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Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages.

Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages. Research Abstract Details 

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  • Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages. Abstract Text:

    toshiko nishimuraToshiko Nishimura,hitoshi hirataHitoshi Hirata,masaya tsujiiMasaya Tsujii,ryu iidaRyu Iida,yoko hokiYoko Hoki,takahiro iinoTakahiro Iino,satoru ogawaSatoru Ogawa,atsumasa uchidaAtsumasa Uchida,toshiko nishimuraToshiko Nishimura,hitoshi hirataHitoshi Hirata,masaya tsujiiMasaya Tsujii,ryu iidaRyu Iida,yoko hokiYoko Hoki,takahiro iinoTakahiro Iino,satoru ogawaSatoru Ogawa,atsumasa uchidaAtsumasa Uchida,

    To examine the pathomechanism of entrapment neuropathy associated with diabetes with special emphasis on the roles of mast cells and Tenascin-C using a rat model of Streptozotocin-induced diabetes. The roles of mast cells and Tenascin-C in development of tarsal tunnel syndrome were analyzed electrophysiologically and histologically in 20 male Ws/Ws-/-rats (mast cell deficient) and 20 of their male wild type counterparts (12-16 weeks old; 250-300 g). Rats were assigned randomly to one of the following three groups; diabetic group and nondiabetic group reared in cages with a wire grid flooring; non-diabetic group in cages with sawdust covered plastic flooring. No significant role for mast cells in entrapment neuropathy was found in the rats with streptozotocin-induced diabetes. Distal latency was prolonged in diabetic rats compared with nondiabetic rats, and positively correlated with increases in blood glucose levels. Tenascin-C expression levels in the endoneurium at the tarsal tunnel in diabetic rats were found to be correlated with distal latency. The anti-alpha-smooth muscle actin (alpha-SMA) positive myofibroblast was scattered in nerve fascicles overexpressing Tenascin-C. It seems likely that Tenascin-C expressing myofibroblasts constrict axons by inducing collagen contraction of the endoneurium. Our data indicate that metabolic and phenotypic abnormalities of endoneurium and perineum lie behind the vulnerability of diabetic patients to entrapment neuropathy.

    Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages. Publishing Authors By Initials

    t nishimuraT Nishimura,h hirataH Hirata,m tsujiiM Tsujii,r iidaR Iida,y hokiY Hoki,t iinoT Iino,s ogawaS Ogawa,a uchidaA Uchida,t nishimuraT Nishimura,h hirataH Hirata,m tsujiiM Tsujii,r iidaR Iida,y hokiY Hoki,t iinoT Iino,s ogawaS Ogawa,a uchidaA Uchida,

    For similar abstracts research abstracts see: abstracts research

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    Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Histology and histopathology

    VOLUME: 23

    Page Numbers: 157-66

    Journal Abbreviation:

    ISSN: 1699-5848

    DAY: 13

    MONTH: Feb

    YEAR: 2008

    Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages. Information

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    LANGUAGE: eng

    NlmUniqueID: 8609357

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    Grant and Affiliation Information for Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages.

    AFFILIATION: Department of Orthopaedic Surgery, Mie University Faculty of Medicine, Tsu, Mie, Japan. nishit41@pref.mie.jp

    Country: Spain

    Spain Research PublicationSpain Research Publication

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    MEDLINETA: Histol Histopathol

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