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1. Wu R, Dong W, Cui X, Zhou M, Simms HH, Ravikumar TS, Wang P: Ghrelin down-regulates proinflammatory cytokines in sepsis through activation of the vagus nerve. Ann Surg; 2007 Mar;245(3):480-6
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  • [Title] Ghrelin down-regulates proinflammatory cytokines in sepsis through activation of the vagus nerve.
  • OBJECTIVE: To test the hypothesis that administration of ghrelin attenuates inflammatory responses in sepsis through vagal nerve stimulation.
  • SUMMARY BACKGROUND DATA: Ghrelin has been demonstrated to possess multiple functions, including stimulation of the vagus nerve.
  • However, it remained unknown whether ghrelin also decreases proinflammatory cytokines in sepsis and, if so, whether the down-regulatory effect of ghrelin is mediated by activation of the vagus nerve.
  • CONCLUSIONS: Ghrelin down-regulates proinflammatory cytokines in sepsis through activation of the vagus nerve.
  • Pharmacologic stimulation of the vagus nerve may offer a novel approach of anti-sepsis therapy.

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  • (PMID = 17435556.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM053008; United States / NIGMS NIH HHS / GM / R01 GM057468; United States / NIGMS NIH HHS / GM / R01 GM053008-12; United States / NIGMS NIH HHS / GM / R01 GM057468-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Interleukin-6; 0 / Peptide Hormones; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1877017
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2. van Maanen MA, Lebre MC, van der Poll T, LaRosa GJ, Elbaum D, Vervoordeldonk MJ, Tak PP: Stimulation of nicotinic acetylcholine receptors attenuates collagen-induced arthritis in mice. Arthritis Rheum; 2009 Jan;60(1):114-22
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  • OBJECTIVE: The parasympathetic nervous system, through the vagus nerve, can down-regulate inflammation in vivo by decreasing the release of cytokines, including tumor necrosis factor alpha (TNFalpha), by activated macrophages.
  • The vagus nerve may exert antiinflammatory actions via a specific effect of its principal neurotransmitter, acetylcholine, on the alpha7 subunit of nicotinic acetylcholine receptors (alpha7nAChR) on macrophages.
  • METHODS: To inhibit the cholinergic antiinflammatory pathway, mice were subjected to unilateral cervical vagotomy or sham surgery, after which arthritis was induced with type II collagen.
  • Moreover, oral nicotine inhibited bone degradation and reduced TNFalpha expression in synovial tissue.
  • This was accompanied by a reduction of TNFalpha levels in both plasma and synovial tissue.
  • [MeSH-major] Arthritis, Experimental / drug therapy. Arthritis, Experimental / metabolism. Macrophages / metabolism. Nicotine / pharmacology. Nicotinic Agonists / pharmacology. Receptors, Nicotinic / metabolism
  • [MeSH-minor] Administration, Oral. Animals. Arthritis, Rheumatoid / drug therapy. Arthritis, Rheumatoid / metabolism. Arthritis, Rheumatoid / pathology. Bridged Compounds / pharmacology. Cartilage / pathology. Disease Models, Animal. Injections, Intraperitoneal. Male. Mice. Mice, Inbred DBA. Parasympathetic Nervous System / physiology. Spiro Compounds / pharmacology. Synovial Membrane / metabolism. Synovitis / drug therapy. Synovitis / metabolism. Synovitis / pathology. Tumor Necrosis Factor-alpha / metabolism. Vagus Nerve / physiology. alpha7 Nicotinic Acetylcholine Receptor

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  • (PMID = 19116908.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR-R 17779; 0 / Bridged Compounds; 0 / Chrna7 protein, mouse; 0 / Nicotinic Agonists; 0 / Receptors, Nicotinic; 0 / Spiro Compounds; 0 / Tumor Necrosis Factor-alpha; 0 / alpha7 Nicotinic Acetylcholine Receptor; 6M3C89ZY6R / Nicotine
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3. Mabley JG, Pacher P, Szabo C: Activation of the cholinergic antiinflammatory pathway reduces ricin-induced mortality and organ failure in mice. Mol Med; 2009 May-Jun;15(5-6):166-72
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  • Activation of the cholinergic antiinflammatory pathway, specifically through the alpha7 nicotinic acetylcholine receptor (either indirectly through vagus nerve stimulation or directly through nicotine treatment) reduces proinflammatory gene expression.
  • The aim of this study was to investigate whether nicotine treatment protected against ricin toxicity in mice.
  • Male Balb/c mice exposed to ricin had increased serum levels of the inflammatory cytokine tumor necrosis factor-alpha and markers of both kidney (blood urea nitrogen, creatine) and liver (alanine tranaminase) dysfunction, with a subsequent increase in mortality.
  • Nicotine administration 2 h after ricin injection significantly delayed and reduced ricin-induced mortality, an effect coupled with reduced serum levels of tumor necrosis factor-alpha and markers of kidney and liver dysfunction.
  • [MeSH-major] Inflammation / chemically induced. Inflammation / drug therapy. Multiple Organ Failure / chemically induced. Multiple Organ Failure / drug therapy. Nicotine / therapeutic use. Ricin / toxicity
  • [MeSH-minor] Alanine Transaminase / blood. Animals. Blood Urea Nitrogen. Male. Malondialdehyde / metabolism. Mice. Mice, Inbred BALB C. Nicotinic Agonists / therapeutic use. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 19209239.001).
  • [ISSN] 1528-3658
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AA000375-02; United States / Intramural NIH HHS / / Z99 AA999999
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nicotinic Agonists; 0 / Tumor Necrosis Factor-alpha; 4Y8F71G49Q / Malondialdehyde; 6M3C89ZY6R / Nicotine; 9009-86-3 / Ricin; EC 2.6.1.2 / Alanine Transaminase
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4. van Westerloo DJ, Giebelen IA, Florquin S, Bruno MJ, Larosa GJ, Ulloa L, Tracey KJ, van der Poll T: The vagus nerve and nicotinic receptors modulate experimental pancreatitis severity in mice. Gastroenterology; 2006 May;130(6):1822-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The vagus nerve and nicotinic receptors modulate experimental pancreatitis severity in mice.
  • BACKGROUND & AIMS: The nervous system, through the vagus nerve, controls inflammation by decreasing the release of tumor necrosis factor-alpha from endotoxin stimulated macrophages.
  • This anti-inflammatory effect is mediated by an interaction of acetylcholine, the principal neurotransmitter of the vagus nerve, with macrophage cholinergic nicotinic receptors expressing the alpha7 subunit.
  • Pancreatitis-associated pulmonary inflammation was independent of the integrity of the vagus nerve and nicotinic receptors.
  • CONCLUSIONS: This study provides the first evidence for a therapeutic potential of the vagus nerve and the "nicotinic anti-inflammatory pathway" in attenuating inflammation and injury during experimental pancreatitis.
  • [MeSH-major] Nicotinic Antagonists / pharmacology. Pancreatitis / drug therapy. Pancreatitis / pathology. Receptors, Nicotinic / metabolism. Vagus Nerve / physiology

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  • (PMID = 16697744.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM057226; United States / NIGMS NIH HHS / GM / R01 GM084125
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nicotinic Antagonists; 0 / Receptors, Nicotinic; 888Y08971B / Ceruletide
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5. Ilgner J, Rojas W, Biesterfeld S, Schürmann K, Zimny M, Westhofen M: [Low-grade malignant peripheral nerve sheath tumor of the neck soft tissues]. Laryngorhinootologie; 2001 Jan;80(1):39-42
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  • [Title] [Low-grade malignant peripheral nerve sheath tumor of the neck soft tissues].
  • BACKGROUND: Malignant Peripheral Nerve Sheath Tumours (MPNST) either grow sporadically, after radiation or chemotherapy respectively.
  • Because of the multiform histologic picture they are often difficult to differentiate from other soft tissue tumours.
  • PATIENT: We present the case of a sporadic MPNST which developed from the vagus nerve of a 39-year-old patient following radiation of the neck 7 years before.
  • With regard to the strong association with Neurofibromatosis I and the difficult differential diagnosis to other soft tissue tumours the emphasis should be put on excluding further manifestations of Neurofibromatosis I and of secondary tumours.
  • [MeSH-major] Cranial Nerve Neoplasms / diagnosis. Head and Neck Neoplasms / diagnosis. Neoplasms, Radiation-Induced / diagnosis. Nerve Sheath Neoplasms / diagnosis. Soft Tissue Neoplasms / diagnosis. Vagus Nerve Diseases / diagnosis
  • [MeSH-minor] Adult. Cell Transformation, Neoplastic / pathology. Diagnosis, Differential. Female. Humans. Neurofibromatosis 1 / diagnosis. Neurofibromatosis 1 / pathology. Neurofibromatosis 1 / surgery. Vagus Nerve / pathology

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  • (PMID = 11272246.001).
  • [ISSN] 0935-8943
  • [Journal-full-title] Laryngo- rhino- otologie
  • [ISO-abbreviation] Laryngorhinootologie
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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6. Emch GS, Hermann GE, Rogers RC: TNF-alpha activates solitary nucleus neurons responsive to gastric distension. Am J Physiol Gastrointest Liver Physiol; 2000 Sep;279(3):G582-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor necrosis factor-alpha (TNF-alpha) is liberated as part of the immune response to antigenic challenge, carcinogenesis, and radiation therapy.
  • In this study, we describe the role of TNF-alpha as a neuromodulator affecting neurons in the nucleus of the solitary tract that are involved in vago-vagal reflex control of gastric motility.
  • The results presented herein suggest that TNF-alpha may induce a persistent gastric stasis by functioning as a hormone that modulates intrinsic vago-vagal reflex pathways during illness.
  • [MeSH-major] Gastric Dilatation / physiopathology. Neurons / physiology. Solitary Nucleus / physiology. Stomach / innervation. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Gastric Emptying / physiology. Male. Microinjections. Rats. Rats, Long-Evans. Reflex / physiology. Vagus Nerve / physiology

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  • (PMID = 10960358.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-52142
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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7. Johnson DR, O'Connor JC, Dantzer R, Freund GG: Inhibition of vagally mediated immune-to-brain signaling by vanadyl sulfate speeds recovery from sickness. Proc Natl Acad Sci U S A; 2005 Oct 18;102(42):15184-9
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  • [Title] Inhibition of vagally mediated immune-to-brain signaling by vanadyl sulfate speeds recovery from sickness.
  • To the ill patient with diabetes, the behavioral symptoms of sickness such as fatigue and apathy are debilitating and can prevent recuperation.
  • Here we report that peripherally administered insulin-like growth factor 1 (IGF-1) attenuates LPS-dependent depression of social exploration (sickness) in nondiabetic (db/+) but not in diabetic (db/db) mice.
  • We show that the insulin/IGF-1 mimetic vanadyl sulfate (VS) is effective at augmenting recovery from sickness in both db/+ and db/db mice.
  • Specifically, peak illness was reached at 2 h for both VS and control animals injected with LPS, and VS mice recovered 50% faster than non-VS-treated animals.
  • Examination of the mechanism of VS action in db/+ mice showed that VS paradoxically augmented peritoneal macrophage responsivity to LPS, increasing both peritoneal and ex vivo macrophage production of IL-1beta and IL-6 but not TNF-alpha.
  • The effects of VS in promoting recovery from sickness were not restricted to LPS, because they were also observed after direct administration of IL-1beta.
  • To explore the possibility that VS impairs immune-to-brain communication via vagal afferents, the vagally mediated satiety-inducing effects of cholecystokinin 8 were tested in db/+ mice.
  • Cholecystokinin decreased food intake in saline-injected mice but not in VS-treated mice.
  • VS also inhibited LPS-dependent up-regulation of IL-1beta and IL-6 mRNA in the brain, while increasing by 50% the cerebral expression of transcripts of the specific antagonist of IL-1 receptors IL-1RA and IL-1R2.
  • Taken together, these data indicate that VS improves recovery from LPS-induced sickness by blocking vagally mediated immune-to-brain signaling and by up-regulating brain expression of IL-1beta antagonists.

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  • (PMID = 16217019.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK064862; United States / NIMH NIH HHS / MH / R01 MH071349; United States / NIDDK NIH HHS / DK / DK064862; United States / NIMH NIH HHS / MH / MH071349
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / IL1RN protein, human; 0 / Il1rn protein, mouse; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Sialoglycoproteins; 0 / Tumor Necrosis Factor-alpha; 0 / Vanadium Compounds; 67763-96-6 / Insulin-Like Growth Factor I; 6DU9Y533FA / vanadyl sulfate; 9011-97-6 / Cholecystokinin
  • [Other-IDs] NLM/ PMC1257721
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8. Konturek PC, Brzozowski T, Burnat G, Kwiecien S, Pawlik T, Hahn EG, Konturek SJ: Role of brain-gut axis in healing of gastric ulcers. J Physiol Pharmacol; 2004 Mar;55(1 Pt 2):179-92
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  • The rats of series C, consisting of animals with intact nerves or those with capsaicin-denervation, received the 7-day treatment with exogenous leptin (10 microg/kg i.p. twice daily) to check whether blockade of sensory nerves could influence the acceleration of ulcer healing by this peptide.
  • Treatment with exogenous leptin significantly accelerated ulcer healing, increased the GBF at ulcer margin and upregulated mRNA for iNOS and these effects were attenuated in rats with capsaicin-deactivation of sensory neurons.
  • [MeSH-major] Brain / physiology. Gastrointestinal Tract / physiology. Stomach Ulcer / drug therapy. Wound Healing / drug effects
  • [MeSH-minor] Acetic Acid / adverse effects. Animals. Antigens, CD31 / biosynthesis. Antigens, CD31 / chemistry. Capsaicin / administration & dosage. Capsaicin / adverse effects. Cell Line, Tumor. Cyclooxygenase 1. Cyclooxygenase 2. Gastric Mucosa / blood supply. Gastric Mucosa / pathology. Gastric Mucosa / physiology. Gene Expression Regulation, Enzymologic / drug effects. Injections, Intraperitoneal. Injections, Subcutaneous. Interleukin-1 / biosynthesis. Interleukin-1 / genetics. Isoenzymes / biosynthesis. Isoenzymes / genetics. Leptin / administration & dosage. Leptin / pharmacokinetics. Leptin / therapeutic use. Membrane Proteins. Neurons, Afferent / drug effects. Neurons, Afferent / physiology. Nitric Oxide Synthase / antagonists & inhibitors. Nitric Oxide Synthase / biosynthesis. Nitric Oxide Synthase / genetics. Nitric Oxide Synthase Type II. Prostaglandin-Endoperoxide Synthases / biosynthesis. Prostaglandin-Endoperoxide Synthases / genetics. RNA, Messenger / antagonists & inhibitors. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics. Up-Regulation / drug effects. Up-Regulation / genetics. Vagotomy / adverse effects. Vagotomy / methods. Vagus Nerve / drug effects. Vagus Nerve / physiology

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  • (PMID = 15082877.001).
  • [ISSN] 0867-5910
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Interleukin-1; 0 / Isoenzymes; 0 / Leptin; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, rat; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs1 protein, rat; Q40Q9N063P / Acetic Acid; S07O44R1ZM / Capsaicin
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9. Ottani A, Giuliani D, Galantucci M, Spaccapelo L, Novellino E, Grieco P, Jochem J, Guarini S: Melanocortins counteract inflammatory and apoptotic responses to prolonged myocardial ischemia/reperfusion through a vagus nerve-mediated mechanism. Eur J Pharmacol; 2010 Jul 10;637(1-3):124-30
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  • [Title] Melanocortins counteract inflammatory and apoptotic responses to prolonged myocardial ischemia/reperfusion through a vagus nerve-mediated mechanism.
  • Here we investigated melanocortin effects, and the role of the vagus nerve-mediated cholinergic protective pathway, in a rat model of prolonged myocardial ischemia/reperfusion associated with marked inflammatory and apoptotic reactions, and a large infarct size.
  • At the end of the 2-h reperfusion, western blot analysis of the inflammatory and apoptotic markers tumor necrosis factor-alpha (TNF-alpha), c-jun N-terminal kinases (JNK) and caspase-3, as well as of the anti-apoptotic extracellular signal-regulated kinases (ERK 1/2), was performed in the left ventricle.
  • Intravenous treatment, during coronary artery occlusion, with the melanocortin analog [Nle(4), D-Phe(7)]alpha-melanocyte-stimulating hormone (NDP-alpha-MSH) produced a reduction in TNF-alpha levels and in the activity of JNK and caspase-3, associated with marked activation of the pro-survival kinases ERK 1/2, and consequent attenuation of infarct size.
  • These results indicate that melanocortins modulate the inflammatory and apoptotic cascades triggered by prolonged myocardial ischemia/reperfusion, and reduce infarct size, seemingly by activation of the vagus nerve-mediated cholinergic protective pathway.
  • [MeSH-major] Apoptosis / drug effects. Inflammation / drug therapy. Inflammation / pathology. Melanocortins / pharmacology. Melanocortins / therapeutic use. Myocardial Reperfusion Injury / drug therapy. Myocardial Reperfusion Injury / pathology. Vagus Nerve / drug effects
  • [MeSH-minor] Animals. Blotting, Western. Caspase 3 / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. JNK Mitogen-Activated Protein Kinases / metabolism. Male. Rats. Rats, Wistar. Time Factors. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20385118.001).
  • [ISSN] 1879-0712
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Melanocortins; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3
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10. Rückert RI, Fleige B, Rogalla P, Woodruff JM: Schwannoma with angiosarcoma. Report of a case and comparison with other types of nerve tumors with angiosarcoma. Cancer; 2000 Oct 1;89(7):1577-85
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  • [Title] Schwannoma with angiosarcoma. Report of a case and comparison with other types of nerve tumors with angiosarcoma.
  • BACKGROUND: Schwannoma with angiosarcomatous change is a rare tumor, the clinical characteristics of which have not been analyzed.
  • METHODS: A patient with schwannoma with angiosarcoma arising in the midneck and clinically mimicking a carotid body paraganglioma is described with a literature review of all previously reported cases and a comparison of their clinical features with those of schwannoma with conventional malignant transformation and cases of neurofibroma and malignant peripheral nerve sheath tumor (MPNST) with angiosarcoma.
  • Three tumors arose from the vagus nerve in the neck.
  • Three of the four angiosarcomas were epithelioid in type.
  • Treatment in all cases was surgical resection followed by radiation and chemotherapy in one case and by radiation alone in another.
  • One patient died with residual local angiosarcoma 5 months after the diagnosis.
  • CONCLUSIONS: Schwannoma with angiosarcoma should be included in the differential diagnosis of presumed carotid body paragangliomas.
  • Recommended treatment is attempted complete surgical resection followed by radiation therapy and chemotherapy, if it can be tolerated by the patient.
  • [MeSH-major] Carotid Body Tumor / pathology. Hemangiosarcoma / pathology. Nerve Sheath Neoplasms / pathology. Neurilemmoma / pathology. Paraganglioma / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic. Diagnosis, Differential. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 11013374.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Number-of-references] 23
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11. Lubbers T, de Haan JJ, Luyer MD, Verbaeys I, Hadfoune M, Dejong CH, Buurman WA, Greve JW: Cholecystokinin/Cholecystokinin-1 receptor-mediated peripheral activation of the afferent vagus by enteral nutrients attenuates inflammation in rats. Ann Surg; 2010 Aug;252(2):376-82
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  • [Title] Cholecystokinin/Cholecystokinin-1 receptor-mediated peripheral activation of the afferent vagus by enteral nutrients attenuates inflammation in rats.
  • Tissue and blood were collected 90 minutes after shock to assess systemic inflammation and intestinal integrity.
  • RESULTS: Deafferentation reversed the inhibitory effect of lipid-rich nutrition on systemic levels of tumor necrosis factor-alpha and interleukin-6, and on intestinal leakage of horseradish peroxidase and bacterial translocation.
  • [MeSH-major] Cholecystokinin / physiology. Enteral Nutrition. Lipids / pharmacology. Receptors, Cholecystokinin / antagonists & inhibitors. Vagus Nerve / physiopathology
  • [MeSH-minor] Animals. Bacterial Translocation. Capsaicin. Inflammation / drug therapy. Inflammation / metabolism. Intestinal Absorption / drug effects. Male. Neural Pathways. Peptide Fragments / pharmacology. Quinolines / pharmacology. Rats. Rats, Sprague-Dawley. Shock, Hemorrhagic / metabolism

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  • [CommentIn] Ann Surg. 2011 Oct;254(4):661-2; author reply 662 [21876433.001]
  • (PMID = 20585240.001).
  • [ISSN] 1528-1140
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipids; 0 / Peptide Fragments; 0 / Quinolines; 0 / Receptors, Cholecystokinin; 108050-84-6 / cholecystokinin 9; 119295-94-2 / A 65186; 9011-97-6 / Cholecystokinin; S07O44R1ZM / Capsaicin
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12. Guarini S, Cainazzo MM, Giuliani D, Mioni C, Altavilla D, Marini H, Bigiani A, Ghiaroni V, Passaniti M, Leone S, Bazzani C, Caputi AP, Squadrito F, Bertolini A: Adrenocorticotropin reverses hemorrhagic shock in anesthetized rats through the rapid activation of a vagal anti-inflammatory pathway. Cardiovasc Res; 2004 Aug 1;63(2):357-65
Hazardous Substances Data Bank. ATROPINE .

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  • The transcription nuclear factor kappaB (NF-kappaB) triggers a potentially lethal systemic inflammatory response, with marked production of tumor necrosis factor-alpha (TNF-alpha), in hemorrhagic shock.
  • Here we investigated whether the hemorrhagic shock reversal produced by the melanocortin ACTH-(1-24) (adrenocorticotropin) depends on the activation of the recently recognized, vagus nerve-mediated, brain "cholinergic anti-inflammatory pathway".
  • In rats intravenously (i.v.) treated with ACTH-(1-24), neural efferent activity along vagus nerve (monitored by means of a standard system for extracellular recordings) was markedly increased, and the restoration of cardiovascular and respiratory functions was associated with blunted NF-kappaB activity and with decreased TNF-alpha mRNA liver content and TNF-alpha plasma levels.
  • CONCLUSIONS: The present data show, for the first time, that the melanocortin ACTH-(1-24) suppresses the NF-kappaB-dependent systemic inflammatory response triggered by hemorrhage, and reverses shock condition, by brain activation (in real-time) of the "cholinergic anti-inflammatory pathway", this pathway seeming to be melanocortin-dependent.
  • [MeSH-major] Cosyntropin / therapeutic use. Shock, Hemorrhagic / drug therapy. Shock, Hemorrhagic / physiopathology. Vagus Nerve / physiopathology
  • [MeSH-minor] Acute Disease. Animals. Atropine / pharmacology. Chlorisondamine / therapeutic use. Electrophoretic Mobility Shift Assay. Female. I-kappa B Proteins / metabolism. Liver / metabolism. Male. NF-kappa B / metabolism. RNA, Messenger / metabolism. Rats. Rats, Wistar. Receptors, Nicotinic / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / analysis. Tumor Necrosis Factor-alpha / genetics

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  • [Copyright] Copyright 2004 European Society of Cardiology
  • (PMID = 15249194.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Receptors, Nicotinic; 0 / Tumor Necrosis Factor-alpha; 16960-16-0 / Cosyntropin; 7C0697DR9I / Atropine; JD3M24F66I / Chlorisondamine
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13. Liu ZH, Ma YF, Wu JS, Gan JX, Xu SW, Jiang GY: Effect of cholinesterase inhibitor galanthamine on circulating tumor necrosis factor alpha in rats with lipopolysaccharide-induced peritonitis. Chin Med J (Engl); 2010 Jul;123(13):1727-30
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  • [Title] Effect of cholinesterase inhibitor galanthamine on circulating tumor necrosis factor alpha in rats with lipopolysaccharide-induced peritonitis.
  • BACKGROUND: The nervous system, through the vagus nerve and its neurotransmitter acetylcholine, can down-regulate the systemic inflammation in vivo, and recently, a role of brain cholinergic mechanisms in activating this cholinergic anti-inflammatory pathway has been indicated.
  • This study aimed to evaluate the effect of galanthamine on circulating tumor necrosis factor alpha (TNF-alpha) in rats with lipopolysaccharide-induced peritonitis and the possible role of the vagus nerve in the action of galanthamine.
  • Galanthamine treatment decreased the level of circulating TNF-alpha in rats with lipopolysaccharide-induced peritonitis, and there was significant difference compared with rats with lipopolysaccharide-induced peritonitis without treatment.
  • CONCLUSION: Cholinesterase inhibitor galanthamine has an inhibitory effect on TNF-alpha release in rats with lipopolysaccharide-induced peritonitis, and the vagus nerve plays a role in the process of the action of galanthamine.
  • [MeSH-major] Cholinesterase Inhibitors / therapeutic use. Galantamine / therapeutic use. Lipopolysaccharides / toxicity. Peritonitis / chemically induced. Peritonitis / drug therapy. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 20819637.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cholinesterase Inhibitors; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 0D3Q044KCA / Galantamine
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14. Minovi A, Basten O, Hunter B, Draf W, Bockmühl U: Malignant peripheral nerve sheath tumors of the head and neck: management of 10 cases and literature review. Head Neck; 2007 May;29(5):439-45
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  • [Title] Malignant peripheral nerve sheath tumors of the head and neck: management of 10 cases and literature review.
  • BACKGROUND: This study analyzes the management and outcomes of a series of 10 malignant peripheral nerve sheath tumors (MPNST) of the head and neck.
  • METHODS: From 1984 to 2004, 10 patients underwent surgical treatment of a MPNST.
  • RESULTS: Eight tumors were located at the lateral skull base; 2 involved the vagus nerve in isolation.
  • Seventy percent of the tumors could be resected completely.
  • Negative prognostic indicators were advanced tumor stage, early recurrence, and presumably also the presence of von Recklinghausen's disease.
  • CONCLUSIONS: Although rare, MPNST is one of the most aggressive tumors in the head and neck area.
  • Complete tumor removal is the mainstay of treatment and most important prognostic factor of MPNST.
  • The role of adjuvant chemotherapy remains controversial.
  • [MeSH-major] Head and Neck Neoplasms / mortality. Head and Neck Neoplasms / therapy. Neoplasm Recurrence, Local / mortality. Nerve Sheath Neoplasms / mortality. Nerve Sheath Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Chemotherapy, Adjuvant. Female. Humans. Male. Middle Aged. Prognosis. Radiotherapy, Adjuvant. Retrospective Studies. Survival Rate

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  • [Copyright] (c) 2006 Wiley Periodicals, Inc.
  • (PMID = 17163467.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 34
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15. Pavlov VA, Ochani M, Yang LH, Gallowitsch-Puerta M, Ochani K, Lin X, Levi J, Parrish WR, Rosas-Ballina M, Czura CJ, Larosa GJ, Miller EJ, Tracey KJ, Al-Abed Y: Selective alpha7-nicotinic acetylcholine receptor agonist GTS-21 improves survival in murine endotoxemia and severe sepsis. Crit Care Med; 2007 Apr;35(4):1139-44
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  • OBJECTIVE: Tumor necrosis factor and high mobility group box 1 are critical cytokine mediators of inflammation.
  • The efferent vagus nerve inhibits cytokine release through alpha7-nicotinic acetylcholine receptor-mediated cholinergic signaling.
  • INTERVENTIONS: RAW 264.7 cells were exposed to endotoxin (4 ng/mL or 10 ng/mL) in the presence or absence of GTS-21 (1-100 muM), and tumor necrosis factor and high mobility group box 1 release and nuclear factor-kappaB activation were analyzed.
  • Mice were treated with GTS-21 (0.4 mg/kg or 4 mg/kg, intraperitoneally) or saline 30 mins before endotoxin (6 mg/kg, intraperitoneally), and serum tumor necrosis factor was analyzed 1.5 hrs after the onset of endotoxemia.
  • In survival experiments, GTS-21 (0.4 or 4 mg/kg) treatment was initiated 24 hrs after CLP and continued twice daily for 3 days.
  • MEASUREMENTS AND MAIN RESULTS: GTS-21 dose-dependently inhibited tumor necrosis factor and high mobility group box 1 release and nuclear factor-kappaB activation in vitro.
  • GTS-21 (4 mg/kg) significantly inhibited serum tumor necrosis factor during endotoxemia and improved survival (p < .0001).
  • CONCLUSION: These findings are of interest for the development of alpha7-nicotinic acetylcholine receptor agonists as a new class of anti-inflammatory therapeutics.
  • [MeSH-major] Benzylidene Compounds / pharmacology. Endotoxemia / drug therapy. Nicotinic Agonists / pharmacology. Pyridines / pharmacology. Receptors, Nicotinic / metabolism. Sepsis / drug therapy
  • [MeSH-minor] Animals. Cell Line. Dose-Response Relationship, Drug. HMGB1 Protein / antagonists & inhibitors. In Vitro Techniques. Male. Mice. Mice, Inbred BALB C. NF-kappa B / antagonists & inhibitors. Severity of Illness Index. Survival Rate. Tumor Necrosis Factor-alpha / antagonists & inhibitors. alpha7 Nicotinic Acetylcholine Receptor

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  • [CommentIn] Crit Care Med. 2007 Aug;35(8):2003-4 [17667267.001]
  • [CommentIn] Crit Care Med. 2007 Apr;35(4):1215-6 [17413799.001]
  • (PMID = 17334244.001).
  • [ISSN] 0090-3493
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR018535
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzylidene Compounds; 0 / Chrna7 protein, mouse; 0 / HMGB1 Protein; 0 / NF-kappa B; 0 / Nicotinic Agonists; 0 / Pyridines; 0 / Receptors, Nicotinic; 0 / Tumor Necrosis Factor-alpha; 0 / alpha7 Nicotinic Acetylcholine Receptor; 156223-05-1 / 3-(2,4-dimethoxybenzylidene)anabaseine
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16. Liu C, Shen FM, Le YY, Kong Y, Liu X, Cai GJ, Chen AF, Su DF: Antishock effect of anisodamine involves a novel pathway for activating alpha7 nicotinic acetylcholine receptor. Crit Care Med; 2009 Feb;37(2):634-41
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Vagus nerve stimulation inhibits proinflammatory cytokine production by signaling through the alpha7 nicotinic acetylcholine receptor (alpha7nAChR).
  • Anisodamine, a muscarinic acetylcholine receptor antagonist, has been used clinically in China for treatment of various shocks, but the mechanism was poorly understood.
  • Mice peritoneal macrophages were pretreated and stimulated with LPS, and tumor necrosis factor (TNF)-alpha in the supernatant was measured by enzyme-linked immunosorbent assay.
  • [MeSH-major] Nicotinic Agonists / pharmacology. Receptors, Nicotinic / drug effects. Shock, Septic / drug therapy. Solanaceous Alkaloids / pharmacology
  • [MeSH-minor] Aconitine / analogs & derivatives. Aconitine / pharmacology. Animals. Base Sequence. Cell Line. China. DNA Primers. Interleukin-1beta / metabolism. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / metabolism. Mice. Nicotinic Antagonists / pharmacology. Polymerase Chain Reaction. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / metabolism. Vagotomy. alpha7 Nicotinic Acetylcholine Receptor

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  • [CommentIn] Crit Care Med. 2009 Feb;37(2):778-9 [19325386.001]
  • (PMID = 19114896.001).
  • [ISSN] 1530-0293
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM077352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chrna7 protein, mouse; 0 / Chrna7 protein, rat; 0 / DNA Primers; 0 / Interleukin-1beta; 0 / Nicotinic Agonists; 0 / Nicotinic Antagonists; 0 / Receptors, Nicotinic; 0 / Solanaceous Alkaloids; 0 / Tumor Necrosis Factor-alpha; 0 / alpha7 Nicotinic Acetylcholine Receptor; 01343Q8EL8 / anisodamine; 21019-30-7 / methyllycaconitine; X8YN71D5WC / Aconitine
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17. Rabussay DP, Nanda GS, Goldfarb PM: Enhancing the effectiveness of drug-based cancer therapy by electroporation (electropermeabilization). Technol Cancer Res Treat; 2002 Feb;1(1):71-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhancing the effectiveness of drug-based cancer therapy by electroporation (electropermeabilization).
  • Many conventional chemotherapeutic drugs, as well as DNA for cancer gene therapy, require efficient access to the cell interior to be effective.
  • The cell membrane is a formidable barrier to many of these drugs, including therapeutic DNA constructs.
  • EP is achieved by the application of short electrical pulses of relatively high local field strength to the target tissue of choice.
  • In cancer therapy, EP can be applied in vivo directly to the tumor to be treated, in order to enhance intracellular uptake of drugs or DNA.
  • Alternatively, EP can be used to deliver DNA into cells of healthy tissue to achieve longer-lasting expression of cancer-suppressing genes.
  • In addition, EP has been used in ex vivo therapeutic approaches for the transfection of a variety of cells in suspension.
  • In this paper, we communicate results related to the development of a treatment for squamous cell carcinomas of the head and neck, using electropermeabilization to deliver the drug bleomycin in vivo directly into the tumor cells.
  • This drug, which is not particularly effective as a conventional therapeutic, becomes highly potent when the intracellular concentration is enhanced by EP treatment.
  • In animal model experiments we found a drug dose of 1 U/cm(3) tumor tissue (delivered in 0.25 mL of an aqueous solution/cm3 tumor tissue) and an electrical field strength of 750 V/cm or higher to be optimal for the treatment of human squamous cell tumors grown subcutaneously in mice.
  • Within 24-48 hours, the majority of tumor cells are rapidly destroyed by this bleomycin-electroporation therapy (B-EPT).
  • This raises the concern that healthy tissue may be similarly affected.
  • In studies with large animals we showed that normal muscle and skin tissue, normal tissue surrounding major blood vessels and nerves, as well as healthy blood vessels and nerves themselves, are much less affected than tumor tissue.
  • Normal tissues did show acute, focal, and transitory effects after treatment, but these effects are relatively minor under standard treatment conditions.
  • The observed histological changes resolved 20 to 40 days after treatment or sooner, even after excessive EP treatment.
  • Thus, B-EPT is distinct from other ablative therapies, such as thermal, cryo, or photodynamic ablation, which equally affect healthy and tumor tissue.
  • In comparison to surgical or radiation therapy, B-EPT also has potential as a tissue-sparing and function-preserving therapy.
  • In clinical studies with over 50 late stage head and neck cancer patients, objective tumor response rates of 55-58%, and complete tumor response rates of 19-30% have been achieved.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Bleomycin / administration & dosage. Carcinoma, Squamous Cell / therapy. Electroporation / methods. Head and Neck Neoplasms / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Animals. Arteries / drug effects. Arteries / pathology. Cell Membrane Permeability / drug effects. Disease Models, Animal. Dogs. Electric Stimulation Therapy / adverse effects. Electric Stimulation Therapy / methods. Female. Fibrosis. Hemorrhage / etiology. Humans. Inflammation / etiology. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Muscles / blood supply. Muscles / drug effects. Muscles / pathology. Necrosis. Skin / drug effects. Skin / pathology. Skin Diseases / etiology. Skin Diseases / pathology. Swine. Vagus Nerve / drug effects. Vagus Nerve / pathology

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  • (PMID = 12614180.001).
  • [ISSN] 1533-0346
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2R44CA62905-02A2
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 11056-06-7 / Bleomycin
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18. Das UN: Beneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how? Prostaglandins Leukot Essent Fatty Acids; 2000 Dec;63(6):351-62
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease.
  • [MeSH-minor] Acetylcholine / physiology. Animals. Arrhythmias, Cardiac / epidemiology. Arrhythmias, Cardiac / prevention & control. Brain / physiopathology. Cell Adhesion Molecules / biosynthesis. Cell Adhesion Molecules / genetics. Cell Division / drug effects. Clinical Trials as Topic. Cohort Studies. Cytokines / metabolism. Eicosanoids / metabolism. Endothelium, Vascular / drug effects. Endothelium, Vascular / metabolism. Exercise. Fatty Acids, Unsaturated / metabolism. Gene Expression Regulation / drug effects. Greenland / epidemiology. Heart / drug effects. Hemostasis / drug effects. Humans. Hypothalamo-Hypophyseal System / drug effects. Hypothalamo-Hypophyseal System / physiopathology. Inflammation / drug therapy. Inflammation / metabolism. Inflammation / prevention & control. Inuits. Japan / epidemiology. Lipid Metabolism. Models, Biological. Myocardium / metabolism. Oxidation-Reduction. Oxidative Stress. Parasympathetic Nervous System / drug effects. Pituitary-Adrenal System / drug effects. Pituitary-Adrenal System / physiopathology. Rats. Sodium Channels / drug effects. Vagus Nerve / physiopathology

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  • [ErratumIn] Prostaglandins Leukot Essent Fatty Acids 2001 Jan;64(1):74
  • (PMID = 11133172.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / Dietary Fats; 0 / Eicosanoids; 0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Unsaturated; 0 / Fish Oils; 0 / Sodium Channels; N9YNS0M02X / Acetylcholine
  • [Number-of-references] 143
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19. Shimaoka M, Park EJ: Advances in understanding sepsis. Eur J Anaesthesiol Suppl; 2008;42:146-53
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  • This dual inflammatory response concomitant with dysregulated coagulation partially accounts for unsuccessful anti-cytokine therapies that have solely targeted early pro-inflammatory mediators (e.g. tumour necrosis factor-alpha).
  • The vagus nerve system has also been shown to suppress innate immune response through endogenous release and exogenous administration of cholinergic agonists, ameliorating inflammation and lethality in sepsis models.

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  • (PMID = 18289433.001).
  • [ISSN] 0952-1941
  • [Journal-full-title] European journal of anaesthesiology. Supplement
  • [ISO-abbreviation] Eur J Anaesthesiol Suppl
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI063421-04; United States / NIAID NIH HHS / AI / R01 AI063421; United States / NIAID NIH HHS / AI / AI063421-04; United States / NHLBI NIH HHS / HL / P01 HL048675-150013; United States / NIAID NIH HHS / AI / AI63421; United States / NHLBI NIH HHS / HL / HL048675-150013
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cholinergic Agonists; 0 / Protein C; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 61
  • [Other-IDs] NLM/ NIHMS56967; NLM/ PMC2490719
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20. Pavlov VA, Parrish WR, Rosas-Ballina M, Ochani M, Puerta M, Ochani K, Chavan S, Al-Abed Y, Tracey KJ: Brain acetylcholinesterase activity controls systemic cytokine levels through the cholinergic anti-inflammatory pathway. Brain Behav Immun; 2009 Jan;23(1):41-5
The Lens. Cited by Patents in .

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  • Recent advances in understanding the biology of cytokine toxicity led to the discovery of the "cholinergic anti-inflammatory pathway," defined as neural signals transmitted via the vagus nerve that inhibit cytokine release through a mechanism that requires the alpha7 subunit-containing nicotinic acetylcholine receptor (alpha7nAChR).
  • Vagus nerve regulation of peripheral functions is controlled by brain nuclei and neural networks, but despite considerable importance, little is known about the molecular basis for central regulation of the vagus nerve-based cholinergic anti-inflammatory pathway.
  • Peripheral administration of the acetylcholinesterase inhibitor galantamine significantly reduced serum TNF levels through vagus nerve signaling, and protected against lethality during murine endotoxemia.
  • Our data also indicate that a clinically used centrally-acting acetylcholinesterase inhibitor can be utilized to suppress abnormal inflammation to therapeutic advantage.

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  • (PMID = 18639629.001).
  • [ISSN] 1090-2139
  • [Journal-full-title] Brain, behavior, and immunity
  • [ISO-abbreviation] Brain Behav. Immun.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM089807; United States / NIGMS NIH HHS / GM / R01 GM0557226
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Atropine Derivatives; 0 / Cholinesterase Inhibitors; 0 / Chrna7 protein, mouse; 0 / Cytokines; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Parasympatholytics; 0 / Receptors, Nicotinic; 0 / Sesquiterpenes; 0 / Tumor Necrosis Factor-alpha; 0 / alpha7 Nicotinic Acetylcholine Receptor; 0111871I23 / huperzine A; 0D3Q044KCA / Galantamine; 80719I460H / methylatropine; EC 3.1.1.7 / Acetylcholinesterase
  • [Other-IDs] NLM/ NIHMS84576; NLM/ PMC4533839
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21. Yeboah MM, Xue X, Duan B, Ochani M, Tracey KJ, Susin M, Metz CN: Cholinergic agonists attenuate renal ischemia-reperfusion injury in rats. Kidney Int; 2008 Jul;74(1):62-9
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  • Local inflammation is modulated by the brain via the vagus nerve and nicotinic acetylcholine receptors such that electrical or pharmacologic stimulation of this cholinergic anti-inflammatory pathway results in suppression of proinflammatory cytokine production.
  • Similarly, tumor necrosis factor-alpha protein expression and leukocyte infiltration of the kidney were markedly reduced following treatment with cholinergic agonists.
  • We found functional nicotinic acetylcholine receptors were present on rat proximal tubule epithelial cells.
  • Cholinergic stimulation significantly decreased tubular necrosis in vagotomized rats after injury, implying an intact vagus nerve is not required for this renoprotective effect.

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  • (PMID = 18401335.001).
  • [ISSN] 1523-1755
  • [Journal-full-title] Kidney international
  • [ISO-abbreviation] Kidney Int.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM070727; United States / NIGMS NIH HHS / GM / R01 GM057226; United States / NIGMS NIH HHS / GM / R01 GM070727-03; United States / NIGMS NIH HHS / GM / R01GM070727; United States / NIGMS NIH HHS / GM / GM070727-02; United States / NIGMS NIH HHS / GM / R01GM0577226; United States / NIGMS NIH HHS / GM / R01 GM070727-02; United States / NIGMS NIH HHS / GM / GM070727-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cholinergic Agonists; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS98400; NLM/ PMC2667336
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22. Parrish WR, Rosas-Ballina M, Gallowitsch-Puerta M, Ochani M, Ochani K, Yang LH, Hudson L, Lin X, Patel N, Johnson SM, Chavan S, Goldstein RS, Czura CJ, Miller EJ, Al-Abed Y, Tracey KJ, Pavlov VA: Modulation of TNF release by choline requires alpha7 subunit nicotinic acetylcholine receptor-mediated signaling. Mol Med; 2008 Sep-Oct;14(9-10):567-74
Hazardous Substances Data Bank. CHOLINE CHLORIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The alpha7 subunit-containing nicotinic acetylcholine receptor (alpha7nAChR) is an essential component in the vagus nerve-based cholinergic anti-inflammatory pathway that regulates the levels of TNF, high mobility group box 1 (HMGB1), and other cytokines during inflammation.
  • ]) treatment prior to endotoxin administration in mice significantly reduced systemic TNF levels.
  • In contrast to its TNF suppressive effect in wild type mice, choline (50 mg/kg, i.p.) failed to inhibit systemic TNF levels in alpha7nAChR knockout mice during endotoxemia.
  • Choline treatment prior to endotoxin resulted in a significantly improved survival rate as compared with saline-treated endotoxemic controls.
  • Choline also suppressed HMGB1 release in vitro and in vivo, and choline treatment initiated 24 h after cecal ligation and puncture (CLP)-induced polymicrobial sepsis significantly improved survival in mice.

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  • (PMID = 18584048.001).
  • [ISSN] 1528-3658
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM057226; United States / PHS HHS / / M01 R018535; United States / NIGMS NIH HHS / GM / R01 GM0557226-08A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Chrna7 protein, human; 0 / Chrna7 protein, mouse; 0 / Endotoxins; 0 / HMGB1 Protein; 0 / Receptors, Nicotinic; 0 / Tumor Necrosis Factor-alpha; 0 / alpha7 Nicotinic Acetylcholine Receptor; N91BDP6H0X / Choline
  • [Other-IDs] NLM/ PMC2435495
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23. Floto RA, Smith KG: The vagus nerve, macrophages, and nicotine. Lancet; 2003 Mar 29;361(9363):1069-70
Hazardous Substances Data Bank. NICOTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The vagus nerve, macrophages, and nicotine.
  • [MeSH-major] Alveolitis, Extrinsic Allergic / immunology. Macrophage Activation / drug effects. Nicotine / adverse effects. Receptors, Nicotinic / drug effects. Sarcoidosis, Pulmonary / immunology. Smoking / adverse effects. Vagus Nerve / drug effects
  • [MeSH-minor] Acupuncture Therapy. Humans. Immune Tolerance / immunology. Interleukin-1 / metabolism. Tumor Necrosis Factor-alpha / metabolism. alpha7 Nicotinic Acetylcholine Receptor

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  • (PMID = 12672307.001).
  • [ISSN] 0140-6736
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chrna7 protein, human; 0 / Interleukin-1; 0 / Receptors, Nicotinic; 0 / Tumor Necrosis Factor-alpha; 0 / alpha7 Nicotinic Acetylcholine Receptor; 6M3C89ZY6R / Nicotine
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