Jos J. Eggermont
- Published in print:
- 2012
- Published Online:
- September 2012
- ISBN:
- 9780199605606
- eISBN:
- 9780191741555
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780199605606.003.0011
- Subject:
- Neuroscience, Sensory and Motor Systems, Development
The scenario of hyperactivity and hypersynchrony suggests that central gain change alone can account for both hyperacusis and tinnitus. The finding that in patients with a primary complaint of ...
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The scenario of hyperactivity and hypersynchrony suggests that central gain change alone can account for both hyperacusis and tinnitus. The finding that in patients with a primary complaint of hyperacusis the prevalence of tinnitus is about 86% supports this. However in patients attending tinnitus clinics with a primary complaint of tinnitus the prevalence of hyperacusis is only about 40%. This suggests a strong link with hyperacusis only for a particular subset of tinnitus patients and it is tempting to suggest that in that group hyperacusis is causal to the tinnitus. More detailed typing of tinnitus etiology is obviously needed to find the reasons why there are so many more patients with tinnitus without accompanying hyperacusis.Less
The scenario of hyperactivity and hypersynchrony suggests that central gain change alone can account for both hyperacusis and tinnitus. The finding that in patients with a primary complaint of hyperacusis the prevalence of tinnitus is about 86% supports this. However in patients attending tinnitus clinics with a primary complaint of tinnitus the prevalence of hyperacusis is only about 40%. This suggests a strong link with hyperacusis only for a particular subset of tinnitus patients and it is tempting to suggest that in that group hyperacusis is causal to the tinnitus. More detailed typing of tinnitus etiology is obviously needed to find the reasons why there are so many more patients with tinnitus without accompanying hyperacusis.
Jerome O. Nriagu and Eric P. Skaar (eds)
- Published in print:
- 2015
- Published Online:
- May 2016
- ISBN:
- 9780262029193
- eISBN:
- 9780262327619
- Item type:
- book
- Publisher:
- The MIT Press
- DOI:
- 10.7551/mitpress/9780262029193.001.0001
- Subject:
- Public Health and Epidemiology, Public Health
Many parts of the world endemic for the most common infectious diseases have the highest prevalence rates of trace metal deficiencies and increasing rates of trace metal pollution. The co-clustering ...
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Many parts of the world endemic for the most common infectious diseases have the highest prevalence rates of trace metal deficiencies and increasing rates of trace metal pollution. The co-clustering of major infectious diseases with trace metal deficiency or toxicity has created a complex web of interactions with serious but poorly understood health repercussions. Infectious diseases can increase human susceptibility to adverse effects of metal exposure while metal excess or deficiency can increase the incidence or severity of infectious diseases. The combined effects of exposure to metals and pathogens on the burden of disease and the mechanisms of interactions between trace metals, pathogens, and the environment have largely been overlooked in animal and human studies. Drawing on expertise from several fields, this book focuses on the distribution, trafficking, fate, and effects of trace metals in biological systems, with the goal of enhancing our understanding of the relationships between homeostatic mechanisms of trace metals and the pathogenesis of infectious diseases. It provides a comprehensive review of current knowledge on vertebrate metal-withholding mechanisms and the strategies employed by different microbes to compete for metals to avoid starvation (or poisoning). State-of-the-art analytical techniques available to investigate pathogen-metal interactions are summarized and open questions highlighted to guide future research. Improving knowledge in these areas will be instrumental to the generation of novel therapeutic countermeasures against infectious diseases.Less
Many parts of the world endemic for the most common infectious diseases have the highest prevalence rates of trace metal deficiencies and increasing rates of trace metal pollution. The co-clustering of major infectious diseases with trace metal deficiency or toxicity has created a complex web of interactions with serious but poorly understood health repercussions. Infectious diseases can increase human susceptibility to adverse effects of metal exposure while metal excess or deficiency can increase the incidence or severity of infectious diseases. The combined effects of exposure to metals and pathogens on the burden of disease and the mechanisms of interactions between trace metals, pathogens, and the environment have largely been overlooked in animal and human studies. Drawing on expertise from several fields, this book focuses on the distribution, trafficking, fate, and effects of trace metals in biological systems, with the goal of enhancing our understanding of the relationships between homeostatic mechanisms of trace metals and the pathogenesis of infectious diseases. It provides a comprehensive review of current knowledge on vertebrate metal-withholding mechanisms and the strategies employed by different microbes to compete for metals to avoid starvation (or poisoning). State-of-the-art analytical techniques available to investigate pathogen-metal interactions are summarized and open questions highlighted to guide future research. Improving knowledge in these areas will be instrumental to the generation of novel therapeutic countermeasures against infectious diseases.
Y. Pichon, N. Joan Abbott, E. R. Brown, Isao Inoue, and Patricia A. Revest
- Published in print:
- 1995
- Published Online:
- March 2012
- ISBN:
- 9780198547907
- eISBN:
- 9780191724299
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198547907.003.0156
- Subject:
- Neuroscience, Invertebrate Neurobiology
In the majority of animal groups, axons release K+ and take up Na+ during action potential production, with a tendency for an accumulation of K+ and depletion of Na+ in the narrow extracellular ...
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In the majority of animal groups, axons release K+ and take up Na+ during action potential production, with a tendency for an accumulation of K+ and depletion of Na+ in the narrow extracellular spaces adjacent to the axon. Homeostatic mechanisms are present to reduce the severity of these changes, and so limit their undesirable effects on neuronal function. This chapter reviews studies in squid giant axons to show that, under normal physiological conditions, the Schwann cell sheath around the axon has powerful mechanisms for regulating the [K+] in the periaxonal space, using a combination of passive diffusion (particularly via the transcellular glial tubular system and across its membranes) and carrier-mediated transport. The significance of this regulation for the normal function of the giant axon system in swimming and escape responses is discussed. Axons in vertebrates and invertebrates use a sequence of voltage-dependent ionic currents to generate propagating action potentials, generally an early inward Na+ current followed by a late outward K+ current. If the axon is surrounded by a narrow interstitial space, there is a tendency for K+ accumulation and Na+ depletion in the space during activity. If the axon is surrounded by a narrow interstitial space, there is a tendency for K+ accumulation and Na+ depletion in the space during activity. The axonal resting potential is relatively insensitive to small changes of [K+] in the physiological range, because the significant Na+ permeability of the membrane flattens the Nernst plot of membrane potential versus log [K+] in this range.Less
In the majority of animal groups, axons release K+ and take up Na+ during action potential production, with a tendency for an accumulation of K+ and depletion of Na+ in the narrow extracellular spaces adjacent to the axon. Homeostatic mechanisms are present to reduce the severity of these changes, and so limit their undesirable effects on neuronal function. This chapter reviews studies in squid giant axons to show that, under normal physiological conditions, the Schwann cell sheath around the axon has powerful mechanisms for regulating the [K+] in the periaxonal space, using a combination of passive diffusion (particularly via the transcellular glial tubular system and across its membranes) and carrier-mediated transport. The significance of this regulation for the normal function of the giant axon system in swimming and escape responses is discussed. Axons in vertebrates and invertebrates use a sequence of voltage-dependent ionic currents to generate propagating action potentials, generally an early inward Na+ current followed by a late outward K+ current. If the axon is surrounded by a narrow interstitial space, there is a tendency for K+ accumulation and Na+ depletion in the space during activity. If the axon is surrounded by a narrow interstitial space, there is a tendency for K+ accumulation and Na+ depletion in the space during activity. The axonal resting potential is relatively insensitive to small changes of [K+] in the physiological range, because the significant Na+ permeability of the membrane flattens the Nernst plot of membrane potential versus log [K+] in this range.
