GING WANG

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Cocaine-induced closures of single batrachotoxin-activated Na+ channels in planar lipid bilayers
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115
    J Gen Physiol 92:747-65. 1988
  2. pmc Block of inactivation-deficient Na+ channels by local anesthetics in stably transfected mammalian cells: evidence for drug binding along the activation pathway
    Sho Ya Wang
    Department of Biology, State University of New York at Albany, NY 12222, USA
    J Gen Physiol 124:691-701. 2004
  3. ncbi request reprint Modification of wild-type and batrachotoxin-resistant muscle mu1 Na+ channels by veratridine
    G K Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, Boston, MA 02115, USA
    Pflugers Arch 439:705-13. 2000
  4. pmc Residues in Na(+) channel D3-S6 segment modulate both batrachotoxin and local anesthetic affinities
    S Y Wang
    Department of Biology, State University of New York, Albany, New York 12222, USA
    Biophys J 79:1379-87. 2000
  5. ncbi request reprint Structure-activity relation of N-alkyl tetracaine derivatives as neurolytic agents for sciatic nerve lesions
    G K Wang
    Department of Anesthesia, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Anesthesiology 88:417-28. 1998
  6. ncbi request reprint Voltage-gated sodium channels as primary targets of diverse lipid-soluble neurotoxins
    Sho Ya Wang
    Department of Biology, State University of New York at Albany, Albany, NY 12222, USA
    Cell Signal 15:151-9. 2003
  7. pmc A mutation in segment I-S6 alters slow inactivation of sodium channels
    S Y Wang
    Department of Biological Sciences, State University of New York at Albany 12222, USA
    Biophys J 72:1633-40. 1997
  8. ncbi request reprint N-butyl tetracaine as a neurolytic agent for ultralong sciatic nerve block
    G K Wang
    Department of Anesthesia, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Anesthesiology 85:1386-94. 1996
  9. doi request reprint Block of persistent late Na+ currents by antidepressant sertraline and paroxetine
    Ging Kuo Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    J Membr Biol 222:79-90. 2008
  10. pmc State-dependent block of wild-type and inactivation-deficient Na+ channels by flecainide
    Ging Kuo Wang
    Department of Anesthesia, Brigham and Women s Hospital, 75 Francis St, Boston, MA 02115, USA
    J Gen Physiol 122:365-74. 2003

Detail Information

Publications52

  1. pmc Cocaine-induced closures of single batrachotoxin-activated Na+ channels in planar lipid bilayers
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115
    J Gen Physiol 92:747-65. 1988
    ..A direct interaction between the receptor and Na+ ions seems minimal...
  2. pmc Block of inactivation-deficient Na+ channels by local anesthetics in stably transfected mammalian cells: evidence for drug binding along the activation pathway
    Sho Ya Wang
    Department of Biology, State University of New York at Albany, NY 12222, USA
    J Gen Physiol 124:691-701. 2004
    ..Our data together illustrate that the Na(+) channel activation pathway, including most, if not all, transient intermediate closed states and the final open state, promotes high-affinity LA binding...
  3. ncbi request reprint Modification of wild-type and batrachotoxin-resistant muscle mu1 Na+ channels by veratridine
    G K Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, Boston, MA 02115, USA
    Pflugers Arch 439:705-13. 2000
    ..The failure of BTX-resistant mutant Na+ channels to trap VTD suggests that segments of D1-S6 and D4-S6 form a common receptor for VTD and BTX...
  4. pmc Residues in Na(+) channel D3-S6 segment modulate both batrachotoxin and local anesthetic affinities
    S Y Wang
    Department of Biology, State University of New York, Albany, New York 12222, USA
    Biophys J 79:1379-87. 2000
    ..Implications of this state-dependent binding model for the S6 alignment are discussed...
  5. ncbi request reprint Structure-activity relation of N-alkyl tetracaine derivatives as neurolytic agents for sciatic nerve lesions
    G K Wang
    Department of Anesthesia, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Anesthesiology 88:417-28. 1998
    ..This study aimed to elucidate the structure-activity relation of various tetracaine derivatives to design better neurolytic agents...
  6. ncbi request reprint Voltage-gated sodium channels as primary targets of diverse lipid-soluble neurotoxins
    Sho Ya Wang
    Department of Biology, State University of New York at Albany, Albany, NY 12222, USA
    Cell Signal 15:151-9. 2003
    ....
  7. pmc A mutation in segment I-S6 alters slow inactivation of sodium channels
    S Y Wang
    Department of Biological Sciences, State University of New York at Albany 12222, USA
    Biophys J 72:1633-40. 1997
    ..These findings together demonstrate that N434 of mu1 Na+ channels is also critical for slow inactivation. We propose that this slow form of Na+ channel inactivation is analogous to the "C-type" inactivation in Shaker K+ channels...
  8. ncbi request reprint N-butyl tetracaine as a neurolytic agent for ultralong sciatic nerve block
    G K Wang
    Department of Anesthesia, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Anesthesiology 85:1386-94. 1996
    ..Studies with such a compound may lead to the design of neurolytic agents that are more effective and more easily administered than phenol and alcohol...
  9. doi request reprint Block of persistent late Na+ currents by antidepressant sertraline and paroxetine
    Ging Kuo Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    J Membr Biol 222:79-90. 2008
    ..Thus, sertraline and paroxetine are potent open channel blockers that target persistent late Na+ currents preferentially, but their block is not mediated via the phenylalanine residue at the known LA/TCA receptor site...
  10. pmc State-dependent block of wild-type and inactivation-deficient Na+ channels by flecainide
    Ging Kuo Wang
    Department of Anesthesia, Brigham and Women s Hospital, 75 Francis St, Boston, MA 02115, USA
    J Gen Physiol 122:365-74. 2003
    ..We conclude that flecainide directly blocks persistent late Na+ currents with a high affinity. The fast-inactivation gate, probably via its S6 docking site, may further stabilize the flecainide-receptor complex in wild-type Na+ channels...
  11. pmc Mexiletine block of wild-type and inactivation-deficient human skeletal muscle hNav1.4 Na+ channels
    Ging Kuo Wang
    Department of Anaesthesia, Harvard Medical School and Brigham and Women s Hospital, Boston, MA, USA
    J Physiol 554:621-33. 2004
    ..Our results together support the hypothesis that the in vivo efficacy of mexiletine is primarily due to the open-channel block of persistent late Na(+) currents, which may arise during various pathological conditions...
  12. ncbi request reprint State-dependent block of voltage-gated Na+ channels by amitriptyline via the local anesthetic receptor and its implication for neuropathic pain
    Ging Kuo Wang
    Department of Anesthesia, Brigham and Women s Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    Pain 110:166-74. 2004
    ....
  13. pmc State- and use-dependent block of muscle Nav1.4 and neuronal Nav1.7 voltage-gated Na+ channel isoforms by ranolazine
    Ging Kuo Wang
    Department of Anesthesia, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Mol Pharmacol 73:940-8. 2008
    ....
  14. pmc Bulleyaconitine A isolated from aconitum plant displays long-acting local anesthetic properties in vitro and in vivo
    Chi Fei Wang
    Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Anesthesiology 107:82-90. 2007
    ..Bulleyaconitine A (BLA) is an active ingredient of Aconitum bulleyanum plants. BLA has been approved for the treatment of chronic pain and rheumatoid arthritis in China, but its underlying mechanism remains unclear...
  15. pmc Time-dependent block and resurgent tail currents induced by mouse beta4(154-167) peptide in cardiac Na+ channels
    Ging Kuo Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, Boston, MA 02115, USA
    J Gen Physiol 127:277-89. 2006
    ....
  16. ncbi request reprint Block of inactivation-deficient cardiac Na(+) channels by acetyl-KIFMK-amide
    Sho Ya Wang
    Department of Biology, State University of New York at Albany, Albany, NY, USA
    Biochem Biophys Res Commun 329:780-8. 2005
    ..Competition experiments showed that acetyl-KIFMK-amide antagonized bupivacaine binding. These results are consistent with a model that two acetyl-KIFMK-amide receptors exist in proximity within the Na(+) channel inner cavity...
  17. pmc Veratridine block of rat skeletal muscle Nav1.4 sodium channels in the inner vestibule
    Ging Kuo Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, Boston, MA, USA
    J Physiol 548:667-75. 2003
    ..We propose that VTD likewise blocks the wild-type open Na+ channel, albeit partially, to decrease the unitary conductance and to stabilize the open conformation for persistent opening...
  18. ncbi request reprint Inactivation-deficient human skeletal muscle Na+ channels (hNav1.4-L443C/A444W) in stably transfected HEK-293 cells
    S Y Wang
    Department of Biology, State University of New York at Albany, Albany, NY, USA
    Receptors Channels 10:131-8. 2004
    ..Stably transfected HEK-293 cells expressing robust inactivation-deficient Na+currents will likely be suitable for screening novel drugs that target persistent late Na+currents selectively...
  19. pmc Point mutations in segment I-S6 render voltage-gated Na+ channels resistant to batrachotoxin
    S Y Wang
    Department of Biological Sciences, State University of New York, Albany, NY 12222, USA
    Proc Natl Acad Sci U S A 95:2653-8. 1998
    ..We propose that the mu1-I433, mu1-N434, and mu1-L437 residues in transmembrane segment I-S6 probably form a part of the BTX receptor...
  20. pmc State-dependent cocaine block of sodium channel isoforms, chimeras, and channels coexpressed with the beta1 subunit
    S N Wright
    Department of Anesthesia Research Laboratories, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115
    Biophys J 76:233-45. 1999
    ..These data, as well as simulations used to predict block, indicate that state-dependent cocaine block depends on both steady-state inactivation and channel activation, although inactivation appears to have the predominant role...
  21. pmc Batrachotoxin-resistant Na+ channels derived from point mutations in transmembrane segment D4-S6
    S Y Wang
    Department of Biological Sciences, State University of New York at Albany, Albany, New York 12222, USA
    Biophys J 76:3141-9. 1999
    ..These two S6 segments may appose too closely to bind BTX and LAs simultaneously when the channel is in its resting closed state...
  22. ncbi request reprint Lysine point mutations in Na+ channel D4-S6 reduce inactivated channel block by local anesthetics
    S N Wright
    Department of Anesthesia Research Laboratories, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Mol Pharmacol 54:733-9. 1998
    ....
  23. ncbi request reprint Point mutations in alpha-subunit of human cardiac Na+ channels alter Na+ current kinetics
    Y F Xiao
    Charles A Dana Research Institute and Harvard Thorndike Laboratory, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
    Biochem Biophys Res Commun 281:45-52. 2001
    ..The effects of PUFAs on these mutant channels will be the subject of subsequent reports...
  24. ncbi request reprint Methanethiosulfonate-modification alters local anesthetic block in rNav1.4 cysteine-substituted mutants S1276C and L1280C
    J P O'Reilly
    Department of Anesthesia Research, Brigham and Women s Hospital, Harvard Medical School, 75 Francis St, Boston, MA 02115, USA
    J Membr Biol 193:47-55. 2003
    ..4 that produces an allosteric, indirect effect on bupivacaine affinity...
  25. ncbi request reprint Disparate role of Na(+) channel D2-S6 residues in batrachotoxin and local anesthetic action
    S Y Wang
    Department of Biology, State University of New York at Albany, Albany, New York, USA
    Mol Pharmacol 59:1100-7. 2001
    ....
  26. ncbi request reprint Slow inactivation of muscle mu1 Na+ channels in permanently transfected mammalian cells
    S Wang
    Department of Biology, State University of New York at Albany, Albany, NY 12222, USA
    Pflugers Arch 432:692-9. 1996
    ..These results together suggest that slow inactivation takes place in the alpha-subunit of mu1 muscle Na+ channels and is governed by a microliter protein region different from that governing fast inactivation...
  27. ncbi request reprint A phenylalanine residue at segment D3-S6 in Nav1.4 voltage-gated Na(+) channels is critical for pyrethroid action
    S Y Wang
    Department of Biological Sciences, State University of New York at Albany, New York, USA
    Mol Pharmacol 60:620-8. 2001
    ..Evidently, distinct residues from multiple S6 segments were critical for deltamethrin and BTX actions...
  28. pmc pH-dependent binding of local anesthetics in single batrachotoxin-activated Na+ channels. Cocaine vs. quaternary compounds
    J Nettleton
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts 02115
    Biophys J 58:95-106. 1990
    ..Our findings support a model in which neutral cocaine can readily cross the membrane barrier, but needs to be protonated internally to bind to its binding site...
  29. ncbi request reprint Block of single batrachotoxin-activated Na+ channels by clofilium
    J Nettleton
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts
    Mol Pharmacol 39:352-8. 1991
    ..Together, our results demonstrate that clofilium is a potent Na+ channel blocker in bilayers and its action is similar to that of other local anesthetics characterized previously...
  30. ncbi request reprint Point mutations at N434 in D1-S6 of mu1 Na(+) channels modulate binding affinity and stereoselectivity of local anesthetic enantiomers
    C Nau
    Department of Anesthesia Research Laboratories, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    Mol Pharmacol 56:404-13. 1999
    ..We propose that in inactivated channels, residue mu1-N434 interacts directly with the positively charged moiety of LAs and that D1-S6 and D4-S6 form a domain-interface site for binding of BTX and LAs in close proximity...
  31. ncbi request reprint Local anesthetic block of batrachotoxin-resistant muscle Na+ channels
    G K Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Mol Pharmacol 54:389-96. 1998
    ..We surmise that the BTX receptor and the LA receptor within segments I-S6 and IV-S6, respectively, may align near or within the Na+ permeation pathway...
  32. ncbi request reprint State-dependent block of human cardiac hNav1.5 sodium channels by propafenone
    T Edrich
    Cellular Electrophysiology Laboratory, Department of Anesthesia, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Membr Biol 207:35-43. 2005
    ..This occurs approximately 4000 and 700 times faster than the binding to the resting and inactivated state, respectively. An established mathematical "gating" model was modified to represent the experimental data...
  33. pmc Altered stereoselectivity of cocaine and bupivacaine isomers in normal and batrachotoxin-modified Na+ channels
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts 02115
    J Gen Physiol 100:1003-20. 1992
    ..The last finding may explain why most LA drugs were reported to be less effective toward BTX-modified Na+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)..
  34. pmc Charged tetracaine as an inactivation enhancer in batrachotoxin-modified Na+ channels
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts
    Biophys J 67:1851-60. 1994
    ....
  35. pmc Binding of benzocaine in batrachotoxin-modified Na+ channels. State-dependent interactions
    G K Wang
    Department of Anesthesia, Harvard Medical School, Boston, Massachusetts 02115
    J Gen Physiol 103:501-18. 1994
    ..This compound also elicits a use-dependent block in unmodified Na+ channels after repetitive depolarizations, whereas benzocaine does not. The implications of these findings for the MRH theory will be discussed...
  36. pmc Inactivation of batrachotoxin-modified Na+ channels in GH3 cells. Characterization and pharmacological modification
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts
    J Gen Physiol 99:1-20. 1992
    ..1 at -70 mV, indicating that benzocaine binds preferentially with inactivated, BTX-modified Na+ channels. Together, these results imply that BTX-modified Na+ channels are governed by an inactivation process...
  37. ncbi request reprint Modifications of human cardiac sodium channel gating by UVA light
    G K Wang
    Department of Anesthesia, Harvard Medical School and Brigham and Women s Hospital, 75 Francis St, Boston, MA 02115, USA
    J Membr Biol 189:153-65. 2002
    ..The potential link between oxidative stress and the impaired Na(+) channel gating may provide valuable clues for ischemia/reperfusion injury in heart and in CNS...
  38. pmc Binding affinity and stereoselectivity of local anesthetics in single batrachotoxin-activated Na+ channels
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts
    J Gen Physiol 96:1105-27. 1990
    ..Possible explanations for this difference are discussed...
  39. pmc Differences in steady-state inactivation between Na channel isoforms affect local anesthetic binding affinity
    S N Wright
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts, USA
    Biophys J 73:779-88. 1997
    ..e., high-affinity) state...
  40. ncbi request reprint Local anesthetic properties of prenylamine
    M G Mujtaba
    Department of Anesthesia Research Laboratories, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Anesthesiology 95:1198-204. 2001
    ..Prenylamine is a known calcium channel blocker, but its local anesthetic blocking effects on voltage-gated sodium channels have not been studied thus far...
  41. pmc Comparison of slow inactivation in human heart and rat skeletal muscle Na+ channel chimaeras
    J P O'Reilly
    Department of Anesthesia, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Physiol 515:61-73. 1999
    ..The results also support previous conclusions that D3 and D4 (and the D3-D4 linker) play an important role in Na+ channel fast inactivation, and that activation may require non-equivalent contributions from all four domains...
  42. ncbi request reprint Coexpression with beta(1)-subunit modifies the kinetics and fatty acid block of hH1(alpha) Na(+) channels
    Y F Xiao
    Charles A Dana Research Institute and Harvard Thorndike Laboratory, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Am J Physiol Heart Circ Physiol 279:H35-46. 2000
    ..Our data demonstrate that functional association of beta(1)-subunit with hH1(alpha) modifies the kinetics and fatty acid block of the Na(+) channel...
  43. ncbi request reprint A common local anesthetic receptor for benzocaine and etidocaine in voltage-gated mu1 Na+ channels
    G K Wang
    Department of Anesthesia, Brigham and Women s Hospital, 75 Francis St Boston, MA 02115, USA
    Pflugers Arch 435:293-302. 1998
    ..We hypothesize that an increase in accessibility of external QX-314 to the mu1-I1575A mutant is accompanied by a reduction of binding towards the charged amine component...
  44. ncbi request reprint Spinal tonicaine: potency and differential blockade of sensory and motor functions
    P Gerner
    Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Anesthesiology 92:1350-60. 2000
    ..The purposes of this study were to measure directly the potency of this charged drug by internal perfusion of cultured neuronal cells, and to evaluate the differential blockade of sensory versus motor function via spinal route in rats...
  45. ncbi request reprint Amitriptyline versus bupivacaine in rat sciatic nerve blockade
    P Gerner
    Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Anesthesiology 94:661-7. 2001
    ..To date there is no report of amitriptyline producing peripheral nerve blockade. The authors therefore investigated the local anesthetic properties of amitriptyline in rats and in vitro...
  46. pmc Residue-specific effects on slow inactivation at V787 in D2-S6 of Na(v)1.4 sodium channels
    J P O'Reilly
    Department of Anesthesia Research, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Biophys J 81:2100-11. 2001
    ..Our results suggest that the V787 position in Na(v)1.4 plays an important role in slow inactivation gating and that molecular rearrangement occurs at or near residue V787 in D2-S6 during NaCh slow inactivation...
  47. pmc A point mutation in domain 4-segment 6 of the skeletal muscle sodium channel produces an atypical inactivation state
    J P O'Reilly
    Department of Anesthesia Research, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Biophys J 78:773-84. 2000
    ....
  48. pmc Irreversible inhibition of sodium current and batrachotoxin binding by a photoaffinity-derivatized local anesthetic
    J McHugh
    Anesthesia Research Laboratories, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Gen Physiol 105:267-87. 1995
    ....
  49. pmc Single point mutations affect fatty acid block of human myocardial sodium channel alpha subunit Na+ channels
    Y F Xiao
    The Charles A. Dana Research Institute and Harvard-Thorndike Laboratory, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Proc Natl Acad Sci U S A 98:3606-11. 2001
    ..Therefore, asparagine at the 406 site in hH1(alpha) may be important for the inhibition by the PUFAs of cardiac voltage-gated Na(+) currents, which play a significant role in the antiarrhythmic actions of PUFAs...
  50. ncbi request reprint Modification of cloned brain Na+ channels by batrachotoxin
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, MA
    Pflugers Arch 427:309-16. 1994
    ..Unexpectedly, steady-state inactivation of BTX-modified NaIIA channels was minimal as measured by the two-pulse protocol, a phenomenon distinctly different from that found in GH3 cells.(ABSTRACT TRUNCATED AT 250 WORDS)..
  51. pmc Quaternary ammonium compounds as structural probes of single batrachotoxin-activated Na+ channels
    G K Wang
    Department of Anesthesia, Harvard Medical School, Boston, Massachusetts
    J Gen Physiol 98:1005-24. 1991
    ..We conclude that amphipathic QA compounds are valuable structural probes to study the permeation pathway of both normal and BTX-activated Na+ channels...
  52. ncbi request reprint Structural determinants of quaternary ammonium blockers for batrachotoxin-modified Na+ channels
    G K Wang
    Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts
    Mol Pharmacol 44:667-76. 1993
    ..These results from GH3 cells mirror those obtained with QA blockers in K+ channels of squid axons and suggest that the QA binding domains in BTX-modified Na+ channels and K+ channels may be structurally conserved...

Research Grants2

  1. THERAPEUTIC NA+ CHANNEL BLOCKERS: RECEPTOR & DRUG DESIGN
    GING WANG; Fiscal Year: 2007
    ..Such drugs, either taken orally or injected locally, may be beneficial for patients with chronic and intractable cancer pain. ..
  2. MOLECULAR BASIS OF LIGAND/SODIUM CHANNEL INTERACTIONS
    GING WANG; Fiscal Year: 2002
    ....