Force and power output of fast and slow skeletal muscles from mdx mice 6-28 months old

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66165/1/j.1469-7793.2001.00591.x.pd

Investigation of Cellular and Molecular Responses to Pulsed Focused Ultrasound in a Mouse Model

Continuous focused ultrasound (cFUS) has been widely used for thermal ablation of tissues, relying on continuous exposures to generate temperatures necessary to induce coagulative necrosis. Pulsed FUS (pFUS) employs non-continuous exposures that lower the rate of energy deposition and allow cooling to occur between pulses, thereby minimizing thermal effects and emphasizing effects created by non-thermal mechanisms of FUS (i.e., acoustic radiation forces and acoustic cavitation). pFUS has shown promise for a variety of applications including drug and nanoparticle delivery; however, little is understood about the effects these exposures have on tissue, especially with regard to cellular pro-homing factors (growth factors, cytokines, and cell adhesion molecules). We examined changes in murine hamstring muscle following pFUS or cFUS and demonstrate that pFUS, unlike cFUS, has little effect on the histological integrity of muscle and does not induce cell death. Infiltration of macrophages was observed 3 and 8 days following pFUS or cFUS exposures. pFUS increased expression of several cytokines (e.g., IL-1α, IL-1β, TNFα, INFγ, MIP-1α, MCP-1, and GMCSF) creating a local cytokine gradient on days 0 and 1 post-pFUS that returns to baseline levels by day 3 post-pFUS. pFUS exposures induced upregulation of other signaling molecules (e.g., VEGF, FGF, PlGF, HGF, and SDF-1α) and cell adhesion molecules (e.g., ICAM-1 and VCAM-1) on muscle vasculature. The observed molecular changes in muscle following pFUS may be utilized to target cellular therapies by increasing homing to areas of pathology

Comedian Hosts and the Demotic Turn

Podcasting is a showcase for what cultural studies scholar Graeme Turner coined “the demotic turn” or the increasing visibility of the ordinary person in the today’s media landscape. Collins argues that the emergence of a particular breed of podcasts – comedian-hosted interviews with celebrities – function in an “off-label” manner as a form of self-help or vicarious therapy. The emergence and rapid growth of this genre can attributed to three main factors: a confessional culture, the triumph of experience over expertise, and the democratization allowed by the form’s technology. She explores the link between emotional intimacy and comedy, and analyzes podcasts like Marc Maron’s WTF that are, in expression, a rejection of the pedestal version of stardom

State rescaling, policy experimentation and path dependency in post-Mao China: a dynamic analytical framework

This paper evaluates the applicability of the state rescaling framework for framing politico-economic evolution in China. It then presents an analytical framework that examines institutional change as driven by the dynamic entwinement of state rescaling, place-specific policy experimentation and institutional path dependency. The framework problematizes simple ‘transition’ models that portray a mechanistic ‘upward’ or ‘downward’ reconfiguration of regulatory relations after market-like rule was instituted in 1978. It emphasizes, instead, a more established pattern of development marked simultaneously by geographically distinct (and enduring) institutional forms and experimental (and capricious) attempts to transcend them

Global energy governance : a review and research agenda

Over the past few years, global energy governance (GEG) has emerged as a major new field of enquiry in international studies. Scholars engaged in this field seek to understand how the energy sector is governed at the global level, by whom and with what consequences. By focusing on governance, they broaden and enrich the geopolitical and hard-nosed security perspectives that have long been, and still are, the dominant perspectives through which energy is analysed. Though still a nascent field, the literature on GEG is thriving and continues to attract the attention of a growing number of researchers. This article reviews the GEG literature as it has developed over the past 10 years. Our aim is to highlight both the progress and limitations of the field, and to identify some opportunities for future research. The article proceeds as follows. First, it traces the origins of the GEG literature (section “Origins and roots of GEG research”). The subsequent sections deal with the two topics that have received the most attention in the GEG literature: Why does energy need global governance (section “The goals and rationale of global energy governance”)? And, who governs energy (section “Mapping the global energy architecture”)? We then address a third question that has received far less attention: How well or poor is energy governed (section “Evaluating global energy governance”)? In our conclusions (section “Conclusions and outlook”), we reflect on the current state of GEG, review recent trends and innovations, and identify some questions that warrant future consideration by scholars. This article is published as part of a thematic collection on global governance

The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia

BACKGROUND: A systems approach to understanding the etiology of schizophrenia requires a theory which is able to integrate genetic as well as neurodevelopmental factors. PRESENTATION OF THE HYPOTHESIS: Based on a co-localization of loci approach and a large amount of circumstantial evidence, we here propose that a functional deficiency of glial growth factors and of growth factors produced by glial cells are among the distal causes in the genotype-to-phenotype chain leading to the development of schizophrenia. These factors include neuregulin, insulin-like growth factor I, insulin, epidermal growth factor, neurotrophic growth factors, erbB receptors, phosphatidylinositol-3 kinase, growth arrest specific genes, neuritin, tumor necrosis factor alpha, glutamate, NMDA and cholinergic receptors. A genetically and epigenetically determined low baseline of glial growth factor signaling and synaptic strength is expected to increase the vulnerability for additional reductions (e.g., by viruses such as HHV-6 and JC virus infecting glial cells). This should lead to a weakening of the positive feedback loop between the presynaptic neuron and its targets, and below a certain threshold to synaptic destabilization and schizophrenia. TESTING THE HYPOTHESIS: Supported by informed conjectures and empirical facts, the hypothesis makes an attractive case for a large number of further investigations. IMPLICATIONS OF THE HYPOTHESIS: The hypothesis suggests glial cells as the locus of the genes-environment interactions in schizophrenia, with glial asthenia as an important factor for the genetic liability to the disorder, and an increase of prolactin and/or insulin as possible working mechanisms of traditional and atypical neuroleptic treatments

Sarcopenia: etiology, clinical consequences, intervention, and assessment

The aging process is associated with loss of muscle mass and strength and decline in physical functioning. The term sarcopenia is primarily defined as low level of muscle mass resulting from age-related muscle loss, but its definition is often broadened to include the underlying cellular processes involved in skeletal muscle loss as well as their clinical manifestations. The underlying cellular changes involve weakening of factors promoting muscle anabolism and increased expression of inflammatory factors and other agents which contribute to skeletal muscle catabolism. At the cellular level, these molecular processes are manifested in a loss of muscle fiber cross-sectional area, loss of innervation, and adaptive changes in the proportions of slow and fast motor units in muscle tissue. Ultimately, these alterations translate to bulk changes in muscle mass, strength, and function which lead to reduced physical performance, disability, increased risk of fall-related injury, and, often, frailty. In this review, we summarize current understanding of the mechanisms underlying sarcopenia and age-related changes in muscle tissue morphology and function. We also discuss the resulting long-term outcomes in terms of loss of function, which causes increased risk of musculoskeletal injuries and other morbidities, leading to frailty and loss of independence

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage