Annals of the New York Academy of Sciences
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Ann. N. Y. Acad. Sci. · Apr 2010
ReviewProthymosin alpha as robustness molecule against ischemic stress to brain and retina.
Following stroke or traumatic damage, neuronal death via both necrosis and apoptosis causes loss of functions, including memory, sensory perception, and motor skills. As necrosis has the nature to expand, while apoptosis stops the cell death cascade in the brain, necrosis is considered to be a promising target for rapid treatment for stroke. We identified the nuclear protein, prothymosin alpha (ProTalpha) from the conditioned medium of serum-free culture of cortical neurons as a key protein-inhibiting necrosis. ⋯ In the ischemic brain or retina, ProTalpha showed a potent inhibition of both necrosis and apoptosis. By use of anti-brain-derived neurotrophic factor or anti-erythropoietin IgG, we found that ProTalpha inhibits necrosis, but causes apoptosis, which is in turn inhibited by ProTalpha-induced neurotrophins under the condition of ischemia. From the experiment using anti-ProTalpha IgG or antisense oligonucleotide for ProTalpha, it was revealed that ProTalpha has a pathophysiological role in protecting neurons in stroke.
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Ann. N. Y. Acad. Sci. · Sep 2014
ReviewThe risk/benefit of predicting a post-antibiotic era: is the alarm working?
There have been concerns about antimicrobial resistance since the first widespread use of antibiotics in humans. More recently, this concern has grown and become the focus of clinical, scientific, and political activity. In part, the political interest is a consequence of publicizing a bleak picture of a post-antibiotic world. ⋯ Many governments now use a risk assessment approach to identify security concerns, based on reasonable worst-case scenarios. There is no doubt that for effective policy-based action to occur, antimicrobial resistance needs to be seen as a national and international security priority, particularly as the major cost of inaction will mostly be felt in the future. We conclude that presenting the evidence in a manner that is used to encourage prioritization of security policy is not only justified, it is essential to drive action in this area.
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Since the first demonstrations that mindfulness-based therapies could have a positive influence on chronic pain patients, numerous studies have been conducted with healthy individuals in an attempt to understand meditative analgesia. This review focuses explicitly on experimental pain studies of meditation and attempts to draw preliminary conclusions based on the work completed in this new field over the past 6 years. Dividing meditative practices into the broad categories of focused attention (FA) and open monitoring (OM) techniques allowed several patterns to emerge. ⋯ The neural pattern underlying pain modulation during OM suggests meditators actively focus on the noxious stimulation while inhibiting other mental processes, consistent with descriptions of mindfulness. A preliminary model is presented for explaining the influence of mindfulness practice on pain. Finally, the potential analgesic effect of the currently unexplored technique of compassion meditation is discussed.
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The pathophysiology of fibromyalgia (FM) is not completely understood. The disease is characterized by a central sensitization with an amplification of pain perception. A combination of interactions among external stressors, behavioral constructs, neurotransmitters, hormones, immune, and sympathetic nervous systems appears to be involved. ⋯ Recent data highlight the putative role of cytokines in the pathogenesis of FM. The autonomic nervous system is implicated in the maintenance of the physiological homeostasis and sympathetic activity appears increased in FM. Neuropeptide Y and its receptors Y1 and Y2 seem to have a complex role in pain modulation.
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Ann. N. Y. Acad. Sci. · Oct 2006
Review Meta Analysis Comparative StudyAssociation of SUMO4, as a candidate gene for IDDM5, with susceptibility to type 1 diabetes in Asian populations.
Recent study demonstrated that M55V variant in SUMO4 at IDDM5 was associated with susceptibility to type 1 diabetes. Subsequent studies, however, showed inconsistency in the association. To clarify the population-wide effect on the association of SUMO4 with type 1 diabetes, we have performed meta-analysis including our own data in Asian populations, which confirmed a highly significant association in Asian populations (summary odds ratio [OR]: 1.29, P = 7.0 x 10(-6)), but indicated significant heterogeneity in the genetic effect of the SUMO4 gene on type 1 diabetes among diverse ethnic groups. These observations indicated the association of SUMO4 with type 1 diabetes in Asian populations.