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1

Anatomical study of lumbar spine innervation

100%
Higuchi K., Sato T.
Folia Morphologica
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2002
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tom 61
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nr 2
71-79
To precisely evaluate low back pain, identification of the detailed innervation of the lumbar spine is necessary. On twenty-five sides of adult cadavers we investigated various patterns of rami communicantes (RC) and their relationship to the psoas major muscle (PM). In ten sides, we focused our dissection on the minute nerve supply of the anterior (ALL) and posterior longitudinal ligaments (PLL), vertebral bodies and the intervertebral discs (IVD). According to the mode of piercing PM, two types of RC were observed: superficial oblique rami (SOR) and deep transverse rami (DTR). SOR ran obliquely between superficial heads of PM, connecting sympathetic trunk (ST) and T12-L2 (3) spinal nerves non-segmentally. DTR ran segmentally close to the vertebral bodies and were situated deep to the PM slips. On the lateral side of the lumbar spine, the vertebral bodies and IVD received branches from DTR and ventral rami segmentally, as well as branches from the sympathetic trunk (ST) and, in the upper lumbar region, SOR non-segmentally. On the anterior aspect of the lumbar spine, ALL received branches from ST and splanchnic nerves non-segmentally. Within the vertebral canal, the posterior aspect of IVD and PLL received the sinu-vertebral nerves originating from DTR. These findings suggest the coexistence of two different types of innervation: one originating directly from the spinal nerve segmentally, and one reaching vertebral structures via the sympathetic nerves non-segmentally. Therefore, sympathetic nerves are likely involved in the proprioception of the spinal column.
2
Content available remote

TGF-beta signalling pathway: its role in gastrointestinal pathophysiology and modulation of ulcer healing

71%
Tanigawa T., Pai R., Arakawa T., Higuchi K., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 1
Gastrointestinal ulcer healing is a complex process, involving cell migration, proliferation, angiogenesis and extracellular matrix deposition, all ultimately leading to reconstruction of tissue architecture within the ulcer scar. These processes are controlled by growth factors, cytokines and hormones. Transforming growth factor-ß (TGF-ß ), one of the multifunctional peptide growth factors, has been reported to positively regulate gastrointestinal ulcer healing. Although TGF-ß inhibits cell proliferation in a variety of cells, it induces cell migration, angiogenesis, and enhances extracellular matrix production necessary for gastrointestinal ulcer healing. TGF-ß exerts its action by binding to its transmembrane serine/threonine kinase receptors, which in turn triggers activation of various intracellular signaling pathways. Smads are intermediate effector proteins that play key roles in biological activities of TGF-ß by transmitting the signals from the cell surface directly into the nucleus and initiating transcription. New insight into the mechanisms underlying TGF-ß-Smad modulation of gastrointestinal ulcer healing will likely enhance our understanding of the mechanisms controlling the healing processes of gastrointestinal ulcers.
3
Content available remote

Prevention by lansoprazole, a proton pump inhibitor, of indomethacin-induced small intestinal ulceration in rats through induction of heme oxygenase-1

51%
Yoda Y., Amagase K., Kato S., Tokioka S., Murano M., Kakimoto K., Nishio H., Umegaki E., Takeuchi K., Higuchi K.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 3
287-294
The effect of lansoprazole, a proton pump inhibitor (PPI), on indomethacin-induced small intestinal ulceration was examined in rats, particularly in relation to heme oxygenase (HO)-1. The animals were administered indomethacin (10 mg/kg, p.o.) and killed 24 h later. Lansoprazole (30-100 mg/kg, p.o.) and omeprazole (30-100 mg/kg, p.o.) were given 30 min before the administration of indomethacin, while tin-protoporphyrin IX (SnPP: 30 mg/kg, i.v.), an inhibitor of HO-1, was injected 10 min before indomethacin or lansoprazole. Indomethacin produced hemorrhagic lesions in the small intestine, accompanied with an increase of mucosal invasion of enterobacteria, inducible nitric oxide synthase (iNOS) expression, and myeloperoxidase (MPO) activity in the mucosa. Pretreatment with lansoprazole dose- dependently reduced the severity of the indomethacin-induced intestinal lesions, with suppression of the increased MPO activity, while omeprazole had no effect. Pretreatment with SnPP significantly exacerbated these intestinal lesions and almost totally abolished the protective effect of lansoprazole. The up-regulation of iNOS mRNA expression following indomethacin was suppressed by lansoprazole in a SnPP-inhibitable manner, although the enhanced enterobacterial invasion remained unaffected. The amount of HO-1 protein in the intestinal mucosa was significantly increased by lansoprazole but not by omeprazole. Prior administration of carbon monoxide (CO)-releasing molecule-2 (CORM-2; 10 mg/kg, i.p.) significantly reduced the severity of these lesions and the enhancement of mucosal iNOS mRNA expression induced in the small intestine by indomethacin. These results suggest that lansoprazole prevents indomethacin-induced small intestinal ulceration, and this effect is associated with inhibition of iNOS expression, through up-regulation of HO-1/CO production in the mucosa.
4
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Lafutidine, a histamine H2 receptor antagonist with mucosal protective properties, attenuates 5-fluorouracil-induced intestinal mucositis in mice through activation of extrinsic primary afferent neurons

51%
Sano T., Utsumi D., Amagase K., Matsumoto K., Tominaga M., Higuchi K., Takeuchi T., Kato S.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 1
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