The past decade has brought great advances in our understanding of the mechanisms underlying auditory pathologies. This volume presents recent developments in research and their potential translation to the clinical setting. It brings together the basic and clinical sciences very nicely in that while most chapters are written by basic scientists, each topic has a pretty direct clinical application or implication.
The past decade has brought great advances in our understanding of the mechanisms underlying auditory pathologies. This volume presents recent developments in research and their potential translation to the clinical setting. It brings together the basic and clinical sciences very nicely in that while most chapters are written by basic scientists, each topic has a pretty direct clinical application or implication.
The experimental animals used during this period for the project, Neural Responses to Injury: Prevention, Protection, and Repair, Subproject: Protecting the Auditory System and Prevention of Hearing Problems, are as follows: Species, Guinea Pig, Number Allowed, 276, Number Used, 83, LSU IACUC# 1061. ANIMAL PROJECT: The SPECIFIC MMS of this study are to demonstrate and explore mechanisms for preventing the effects of intense sound. In years 01, and 02 we discovered that continuous, ipsilateral primary stimulation (CM-LIPS) will produce complex changes in the mechanics of the cochlea, possibly related to toughening In year 03 we discovered that ATP is involved in generating this complex mechanics. We extended the noise exposure studies and found that continuous noise is less effective than interrupted noise in inducing "toughing" Cellular mechanism studies discovered that ATP kills outer hair cells in vitro and in vivo, indicating that ATP may be a key player in noise-induced deafness and toughening. HUMAN PROJECT: We have found that binaural noise suppresses linear click evoked emissions twice as much as ipsilateral noise and 3 times as much as contralateral noise. However, subjects with noise exposure often show poor or reduced emissions when the stimulus is a click. Of 20 subjects enrolled and 13 completely tested so far in the multi-day protocol, subjects with noise exposure effects at higher frequencies show MORE suppression at and around 1500 Hz than do subjects with no hearing loss. This may support the original hypothesis in this program that "Noise Tender Ears" will show different emission suppression patterns from ears that are tough.
ANIMAL PROJECT: The SPECIFIC AIMS of this study are to demonstrate and explore mechanisms for preventing the effects of intense sound. In years 01, 02, 03 we discovered that continuous, ipsilateral sound stimulation (CM-LIPS) will produce complex changes in the mechanics of the cochlea. In year 04 we obtained additional evidence that ATP is involved in generating this mechanics. We completed the noise exposure studies and found that continuous noise is less effective than interrupted noise in inducing.
Exposure to loud noise continues to be the largest cause of hearing loss in the adult population. The problem of NIHL impacts a number of disciplines. US standards for permissible noise exposure were originally published in 1968 and remain largely unchanged today. Indeed, permissible noise exposure for US personnel is significantly greater than that allowed in numerous other countries, including for example, Canada, China, Brazil, Mexico, and the European Union. However, there have been a number of discoveries and advances that have increased our understanding of the mechanisms of NIHL. These advances have the potential to impact how NIHL can be prevented and how our noise standards can be made more appropriate.
The brain is the most complex organ in our body. Indeed, it is perhaps the most complex structure we have ever encountered in nature. Both structurally and functionally, there are many peculiarities that differentiate the brain from all other organs. The brain is our connection to the world around us and by governing nervous system and higher function, any disturbance induces severe neurological and psychiatric disorders that can have a devastating effect on quality of life. Our understanding of the physiology and biochemistry of the brain has improved dramatically in the last two decades. In particular, the critical role of cations, including magnesium, has become evident, even if incompletely understood at a mechanistic level. The exact role and regulation of magnesium, in particular, remains elusive, largely because intracellular levels are so difficult to routinely quantify. Nonetheless, the importance of magnesium to normal central nervous system activity is self-evident given the complicated homeostatic mechanisms that maintain the concentration of this cation within strict limits essential for normal physiology and metabolism. There is also considerable accumulating evidence to suggest alterations to some brain functions in both normal and pathological conditions may be linked to alterations in local magnesium concentration. This book, containing chapters written by some of the foremost experts in the field of magnesium research, brings together the latest in experimental and clinical magnesium research as it relates to the central nervous system. It offers a complete and updated view of magnesiums involvement in central nervous system function and in so doing, brings together two main pillars of contemporary neuroscience research, namely providing an explanation for the molecular mechanisms involved in brain function, and emphasizing the connections between the molecular changes and behavior. It is the untiring efforts of those magnesium researchers who have dedicated their lives to unraveling the mysteries of magnesiums role in biological systems that has inspired the collation of this volume of work.
