highly differentiated aspects of skeletal muscle in an in vitro system. Indirect immunofluorescence of FDB myofibers allowed us to better determine the subcellular localization of KLHL41, a new nemaline myopathy (NM) gene product, to ER-like subdomains of the sarcoplasmic retiuculum. By comparing FDB myofibers from wild type and myotubularin knockout mice with X-linked myotubular myopathy (XLMTM), we were also able to analyze satellite cell populations, showing that the knockout mice suffered a marked decrease in associated myogenic satellite cells. This supports concurrent data from our lab indicating a disease progression-related increase in apoptosis and a decrease in satellite cell proliferation in XLMTM.
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Analysis, Implementation and Enhancement of Vendor dependent and independent Layer-2 Network Topology Discovery / Analyse, Implementierung und Verbesserung von Hersteller abhängigem und unabhängigem Layer-2 Netzwerk Topologie ErkennungBarthel, Alexander 26 May 2005 (has links) (PDF)
This work shows and implements possibilities of OSI Layer-2 Network Topology Discovery based on information from Cisco Discovery Protocol, Spanning Tree Protocol and Switches' Filtering Databases. / Diese Arbeit zeigt und implementiert Möglichkeiten zur OSI Layer-2 Netzwerk Topologie Erkennung basierend auf Informationen des Cisco Discovery Protocol, Spanning Tree Protocol und Switch Filter Datenbanken.
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Regulation of Myoplasmic Ca2+ During Fatigue in KATP Channel Deficient FDB Muscle FibresSelvin, David 23 September 2013 (has links)
It is known that muscles that lack KATP channel activity generate much greater unstimulated [Ca2+]i and force than normal muscles during fatigue. The increase in unstimulated force in KATP channel deficient muscles is abolished by a partial inhibition of L-type Ca2+ channels, suggesting that it is due to a Ca2+ influx through L-type Ca2+ channels and a subsequent increased myoplasmic Ca2+. However, there is also evidence that the increase in resting force is abolished by NAC, a ROS scavenger. The objective of this study was to reconcile these observations by studying the hypothesis that “the increase in resting [Ca2+]i during fatigue in KATP channel deficient muscles starts with an excess Ca2+ influx through L-type Ca2+ channels, followed by an excess ROS production that causes a further increase in resting [Ca2+]i”. To test the hypothesis, single FDB fibres were fatigued with one tetanic contraction/sec for 180 sec. KATP channel deficient fibres were obtained i) by exposing wild type muscle fibers to glibenclamide, a KATP channel blocker and ii) by using fibres from Kir6.2-/- mice, which are null mice for the Kir6.2 gene that encodes for the protein forming the channel pore. Verapamil, a L-type Ca2+ channel blocker, applied at 1 μM, significantly reduced resting [Ca2+]i during fatigue in glibenclamide-exposed wild type fibres. NAC (1 mM) also reduced resting [Ca2+]i in glibenclamide-exposed muscles. The results suggest that the increase in resting [Ca2+]i during fatigue in KATP channel deficient FDB fibres is due to an influx through L-type Ca2+ channels, and an excess ROS production.
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Regulation of Myoplasmic Ca2+ During Fatigue in KATP Channel Deficient FDB Muscle FibresSelvin, David January 2013 (has links)
It is known that muscles that lack KATP channel activity generate much greater unstimulated [Ca2+]i and force than normal muscles during fatigue. The increase in unstimulated force in KATP channel deficient muscles is abolished by a partial inhibition of L-type Ca2+ channels, suggesting that it is due to a Ca2+ influx through L-type Ca2+ channels and a subsequent increased myoplasmic Ca2+. However, there is also evidence that the increase in resting force is abolished by NAC, a ROS scavenger. The objective of this study was to reconcile these observations by studying the hypothesis that “the increase in resting [Ca2+]i during fatigue in KATP channel deficient muscles starts with an excess Ca2+ influx through L-type Ca2+ channels, followed by an excess ROS production that causes a further increase in resting [Ca2+]i”. To test the hypothesis, single FDB fibres were fatigued with one tetanic contraction/sec for 180 sec. KATP channel deficient fibres were obtained i) by exposing wild type muscle fibers to glibenclamide, a KATP channel blocker and ii) by using fibres from Kir6.2-/- mice, which are null mice for the Kir6.2 gene that encodes for the protein forming the channel pore. Verapamil, a L-type Ca2+ channel blocker, applied at 1 μM, significantly reduced resting [Ca2+]i during fatigue in glibenclamide-exposed wild type fibres. NAC (1 mM) also reduced resting [Ca2+]i in glibenclamide-exposed muscles. The results suggest that the increase in resting [Ca2+]i during fatigue in KATP channel deficient FDB fibres is due to an influx through L-type Ca2+ channels, and an excess ROS production.
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Analysis, Implementation and Enhancement of Vendor dependent and independent Layer-2 Network Topology DiscoveryBarthel, Alexander 15 April 2005 (has links)
This work shows and implements possibilities of OSI Layer-2 Network Topology Discovery based on information from Cisco Discovery Protocol, Spanning Tree Protocol and Switches' Filtering Databases. / Diese Arbeit zeigt und implementiert Möglichkeiten zur OSI Layer-2 Netzwerk Topologie Erkennung basierend auf Informationen des Cisco Discovery Protocol, Spanning Tree Protocol und Switch Filter Datenbanken.
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