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1.
Journal of Audiology and Speech Pathology ; (6): 256-260, 2015.
Article in Chinese | WPRIM | ID: wpr-463160

ABSTRACT

Objective To investigate the morphology change of posterior cricoarytenoid muscle myofiber in patients with idiopathic vocal fold paralysis and to provide experimental evidence for the clinical treatment of idio‐pathic vocal cord paralysis .Methods Thirty -nine cases of vocal fold paralysis patients were recruited into and di‐vided into 2 groups :idiopathic vocal cord paralysis group(n=16) ,and traumatic vocal cord paralysis group(n=23) . Both groups were further divided into 3 subgroups:0 .5~1 year(5 cases and 7 cases) ,>1~2 years(5 cases and 10 cases) ,>2 years(6 cases and 6 cases) .Part of posterior cricoarytenoid muscle(PCAM ) were acquired from all of vo‐cal cord paralysis patients .Normal human posterior cricoarytenoid muscles were treated as the control group (n=5) . They were all stained with Masson three-color staining ,the fiber crosssectional area of muscle tissue and collagen connective tissue were quantitatively analyzed with the image pro plus analysis system .Differences of two observa‐tion indexes were compared with each other among groups and subgroups .Results The number of myofibers was decreased ,but the numbers of the collagen fibers was increased with the onset time course extension ,the ratio of cross sectional area of myofibers to those of collagen fibers was progressively decreasd with increased time course of denervation and more decrease within 1 year .There was obvious difference between the control group and 0 .5~1 year ,>1~2 years ,>2 years subgroup of idiopathic vocal cord paralysis (P1~2 years subgroup and >2 years subgroup ,the trend of shrinking still existed .Com‐pared two observation indexes of traumatic vocal cord paralysis with the same period subgroup indexes of idiopathic vocal fold paralysis ,there was no significant difference about these two observation indexes (P>0 .05) .In some special cases with 10 years duration in idiopathic vocal cord paralysis group ,the posterior cricoarytenoid muscle at‐rophy fibrosis was not serious .However ,in some case which the course lasted for only 1 .5 years ,the muscle atrophy was very obvious .There were great individual differences among idiopathic vocal cord paralysis patients .Conclusion If there is no recovery after half year treatment ,for PCA muscle function recovery ,the recurrent laryngeal nerve injury repair surgery could be considered to carry out within 1 year .In some cases with long disease duration (>2 years) ,they may still have the muscle morphological basis for nerve repair .

2.
Space Medicine & Medical Engineering ; (6): 240-244, 2008.
Article in Chinese | WPRIM | ID: wpr-407280

ABSTRACT

Objective To investigate the intervention of ciliary enurotrophic factors(CNTF)on weightlessness-induced muscle atrophy and its myofiber phenotype transition.Methods Tail-suspended (hindlimb unloading)of adult male Wistar rats were used to create the mode J of weightlessness-induced muscle atrophy.The effect of CNTF treatment on weightlessness-induced muscle atrophy and its myofiber phenotype transition was determined by analyzing the expression changes of MHCI/IIb and p130 or Myf5 with RT-PCR and Western blot.Results CNTF treatment in vivo markedly reversed weightlessness-induced muscle weight IOSS selectively in the slow-twitch muscle soleus.Moreover,during tail suspension,soleus weight loss and myofiber phenotype transition indicated that CNTF treatment could sigificantly attenuate the weight loss and slow to fast myofiber phenotrype transition in soleus compared with control(CNTF untreated and tail suspended).Furthermore,it was showed that the CNTF-induced intervention effect was associated with the protein level upregulation of muscle satellite cell-specific markers,P130 and Myf5.The satellite cell pool in CNTFtreated soleus was increased.Conclusion It iS firstly demonstrated that CNTF can attenuate weightlessness-induced muscle atrophy and its myofiber phenotype transition to be through the increase of satellite cell pool in soleus.

3.
Journal of Veterinary Science ; : 425-427, 2008.
Article in English | WPRIM | ID: wpr-65384

ABSTRACT

Histopathological findings of eosinophilic myositis in the carcass of a slaughtered Korean native cow are presented. Lesions contained massive fibrous septae with vacuolar changes in some lesions, and the hypercontraction and rupturing of muscle bundles, with replacement by eosinophils. Necrosis and severe eosinophil infiltration were observed. Sarcoplasmic fragmentation and atrophy developed. Typical of granuloma, calcified myofibers were focally surrounded by macrophages and numerous inflammatory cells, and multinucleated giant cell formation was evident.


Subject(s)
Animals , Cattle , Female , Cattle Diseases/pathology , Eosinophilia/pathology , Muscle, Skeletal/pathology , Muscular Diseases/pathology
4.
Japanese Journal of Physical Fitness and Sports Medicine ; : 269-277, 2005.
Article in Japanese | WPRIM | ID: wpr-362341

ABSTRACT

Markedly smaller myofibers including branched myofibers (SF) were contained in regenerated skeletal muscles. However, its functional properties are not yet sufficiently understood. The present study examined the metabolic, contractile properties and hypertrophy of SF included in rat skeletal plantaris muscles regenerated from eccentric contraction-induced muscle injury. Succinate dehydrogenase and alpha-glycerophosphate dehydrogenase activity of SF were respectively similar to that of other normal size myofibers (NF) within regenerated muscles. The shortening velocity of skinned fibers prepared from branched myofibers isolated from regenerated muscles was slightly slower than that of control muscles. In addition, the extent of glycogen depletion in SF was similar to that of NF after exhaustive running. Therefore, SF were innervated by motoneurons and recruited during the contractile activity of the skeletal muscle. No matter when the regenerated muscle was loaded by synergistic ablation, the continued existence of SF was observed. Therefore, the ability of hypertrophy in SF may be distinct from that in NF. The physiological properties of SF were similar to that of normal myofiber, except for the ability to regulate hypertrophy.

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