Surgical intervention for tbc p

1930 ◽  
Vol 26 (12) ◽  
pp. 1248-1249
Author(s):  
M. Davies
Keyword(s):  
Muscle Fiber ◽  
Surgical Intervention ◽  
Muscle Fibers ◽  
Muscle Spasm ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy ◽  
Respiratory Movements

Abstracts. Tuberculosis. Surgical intervention for tbc p. Morr Davies (British med Journ. No. 3614), dwelling briefly on the claim. pneumothorax, examines other methods. A. prefers phrenicoexeresis to phrenicotomy, since the first is possible to destroy the connections of the additional branches of n. phrenic with the intra'thoracic part of the nerve. As a result of paralysis of the dome of the diaphragm and atrophy of muscle fibers, muscle spasm disappears, respiratory movements decrease; the rise of the dome of the diaphragm upward continues for 2-3 months. after muscle fiber atrophy. The collapse is not limited only to the base of the lungs, but also leads to a decrease in the volume of the cavities in the upper section. Indications for f. BC: 1. Cases of basal tbc. 2. In cases of chronic basal effusions.

scholarly journals Inhibition of FoxO transcriptional activity prevents muscle fiber atrophy during cachexia and induces hypertrophy

2011 ◽  
Vol 26 (3) ◽  
pp. 987-1000 ◽  
Author(s):  
Sarah A. Reed ◽  
Pooja B. Sandesara ◽  
Sarah M. Senf ◽  
Andrew R. Judge
Keyword(s):  
Muscle Fiber ◽  
Transcriptional Activity ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy

scholarly journals Muscle fiber atrophy

2012 ◽  
Vol 52 (11) ◽  
pp. 1315-1317
Author(s):  
Ikuya Nonaka
Keyword(s):  
Muscle Fiber ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy

scholarly journals FOXO signaling is required for disuse muscle atrophy and is directly regulated by Hsp70

2010 ◽  
Vol 298 (1) ◽  
pp. C38-C45 ◽  
Author(s):  
Sarah M. Senf ◽  
Stephen L. Dodd ◽  
Andrew R. Judge
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Fiber ◽  
Muscle Wasting ◽  
Dominant Negative ◽  
Disuse Muscle Atrophy ◽  
Rat Soleus Muscle ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy

The purpose of the current study was to determine whether heat shock protein 70 (Hsp70) directly regulates forkhead box O (FOXO) signaling in skeletal muscle. This aim stems from previous work demonstrating that Hsp70 overexpression inhibits disuse-induced FOXO transactivation and prevents muscle fiber atrophy. However, although FOXO is sufficient to cause muscle wasting, no data currently exist on the requirement of FOXO signaling in the progression of physiological muscle wasting, in vivo. In the current study we show that specific inhibition of FOXO, via expression of a dominant-negative FOXO3a, in rat soleus muscle during disuse prevented >40% of muscle fiber atrophy, demonstrating that FOXO signaling is required for disuse muscle atrophy. Subsequent experiments determined whether Hsp70 directly regulates FOXO3a signaling when independently activated in skeletal muscle, via transfection of FOXO3a. We show that Hsp70 inhibits FOXO3a-dependent transcription in a gene-specific manner. Specifically, Hsp70 inhibited FOXO3a-induced promoter activation of atrogin-1, but not MuRF1. Further studies showed that a FOXO3a DNA-binding mutant can activate MuRF1, but not atrogin-1, suggesting that FOXO3a activates these two genes through differential mechanisms. In summary, FOXO signaling is required for physiological muscle atrophy and is directly inhibited by Hsp70.

scholarly journals Satellite cell content is specifically reduced in type II skeletal muscle fibers in the elderly

2007 ◽  
Vol 292 (1) ◽  
pp. E151-E157 ◽  
Author(s):  
Lex B. Verdijk ◽  
René Koopman ◽  
Gert Schaart ◽  
Kenneth Meijer ◽  
Hans H. C. M. Savelberg ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Fiber Type ◽  
The Elderly ◽  
Type I ◽  
Type Ii ◽  
Fiber Area ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy ◽  
Type Ii Fibers

Satellite cells (SC) are essential for skeletal muscle growth and repair. Because sarcopenia is associated with type II muscle fiber atrophy, we hypothesized that SC content is specifically reduced in the type II fibers in the elderly. A total of eight elderly (E; 76 ± 1 yr) and eight young (Y; 20 ± 1 yr) healthy males were selected. Muscle biopsies were collected from the vastus lateralis in both legs. ATPase staining and a pax7-antibody were used to determine fiber type-specific SC content (i.e., pax7-positive SC) on serial muscle cross sections. In contrast to the type I fibers, the proportion and mean cross-sectional area of the type II fibers were substantially reduced in E vs. Y. The number of SC per type I fiber was similar in E and Y. However, the number of SC per type II fiber was substantially lower in E vs. Y (0.044 ± 0.003 vs. 0.080 ± 0.007; P < 0.01). In addition, in the type II fibers, the number of SC relative to the total number of nuclei and the number of SC per fiber area were also significantly lower in E. This study is the first to show type II fiber atrophy in the elderly to be associated with a fiber type-specific decline in SC content. The latter is evident when SC content is expressed per fiber or per fiber area. The decline in SC content might be an important factor in the etiology of type II muscle fiber atrophy, which accompanies the loss of skeletal muscle with aging.

Effects of Emphysema on Skeletal Muscle Fiber Atrophy in Hamsters

2004 ◽  
Vol 36 (Supplement) ◽  
pp. S332
Author(s):  
John P. Mattson ◽  
Michael D. Delp ◽  
David C. Poole
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Skeletal Muscle Fiber ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy

The transcription factor ATF4 promotes skeletal muscle fiber atrophy during fasting

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Scott Matthew Ebert ◽  
Daniel K Fox ◽  
Kale S Bongers ◽  
Sharon E Malmberg ◽  
Christopher M Adams
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factor ◽  
Muscle Fiber ◽  
Skeletal Muscle Fiber ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy

scholarly journals Skeletal muscle denervation causes skeletal muscle atrophy through a pathway that involves both Gadd45a and HDAC4

2013 ◽  
Vol 305 (7) ◽  
pp. E907-E915 ◽  
Author(s):  
Kale S. Bongers ◽  
Daniel K. Fox ◽  
Scott M. Ebert ◽  
Steven D. Kunkel ◽  
Michael C. Dyle ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Fiber ◽  
Molecular Mechanisms ◽  
Skeletal Muscle Atrophy ◽  
Muscle Denervation ◽  
Mrna Induction ◽  
Convergence Point ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy

Skeletal muscle denervation causes muscle atrophy via complex molecular mechanisms that are not well understood. To better understand these mechanisms, we investigated how muscle denervation increases growth arrest and DNA damage-inducible 45α ( Gadd45a) mRNA in skeletal muscle. Previous studies established that muscle denervation strongly induces Gadd45a mRNA, which increases Gadd45a, a small myonuclear protein that is required for denervation-induced muscle fiber atrophy. However, the mechanism by which denervation increases Gadd45a mRNA remained unknown. Here, we demonstrate that histone deacetylase 4 (HDAC4) mediates induction of Gadd45a mRNA in denervated muscle. Using mouse models, we show that HDAC4 is required for induction of Gadd45a mRNA during muscle denervation. Conversely, forced expression of HDAC4 is sufficient to increase skeletal muscle Gadd45a mRNA in the absence of muscle denervation. Moreover, Gadd45a mediates several downstream effects of HDAC4, including induction of myogenin mRNA, induction of mRNAs encoding the embryonic nicotinic acetylcholine receptor, and, most importantly, skeletal muscle fiber atrophy. Because Gadd45a induction is also a key event in fasting-induced muscle atrophy, we tested whether HDAC4 might also contribute to Gadd45a induction during fasting. Interestingly, however, HDAC4 is not required for fasting-induced Gadd45a expression or muscle atrophy. Furthermore, activating transcription factor 4 (ATF4), which contributes to fasting-induced Gadd45a expression, is not required for denervation-induced Gadd45a expression or muscle atrophy. Collectively, these results identify HDAC4 as an important regulator of Gadd45a in denervation-induced muscle atrophy and elucidate Gadd45a as a convergence point for distinct upstream regulators during muscle denervation and fasting.

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