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2-Minute Neuroscience: Long-Term Potentiation (LTP)

Annual Review of Medicine. It is produced by endothelial cells to mediate blood vessel relaxation; it mediates, in part, the immune functions of activated macrophages; and in the central and peripheral nervous system it serves as a neurotransmitter. In the nervous system, nitric oxide may regulate neurotransmitter release, it may play a key role in synaptic plasticity and morphogenesis, and it may regulate sexual and aggressive behavior.

Nitric Oxide in Brain Development, Plasticity, and Disease, Volume 118

Under conditions of excessive formation, nitric oxide is emerging as an important neurotoxin. Gene therapies are gaining momentum as promising early successes in clinical studies accumulate and examples of regulatory approval for licensing increase. Investigators are advancing with cautious optimism that effective, durable, and safe therapies will Read More. Figure 1: Indications in gene therapy clinical trials.


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The bar graph classifies clinical gene transfer studies by disease. Adapted from Reference 1. Figure 2: a The goal of gene augmentation is to restore normal cellular function by providing a functional copy of a gene in trans i. Figure 3: Genetic engineering of T cells. TCRs have the ability to recognize any protein expressed by a cell and can potentially distinguish healthy cells from tumor cells through the specific recogni The field of cancer immunotherapy has been re-energized by the application of chimeric antigen receptor CAR T cell therapy in cancers.

These CAR T cells are engineered to express synthetic receptors that redirect polyclonal T cells to surface antigens Figure 1: Immunosuppressive tumor microenvironment. This diagram depicts the multiple challenges for chimeric antigen receptor CAR T cells.

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In addition to proper trafficking and successful infiltrat Alzheimer's disease AD is the primary cause of age-related dementia. Effective strategies to prevent and treat AD remain elusive despite major efforts to understand its basic biology and clinical pathophysiology.

Significant investments in therapeutic Figure 1: Alzheimer's disease AD is characterized by neuronal death, which is usually correlated with the appearance of amyloid plaques and neurofibrillary tangles NFTs. In response, the US National Figure 1: Ethical formulations of human genome editing. Acute kidney injury AKI is a global public health concern associated with high morbidity, mortality, and healthcare costs.

Mechanisms of formation and accumulation of mitochondrial DNA deletions in aging neurons. Gabbita, S.

R. Ranney Mize, Ph.D.- LSUHSC School of Medicine

Garthwaite, J. Endothelium-derived relaxing factor release on activation of NMDA receptors suggests role as intercellular messenger in the brain. Nature , — Gibson, G. Greaves, L.


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Comparison of mitochondrial mutation spectra in ageing human colonic epithelium and disease: absence of evidence for purifying selection in somatic mitochondrial DNA point mutations. PLoS Genet. Greilberger, J. Guo, S. Halim, N. Phosphorylation status of pyruvate dehydrogenase distinguishes metabolic phenotypes of cultured rat brain astrocytes and neurons.

Glia 58, — Hamel, E. Harris, M.

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Harris, J. Synaptic energy use and supply. Neuron 75, — Hensley, K. Herrero-Mendez, A. Cell Biol. Hertz, L. Kinetic characteristics of the glutamate uptake into normal astrocytes in cultures. Hoge, R. Simultaneous recording of task-induced changes in blood oxygenation, volume, and flow using diffuse optical imaging and arterial spin-labeling MRI. Neuroimage 25, — Horton, T. Neurology 45, — Hsiao, H.

I. Nitric oxide: Brain distribution, production and signaling

Aberrant astrocytes impair vascular reactivity in Huntington disease. Hunsberger, J. Gene profiling the response to kainic acid induced seizures. Hyder, F. Cortical energy demands of signaling and nonsignaling components in brain are conserved across mammalian species and activity levels. Ivan, M. Jaakkola, P. Jeitner, T. Johnson, G. Junn, E. Kasischke, K. Neural activity triggers neuronal oxidative metabolism followed by astrocytic glycolysis. Science , 99— Kim, S. Mitochondrial aconitase is a transglutaminase 2 substrate: transglutamination is a probable mechanism contributing to high-molecular-weight aggregates of aconitase and loss of aconitase activity in Huntington disease brain.

Kim, J. HIFmediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia. Cell Metab. Klivenyi, P. Mice deficient in dihydrolipoamide dehydrogenase show increased vulnerability to MPTP, malonate and 3-nitropropionic acid neurotoxicity. Koong, A. Candidate genes for the hypoxic tumor phenotype. Cancer Res.

Google Scholar. Kraytsberg, Y. Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons. Kumar-Singh, S. Kvamme, E. Synthesis of glutamate and its regulation. Langston, J. Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. Lee, H. Li, X. Oxidative stress induces the decline of brain EPO expression in aging rats.

Li-Byarlay, H. Socially responsive effects of brain oxidative metabolism on aggression. Lin, A. Nonlinear coupling between cerebral blood flow, oxygen consumption and ATP production in human visual cortex. Liu, L. Lovell, M. Elevated zinc transporter-6 in mild cognitive impairment, Alzheimer disease, and pick disease. Lu, H. Sustained poststimulus elevation in cerebral oxygen utilization after vascular recovery. Lundgaard, I.

www.sibteplokomplekt.ru/includes/znakomstva/104-klub-znakomstv.php Direct neuronal glucose uptake heralds activity-dependent increases in cerebral metabolism. Macas, J. Increased generation of neuronal progenitors after ischemic injury in the aged adult human forebrain. Machler, P. In vivo evidence for a lactate gradient from astrocytes to neurons. Maddock, R. Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study.

Psychiatry 14, — Manczak, M. Mangia, S.