Combination Of Denervation Research Articles

13. Combination of Denervation with Autologous Fat Transfer (CoDRAFT): A Novel Technique and Outcomes in the Treatment of Thumb Carpometacarpal Arthritis

13. Combination of Denervation with Autologous Fat Transfer (CoDRAFT): A Novel Technique and Outcomes in the Treatment of Thumb Carpometacarpal Arthritis

Sarcopenia in stroke-facts and numbers on muscle loss accounting for disability after stroke.

Stroke is the third leading cause of death and the leading cause of disability in Western countries. More than 60% of patients remain disabled, 50% of patients suffer from some hemiparesis and 30% remain unable to walk without assistance. The skeletal muscle is the main effector organ accountable for disability in stroke. This disability is, however, traditionally attributed to the brain injury itself and less attention is paid to structural, metabolic and functional aspects of muscle tissue. Hemiparetic stroke leads to various muscle abnormalities. A combination of denervation, disuse, inflammation, remodelling and spasticity account for a complex pattern of muscle tissue phenotype change and atrophy. While the molecular mechanisms of muscle degradation after stroke are only incompletely understood, a stroke-related sarcopenia may be concluded. Reinnervation, fiber-type shift, disuse atrophy and local inflammatory activation are only some of the key features to be addressed. Despite the importance for optimum post stroke recovery, stroke-related sarcopenia is not recognised in current guidelines for stroke therapy and rehabilitation. A total of not more than 500 patients forms the basis for all available evidence on clinical muscle changes after stroke. A lack of robust evidence on muscle pathology after stroke and on treatment strategies becomes apparent that needs to be addressed in an interdisciplinary integrated approach.

Neural control of glutamine synthetase activity in rat skeletal muscles

The mechanism of glutamine synthetase induction in rat skeletal muscle after denervation or limb immobilization was investigated. Adult male rats were subjected to midthigh section of the sciatic nerve. At 1, 2, and 5 h and 1, 2, and 7 days after denervation, rats were killed and denervated, and contralateral control soleus and plantaris muscles were excised, weighted, homogenized, and assayed for glutamine synthetase. Glutamine synthetase activity increased approximately twofold 1 h after denervation in both muscles. By 7 days postdenervation enzyme activity had increased to three times the control level in plantaris muscle and to four times the control level in soleus muscle. Increased enzyme activity after nerve section was associated with increased maximum velocity with no change in apparent Michaelis constant. Immunotitration with an antiglutamine synthetase antibody suggested that denervation caused an increase in the number of glutamine synthetase molecules in muscle. However, Northern-blot analysis revealed no increase in the steady-state level of glutamine synthetase mRNA after denervation. A mixing experiment failed to yield evidence for the presence of a soluble factor involved in regulating the activity of glutamine synthetase in denervated muscle. A combination of denervation and dexamethasone injections resulted in additive increases in glutamine synthetase. Thus the mechanism underlying increased glutamine synthetase after denervation appears to be posttranscriptional and is distinct from that of the glucocorticoid-mediated glutamine synthetase induction previously described by us.

Effects of some pharmacological agents on bovine intramuscular fat deposition.

The effects of several pharmacological agents on bovine lipid deposition in the longissimus and semimembranosus muscles were assessed in this study. Data revealed that the deposition of extractable intramuscular lipid was significantly increased by injections of alcohol, glycerol, or fatty acids into the aforementioned muscles. The resultant increased lipid was not evenly distributed and therefore was not desirable from the standpoint of appearance. The fatty acid composition of the treated muscles was generally similar to that of the untreated muscles. Generally, muscle sites posterior to the treated area possessed more lipid than similar sites of the untreated control muscles. The mechanisms responsible for the increased lipid were probably a combination of denervation, capillary rupture and trauma to the treated area. It was observed that the most irritating compounds effected the greatest response.