✦ LIBER ✦

Ca2+Channels as Targets of Neurological Disease: Lambert–Eaton Syndrome and Other Ca2+Channelopathies

✍ Scribed by Michael T. Flink; William D. Atchison

Book ID: 111591575
Publisher: Springer US
Year: 2003
Tongue: English
Weight: 180 KB
Volume: 35
Category: Article
ISSN: 0145-479X
DOI: 10.1023/b:jobb.0000008033.02320.10

No coin nor oath required. For personal study only.

📜 SIMILAR VOLUMES

Sera from Patients with Lambert-Eaton My

Sera from Patients with Lambert-Eaton Myasthenic Syndrome Recognize the β-Subunit of Ca2+ Channel Complexes

✍ MYRNA R. ROSENFELD; ELLEN WONG; JOSEP DALMAU; GEOFF MANLEY; DAVID EGAN; JEROME B 📂 Article 📅 1993 🏛 John Wiley and Sons 🌐 English ⚖ 255 KB

Lambert-Eaton syndrome antibodies inhibi

Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings

✍ Yasushi Satoh; Naohide Hirashima; Hiroshi Tokumaru; Masanori P. Takahashi; Jin K 📂 Article 📅 1998 🏛 Cambridge University Press 🌐 English ⚖ 502 KB

Lambert-eaton myasthenic syndrome: Immun

Lambert-eaton myasthenic syndrome: Immunoglobulin G inhibition of Ca2+ flux in tumor cells correlates with disease severity

✍ B. Lang; A. Vincent; N. M. F. Murray; Dr. J. Newsom-Davis 📂 Article 📅 1989 🏛 John Wiley and Sons 🌐 English ⚖ 653 KB

Lambert-Eaton myasthenic syndrome: Immun

Lambert-Eaton myasthenic syndrome: Immunoglobulin G inhibition of Ca2+ flux in tumor cells correlates with disease severity

📂 Article 📅 1989 🏛 Elsevier Science 🌐 English ⚖ 175 KB

Inhibition of low- and high-threshold Ca

Inhibition of low- and high-threshold Ca2+ channels of human neuroblastoma IMR32 cells by Lambert-Eaton myasthenic syndrome (LEMS) IgGs

✍ Grassi, C.; Magnelli, V.; Carabelli, V.; Sher, E.; Carbone, E. 📂 Article 📅 1994 🏛 Elsevier Science 🌐 English ⚖ 625 KB

Central type Ca2+ channel modulators as

Central type Ca2+ channel modulators as targets for the novel treatment of psychiatric diseases

✍ Yasuo Watanabe 📂 Article 📅 1998 🏛 John Wiley and Sons 🌐 English ⚖ 77 KB 👁 2 views

In order to develop novel central acting drugs, the modulation of intracellular Ca 2 dynamics must be considered as an essential factor, since following excessive Ca 2 in¯ux to neuronal cells, abnormal intracellular Ca 2 concentrations induce several types of mental and neurological disorders. This