1,721,270 research outputs found
Maternal fish oil supplementation: the prodrom of synaptic protection in Alzheimer's disease
No full textPain and depression: the egg and the chicken story revisited
No full textThe prevalence of pain in depressed individuals and the prevalence of depression in patients with pain are higher than when these conditions are considered individually. When pain is severe, impairs function, and/or is refractory to treatment, it is associated with more depressive symptoms and worse depression outcomes. Similarly, depression in patients with pain is associated with more complaints and greater functional impairment. Whether alleviation of pain helps depressive symptoms or, likewise, whether relief of depression improves pain, are questions still incompletely clarified. However, there is growing evidence that depression and pain share genetic factors, biological pathways and neurotransmitters. Thus, the most promising area of future research is elucidating the neurobiological alterations in pain pathways that intersect with those involved in depression
Association of community-acquired pneumonia with antipsychotic drug in elderly: a nested case-control study.
No full text[Stimulation of the alpha-1 adrenergic receptors during simulated reperfusion after myocardial acidosis. The evidence for an arrhythmogenic role of the Na+/H+ exchanger]
No full textMyocardial ischemia is associated with an intracellular acidosis recovering after reperfusion. Alpha 1-adrenergic stimulation (alpha 1) exacerbates ischemic injury and triggers ventricular arrhythmias during the reperfusion phase. We have tested the hypothesis that the arrhythmogenic effect of alpha 1 is due to a cytosolic alkalinization secondary to proteinkinase C (PKC)-dependent activation of the sarcolemmal Na+/H+ exchanger. In addition, the effect of the 2 distinct receptor subtypes, alpha 1A and alpha 1B, has also been evaluated. We used single, enzymatically dissociated, adult rat ventricular myocytes. Cells were loaded with the ester derivative of the Ca2+ probe, indo-1 or with the intracellular pH probe SNARF-1. Fluorescence was monitored simultaneously with contractility and was taken as an index of intracellular [Ca2+] or as pHi value. Cells on a stage of an inverted microscope were superfused with a bicarbonate buffer continuously gassed with 95% O2 and 5% CO2 (pH = 7.37; Ca2+ 1.5 mM) and electrically stimulated at 0.5 Hz, at 25 degrees C. Alpha 1 (phenylephrine 50 microM + nadolol 1 microM) increased twitch amplitude and pHi (delta pHi = 0.05 +/- 0.01; pHi in control = 7.24 +/- 0.06, n = 10; p < 0.05). This effect was abolished by the PKC inhibitor staurosporine (5 nM), by overnight (12-24 hours) exposure to 0.2 microM phorbol esters and by the perfusion with 10 microM ethylisopropylamiloride (EIPA), a Na+/H+ exchange inhibitor. During 15 min of hypercarbic acidosis, achieved by switching to a buffer equilibrated with 85% O2 and 15% CO2 (pH = 7.01), alpha 1 had a more pronounced effect on pHi (delta pHi = 0.11 +/- 0.02; pHi in control = 7.02 +/- 0.04, n = 10; p < 0.05). During the 10 min following the removal of acidosis, alpha 1 induced aftercontractions in 75% (n = 20) versus only 25% (n = 8) of the cells in the absence of phenylephrine (p < 0.05). Superfusion with 10 microM EIPA (n = 6) abolished the occurrence of aftercontractions. Selective alpha 1A-adrenergic receptors stimulation (alpha 1 + 2 microM CEC, which inactivates alpha 1B receptors) further increased them (92%, n = 12) whereas selective alpha 1B-adrenergic receptors stimulation (alpha 1 + 2 microM WB-4101, a alpha 1A receptors antagonist) greatly reduced the occurrence of aftercontractions (11%, n = 18). These results show that the PKC-mediated activation of the Na+/H+ exchanger is the mechanism for the arrhythmias induced by alpha 1 during simulated reperfusion after a period of acidosis.(ABSTRACT TRUNCATED AT 400 WORDS
Pain in European long-term care facilities: study in Finland, Italy and The Netherlands.
No full textElderly patients, use of antidepressants, and hip fracture
No full textElderly patients, use of antidepressants, and hip fractur
[Acidosis is associated with an intracellular accumulation of Ca2+. Its role in the modulation of myocardial contractility]
No full textMyocardial acidosis, as during ischemia, profoundly modifies excitation-contraction mechanisms. The decreased myofilament sensitivity to Ca2+ reduces contractility regardless of an intracellular accumulation of Ca2+. To determine the source for this increase in Ca2+ we evaluated the effect of acidosis on diastolic [Ca2+] and mitochondrial [Ca2+]. We used single cardiac cells loaded with the fluorescent probes, indo-1 for Ca2+ and SNARF-1 for pH. Acidosis increases [Ca2+] both in cytosol and mitochondria. The cytosolic accumulation depends, most likely, on an active release from mitochondria. A competition among Ca2+ and H+ ions may, instead, explains the increase in mitochondrial [Ca2+]
[The effect of alpha 1-adrenergic stimulation of the myocardium depends on the opposite actions of 2 receptor subtypes]
No full textTwo different myocardial alpha 1-adrenergic receptor subtypes have been recently described. Since their functional role is still unknown we examined the effect of alpha 1A and alpha 1B on contractile properties, cell Ca2+ homeostasis and myofilament sensitivity to Ca2+ in indo-1 loaded ventricular myocytes. Non selective alpha 1-adrenergic stimulation increases twitch amplitude, systolic Ca2+ and myofilament sensitivity. Same effects but amplified are associated with alpha 1A-receptors stimulation. In contrast, alpha 1B-receptors stimulation decreases twitch amplitude and systolic Ca2+ below control value. Myocardial alpha 1-adrenergic stimulation results from the opposite actions of the 2 subtypes
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