A life without pain? Hedonists take note

Young, Frances

doi:10.1111/j.1399-0004.2007.00921.x

Cited by 8 publications

(8 citation statements)

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“…Given the intense interest in human Na v 1.7 as a target for pain (4)(5)(6)(7)15) and growing interest in clinical applications of guanidinium toxins as antinociceptive agents (16)(17)(18)(19)(20)(21)(22)(23), we began a series of electrophysiology recordings with TTX, STX, and gonyautoxin-III (GTX-III) against recombinant hNa v 1.7 α-subunit expressed in CHO cells. For comparative purposes, an identical series of measurements was made using rat Na v 1.4 (CHO).…”

Section: Resultsmentioning

confidence: 99%

Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na _v 1.7)

Walker¹,

Novick²,

Parsons³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

102

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Human nociceptive voltage-gated sodium channel (Na v 1.7), a target of significant interest for the development of antinociceptive agents, is blocked by low nanomolar concentrations of (−)-tetrodotoxin(TTX) but not (+)-saxitoxin (STX) and (+)-gonyautoxin-III (GTX-III). These findings question the long-accepted view that the 1.7 isoform is both tetrodotoxin– and saxitoxin-sensitive and identify the outer pore region of the channel as a possible target for the design of Na v 1.7-selective inhibitors. Single- and double-point amino acid mutagenesis studies along with whole-cell electrophysiology recordings establish two domain III residues (T1398 and I1399), which occur as methionine and aspartate in other Na v isoforms, as critical determinants of STX and gonyautoxin-III binding affinity. An advanced homology model of the Na v pore region is used to provide a structural rationalization for these surprising results.

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Section: Resultsmentioning

confidence: 99%

Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na _v 1.7)

Walker¹,

Novick²,

Parsons³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

102

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“…Young insists on the compatibility between deliberative democracy and guarantees of group representation. 40 But if women fail to gain respect for their methods of articulation, or if the very deliberation of the issues they wish to raise is placed in question, then group representation becomes essential. As Jane Mansbridge points out, it is precisely in situations marked by histories of distrust and where interests are uncrystallized that descriptive representation matters.…”

Section: New Democratic Spacesmentioning

confidence: 99%

Democratizing democracy: Feminist perspectives

Cornwall

Goetz

2005

Democratization

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Increasing numbers of women have gained entry into the arena of representative politics in recent times. Yet the extent to which shifts in the sex ratio within formal democratic spaces translates into political influence, and into gains in policies that redress gendered inequities and inequalities remains uncertain. At the same time, a plethora of new democratic spaces have been created -whether through the promotion of 'civil society organizations' or the institutionalization of participatory governance mechanisms -which hold the prospect of democratizing other political spaces beyond those of formal politics. This study examines factors that constrain and enable women's political effectiveness in these different democratic arenas. We suggest that 'engendering democracy' by adding women or multiplying democratic spaces is necessary but not sufficient to address historically and culturally embedded forms of disadvantage that have been the focus for feminist politics. We suggest that an important, but neglected, determinant of political effectiveness is women's political apprenticeshiptheir experiences in political parties, civil society associations and the informal arenas in which political skills are learned and constituencies built. Enhancing the democratizing potential of women's political participation calls, we argue, for democratizing democracy itself: building new pathways into politics, fostering political learning and creating new forms of articulation across and beyond existing democratic spaces.

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“…The genetic basis of this disorder also lies in the mutations of the SCN9A gene [2]. Some of these mutations are S459X, I767X, W897X, M899I, and M932L [10,[26][27][28]. Research conducted by Yuan et al included the analysis of the sequences of the candidate genes.…”

Section: Congenital Analgesia and Mutations On Scn9a Genementioning

confidence: 99%

Mutations in Sodium Channel Gene SCN9A and the Pain Perception Disorders

Marković

Janković

Veselinović

2015

Advances in Anesthesiology

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Voltage-gated sodium channels (NaV) play a crucial role in development and propagation of action potentials in neurons and muscle cells. NaV1.7 channels take a special place in modern science since it is believed that they contribute to nerve hyperexcitability. Mutations of the gene SCN9A, which codes theαsubunit of NaV1.7 channels, are associated with pain perception disorders (primary erythermalgia, congenital analgesia, and paroxysmal pain disorder). It is considered that the SCN9A gene mutations may cause variations in sensitivity to pain, from complete insensitivity to extreme sensitivity. Further research of the SCN9A gene polymorphism influence on pain sensitivity is essential for the understanding of the pathophysiology of pain and the development of the appropriate targeted pain treatment.

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A life without pain? Hedonists take note

Cited by 8 publications

References 0 publications

Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na _v 1.7)

Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na _v 1.7)

Democratizing democracy: Feminist perspectives

Mutations in Sodium Channel Gene SCN9A and the Pain Perception Disorders

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A life without pain? Hedonists take note

Cited by 8 publications

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Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na v 1.7)

Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na v 1.7)

Democratizing democracy: Feminist perspectives

Mutations in Sodium Channel Gene SCN9A and the Pain Perception Disorders

Contact Info

Product

Resources

About

Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na _v 1.7)

Marked difference in saxitoxin and tetrodotoxin affinity for the human nociceptive voltage-gated sodium channel (Na _v 1.7)