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7. Safinamide's potential in treating nondystrophic myotonias: Inhibition of skeletal muscle voltage-gated sodium channels and skeletal muscle hyperexcitability in vitro and in vivo

9. A c.1775C > T Point Mutation of Sodium Channel Alfa Subunit Gene (SCN4A) in a Three-Generation Sardinian Family with Sodium Channel Myotonia

12. Immunoglobulin Replacement Therapy: Insights into Multiple Myeloma Management.

13. Effects of Benzothiazolamines on Voltage-Gated Sodium Channels

15. A c.1775C?>?T Point Mutation of Sodium Channel Alfa Subunit Gene (SCN4A) in a Three-Generation Sardinian Family with Sodium Channel Myotonia

16. ECM Composition Differentially Regulates Intracellular and Extracellular pH in Normal and Cancer Pancreatic Duct Epithelial Cells

17. Uptake-Dependent and -Independent Effects of Fibroblasts-Derived Extracellular Vesicles on Bone Marrow Endothelial Cells from Patients with Multiple Myeloma: Therapeutic and Clinical Implications

22. Development of Riluzole Analogs with Improved Use-Dependent Inhibition of Skeletal Muscle Sodium Channels.

29. Corrigendum: Bioisosteric Modification of To042: Synthesis and Evaluation of Promising Use‐Dependent Inhibitors of Voltage‐Gated Sodium Channels

31. The Treatabolome Database and Platform: enhancing Rare Diseases’ treatment visibility

32. Bioisosteric Modification of To042: Synthesis and Evaluation of Promising Use‐Dependent Inhibitors of Voltage‐Gated Sodium Channels

37. Musculoskeletal Features without Ataxia Associated with a Novel de novo Mutation in KCNA1 Impairing the Voltage Sensitivity of Kv1.1 Channel

38. Synthesis and Evaluation of Voltage‐Gated Sodium Channel Blocking Pyrroline Derivatives Endowed with Both Antiarrhythmic and Antioxidant Activities

39. Pathomechanisms of a CLCN1 Mutation Found in a Russian Family Suffering From Becker's Myotonia

40. Synthesis and Evaluation of Voltage‐Gated Sodium Channel Blocking Pyrroline Derivatives Endowed with Both Antiarrhythmic and Antioxidant Activities.

41. The analysis of myotonia congenita mutations discloses functional clusters of amino acids within the CBS2 domain and the C-terminal peptide of the ClC-1 channel

42. Multidisciplinary study of a new CIC‐1 mutation causing myotonia congenita: a paradigm to understand and treat ion channelopathies

44. The analysis of myotonia congenita mutations discloses functional clusters of amino acids within the CBS2 domain and the C-terminal peptide of the ClC-1 channel

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