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- 1. 線維筋痛症の病因 pathogenesis of fibromyalgia
- 2. コレシストキニンの生理学 physiology of cholecystokinin
- 3. 過敏性腸症候群に対するアロセトロン塩酸塩（Lotronex） alosetron hydrochloride lotronex for irritable bowel syndrome
- 4. 脆弱X症候群：小児および思春期におけるマネージメント fragile x syndrome management in children and adolescents
- 5. 癌疼痛のマネージメント：介入的治療 cancer pain management interventional therapies
- Negative cerebral blood volume fMRI response coupled with Ca(2+)-dependent brain activity in a dopaminergic road map of nociception.
- Hsu YH1, Chang C1, Chen CC2.Author information 1Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan; Institute of Biomedical Sciences, Academic Sinica, Taipei, Taiwan.2Institute of Biomedical Sciences, Academic Sinica, Taipei, Taiwan. Electronic address: firstname.lastname@example.org.AbstractDecreased cerebral blood volume/flow (CBV/CBF) contributes to negative blood-oxygen-level-dependent (BOLD) functional MRI (fMRI) signals. But it is still strongly debated whether these negative BOLD or CBV/CBF signals are indicative of decreased or increased neuronal activity. The fidelity of Ca(2+) signals in reflecting neuronal excitation is well documented. However, the roles of Ca(2+) signals and Ca(2+)-dependent activity in negative fMRI signals have never been explored; an understanding of this is essential to unraveling the underlying mechanisms and correctly interpreting the hemodynamic response of interest. The present study utilized a nociception-induced negative CBV fMRI response as a model. Ca(2+) signals were investigated in vivo using Mn(2+)-enhanced MRI (MEMRI), and the downstream Ca(2+)-dependent signaling was investigated using phosphorylated cAMP response-element-binding (pCREB) immunohistology. The results showed that nociceptive stimulation led to (1) striatal CBV decreases, (2) Ca(2+) increases via the nigrostriatal pathway, and (3) substantial expression of pCREB in substantia nigra dopaminergic neurons and striatal neurons. Interestingly, the striatal negative fMRI response was abolished by blocking substantia nigra activity but was not affected by blocking the striatal activity. This suggests the importance of input activity other than output in triggering the negative CBV signals. These findings indicate that the striatal negative CBV fMRI signals are associated with Ca(2+) increases and Ca(2+)-dependent signaling along the nigrostriatal pathway. The obtained data reveal a new brain road map in response to nociceptive stimulation of hemodynamic changes in association with Ca(2+) signals within the dopaminergic system.
- NeuroImage.Neuroimage.2014 Apr 15;90:43-51. doi: 10.1016/j.neuroimage.2013.12.028. Epub 2013 Dec 22.
- Decreased cerebral blood volume/flow (CBV/CBF) contributes to negative blood-oxygen-level-dependent (BOLD) functional MRI (fMRI) signals. But it is still strongly debated whether these negative BOLD or CBV/CBF signals are indicative of decreased or increased neuronal activity. The fidelity of Ca(2+)
- PMID 24369291
- The role of kinin receptors in cancer and therapeutic opportunities.
- da Costa PL1, Sirois P2, Tannock IF3, Chammas R4.Author information 1Laboratório de Oncologia Experimental, Faculdade de Medicina da Universidade de São Paulo and Instituto do Câncer do Estado de São Paulo, Brazil.2CHUL Research Center, Laval University, Quebec City, Canada.3Princess Margaret Cancer Centre and University of Toronto, Toronto, ON, Canada.4Laboratório de Oncologia Experimental, Faculdade de Medicina da Universidade de São Paulo and Instituto do Câncer do Estado de São Paulo, Brazil. Electronic address: email@example.com.AbstractKinins are generated within inflammatory tissue microenvironments, where they exert diverse functions, including cell proliferation, leukocyte activation, cell migration, endothelial cell activation and nociception. These pleiotropic functions depend on signaling through two cross talking receptors, the constitutively expressed kinin receptor 2 (B2R) and the inducible kinin receptor 1 (B1R). We have reviewed evidence, which supports the concept that kinin receptors, especially kinin receptor 1, are promising targets for cancer therapy, since (1) many tumor cells express aberrantly high levels of these receptors; (2) some cancers produce kinins and use them as autocrine factors to stimulate their growth; (3) activation of kinin receptors leads to activation of macrophages, dendritic cells and other cells from the tumor microenvironment; (4) kinins have pro-angiogenic properties; (5) kinin receptors have been implicated in cancer migration, invasion and metastasis; and (6) selective antagonists for either B1R or B2R have shown anti-proliferative, anti-inflammatory, anti-angiogenic and anti-migratory properties. The multiple cross talks between kinin receptors and renin-angiotensin system (RAS) as well as its implications for targeting KKS or RAS for the treatment of malignancies are also discussed. It is expected that B1R antagonists would interfere less with housekeeping functions and therefore would be attractive compounds to treat selected types of cancer. Reliable clinical studies are needed to establish the translatability of these data to human settings and the usefulness of kinin receptor antagonists.
- Cancer letters.Cancer Lett.2014 Apr 1;345(1):27-38. doi: 10.1016/j.canlet.2013.12.009. Epub 2013 Dec 11.
- Kinins are generated within inflammatory tissue microenvironments, where they exert diverse functions, including cell proliferation, leukocyte activation, cell migration, endothelial cell activation and nociception. These pleiotropic functions depend on signaling through two cross talking receptors,
- PMID 24333733
- Deletion of GABA-B Receptor in Schwann Cells Regulates Remak Bundles and Small Nociceptive C-fibers.
- Faroni A1, Castelnovo LF, Procacci P, Caffino L, Fumagalli F, Melfi S, Gambarotta G, Bettler B, Wrabetz L, Magnaghi V.Author information 1Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133, Milan, Italy; Blond McIndoe Laboratories, The University of Manchester, Institute of Inflammation and Repair, M13 9PT, Manchester, United Kingdom.AbstractThe mechanisms regulating the differentiation into non-myelinating Schwann cells is not completely understood. Recent evidence indicates that GABA-B receptors may regulate myelination and nociception in the peripheral nervous system. GABA-B receptor total knock-out mice exhibit morphological and molecular changes in peripheral myelin. The number of small myelinated fibers is higher and associated with altered pain sensitivity. Herein, we analyzed whether these changes may be produced by a specific deletion of GABA-B receptors in Schwann cells. The conditional mice (P0-GABA-B1(fl/fl) ) show a morphological phenotype characterized by a peculiar increase in the number of small unmyelinated fibers and Remak bundles, including nociceptive C-fibers. The P0-GABA-B1(fl/fl) mice are hyperalgesic and allodynic. In these mice, the morphological and behavioral changes are associated with a downregulation of neuregulin 1 expression in nerves. Our findings suggest that the altered pain sensitivity derives from a Schwann cell-specific loss of GABA-B receptor functions, pointing to a role for GABA-B receptors in the regulation of Schwann cell maturation towards the non-myelinating phenotype. GLIA 2014;62:548-565.
- Glia.Glia.2014 Apr;62(4):548-65. doi: 10.1002/glia.22625. Epub 2014 Jan 29.
- The mechanisms regulating the differentiation into non-myelinating Schwann cells is not completely understood. Recent evidence indicates that GABA-B receptors may regulate myelination and nociception in the peripheral nervous system. GABA-B receptor total knock-out mice exhibit morphological and mol
- PMID 24474699
- Nociceptor-Enriched Genes Required for Normal Thermal Nociception
- Cell reports 16(2), 295-303, 2016-07
- NAID 120005838217
- 日本ペインクリニック学会誌 23(2), 93-96, 2016
- NAID 130005160437
- The use of autologous neurogenically-induced bone marrow-derived mesenchymal stem cells for the treatment of paraplegic dogs without nociception due to spinal trauma
- Journal of Veterinary Medical Science advpub(0), 2016
- NAID 130005156401
- 表在痛 皮膚の痛み
- pain sense