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      Skeletal Muscle Metabolic Dysfunction in Patients With Malignant Hyperthermia Susceptibility :

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          Java-based graphical user interface for MRUI, a software package for quantitation of in vivo/medical magnetic resonance spectroscopy signals.

          This article describes a Java-based graphical user interface for the magnetic resonance user interface (MRUI) quantitation package. This package allows MR spectroscopists to easily perform time-domain analysis of in vivo/medical MR spectroscopy data. We have found that the Java programming language is very well suited for developing highly interactive graphical software applications such as the MRUI system. We also have established that MR quantitation algorithms, programmed in the past in other languages, can easily be embedded into the Java-based MRUI by using the Java native interface (JNI).
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            Stac3 is a component of the excitation-contraction coupling machinery and mutated in Native American myopathy

            Excitation-contraction coupling, the process that regulates contractions by skeletal muscles, transduces changes in membrane voltage by activating release of Ca2+ from internal stores to initiate muscle contraction. Defects in EC coupling are associated with muscle diseases. Here we identify Stac3 as a novel component of the EC coupling machinery. Using a zebrafish genetic screen, we generate a locomotor mutation that is mapped to stac3. We provide electrophysiological, Ca2+ imaging, immunocytochemical and biochemical evidence that Stac3 participates in excitation-contraction coupling in muscles. Furthermore, we reveal that a mutation in human STAC3 as the genetic basis of the debilitating Native American myopathy (NAM). Analysis of NAM stac3 in zebrafish shows that the NAM mutation decreases excitation-contraction coupling. These findings enhance our understanding of both excitation-contraction coupling and the pathology of myopathies.
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              Calcium and mitochondrial reactive oxygen species generation: how to read the facts.

              A number of recent discoveries indicate that abnormal Ca2+ signaling, oxidative stress, and mitochondrial dysfunction are involved in the neuronal damage in Alzheimer's disease. However, the literature on the interactions between these factors is controversial especially in the interpretation of the cause-effect relationship between mitochondrial damage induced by Ca2+ overload and the production of reactive oxygen species (ROS). In this review, we survey the experimental observations on the Ca2+-induced mitochondrial ROS production, explain the sources of controversy in interpreting these results, and discuss the different molecular mechanisms underlying the effect of Ca2+ on the ROS emission by brain mitochondria.
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                Author and article information

                Journal
                Anesthesia & Analgesia
                Anesthesia & Analgesia
                Ovid Technologies (Wolters Kluwer Health)
                0003-2999
                2017
                August 2017
                : 125
                : 2
                : 434-441
                Article
                10.1213/ANE.0000000000002232
                28682948
                885f4b8a-0f21-4e26-9096-278bf8346b2d
                © 2017
                History

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