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Books on the topic 'Genes, Immediate-Early'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 January 2023

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1

Tölle, T. R., J. Schadrack, and W. Zieglgänsberger, eds. Immediate-Early Genes in the Central Nervous System. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79562-6.

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2

R, Tölle T., Schadrack J. 1965-, and Zieglgänsberger W. 1940-, eds. Immediate early genes in the central nervous system. New York: Springer-Verlag, 1995.

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3

Schadrack, J., T. R. Tölle, and W. Zieglgänsberger. Immediate-Early Genes in the Central Nervous System. Springer London, Limited, 2012.

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4

Schadrack, J., T. R. Tölle, and W. Zieglgänsberger. Immediate-Early Genes in the Central Nervous System. Springer London, Limited, 2012.

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5

Reinhard, Grzanna, Brown Roger M, and National Institute on Drug Abuse., eds. Activation of immediate early genes by drugs of abuse. Rockville, MD (5600 Fishers Lane, Rockville 20857): U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute on Drug Abuse, 1993.

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6

Gallitano, Amelia L., ed. The Role of Immediate Early Genes in Neuropsychiatric Illness. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-617-4.

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7

(Editor), Raphael Pinaud, and Liisa A. Tremere (Editor), eds. Immediate Early Genes in Sensory Processing, Cognitive Performance and Neurological Disorders. Springer, 2006.

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8

Pinaud, Raphael, and Liisa A. Tremere. Immediate Early Genes in Sensory Processing, Cognitive Performance and Neurological Disorders. Springer London, Limited, 2006.

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9

Pinaud, Raphael, and Liisa A. Tremere. Immediate Early Genes in Sensory Processing, Cognitive Performance and Neurological Disorders. Springer, 2014.

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10

Pinaud, Raphael, and Liisa A. Tremere, eds. Immediate Early Genes in Sensory Processing, Cognitive Performance and Neurological Disorders. Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-33604-6.

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11

L, Kaczmarek, and Robertson Harold A, eds. Immediate early genes and inducible transcription factors in mapping of the central nervous system function and dysfunction. Amsterdam: Elsevier, 2002.

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12

Robertson, H. A., and L. Kaczmarek. Immediate Early Genes and Inducible Transcription Factors in Mapping of the Central Nervous System Function and Dysfunction. Elsevier Science & Technology Books, 2002.

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13

Immediate early genes and inducible transcription factors in mapping of the central nervous system function and dysfunction. Elsevier, 2002. http://dx.doi.org/10.1016/s0924-8196(02)x8010-5.

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14

(Editor), L. Kaczmarek, and H. A. Robertson (Editor), eds. Immediate Early Genes and Inducible Transcription Factors in Mapping of the Central Nervous System Function and Dysfunction (Handbook of Chemical Neuroanatomy). Elsevier Science, 2002.

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15

Stoddard, Frederick J., and Robert L. Sheridan. Wound Healing and Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0009.

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Abstract:
Depression and wound healing are bidirectional processes for adults and children consistent with the conception of depression as systemic. This systemic interaction is similar to the “bidirectional impact of mood disorder on risk for development, progression, treatment, and outcomes of medical illness” generally. And, evidence is growing that the bidirectional impact of mood disorder may be true for injuries and for trauma surgery. Animal models have provided some support that treatment of depression may improve wound healing. An established biological model for a mechanism delaying wound healing is increased cortisol secretion secondary to depression and/or stress, and impaired immune response, in addition or together with the other factors such as genetic or epigenetic risk for depression. Cellular models relate both to wound healing and to depression include cytokines, the inflammatory response (Miller et al, 2008), and cellular aging (Telgenhoff and Shroot, 2005) reflected in shorter leukocyte telomere length (LTL) (Verhoeven et al, 2016). Another model of stress impacting wound healing investigated genetic correlates—immediate early gene expression or IEG from the medial prefrontal cortex, and locomotion, in isolation-reared juvenile rats. Levine et al (2008) compared isolation reared to group reared samples, and found that, immediate gene expression in the medial prefrontal cortex (mPFC) was reduced, and behavioral hyperactivity increased, in juvenile rats with 20% burn injuries. Wound healing in the isolation reared rats was significantly impaired. They concluded that these results provide candidates for behavioral biomarkers of isolation rearing during physical injury, i.e. reduced immediate mPFC gene expression and hyperactivity. They suggested that a biomarker such as IEGs might aid in demarcating patients with resilient and adaptive responses to physical illness from those with maladaptive responses
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