INT21609
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Clinical evaluation of the patient requires correct diagnosis of RAS and classification of the disease based on morphology (MiAU, MjAU, HU) and severity (simple versus complex). | |||||||||||||||
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This association raises the possibility that sepsis stimulates RAS, which contributes to microvascular perfusion heterogeneity (manifested as impaired response to local ischemia), and that perfusion heterogeneity contributes to organ failure. | |||||||||||||||
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Although we did identify a relationship between arterial hypotension and circulating Ang II after the first day of severe sepsis, the modest statistical significance and lack of a similar relationship between hypotension and PRA (a biologic precursor to Ang II) temper our enthusiasm to declare arterial pressure a dominant factor leading to persistent RAS activation during sepsis. | |||||||||||||||
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We note that the levels of PRA and Ang II measured in our septic subjects are elevated nearly two-fold compared to outpatients with risk factors for vascular disease [33,34], arguing that the acute septic state contributes to RAS activation. | |||||||||||||||
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Similarly, preexisting hypertension, diabetes, and coronary disease are associated with increased RAS activity, and no doubt are co-morbid conditions in clinical sepsis. | |||||||||||||||
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Circulating mediators of RAS were measured and compared to both microvascular responses during reactive hyperemia as well as to organ dysfunction.
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We considered that RAS activation might simply reflect glomerular hypoperfusion due to hypovolemia, hypotension, or insufficient resuscitation. | |||||||||||||||
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The renin-angiotensin system (RAS) is activated in sepsis, and recent studies implicate Ang II in the pathogenesis of acute lung injury in animal models [14]. | |||||||||||||||
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We cautiously note that our studies do not define a causal role of RAS in the pathogenesis of septic microvascular dysfunction, and RAS activation may be unrelated or even compensatory for microvascular dysfunction. | |||||||||||||||
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We hypothesize that RAS activation is associated with impaired microvascular regulation and organ dysfunction in patients with sepsis. | |||||||||||||||
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Since elevated activation of the RAS signaling pathway, including overexpression of HER-2/neu and mutations of RAS and BRAF, is common in human ovarian carcinoma, we examined the cellular effect of oncogenic RAS on the expression status of OPCML in a genetically defined human ovarian cancer model. | |||||||||||||||
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The key question for future research on the matter should be: are results in CES or RAS improved by adding haptic feedback? | |||||||||||||||
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Further results, which indicate the huge value of three-dimensional vision restoration that occurs in RAS, also seem logical. | |||||||||||||||
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Their response to RAs at the cellular level was also evaluated. | |||||||||||||||
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There was no relationship between serum creatinine and either measure of RAS activation. | |||||||||||||||
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RAS is activated in clinical severe sepsis. | |||||||||||||||
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Coincident induction of K rev-1/rap 1A, rap 1B and H-ras mRNAs in the rat spinal cord by noxious stimulation. | |||||||||||||||
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We report here using Northern blot analysis with these cDNA probes that noxious stimulation causes a marked and coincident increase in rap 1A, rap 1B and H-ras mRNAs in the rat spinal cord. | |||||||||||||||
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Further studies analyzing non-ACE pathways contributing to RAS activity in human pancreatic disorders are needed.
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Neurohormonal activation, primarily of the sympathetic nervous system and the RAS, counteracts myocardial dysfunction initially, but may eventually aggravate the underlying pathophysiology, causing a further deterioration of cardiac function. | |||||||||||||||
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