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 : 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: Publisher: ISBN: Category : Languages : en Pages : 78
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. JMD.
Author: Publisher: ISBN: Category : Languages : en Pages : 0
Book Description
The hypothesis on which this investigation is based is that stressors such as transient temperature changes and restraint signal the central nervous system eliciting the release of catecholamines and adrenal steroids which, in turn, affect the immune system resulting in the reactivation of latent viruses. Employing a mouse model of stress-induced reactivation of herpes simplex virus type 1 (HSV-1), we are determining the time course of viral reactivation relative to the alteration of immune parameters including lymphocyte functions and numbers. Specifically, we are correlating the expression of various immunomodulatory cytokine genes with the levels of neuroendocrine monoamines, as well as the activation of the hypothalamic-pituitary-adrenal (HPA) axis and relating these to the reactivation of infectious virus in the nervous system. Alterations in serum corticosterone and shifts in monoamines in the brains, trigeminal ganglia, and brain stems of latently infected and reactivated mice following the application of stress are being studied. Differences between control (not stressed) and stressed animals are being determined relative to the incidence of viral reactivation and the affect of stress on immunological regulation of the reactivation process.
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 : 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 : 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 : 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: Nicolas Bazan
Author: 
Author: 
Author: 
Author: 
Author: Nicolas Bazan
Author: ![Gedenkboek der vaste keuringscommissie [van de] Koninklijke Nederlandsche Maatschappij voor tuinbouw en plantkunde 1889-1939 PDF](https://books.google.com/books/content/images/frontcover/gkXgjwEACAAJ?fife=w80-h100)
Author: 
Author: Nicolas Bazan
Author: