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Physiological Activation (physiological + activation)
Selected AbstractsInteraction of Artificial and Physiological Activation of the Gastrocnemius During GaitNEUROMODULATION, Issue 2 2008Colleen C. Monaghan BSc ABSTRACT Objectives., The purpose of this research was to understand the effects of surface functional electrical stimulation (FES) of the tibial nerve on the activation of the gastrocnemius medialis of the stimulated side. Methods., FES was carried out on six healthy subjects, initiated at three different times during gait: early, mid, and late stance. Each stimulation burst consisted of 15 pulses, applied for 300 msec, at 50 Hz stimulation frequency. Mixed model statistical analysis was carried out on the median onset and offset times of the gastrocnemius medialis and the root mean square of the interpulse interval responses. Results., Results indicate that the electromyography response to FES is dependent on the time of application. The most prominent effects found in the intervals between the stimulation pulses (interpulse intervals) were found when stimulation was applied early in the stance phase. This study revealed that the only statistically significant effect on burst timing was a delay in offset timing due to mid-timed stimulation. Conclusions., We conclude that additional activation may have been compensated, at least in part, by blocking of the physiological activation during the stimulation burst. [source] Calcium influx mechanisms underlying calcium oscillations in rat hepatocytes,HEPATOLOGY, Issue 4 2008Bertina F. Jones The process of capacitative or store-operated Ca2+ entry has been extensively investigated, and recently two major molecular players in this process have been described. Stromal interacting molecule (STIM) 1 acts as a sensor for the level of Ca2+ stored in the endoplasmic reticulum, and Orai proteins constitute pore-forming subunits of the store-operated channels. Store-operated Ca2+ entry is readily demonstrated with protocols that provide extensive Ca2+ store depletion; however, the role of store-operated entry with modest and more physiological cell stimuli is less certain. Recent studies have addressed this question in cell lines; however, the role of store-operated entry during physiological activation of primary cells has not been extensively investigated, and there is little or no information on the roles of STIM and Orai proteins in primary cells. Also, the nature of the Ca2+ influx mechanism with hormone activation of hepatocytes is controversial. Hepatocytes respond to physiological levels of glycogenolytic hormones with well-characterized intracellular Ca2+ oscillations. In the current study, we have used both pharmacological tools and RNA interference (RNAi)-based techniques to investigate the role of store-operated channels in the maintenance of hormone-induced Ca2+ oscillations in rat hepatocytes. Pharmacological inhibitors of store-operated channels blocked thapsigargin-induced Ca2+ entry but only partially reduced the frequency of Ca2+ oscillations. Similarly, RNAi knockdown of STIM1 or Orai1 substantially reduced thapsigargin-induced calcium entry, and more modestly diminished the frequency of vasopressin-induced oscillations. Conclusion: Our findings establish that store-operated Ca2+ entry plays a role in the maintenance of agonist-induced oscillations in primary rat hepatocytes but indicate that other agonist-induced entry mechanisms must be involved to a significant extent. (HEPATOLOGY 2008.) [source] Induction of 150-kDa adenosine deaminase that acts on RNA (ADAR)-1 gene expression in normal T lymphocytes by anti-CD3-, and anti-CD28IMMUNOLOGY, Issue 4 2007Dama Laxminarayana Summary We and other investigators have demonstrated up-regulation of the expression of the RNA-editing gene 150-kDa adenosine deaminase that acts on RNA (ADAR1) in systemic lupus erythematosus (SLE) T cells and B cells, peripheral blood mononuclear cells (PBMC), natural killer (NK) cells. The presence of a small proportion of activated T cells is the hallmark of SLE. Therefore, it was hypothesized that 150-kDa ADAR1 gene expression is induced by the physiological activation of T cells. To examine this hypothesis, normal T cells were activated by anti-CD3-, plus anti-CD28 for various time periods from 0 to 48 hr. The expression of 110-kDa and 150-kDa ADAR1, and interleukin (IL)-2 and ,-actin gene transcripts was analysed. An approximately fourfold increase in 150-kDa ADAR1 gene expression was observed in activated T cells. ADAR2 gene transcripts are substrates for ADAR1 and ADAR2 enzymes. Therefore, we assessed the role of the 150-kDa ADAR enzyme in editing of ADAR2 gene transcripts. In activated T cells, site-selective editing of the ,2 site was observed. Previous studies indicate that this site is predominantly edited by ADAR1. In addition to this, novel editing sites at base positions ,56, ,48, ,45, ,28, ,19, ,15, +46 and +69 were identified in activated T cells. On the basis of these results, it is proposed that 150-kDa ADAR1 gene expression is selectively induced in T cells by anti-CD3-, and anti-CD28 stimulation and that it may play a role in site-selective editing of gene transcripts and in altering the functions of several gene products of T cells during activation and proliferation. [source] Interaction of Artificial and Physiological Activation of the Gastrocnemius During GaitNEUROMODULATION, Issue 2 2008Colleen C. Monaghan BSc ABSTRACT Objectives., The purpose of this research was to understand the effects of surface functional electrical stimulation (FES) of the tibial nerve on the activation of the gastrocnemius medialis of the stimulated side. Methods., FES was carried out on six healthy subjects, initiated at three different times during gait: early, mid, and late stance. Each stimulation burst consisted of 15 pulses, applied for 300 msec, at 50 Hz stimulation frequency. Mixed model statistical analysis was carried out on the median onset and offset times of the gastrocnemius medialis and the root mean square of the interpulse interval responses. Results., Results indicate that the electromyography response to FES is dependent on the time of application. The most prominent effects found in the intervals between the stimulation pulses (interpulse intervals) were found when stimulation was applied early in the stance phase. This study revealed that the only statistically significant effect on burst timing was a delay in offset timing due to mid-timed stimulation. Conclusions., We conclude that additional activation may have been compensated, at least in part, by blocking of the physiological activation during the stimulation burst. [source] The pattern-recognition molecule Nod1 is localized at the plasma membrane at sites of bacterial interactionCELLULAR MICROBIOLOGY, Issue 2 2008Thomas A. Kufer Summary The pattern-recognition molecule Nod1 is a critical sensor for bacterial derived diaminopimelic acid-containing peptidoglycan fragments which induces innate immune responses in epithelial cells. Here we report the subcellular localization of this protein in human epithelial cells. Nod1 is localized in the cytosol and at the plasma membrane in human cells. This membrane association is dependent on the integrity of the protein, on its signalling capacity and on an intact actin cytoskeleton. Signalling-inactive mutants of Nod1 or disruption of the actin cytoskeleton interferes with this localization pattern and impacts on downstream NF-,B activation. Moreover, the invasive bacterium Shigella flexneri was used as a model for physiological activation of Nod1. Imaging revealed that Nod1 is recruited to the site of bacterial entry, where it colocalizes with NEMO. Our data provide evidence that membrane association is linked to Nod1 function and, in view of recent findings on Nod2, that this may be a common feature of NLR family members. [source] NEURAL CONTROL OF RENAL MEDULLARY PERFUSIONCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004Gabriela A Eppel Summary 1.,There is strong evidence that the renal medullary circulation plays a key role in long-term blood pressure control. This, and evidence implicating sympathetic overactivity in development of hypertension, provides the need for understanding how sympathetic nerves affect medullary blood flow (MBF). 2.,The precise vascular elements that regulate MBF under physiological conditions are unknown, but likely include the outer medullary portions of descending vasa recta and afferent and efferent arterioles of juxtamedullary glomeruli, all of which receive dense sympathetic innervation. 3.,Many early studies of the impact of sympathetic drive on MBF were flawed, both because of the methods used for measuring MBF and because single and often intense neural stimuli were tested. 4.,Recent studies have established that MBF is less sensitive than cortical blood flow (CBF) to electrical renal nerve stimulation, particularly at low stimulus intensities. Indeed, MBF appears to be refractory to increases in endogenous renal sympathetic nerve activity within the physiological range in all but the most extreme cases. 5.,Multiple mechanisms appear to operate in concert to blunt the impact of sympathetic drive on MBF, including counter-regulatory roles of nitric oxide and perhaps even paradoxical angiotensin II-induced vasodilatation. Regional differences in the geometry of glomerular arterioles are also likely to predispose MBF to be less sensitive than CBF to any given vasoconstrictor stimulus. 6.,Failure of these mechanisms would promote reductions in MBF in response to physiological activation of the renal nerves, which could, in turn, lead to salt and water retention and hypertension. [source] | ||||||||||