[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 12 of about 12
1. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • Hazardous Substances Data Bank. BLEOMYCIN .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


2. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Hazardous Substances Data Bank. CAPSAICIN .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


3. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


Advertisement
4. Li T, Zuo X, Zhou Y, Wang Y, Zhuang H, Zhang L, Zhang H, Xiao X: The vagus nerve and nicotinic receptors involve inhibition of HMGB1 release and early pro-inflammatory cytokines function in collagen-induced arthritis. J Clin Immunol; 2010 Mar;30(2):213-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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 involve inhibition of HMGB1 release and early pro-inflammatory cytokines function in collagen-induced arthritis.
  • OBJECTIVES: The cholinergic anti-inflammatory pathway, a vagus nerve-dependent mechanism, inhibits cytokine releases in models of acute inflammatory disease.
  • The concentration of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-10 in serum were evaluated by ELISA.
  • Study of this pathway could be used for RA therapy.
  • [MeSH-major] Arthritis, Experimental / immunology. HMGB1 Protein / antagonists & inhibitors. Nicotine / administration & dosage. Receptors, Nicotinic / metabolism. Vagus Nerve / immunology
  • [MeSH-minor] Animals. Cattle. Cholinergic Agents / administration & dosage. Collagen Type II / administration & dosage. Cytokines / antagonists & inhibitors. Cytokines / blood. Disease Progression. Inflammation. Male. Mice. Mice, Inbred DBA. Synovial Membrane / pathology. Vagotomy

  • Hazardous Substances Data Bank. NICOTINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arthritis Rheum. 2009 Jan;60(1):114-22 [19116908.001]
  • [Cites] Shock. 2008 Oct;30(4):468-72 [18391858.001]
  • [Cites] Rheumatology (Oxford). 2005 Aug;44(8):1026-31 [15870150.001]
  • [Cites] Arthritis Rheum. 2003 Apr;48(4):971-81 [12687539.001]
  • [Cites] Nature. 2003 Jan 23;421(6921):384-8 [12508119.001]
  • [Cites] Nat Immunol. 2005 Aug;6(8):844-51 [16025117.001]
  • [Cites] Rheumatology (Oxford). 2002 Mar;41(3):329-37 [11934972.001]
  • [Cites] J Immunol. 1998 Nov 1;161(9):4652-60 [9794394.001]
  • [Cites] Nat Rev Immunol. 2005 Apr;5(4):331-42 [15803152.001]
  • [Cites] Clin Exp Immunol. 2000 May;120(2):375-83 [10792391.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):853-9 [12490958.001]
  • [Cites] Curr Opin Rheumatol. 2004 May;16(3):218-22 [15103248.001]
  • [Cites] Clin Exp Immunol. 1997 Mar;107(3):507-12 [9067525.001]
  • [Cites] Clin Exp Immunol. 1999 Jan;115(1):32-41 [9933418.001]
  • [Cites] J Infect Dis. 2005 Jun 15;191(12):2138-48 [15898001.001]
  • [Cites] Brain Behav Immun. 2005 Nov;19(6):493-9 [15922555.001]
  • [Cites] J Immunol. 1998 Oct 1;161(7):3639-44 [9759887.001]
  • [Cites] Nature. 2000 May 25;405(6785):458-62 [10839541.001]
  • [Cites] Arthritis Rheum. 2006 Jan;54(1):158-68 [16385511.001]
  • [Cites] Cancer Immunol Immunother. 1994 Feb;38(2):119-26 [8306367.001]
  • [Cites] Mol Med. 2007 Mar-Apr;13(3-4):210-5 [17597834.001]
  • [Cites] Cytokine. 2000 Mar;12(3):281-8 [10704256.001]
  • [Cites] Ann Rheum Dis. 2008 Nov;67(11):1516-23 [18625622.001]
  • [Cites] Nat Rev Drug Discov. 2005 Aug;4(8):673-84 [16056392.001]
  • [Cites] Nature. 2003 May 15;423(6937):356-61 [12748655.001]
  • [Cites] Nat Med. 2004 Nov;10(11):1216-21 [15502843.001]
  • [Cites] Clin Exp Immunol. 1997 Mar;107(3):485-93 [9067522.001]
  • [Cites] Rheumatology (Oxford). 2004 Jun;43(6):712-8 [15039494.001]
  • [Cites] Arthritis Rheum. 2003 Jun;48(6):1693-700 [12794838.001]
  • [Cites] Arthritis Rheum. 2002 Oct;46(10):2598-603 [12384917.001]
  • [Cites] Ann N Y Acad Sci. 2005 Dec;1062:209-19 [16461803.001]
  • [Cites] Mol Med. 2003 May-Aug;9(5-8):125-34 [14571320.001]
  • [Cites] Arthritis Rheum. 2003 Jul;48(7):2052-8 [12847700.001]
  • [Cites] N Engl J Med. 2001 Mar 22;344(12):907-16 [11259725.001]
  • (PMID = 19890701.001).
  • [ISSN] 1573-2592
  • [Journal-full-title] Journal of clinical immunology
  • [ISO-abbreviation] J. Clin. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cholinergic Agents; 0 / Collagen Type II; 0 / Cytokines; 0 / HMGB1 Protein; 0 / Receptors, Nicotinic; 6M3C89ZY6R / Nicotine
  •  go-up   go-down


5. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


6. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • MedlinePlus Health Information. consumer health - Diabetes Medicines.
  • MedlinePlus Health Information. consumer health - Immune System and Disorders.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VANADIUM COMPOUNDS .
  • Hazardous Substances Data Bank. VANADYL SULFATE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Adv Intern Med. 1979;24:23-52 [218432.001]
  • [Cites] Physiol Behav. 1982 Oct;29(4):599-604 [6294698.001]
  • [Cites] Neurosci Biobehav Rev. 1988 Summer;12(2):123-37 [3050629.001]
  • [Cites] Nature. 1990 Jan 25;343(6256):336-40 [2137200.001]
  • [Cites] Brain Res. 1995 Apr 17;677(1):171-6 [7606464.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Sep 13;226(2):506-11 [8806664.001]
  • [Cites] Mol Cell Biochem. 1995 Dec 6-20;153(1-2):103-12 [8927024.001]
  • [Cites] Biochemistry. 1999 Nov 2;38(44):14667-75 [10545192.001]
  • [Cites] Eur J Endocrinol. 1999 Nov;141(5):546-54 [10576774.001]
  • [Cites] J Biol Chem. 2000 Feb 11;275(6):4283-9 [10660596.001]
  • [Cites] Inflammation. 2000 Apr;24(2):127-39 [10718115.001]
  • [Cites] Diabetes. 1990 Sep;39(9):1028-32 [2166697.001]
  • [Cites] EMBO J. 1991 Oct;10(10):2821-32 [1833184.001]
  • [Cites] FASEB J. 1991 Sep;5(12):2661-7 [1916090.001]
  • [Cites] Trends Pharmacol Sci. 1992 Jan;13(1):24-8 [1542935.001]
  • [Cites] Eur J Pharmacol. 1991 Dec 17;209(3):281-3 [1839150.001]
  • [Cites] Ann N Y Acad Sci. 1992 Apr 15;650:268-75 [1605483.001]
  • [Cites] Brain Res. 1992 Feb 28;573(2):318-20 [1387028.001]
  • [Cites] Brain Res. 1992 Aug 21;588(2):291-6 [1393581.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9117-20 [1409612.001]
  • [Cites] J Biol Chem. 1993 Feb 5;268(4):2513-24 [8428929.001]
  • [Cites] Brain Res. 1993 Oct 8;624(1-2):291-4 [8252403.001]
  • [Cites] Psychoneuroendocrinology. 1994;19(2):197-207 [8190839.001]
  • [Cites] Brain Res Mol Brain Res. 1994 Nov;27(1):157-62 [7877446.001]
  • [Cites] J Clin Invest. 1995 Jun;95(6):2806-12 [7769120.001]
  • [Cites] J Biol Chem. 2000 Aug 4;275(31):23642-7 [10807907.001]
  • [Cites] N Engl J Med. 2000 Sep 7;343(10):732-4 [10974140.001]
  • [Cites] Biochem Pharmacol. 2000 Oct 1;60(7):877-83 [10974195.001]
  • [Cites] Life Sci. 2000 Jun 8;67(3):291-300 [10983873.001]
  • [Cites] Physiol Behav. 2000 Aug-Sep;70(3-4):367-73 [11006436.001]
  • [Cites] Eur J Neurosci. 2000 Dec;12(12):4434-46 [11122354.001]
  • [Cites] Eur J Neurosci. 2000 Dec;12(12):4447-56 [11122355.001]
  • [Cites] Auton Neurosci. 2000 Dec 20;85(1-3):127-32 [11189019.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Mar;86(3):1410-7 [11238540.001]
  • [Cites] Hum Mol Genet. 2001 Mar 15;10(6):605-16 [11230180.001]
  • [Cites] JAMA. 2001 Jul 18;286(3):327-34 [11466099.001]
  • [Cites] Diabetes. 2001 Oct;50(10):2384-9 [11574423.001]
  • [Cites] Neuropsychopharmacology. 2002 Jan;26(1):86-93 [11751035.001]
  • [Cites] Trends Neurosci. 2002 Mar;25(3):154-9 [11852148.001]
  • [Cites] Cardiovasc Drugs Ther. 2001 Sep;15(5):445-52 [11855663.001]
  • [Cites] Diabetes. 2002 Apr;51(4):1131-7 [11916936.001]
  • [Cites] Ann N Y Acad Sci. 2001 Mar;933:222-34 [12000023.001]
  • [Cites] Brain Behav Immun. 2002 Oct;16(5):513-24 [12401465.001]
  • [Cites] Neuroreport. 1996 Jun 17;7(9):1485-8 [8856703.001]
  • [Cites] FEBS Lett. 1997 Mar 3;404(1):37-40 [9074633.001]
  • [Cites] Pharmacol Toxicol. 1997 Apr;80(4):202-6 [9140141.001]
  • [Cites] J Clin Invest. 1997 May 15;99(10):2538-44 [9153298.001]
  • [Cites] J Toxicol Environ Health. 1997 Aug 29;51(6):591-608 [9242230.001]
  • [Cites] Ann N Y Acad Sci. 1997 Aug 14;823:234-46 [9292049.001]
  • [Cites] Crit Rev Biochem Mol Biol. 1998;33(1):1-52 [9543627.001]
  • [Cites] Mol Cell Biochem. 1998 May;182(1-2):101-8 [9609119.001]
  • [Cites] Neurosci Lett. 1998 Apr 24;246(2):101-4 [9627190.001]
  • [Cites] Ann N Y Acad Sci. 1998 May 1;840:586-90 [9629285.001]
  • [Cites] Neuroimmunomodulation. 1998 Sep-Oct;5(5):234-40 [9730691.001]
  • [Cites] Brain Res. 1998 Sep 7;804(2):306-10 [9757071.001]
  • [Cites] J Biol Chem. 1998 Oct 9;273(41):26908-14 [9756938.001]
  • [Cites] Am J Physiol. 1999 Mar;276(3 Pt 2):R652-8 [10070124.001]
  • [Cites] Neuroscience. 1999 Mar;89(2):535-48 [10077334.001]
  • [Cites] J Neurosci. 1999 Apr 1;19(7):2799-806 [10087091.001]
  • [Cites] Sports Med. 1999 Feb;27(2):97-110 [10091274.001]
  • [Cites] Psychoneuroendocrinology. 1999 Apr;24(3):301-11 [10101735.001]
  • [Cites] Neuroreport. 1999 Feb 5;10(2):289-92 [10203323.001]
  • [Cites] Adv Exp Med Biol. 1999;461:83-105 [10442169.001]
  • [Cites] Crit Rev Food Sci Nutr. 1999 Jul;39(4):317-28 [10442270.001]
  • [Cites] Mol Endocrinol. 1999 Oct;13(10):1784-98 [10517679.001]
  • [Cites] Phys Med Rehabil Clin N Am. 1999 Aug;10(3):673-703 [10516985.001]
  • [Cites] Am J Clin Nutr. 1963 Jan;12:49-53 [14027941.001]
  • [Cites] Horm Res. 2004;62 Suppl 1:77-82 [15761237.001]
  • [Cites] J Immunol. 2005 Apr 15;174(8):4991-7 [15814729.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):853-9 [12490958.001]
  • [Cites] Diabet Med. 2003 Jan;20(1):3-15 [12519314.001]
  • [Cites] Diabetes. 2003 Mar;52(3):812-7 [12606524.001]
  • [Cites] Free Radic Biol Med. 2003 May 15;34(10):1333-42 [12726921.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2003 Jun;284(6):E1055-64 [12569083.001]
  • [Cites] Nat Neurosci. 2004 Apr;7(4):335-6 [15034587.001]
  • [Cites] Toxicol Lett. 2004 Apr 21;150(2):135-43 [15093669.001]
  • [Cites] Biol Pharm Bull. 2004 Jun;27(6):789-96 [15187419.001]
  • [Cites] J Biol Chem. 2004 Jul 2;279(27):28045-50 [15123681.001]
  • (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
  •  go-up   go-down


7. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Schwannoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


8. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CHOLINE CHLORIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 May 25;405(6785):458-62 [10839541.001]
  • [Cites] Kidney Int. 2008 Jul;74(1):62-9 [18401335.001]
  • [Cites] Food Chem Toxicol. 2002 Apr;40(4):545-9 [11893413.001]
  • [Cites] Br J Pharmacol. 2002 Sep;137(1):49-61 [12183330.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):853-9 [12490958.001]
  • [Cites] Nature. 2003 Jan 23;421(6921):384-8 [12508119.001]
  • [Cites] Mol Med. 2003 May-Aug;9(5-8):125-34 [14571320.001]
  • [Cites] J Intern Med. 2004 Mar;255(3):320-31 [14871456.001]
  • [Cites] Proc Soc Exp Biol Med. 1968 Oct;129(1):29-31 [5686530.001]
  • [Cites] Science. 1986 Oct 24;234(4775):470-4 [3764421.001]
  • [Cites] Am J Pathol. 1991 Feb;138(2):395-402 [1992764.001]
  • [Cites] Nutr Rev. 1994 Oct;52(10):327-39 [7816350.001]
  • [Cites] J Neurophysiol. 1995 Sep;74(3):1212-21 [7500145.001]
  • [Cites] Neurosci Lett. 1996 Aug 9;213(3):201-4 [8873149.001]
  • [Cites] Alcohol Clin Exp Res. 1997 Sep;21(6):1037-41 [9309314.001]
  • [Cites] Eur J Neurosci. 1997 Dec;9(12):2734-42 [9517478.001]
  • [Cites] Science. 1998 Aug 7;281(5378):794-5 [9714685.001]
  • [Cites] Am J Physiol. 1998 Oct;275(4 Pt 1):G862-7 [9756519.001]
  • [Cites] Immunity. 2005 Jan;22(1):93-104 [15664162.001]
  • [Cites] Nat Rev Immunol. 2005 Apr;5(4):331-42 [15803152.001]
  • [Cites] J Exp Med. 2005 Apr 4;201(7):1113-23 [15809354.001]
  • [Cites] Shock. 2005 Sep;24(3):288-93 [16135970.001]
  • [Cites] Brain Behav Immun. 2005 Nov;19(6):493-9 [15922555.001]
  • [Cites] Eur J Pharmacol. 2005 Nov 7;524(1-3):11-8 [16266703.001]
  • [Cites] Shock. 2006 Jan;25(1):73-9 [16369190.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5219-23 [16549778.001]
  • [Cites] Gastroenterology. 2006 May;130(6):1822-30 [16697744.001]
  • [Cites] Annu Rev Nutr. 2006;26:229-50 [16848706.001]
  • [Cites] Methods Mol Biol. 2007;361:145-62 [17172710.001]
  • [Cites] J Clin Invest. 2007 Feb;117(2):289-96 [17273548.001]
  • [Cites] J Leukoc Biol. 2007 Mar;81(3):599-606 [17108054.001]
  • [Cites] Crit Care Med. 2007 Apr;35(4):1139-44 [17334244.001]
  • [Cites] Life Sci. 2007 May 30;80(24-25):2325-9 [17289087.001]
  • [Cites] Life Sci. 2007 May 30;80(24-25):2314-9 [17383684.001]
  • [Cites] Am J Respir Cell Mol Biol. 2007 Aug;37(2):186-92 [17431097.001]
  • [Cites] Crit Care Med. 2007 Dec;35(12):2762-8 [17901837.001]
  • [Cites] Nutrition. 2000 Jul-Aug;16(7-8):669-71 [10906592.001]
  • (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
  •  go-up   go-down


9. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Malignant peripheral nerve sheath tumor.
  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


10. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Dietary Fats.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


11. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GALANTAMINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • Hazardous Substances Data Bank. NICOTINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down






Advertisement