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Author: Nicolas Bazan Publisher: ISBN: Category : Languages : en Pages : 17
Book Description
The addition of two floors to the existing building housing the LSU Eye Center and the Lions Eye Research Laboratories is now nearing completion. The Neuroscience Center will be occupying this space in February - March 1997. Plans for floors eight and nine have been included as an appendix of this volume. The additional space will greatly enhance the capabilities of the research program of the Neuroscience Center. Many components of the eight research projects, as well as the associated Core research facilities and administrative units, will be housed in the new space. The benefits of the synergy created by proximity in the development of exciting new approaches to research problems related with Neural Responses to Injury: Prevention, Protection, and Repair will soon be realized. The centralization of the Core Research Facilities will allow cooperative usage and simply oversight, reducing costs and eliminating duplication. Finally, the location of administrative functions in constant contact with the research facilities will permit efficient management and minimize wasteful miscommunication.
Author: Nicolas Bazan Publisher: ISBN: Category : Languages : en Pages : 17
Book Description
The addition of two floors to the existing building housing the LSU Eye Center and the Lions Eye Research Laboratories is now nearing completion. The Neuroscience Center will be occupying this space in February - March 1997. Plans for floors eight and nine have been included as an appendix of this volume. The additional space will greatly enhance the capabilities of the research program of the Neuroscience Center. Many components of the eight research projects, as well as the associated Core research facilities and administrative units, will be housed in the new space. The benefits of the synergy created by proximity in the development of exciting new approaches to research problems related with Neural Responses to Injury: Prevention, Protection, and Repair will soon be realized. The centralization of the Core Research Facilities will allow cooperative usage and simply oversight, reducing costs and eliminating duplication. Finally, the location of administrative functions in constant contact with the research facilities will permit efficient management and minimize wasteful miscommunication.
Author: Nicolas Bazan Publisher: ISBN: Category : Languages : en Pages : 130
Book Description
In Year 4 of the DOD Agreement, the calcium Imaging Facility has continued to support DOD-Funded projects and to serve as a core facility for Neuroscientists throughout the LSUMC campus. Usage of the Facility has been divided up at approximately 20 percent hardware and software maintenance and development, 40 percent DoD-Funded investigations, and 40 percent other neuroscience projects.
Author: Nicolas Bazan Publisher: ISBN: Category : Languages : en Pages : 161
Book Description
The fibroblast growth factors (FGFs) are a family of nine structurally related polypeptides. The best characterized members are acidic FGF (FGF-1) and basic FGF (FGF-2). Other members of the FGF family include FGF-3 (int-2), FGF-4 (hstlkfgf), FGF-5, FGF-6, FGF-7 (keratinocyte growth factor, KGF), FGF-8 (AlGF) and FGF-9 (glial-activating factor, GAF) (1-3). FGF types I and 2 share 53% amino acid sequence homology (4), suggesting that they are derived from a common ancestral gene. They also have a strong affinity for heparin (5,6) and bind to the same cell surface receptor (7). FGFs are involved in various biological activities, including angiogenesis, mitogenesis, cellular differentiation, tumorigenesis, and repair of tissue injury (5, 8, 9). These actions are mediated through specific, high affinity, transmembrane receptors. Four structurally related genes encoding high affinity receptors have been identified (10-13). The FGF receptor has diverse forms, FGFR-1, FGFR-2, FGFR-3 and FGFR-4. FGF-1 binds to all four members of the FGF receptor family and FGF-2 binds to all but FGFR (14-15). FGF is found in many tissues including peripheral nerve, and it is suggested that due to its action on fibroblasts may participate in neuroma formation, a complication of peripheral nerve injury and characterized by accumulation of collagen and extracellular matrix which form a barrier thar regenerating axons cannot penetrate, resulting in bulb- like enlargement or neuroma (1 6), The mechanism of neuroma formation is not understood.
Author: Publisher: ISBN: Category : Languages : en Pages : 34
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. Converging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuropharmacology, molecular biology and virology are proposed.
Author: Nicolas Bazan Publisher: ISBN: Category : Languages : en Pages : 171
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 : 122
Book Description
The overall focus of this project has been to understand the cellular and molecular biology of neuroma formation as a complication of damage and repair to peripheral nerves. As part of this, a secondary focus has been to establish in vitro models of cell lines of fibroblasts from peripheral nerves that can be used to uncover the molecular mechanisms of peripheral nerve fibroblast response to damage and also to their interaction with cell signaling molecules that may be present in the repair process. A third objective has been to understand the origin of pain that accompanies neuroma formation. It has not been known how the cellular developments affect the physiology of the entrapped nerve endings. Electrophysiological and immunohistochemical studies have been carried out on human neuroma tissue to determine how the ion channels change as the neuroma develops.
Author: Publisher: ISBN: Category : Languages : en Pages : 23
Book Description
The LSU Neuroscience Center is a comprehensive, multidisciplinary, and trans-departmental 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 this program is to find solutions to neuroscience-related problems of interest to the US 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. Converging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuroppharmacology, molecular biology and virology are ongoing. Over the four years covered in this proposal, this program aims to: (1) carry out seven research projects in the basic and clinical neurosciences; (2) expand central, shared facilities with the addition of highly specialized instrumentation not currently available to our scientists; (3) develop laboratory space to permit the physical consolidation and coordination of this research effort; and (4) institute a coordination unit to monitor, facilitate, and administrate the cooperative research programs, as well as to meet the associated budgetary, human resources, facilities, and communications needs for the attainment of the program goals.
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: 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: Publisher: ISBN: Category : Languages : en Pages : 0
Book Description
The overall focus of this project has been to understand the cellular and molecular biology of neuroma formation as a complication of damage to peripheral nerves. Several objectives have been clarified: 1) to establish in vitro models of cell lines of fibroblasts from normal peripheral nerves and neuromas that can be used to uncover the molecular mechanisms of the peripheral nerve fibroblast response to damage; 2) to understand the interactions of fibroblasts of peripheral nerve origin with cell signaling molecules in the neural environment after an injury and during the repair process; and 3) to understand the origin of pain that accompanies neuroma formation. It is not known how the cellular physiology of the entrapped nerve endings is affected by the dense collagenous mass of tissue that makes up the neuroma. However, it is clear that abnormalities develop in gated ion channels in the entrapped nerve endings and that the neuroma is formed by an exaggerated fibroblast response to nerve damage. Studies using fibroblasts cultured from peripheral human nerves have shown that these cells express basic fibroblast growth factor and its receptor. Immunohistochemical studies and quantitative Western blots have shown that basic fibroblast growth factor and its receptor are found in all tissue samples taken directly from human neuromas. The goal of these ongoing studies is to elucidate the mechanisms that regulate the activities of these cells in injury and repair and ultimately to determine potential approaches to modification of these mechanisms that may prevent the development of neuromas and their associated morbidities in traumatized tissues.
Author: Nicolas Bazan
Author: Nicolas Bazan
Author: Nicolas Bazan
Author: Nicolas Bazan
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Author: Nicolas Bazan
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Author: Nicolas Bazan
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