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      In Vivo35Cl MR Imaging in Humans: A Feasibility Study

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          Abstract

          To implement chlorine 35 ((35)Cl) magnetic resonance (MR) at a 7-T whole-body MR system and evaluate its feasibility for imaging humans.

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          Most cited references24

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          Selection of a convolution function for Fourier inversion using gridding [computerised tomography application].

          In the technique known as gridding, the data samples are weighted for sampling density and convolved with a finite kernel, then resampled on a grid preparatory to a fast Fourier transform. The authors compare the artifact introduced into the image for various convolving functions of different sizes, including the Kaiser-Bessel window and the zero-order prolate spheroidal wave function (PSWF). They also show a convolving function that improves upon the PSWF in some circumstances.
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            The skeletal muscle chloride channel in dominant and recessive human myotonia.

            Autosomal recessive generalized myotonia (Becker's disease) (GM) and autosomal dominant myotonia congenita (Thomsen's disease) (MC) are characterized by skeletal muscle stiffness that is a result of muscle membrane hyperexcitability. For both diseases, alterations in muscle chloride or sodium currents or both have been observed. A complementary DNA for a human skeletal muscle chloride channel (CLC-1) was cloned, physically localized on chromosome 7, and linked to the T cell receptor beta (TCRB) locus. Tight linkage of these two loci to GM and MC was found in German families. An unusual restriction site in the CLC-1 locus in two GM families identified a mutation associated with that disease, a phenylalanine-to-cysteine substitution in putative transmembrane domain D8. This suggests that different mutations in CLC-1 may cause dominant or recessive myotonia.
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              Ion channels and transporters [corrected] in cancer. 2. Ion channels and the control of cancer cell migration.

              A hallmark of high-grade cancers is the ability of malignant cells to invade unaffected tissue and spread disease. This is particularly apparent in gliomas, the most common and lethal type of primary brain cancer affecting adults. Migrating cells encounter restricted spaces and appear able to adjust their shape to accommodate to narrow extracellular spaces. A growing body of work suggests that cell migration/invasion is facilitated by ion channels and transporters. The emerging concept is that K(+) and Cl(-) function as osmotically active ions, which cross the plasma membrane in concert with obligated water thereby adjusting a cell's shape and volume. In glioma cells Na(+)-K(+)-Cl(-) cotransporters (NKCC1) actively accumulate K(+) and Cl(-), establishing a gradient for KCl efflux. Ca(2+)-activated K(+) channels and voltage-gated Cl(-) channels are largely responsible for effluxing KCl promoting hydrodynamic volume changes. In other cancers, different K(+) or even Na(+) channels may function in concert with a variety of Cl(-) channels to support similar volume changes. Channels involved in migration are frequently regulated by Ca(2+) signaling, most likely coupling extracellular stimuli to cell migration. Importantly, the inhibition of ion channels and transporters appears to be clinically relevant for the treatment of cancer. Recent preclinical data indicates that inhibition of NKCC1 with an FDA-approved drug decreases neoplastic migration. Additionally, ongoing clinical trials demonstrate that an inhibitor of chloride channels may be a therapy for the treatment of gliomas. Data reviewed here strongly indicate that ion channels are a promising target for the development of novel therapeutics to combat cancer.
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                Author and article information

                Journal
                Radiology
                Radiology
                Radiological Society of North America (RSNA)
                0033-8419
                1527-1315
                May 2014
                May 2014
                : 271
                : 2
                : 585-595
                Article
                10.1148/radiol.13131725
                24495267
                098a084e-d135-42ea-9cde-6737edb6cf16
                © 2014
                History

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