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The municipal market roundtable brings together authorities from the market's principle regulatory bodies along with industry leaders to discuss key issues of the day, notably the Financial Disclosure Transparency Act, trends in disclosure, pending and potential regulatory rule changes such as the forthcoming GASB standards and MSRB rule G14 on time of trade reporting, and possible legislative changes in light of Congress taking up expiring provisions of the Tax Cuts and Jobs Act of 2017. [ABSTRACT FROM AUTHOR]

Gain-of-function mutations or dysregulated expression of voltage-gated sodium channels can produce neuronal hyperexcitability, leading to acute or chronic pain. The sodium channel [Na.sub.v]1.7 is expressed preferentially in most slowly conducting nociceptive neurons and in sympathetic neurons. Gain-of-function mutations in the [Na.sub.v]1.7 channel lead to DRG neuron hyperexcitability associated with severe pain, whereas loss of the [Na.sub.v]1.7 channel in patients leads to indifference to pain. The contribution of [Na.sub.v]l.7 to acquired and inherited pain states and the absence of motor, cognitive and cardiac deficits in patients lacking this channel make it an attractive target for the treatment of neuropathic pain.

Jeffrey Ruoff, ed. Virtual Voyages: Cinema and Travel. Durham: Duke UP, 2006. xiv + 298 pp. ISBN 0-8223-3713-4, $22.95. Billed as 'the first book of travelogues,' Virtual Voyages examines an [...]

Disease-producing mutations of ion channels are usually characterized as producing hyperexcitability or hypoexcitability. We show here that a single mutation can produce hyperexcitability in one neuronal cell type and hypoexcitability in another neuronal cell type. We studied the functional effects of a mutation of sodium channel [Na.sub.v]1.7 associated with a neuropathic pain syndrome, erythermalgia, within sensory and sympathetic ganglion neurons, two cell types where [Na.sub.v]1.7 is normally expressed. Although this mutation depolarizes resting membrane potential in both types of neurons, it renders sensory neurons hyperexcitable and sympathetic neurons hypoexcitable. The selective presence, in sensory but not sympathetic neurons, of the [Na.sub.v]1.8 channel, which remains available for activation at depolarized membrane potentials, is a major determinant of these opposing effects. These results provide a molecular basis for the sympathetic dysfunction that has been observed in erythermalgia. Moreover, these findings show that a single ion channel mutation can produce opposing phenotypes (hyperexcitability or hypoexcitability) in the different cell types in which the channel is expressed. inherited erythermalgia | neuropathic pain | primary erythromelalgia | sodium channelopathy

Following the loss of myelin from axons in multiple sclerosis, some axons recover the ability to conduct impulses despite the absence of an insulating sheath, providing a basis for remission of clinical deficits, By contrast, other axons degenerate and contribute to non-remitting clinical deficits and, thus, disability, Investigations using laboratory models of multiple sclerosis indicate that altered expression of two distinct isoforms of Na+ channels underlies these two processes, and the study of human tissue reveals similar changes in multiple sclerosis.

Although voltage-gated sodium channels are known to be deployed along experimentally demyelinated axons, the molecular identities of the sodium channels expressed along axons in human demyelinating diseases such as multiple sclerosis (MS) have not been determined. Here we demonstrate changes in the expression of sodium channels in demyelinated axons in MS, with [Na.sub.v]1.6 confined to nodes of Ranvier in controls but with diffuse distribution of [Na.sub.v]1.2 and [Na.sub.v]1.6 along extensive regions of demyelinated axons within acute MS plaques. Using triple-labeled fluorescent immunocytochemistry, we also show that [Na.sub.v]1.6, which is known to produce a persistent sodium current, and the [Na.sup.+]/ [Ca.sup.2+] exchanger, which can be driven by persistent sodium current to import damaging levels of calcium into axons, are colocalized with [beta]-amyloid precursor protein, a marker of axonal injury, in acute MS lesions. Our results demonstrate the molecular identities of the sodium channels expressed along demyelinated and degenerating axons in MS and suggest that coexpression of [Na.sub.v]1.6 and [Na.sup.+]/[Ca.sup.2+] exchanger is associated with axonal degeneration in MS. demyelinating diseases | action potential conduction | axonal degeneration