Clinical significance and developmental changes of auditory-language-related gamma activity

ObjectiveWe determined the clinical impact and developmental changes of auditory-language-related augmentation of gamma activity at 50–120 Hz recorded on electrocorticography (ECoG).MethodsWe analyzed data from 77 epileptic patients ranging 4–56 years in age. We determined the effects of seizure-onset zone, electrode location, and patient-age upon gamma-augmentation elicited by an auditory-naming task.ResultsGamma-augmentation was less frequently elicited within seizure-onset sites compared to other sites. Regardless of age, gamma-augmentation most often involved the 80–100 Hz frequency band. Gamma-augmentation initially involved bilateral superior-temporal regions, followed by left-side dominant involvement in the middle-temporal, medial-temporal, inferior-frontal, dorsolateral-premotor, and medial-frontal regions and concluded with bilateral inferior-Rolandic involvement. Compared to younger patients, those older than 10 years had a larger proportion of left dorsolateral-premotor and right inferior-frontal sites showing gamma-augmentation. The incidence of a post-operative language deficit requiring speech therapy was predicted by the number of resected sites with gamma-augmentation in the superior-temporal, inferior-frontal, dorsolateral-premotor, and inferior-Rolandic regions of the left hemisphere assumed to contain essential language function (r² = 0.59; p = 0.001; odds ratio = 6.04 [95% confidence-interval: 2.26–16.15]).ConclusionsAuditory-language-related gamma-augmentation can provide additional information useful to localize the primary language areas.SignificanceThese results derived from a large sample of patients support the utility of auditory-language-related gamma-augmentation in presurgical evaluation.     

Exercise and nutritional interventions for improving aging muscle health

Skeletal muscle mass declines with age (i.e., sarcopenia) resulting in muscle weakness and functional limitations. Sarcopenia has been associated with physiological changes in muscle morphology, protein and hormonal kinetics, insulin resistance, inflammation, and oxidative stress. The purpose of this review is to highlight how exercise and nutritional intervention strategies may benefit aging muscle. It is well known that resistance exercise training increases muscle strength and size and evidence also suggests that resistance training can increase mitochondrial content and decrease oxidative stress in older adults. Recent findings suggest that fast-velocity resistance exercise may be an effective intervention for older adults to enhance muscle power and functional capacity. Aerobic exercise training may also benefit aging skeletal muscle by enhancing mitochondrial bioenergetics, improving insulin sensitivity, and/or decreasing oxidative stress. In addition to exercise, creatine monohydrate, milk-based proteins, and essential fatty acids all have biological effects which could enhance some of the physiological adaptations from exercise training in older adults. Additional research is needed to determine whether skeletal muscle adaptations to increased activity in older adults are further enhanced with effective nutritional interventions and whether this is due to enhanced muscle protein synthesis, improved mitochondrial function, and/or a reduced inflammatory response.     

Effect of nutritional interventions and resistance exercise on aging muscle mass and strength

Sarcopenia, defined as the age-related loss of muscle mass, has a negative effect on strength, functional independence and overall quality of life. Sarcopenia is a multifactorial phenomenon characterized by changes in muscle morphology, protein and hormonal kinetics, oxidative stress, inflammation, physical activity and nutrition. It is well known that resistance exercise increases aging muscle mass and strength and these physiological adaptations from exercise may be further enhanced with certain nutritional interventions. Research indicates that essential amino acids and milk-based proteins, creatine monohydrate, essential fatty acids, and vitamin D may all have beneficial effects on aging muscle biology.     

The role of oxygen as a regulator of stem cell fate during fracture repair in TSP2‐null mice

It is often difficult to decouple the relative importance of different factors in regulating MSC differentiation. Genetically modified mice provide model systems whereby some variables can be manipulated while others are kept constant. Fracture repair in thrombospondin‐2 (TSP2)‐null mice is characterized by reduced endochondral ossification and enhanced intramembranous bone formation. The proposed mechanism for this shift in MSC fate is that increased vascular density and hence oxygen availability in TSP2‐null mice regulates differentiation. However, TSP2 is multifunctional and regulates other aspects of the regenerative cascade, such as MSC proliferation. The objective of this study is to use a previously developed computational model of tissue differentiation, in which substrate stiffness and oxygen tension regulate stem cell differentiation, to simulate potential mechanisms which may drive alterations in MSC fate in TSP2‐null mice. Four models (increased cell proliferation, increased numbers of MSCs in the marrow decreased cellular oxygen consumption, and an initially stiffer callus) were not predictive of experimental observations in TSP2‐null mice. In contrast, increasing the rate of angiogenic progression led to a prediction of greater intramembranous ossification, diminished endochondral ossification, and a reduced region of hypoxia in the fracture callus similar to that quantified experimentally by the immunohistochemical detection of pimonidazole adducts that develop with hypoxia. This study therefore provides further support for the hypothesis that oxygen availability during early fracture healing is a key regulator of MSC bipotential differentiation, and furthermore, it highlights the advantages of integrating computational models with genetically modified mouse studies for further elucidating mechanisms regulating stem cell fate. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31:1585–1596, 2013.     

Non-tuberculous mycobacterial PD peritonitis in Australia

Purpose

Peritonitis can be a severe complication of peritoneal dialysis (PD) due to associated morbidity and mortality. Non-tuberculous mycobacteria (NTM) are a rare cause of PD peritonitis, with high rates of catheter removal and conversion to haemodialysis, and a reported mortality as high as 40 %. The incidence, culprit NTM species, and outcomes associated with PD peritonitis have not been described in many countries, including Australia.

Methods

We examined the Australia and New Zealand Dialysis and Transplant Registry from 1 October 2003 to 31 December 2009 for all prevalent peritoneal dialysis patients. Patient characteristics, organisms, treatment and outcome for all NTM PD peritonitis episodes were obtained.

Results

Twelve cases of NTM PD peritonitis were reported, including the first reports of infection due to Mycobacterium hassiacum and Mycobacterium neoaurum. The incidence of NTM PD peritonitis was approximately 1 per 1000 PD patient-years. Recovery occurred in 11 patients, including 3 without removal of their Tenckhoff catheters. A range of antibiotics were utilised. One patient died of sclerosing peritonitis 5 months after diagnosis of PD peritonitis.

Conclusion

Non-tuberculous mycobacteria PD peritonitis is a rare cause of peritonitis, and mortality may be lower than previously reported. Catheter removal occurred in the majority of patients, and adverse outcomes were not observed for those in whom it was retained.