Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Allostasis designates processes of bodily adaptation to stressful challenges, whereas allostatic load means the costs of wear and tear to the body as a consequence of inefficient allostasis. In distressed dementia caregivers, an acute procoagulant stress response might be one dynamic mediator of allostatic load relevant to cardiovascular endpoints. An interviewer assessed the number of negative life-events independent from caregiving over 4 weeks in 37 spousal Alzheimer caregivers (M age +/- SD = 72 +/- 6 years). Baseline procoagulability scores and procoagulability scores in response to a 15-min speech task included plasma thrombin/antithrombin III complex, D-dimer, von Willebrand factor, tissue-type plasminogen activator, and plasminogen activator inhibitor 1 levels. Allostatic load was defined as the difference in procoagulability scores from baseline to speech, using standardized (z-score) transformations. Speech stress significantly increased heart rate (p =.017), systolic blood pressure (p =.002), and diastolic blood pressure (p <.001). The number of negative life-events (M +/- SD 2.8 +/- 2.0) correlated with allostatic load (r =.367, p =.026). After controlling for age and smoking, which together explained 32% of the variance in the allostatic load (R2 =.324), F(2, 34) = 8.14, p =.001, the number of negative life-events accounted for an additional 13% of that variance (Delta R2=.125), Delta F(1, 33) = 7.49, p =.010. The finding is compatible with the concept of allostasis and allostatic load, suggesting that higher combined caregiving and life distress levels are associated with more dysfunctional hemostatic responses to acute mental stress. The acute procoagulant stress response might constitute a dynamic mediator of allostatic load in Alzheimer caregivers.
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PMID:Acute procoagulant stress response as a dynamic measure of allostatic load in Alzheimer caregivers. 1286 53

Depression and anxiety are prospectively associated with cardiac morbidity and mortality. Increased clotting diathesis may mediate this link. We hypothesized that there would be an association between mood and hemostatic changes that occur during and following recovery from acute mental stress. Forty-eight community-dwelling elderly subjects underwent a laboratory speech stressor task. Plasma von Willebrand factor (vWF), thrombin/antithrombin III (TAT) complexes, D-dimer, tissue-type plasminogen activator (t-PA), and type I plasminogen activator inhibitor (PAI-1) were measured at rest, after conclusion of the speech, and 14 min afterwards (recovery). Mood was assessed with the Hamilton Rating Scales for Depression (Ham-D) and Anxiety (Ham-A). Mental stress elicited a hypercoagulable state as evidenced by increases in TAT and D-dimer, and by a decrease in t-PA. Overall, hypercoagulability had increased after recovery. Ham-D scores and Ham-A scores correlated with increases in D-dimer over the testing interval (i.e. area under the curve). Ham-A (but not Ham-D) uniquely explained 8% and 17% of the variance in resting D-dimer and D-dimer area under the curve, respectively. The independent association of anxiety symptoms with resting and stress-induced fibrin formation (D-dimer) may be a mechanism linking mood with cardiovascular disease risk in the elderly.
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PMID:Effects of depressive symptoms and anxiety on hemostatic responses to acute mental stress and recovery in the elderly. 1515 51

Epidemiological, genetic and clinical studies have demonstrated an association between major depressive disorder (MDD) and cardiovascular disease (CVD). For example, MDD is a risk factor for the development of CVD, while around one fifth of patients with CVD have MDD and a significantly larger percentage have subsyndromal symptoms of depression. Furthermore, patients with CVD and depression have an increased risk of future cardiac events compared to similar cohorts without depression, independent of baseline cardiac dysfunction. Despite evidence that CVD and MDD are epidemiologically linked, the cause of this correlation is still unknown. Several risk factors including physical and psychological stress, smoking, physical inactivity and inflammation have been proposed to mediate the interaction between MDD and CVD. The tissue-type plasminogen activator (tPA)-plasminogen proteolytic cascade is widely expressed in the brain. Accumulating evidence from preclinical and clinical studies suggests that tPA and its inhibitor, plasminogen activator inhibitor-1, are related to stress reaction and depression. In addition, brain-derived neurotrophic factor (BDNF) is important for the pathogenesis of MDD and the tPA-plasminogen proteolytic cascade has been implicated in the cleavage of proBDNF to BDNF in the brain, by which the direction of BDNF action is controlled. Thus, it is proposed that tPA-plasmin pathway dysfunction may play a role in the link between MDD and CVD. Future study of the components in the tPA-plasminogen system in CVD patients comorbid with MDD may lead to new, potentially important insights into the link between MDD and CVD, and might also contribute to novel strategies for the management of these two common and devastating diseases.
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PMID:Is dysfunction of the tissue plasminogen activator (tPA)-plasmin pathway a link between major depression and cardiovascular disease? 1892 45


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