Neural Responses to Injury: Prevention, Protection and Repair; Volume 6: Protecting the Auditory System and Prevention of Hearing Problems PDF Download
Are you looking for read ebook online? Search for your book and save it on your Kindle device, PC, phones or tablets. Download Neural Responses to Injury: Prevention, Protection and Repair; Volume 6: Protecting the Auditory System and Prevention of Hearing Problems PDF full book. Access full book title Neural Responses to Injury: Prevention, Protection and Repair; Volume 6: Protecting the Auditory System and Prevention of Hearing Problems by . Download full books in PDF and EPUB format.
Author: Publisher: ISBN: Category : Languages : en Pages : 0
Book Description
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.
Author: Publisher: ISBN: Category : Languages : en Pages : 0
Book Description
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.
Author: Publisher: ISBN: Category : Languages : en Pages : 108
Book Description
The LSU Neuroscience Center is a comprehensive, multidisciplinary, and transdepartmental entity that unites fundamental neurobiology and the clinical neurosciences in the common goal of elucidating the workings of the brain and contributing to the treatment of currently incurable diseases of the nervous system. The objective of the present program is to find solutions to neuroscience-related problems of interest to the U.S. Army Medical Research and Development Command. The program is focused on exploiting novel neuroprotective strategies that lead to prevention of and repair after neural injury. Corwerging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuropharmacology, molecular biology and virology are proposed. JMD.
Author: Nicolas Bazan Publisher: ISBN: Category : Languages : en Pages : 292
Book Description
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.
Author: Publisher: ISBN: Category : Languages : en Pages : 169
Book Description
The LSU Neuroscience Center is a comprehensive, multidisciplinary, and transdepartmental entity that unites fundamental neurobiology and the clinical neurosciences in the common goal of elucidating the workings of the brain and contributing to the treatment of currently incurable diseases of the nervous system. The objective of the present program is to find solutions to neuroscience-related problems of interest to the U.S. Army Mo%%na3 Research and Development Command. The program is focused on exploiting novel neuroprotective strategies that lead to prevention of and repair after neural injury. Converging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuropharmacology, molecular biology and virology are proposed. JMD.
Author: Nicolas Bazan Publisher: ISBN: Category : Languages : en Pages : 126
Book Description
The experimental animals used during this period for the project, Neural Responses to Injury: Prevention, Protection, and Repair, Subproject: Role of Growth Factors and Cell Signaling in the Response of Brain and Retina to Injury, are as follows: Species Rat(Albino Wistar), Number Allowed: 78, Number Used, 78, LSU IACUC# 1032. The objective of this study is to assay for changes in expression of genes involved in neural growth and differentiation as a flinction of wound healing. We have used the Chalifour procedure (1) to assay for changes in panels of brain cortex RNAs. Materials and Methods Rat Brain Cryogenic Injury Winstar rats weighing 250-275 g were ether anesthetized and a 9 mm diameter probe cooled in liquid nitrogen was placed on the right parietal region of the rat skull for 1 min. The animals were then euthanized and the brains dissected at the specified times. Analysis of Gene Expression Pafterns Double-stranded radiolabeled cDNAs were synthesized from rat cortex RNAs isolated at various time points following brain injury. Panels of nitrocellulose filter-fixed cDNA clones were then screened according to the method of Chalifour et al. (1). Modifications included the use of 50 g of RNA, 2000u reverse transcriptase, 120 Ci 32P-dCTP, and 2u of klenow per sample. Nitrocellulose filters were hybridized to 106 cpm/ml of brain cDNA in 10 ml of hybridization solution. RNA Collection and Northern Blots RNAs from rat brain were collected by the method of Chomczynski and Sacchi (2). Northern blots were performed using standard techniques.
Author: Robert Vink Publisher: University of Adelaide Press ISBN: 0987073052 Category : Medical Languages : en Pages : 354
Book Description
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.
Author: Publisher: ISBN: Category : Languages : en Pages : 0
Book Description
The experimental animals used during this period for the project, Neural Responses to Injury: Prevention, Protection, and Repair, Subproject: Neurochemical Protection of the Brain, Neural Plasticity and Repair, are as follows: Species Number Allowed Number Used LSU IACUC# Rat (sprague-Dawle) 125 125 1046 Rat (Sprague-Dawle) 91 91 1045 The development of chronic epilepsy is a very serious complication of head injury, neurodegenerative diseases, brain tumors, and exposure to neurotoxic agents. Head injury is often associated with loss of short-term memory, indicating trauma to the hippocampal formation, the brain region most commonly associated with epileptic brain damage. Underlying the formation of epilepsy (epileptogenesis) is proposed to be a vicious cycle initiated by the loss of neurons. In an attempt to repair and/or replace lost synaptic connections, the brain can develop aberrant synaptic circuits that permit the propagation and amplification of waves of excitatory neurotransmission, eventually resulting in prolonged or repeated seizures (status epilepticus). The massive amounts of excitatory amino acids released during these episodes can stimulate further neuronal loss (excitotoxic damage), the formation of more aberrant synaptic circuits, and further seizures (Choi and Rothinan, 1990). Excitotoxic damage has been demonstrated in several experimental models of status epilepticus (Meldmm et al, 1973; Ben-Ari, 1995; Sloviter, 1987).
Author: Publisher: ISBN: Category : Languages : en Pages : 0
Book Description
The experimental animals used during this period for the project, Neural Responses to Injury: Prevention, Protection, and Repair, Subproject: Role of Growth Factors and Cell Signaling in the Response of Brain and Retina to Injury, are as follows: Species Rat(Albino Wistar), Number Allowed: 78, Number Used, 78, LSU IACUC# 1032. The objective of this study is to assay for changes in expression of genes involved in neural growth and differentiation as a flinction of wound healing. We have used the Chalifour procedure (1) to assay for changes in panels of brain cortex RNAs. Materials and Methods Rat Brain Cryogenic Injury Winstar rats weighing 250-275 g were ether anesthetized and a 9 mm diameter probe cooled in liquid nitrogen was placed on the right parietal region of the rat skull for 1 min. The animals were then euthanized and the brains dissected at the specified times. Analysis of Gene Expression Pafterns Double-stranded radiolabeled cDNAs were synthesized from rat cortex RNAs isolated at various time points following brain injury. Panels of nitrocellulose filter-fixed cDNA clones were then screened according to the method of Chalifour et al. (1). Modifications included the use of 50 g of RNA, 2000u reverse transcriptase, 120 Ci 32P-dCTP, and 2u of klenow per sample. Nitrocellulose filters were hybridized to 106 cpm/ml of brain cDNA in 10 ml of hybridization solution. RNA Collection and Northern Blots RNAs from rat brain were collected by the method of Chomczynski and Sacchi (2). Northern blots were performed using standard techniques.
Author: Publisher: ISBN: Category : Languages : en Pages : 0
Book Description
Traumatic brain injury is characterized by multiple phases of damage; including primary tissue damage and bleeding at the site of impact; secondary damage, including brain edema, ischemia, the diffusion of toxic substances beyond the initial site of injury and delayed neuronal death; and long-term epileptogenic changes in synaptic plasticity. A common motif at the cellular level of these various forms of neurotrauma is the over-release of neurotransmitters, the stimulation of post-synaptic receptors, and the subsequent accumulation of abnormally high concentrations of second messengers. The major neurotransmitter involved in neuronal damage is thought to be the excitatory amino acid L-glutamate. Glutamate triggers calcium entry into post-synaptic neurons via the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors (Rotlunan and Olney, 1986, 1987; Choi 1988), and so the activation of many calcium-dependent signaling pathways. The major focus of research in our laboratory has been the activation of calcium- dependent phospholipases A2, the release from membrane phospholipids of bioactive lipids, including free arachidonic acid (AA) and platelet-activating factor (PAF), and the signaling pathways then activated. We and other groups have shown the neuroprotective properties of pharmacological agents targeting bioactive lipid signaling cascades. Detailed characterization of these processes, and the downstream events that link the over-accumulation of bioactive lipids to long-term changes in brain physiology, is important in identifying the best therapeutic targets for the treatment of traumatic brain injury.
Author: 
Author: 
Author: 
Author: 
Author: Nicolas Bazan
Author: 
Author: Nicolas Bazan
Author: Robert Vink
Author: 
Author: 
Author: