The historical lineage of therapeutic hypnosis in James Braid's "psychophysiology", Pierre Janet's "physiological modification", and Milton Erickson's "neuro-psycho-physiology" is extended to include current neuroscience research on activity-dependent gene expression, neurogenesis, and stem cells in memory, learning, behavior change, and healing.
A new perspective on how therapeutic hypnosis and neuroscience may be integrated on the molecular-genomic level is offered as a guide for basic research and clinical applications. An update of Watson and Crick's original formulation of molecular biology is proposed to illustrate how psychosocial experiences modulate gene expression, protein synthesis, and brain plasticity during memory trace reactivation for the reorganization of neural networks that encode fear, stress, and traumatic symptoms.
This paean composed on the occasion of the inaugural Bernauer W. Newton Trust presentation celebrates the personal and professional culture of 50 years of mentorship, teaching, and research by the American Society for Clinical Hypnosis (ASCH). This review of current neuroscience concepts of therapeutic hypnosis and psychotherapy is made possible by the cooperation and dedication of all members of our society.
It has been reported that the sedative component of pentobarbital is mediated by GABA receptors in an endogenous sleep pathway and the ventrolateral preoptic area (VLPO)-tuberomammillary nucleus (TMN) or VLPO-dorsal raphe nucleus (DRN) neural circuit is important in the sedative response to pentobarbital. Our previous findings indicated that the VLPO-TMN neuronal circuit may play crucial part in the augmentative effect of diltiazem on pentobarbital sleep and the serotonergic system may be involved.
The authors present empirical data on therapeutic hypnosis and brief psychotherapy as a 4-Stage Creative Process of focused attention and positive expectancy in professional training workshops of the American Society of Clinical Hypnosis, the National Institute for the Clinical Applications of Behavioral Medicine, and the Milton H. Erickson Foundation. The authors developed a brief protocol for assessing the 4-Stage Creative Process, which is the core dynamic of the Creative Psychosocial Genomic Healing Experience.
The classical benzodiazepine diazepam (DZ) induces anxiolysis at low doses and sedation and hypnosis at higher doses. Different brain areas and neuronal populations most likely mediate these different behavioral effects. We used c-Fos immunohistochemistry as an indirect way to study neuronal activation or inhibition induced by DZ at anxiolytic and sedative doses (0.5 and 5mg/kg, respectively) in various brain areas involved in anxiety, arousal, sedation and addiction in C57BL/6J mice.
Zhongguo Yao Li Xue Bao = Acta Pharmacologica Sinica
Immunoregulatory properties of a novel antimalarial drug dihydroartemisinin (DHA) were investigated in vitro. DHA 0.5-5 mumol.L-1 enhanced the lymphocyte proliferation induced by Con A. Interleukin 2 (IL-2) production and its mRNA expression by both Con A-stimulated mouse splenocytes and a T cell line LBRM-33-1A5 were also augmented by DHA. In contrast, DHA 0.5-5 mumol.L-1 did not show any effect on the lipopolysaccharides (LPS)-induced lymphocyte proliferation and the spontaneous and mitogen-induced proliferation of transformed T cells.
Drug Metabolism and Disposition: The Biological Fate of Chemicals
Fa2N-4 cells have been proposed as a tool to identify CYP3A4 inducers. To evaluate whether Fa2N-4 cells are a reliable surrogate for cryopreserved human hepatocytes, we assessed the basal mRNA expression of 64 drug disposition genes in Fa2N-4 cells. Significant differences were found in the expression of major drug-metabolizing enzymes, nuclear receptors, and transporters between both cell types.
MCF7 cells are an estrogen-responsive human breast cancer cell line that expresses both estrogen receptor (ER) alpha and ERbeta. Treatment of MCF7 cells with artemisinin, an antimalarial phytochemical from the sweet wormwood plant, effectively blocked estrogen-stimulated cell cycle progression induced by either 17beta-estradiol (E(2)), an agonist for both ERs, or by propyl pyrazole triol (PPT), a selective ERalpha agonist. Artemisinin strongly downregulated ERalpha protein and transcripts without altering expression or activity of ERbeta.