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Journal of Submicroscopic Cytology and... Oct 1989Fast twitch extensor digitorum longus (EDL) and slow twitch soleus (S) muscles were studied after 5 and 16 days of denervation. Elemental contents of single muscle...
Fast twitch extensor digitorum longus (EDL) and slow twitch soleus (S) muscles were studied after 5 and 16 days of denervation. Elemental contents of single muscle fibres were obtained with energy dispersive X-ray microanalyses (XRMA) applied on cryosections visualised in the scanning or scanning-transmission mode of electron microscopy. Cross sections in series with those produced for analytical electron microscopy were stained for enzyme histochemical fibre typing. A similar increase of Na and Cl was observed in EDL and S fibres after 16 days of denervation and a decrease of K was observed as well in EDL. This time after denervation is known to correspond to the maximal acetylcholine receptor synthesis extrajunctionally. There were no changes of elemental content after 5 days and thus the early membrane changes as i.a. fall in resting membrane potential and increased permeability for Na as well as increased endocytosis did not correspond to changes detectable by XRMA. Time course of atrophy differed between histochemical fibre types in EDL. In S all the muscle fibres atrophied earlier than in EDL and without any difference between fibre types. Then changes in elemental composition of muscle fibres after denervation do not seem to be related to degree and time course of muscle fibre atrophy.
Topics: Animals; Electron Probe Microanalysis; Elements; Muscle Denervation; Muscles; Muscular Atrophy; Rats; Rats, Inbred Strains; Time Factors
PubMed: 2804954
DOI: No ID Found -
Nederlands Tijdschrift Voor Geneeskunde Oct 1955
Topics: Atrophy; Humans; Liver; Liver Diseases; Regeneration
PubMed: 13279974
DOI: No ID Found -
Veterinary Pathology Nov 1979The histologic features of male accessory genital glands of entire sheep (group I), castrated sheep (group II), castrated sheep treated with 40 daily intramuscular...
The histologic features of male accessory genital glands of entire sheep (group I), castrated sheep (group II), castrated sheep treated with 40 daily intramuscular injections of 50 milligrams testosterone propionate (group III), and castrated sheep treated with 600 milligrams testosterone propionate 72 hours before death (group IV) were compared. Sheep were castrated at 3 months old and all sheep were killed when 15 months old. Volume fractions of glandular tissue, intralobular fibromuscular tissue and perilobular fibromuscular tissue of the seminal vesicles and Cowper's glands fluctuated significantly (P less than 0.05) during postcastration atrophy and after repeated testosterone treatment. Atrophy in sheep in group II was least in the prostate but greatest in Cowper's glands, seminal vesicles and ampullae of vasa deferentia. Seminal vesicle plexi, whose cytons had a statistically significant (P less than 0.05) degree of shrinkage, also were atrophied. After treatment with testosterone the postcastration atrophy of plexal neurons was almost reversed in sheep in group III. There also was hypertrophy of epithelial cells but the testosterone treatment failed to reduce to normal the fibromuscular volume fraction of the accessory genital glands. Testosterone propionate treatment of sheep in group IV failed to elicit appreciable morphologic changes. These results are compared with our previous findings on the content and uptake of zinc by the accessory genital glands. It is suggested that accumulation of zinc in the accessory genital glands of sheep is not necessarily closely linked to normal histologic appearance.
Topics: Animals; Atrophy; Castration; Genital Diseases, Male; Genitalia, Male; Male; Sheep; Sheep Diseases; Testosterone
PubMed: 505896
DOI: 10.1177/030098587901600610 -
Archives Internationales de Neurologie,... 1948
Topics: Atrophy; Brain; Brain Diseases; Brain Injuries; Humans
PubMed: 18892866
DOI: No ID Found -
Bulletins Et Memoires de La Societe...
Topics: Atrophy; Brain; Brain Diseases; Humans; Neurodegenerative Diseases; Walking
PubMed: 14954451
DOI: No ID Found -
Skeletal Muscle Jun 2021Diabetes-related muscle wasting is one of the devastating complications of diabetes, which is associated with muscle autophagy due to insulin-mediated glucose...
BACKGROUND
Diabetes-related muscle wasting is one of the devastating complications of diabetes, which is associated with muscle autophagy due to insulin-mediated glucose starvation. However, treatment for diabetes-related muscle wasting is limited. Our previous study already found that niclosamide ethanolamine salt has the therapeutic effects on insulin deficiency of type 1 diabetes mice and muscle wasting induced by doxorubicin. Therefore, we aim to investigate the therapeutic effects of niclosamide ethanolamine salt on diabetes-induced muscle wasting and to explore whether the mechanism is associated with muscle autophagy.
METHODS
Type 1 diabetes mice were induced by intraperitoneal injection of streptozotocin, then were fed with regular diet supplemented with 10 g/kg niclosamide ethanolamine salt. The whole experiment lasted for 8 weeks. At the end of the study, grip strength, weights of tibialis anterior, gastrocnemius, soleus, and extensor digitorum longus muscle were measured. Tibialis anterior muscles stained with PAS were used for evaluating the fiber cross sectional area. Immunofluorescence analysis of myosin heavy chain expression in extensor digitorum longus and soleus muscle was used for determining the composition of the muscle fiber type. Electronic microscopy was applied to observe the autophagy in the atrophied muscle. Serum insulin levels and fasting blood glucose were also measured. Tissues of gastrocnemius muscle were used for detecting the expression of the proteins related to autophagy.
RESULTS
In this study, we found that niclosamide ethanolamine salt could ameliorate muscle atrophy in the type 1 diabetes mice as well, such as enhancing the declined grip strength, improving limb weight and increasing the numbers of glycolytic muscle fiber. Electron microscopy also confirmed that there did exist abundant autophagic vacuoles in the atrophied muscle of the type 1 diabetes mice. Specifically, niclosamide ethanolamine salt could reduce the over expression of autophagy-related proteins, including p-AMPK (Thr172), FoxO3a, p-ULK1 (Ser555), LC3B II, and p-p38 in gastrocnemius muscle of the type 1 diabetes mice.
CONCLUSION
Niclosamide ethanolamine salt could ameliorate muscle wasting. The mechanisms underlying might be associated with inhibition of muscle autophagy.
Topics: Animals; Autophagy; Diabetes Mellitus; Ethanolamine; Ethanolamines; Mice; Muscle, Skeletal; Muscles; Muscular Atrophy; Niclosamide
PubMed: 34107998
DOI: 10.1186/s13395-021-00272-7 -
Der Nervenarzt Jun 1947
Topics: Atrophy; Humans
PubMed: 20271582
DOI: No ID Found -
Revue Neurologique Oct 1950
Topics: Atrophy; Humans; Muscles; Muscular Atrophy; Spinal Muscular Atrophies of Childhood
PubMed: 14816911
DOI: No ID Found -
American Journal of Ophthalmology Sep 1971
Topics: Adolescent; Adult; Age Factors; Angiography; Atrophy; Basement Membrane; Capillaries; Child, Preschool; Choroid; Color Perception Tests; Dark Adaptation; Electrooculography; Electroretinography; Eye Diseases; Female; Fluoresceins; Fundus Oculi; Genes, Recessive; Humans; Male; Middle Aged; Myopia; Night Blindness; Pedigree; Scotoma; Sex Chromosomes; Vascular Diseases; Visual Fields
PubMed: 5315093
DOI: 10.1016/0002-9394(71)90854-3 -
American Journal of Physiology. Cell... Jun 2002In this study, the role of the calcineurin pathway in skeletal muscle atrophy and atrophy-reducing interventions was investigated in rat soleus muscles. Because...
In this study, the role of the calcineurin pathway in skeletal muscle atrophy and atrophy-reducing interventions was investigated in rat soleus muscles. Because calcineurin has been suggested to be involved in skeletal and cardiac muscle hypertrophy, we hypothesized that blocking calcineurin activity would eliminate beneficial effects of interventions that maintain muscle mass in the face of atrophy-inducing stimuli. Hindlimb suspension and spinal cord transection were used to induce atrophy, and intermittent reloading and exercise were used to reduce atrophy. Cyclosporin (CsA, 25 mg x kg(-1) x day(-1)) was administered to block calcineurin activity. Soleus muscles were studied 14 days after the onset of atrophy. CsA administration did not inhibit the beneficial effects of the two muscle-maintaining interventions, nor did it change muscle mass in control or atrophied muscles, suggesting that calcineurin does not play a role in regulating muscle size during atrophy. However, calcineurin abundance was increased in atrophied soleus muscles, and this was associated with nuclear localization of NFATc1 (a nuclear factor of activated T cells). Therefore, results suggest that calcineurin may be playing opposing roles during skeletal muscle atrophy and under muscle mass-maintaining conditions.
Topics: Animals; Atrophy; Axotomy; Calcineurin; Calcineurin Inhibitors; Cell Nucleus; Cyclosporine; DNA-Binding Proteins; Exercise Therapy; Female; Hindlimb Suspension; MEF2 Transcription Factors; Male; Muscle, Skeletal; Myogenic Regulatory Factors; NFATC Transcription Factors; Nuclear Proteins; RNA, Messenger; Rats; Rats, Sprague-Dawley; Signal Transduction; Spinal Cord; Transcription Factors
PubMed: 11997253
DOI: 10.1152/ajpcell.00424.2001