Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the effects of vibrating-tool operation on the autonomic and peripheral nervous system, we measured the variability in the electrocardiographic R-R interval (CVRR) and the distribution of nerve conduction velocities (DCV) in 24 men who were vibrating-tool operators and in 17 healthy adult men (control group). Of the 24 tool operators, 13 had a history of vibration-induced white finger [VWF(+) group] and 11 had no such history [VWF(-) group]. Two components of CVRR, i.e. C-CVRSA and C-CVMWSA, which have been considered to reflect parasympathetic and sympathetic activities, respectively, were also examined. Both the CVRR and the C-CVRSA in the VWF(+) group and the CVRR in the VWF(-) group were found to be significantly depressed as compared with the control values; moreover, a significant difference in the C-CVRSA was observed between the VWF(+) group and the VWF(-) group. The faster DCVs and the sensory median nerve conduction velocity were significantly slowed in the VWF(+) and VWF(-) groups. The C-CVMWSA was significantly correlated with most of the DCV parameters and with the median nerve conduction velocities in all 24 vibrating-tool operators. These data suggest that operation of vibrating tools, which involves exposure to combined stressors of local vibration, heavy work, climate, and noise, affects both the faster myelinated nerve-fiber activity and the parasympathetic activity; the sympathetic activity at rest in workers exposed to hand-arm vibration may be related to depression of peripheral nerve conduction.
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PMID:Autonomic and peripheral nervous system dysfunction in workers exposed to hand-arm vibration: a study of R-R interval variability and distribution of nerve conduction velocities. 165 54

1. Potential mechanisms responsible for the prominent depression of atrioventricular conduction by adenosine have been investigated in guinea-pig heart. 2. Adenosine A1 receptors and nucleoside transport (NT) sites were identified and enumerated in cardiac myocytes, atrioventricular conduction cells and coronary endothelial cells in 10 microns sections by autoradiographical analysis of the binding of the A1 selective antagonist 8-cyclopentyl-1,3-[3H]-dipropylxanthine ([3H]-DPCPX) and the NT ligand [3H]-nitrobenzylthioinosine ([3H]-NBMPR), respectively. 3. Atrioventricular conduction cells were identified by acetylcholinesterase histochemistry and endothelial cells by von Willebrand factor immunohistochemistry. 4. Site-specific binding of [3H]-DPCPX, when expressed as grains per cell nucleus was significantly higher (30 fold) in conduction cells than in surrounding myocytes. [3H]-DPCPX site density on endothelial cells in adjacent coronary vessels was not significantly different from myocytes. 5. In contrast, autoradiography of [3H]-NBMPR sites in these areas indicated that, relative to myocytes, conduction cells and endothelial cells were significantly enriched (2 fold and 4.5 fold, respectively) in NT sites. 6. The pronounced dromotropic effect of adenosine in guinea-pig heart is correlated with a higher density of adenosine A1 receptors in atrioventricular conduction cells than in myocytes. The NT capacity of these cells, as estimated by [3H]-NBMPR binding site density, is not increased in proportion to A1 receptors.
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PMID:Adenosine receptors and nucleoside transport sites in cardiac cells. 179 6

In most of the epidemiologic studies conducted during the last 20 years, impulse noise caused increased risk of hearing loss in comparison to continuous noise with the same acoustical energy. The interaction between noise exposure (broadband at 100 dB(A)) and hand-arm vibration (125 Hz at 2 ms-2 acceleration level) has been proven for people having vibration-induced white finger symptoms. This interaction is evidenced as a permanent hearing loss. However, why the interaction is seen only in people with VWF is not known. The mechanisms may be related to individual susceptibility, and hypotheses are given on the role of the autonomous nervous system regulating the peripheral vascular reaction. Whole-body vibration (2-10 Hz, at 10 ms-2 level) seems to increase the TTS when noise (broadband at 90 dB(A)) is present. This effect is more pronounced at higher temperatures. The hypothermia protects hearing against the effects of noise in animal studies. The interaction between noise and temperature decrease seems obvious in animal studies. Exercise has both increased and decreased the TTS during noise exposure. The effects have been successfully explained as the depression of the stapedius reflex. Thus, less protection against noise is provided for the inner ear in exercise conditions. The increase of the blood temperature also has been suggested to increase noise-induced TTS during exercise. Electromagnetic fields have been found to cause acoustical interactions in the inner ear. Animal studies and human studies have given contradictory results on the effects of magnetic coil devices on hearing. The MR imaging devices produce noise levels of 82-93 dB, which is not sufficient to produce the risk of permanent hearing loss when short exposure durations are taken into consideration. More systematic research is needed with accurately defined electromagnetic characteristics to reveal the potential interactions. The interactions seem to exist, but relatively high levels and durations of exposure are needed to produce an observable effect on hearing. More investigations are still needed on the permanent hearing loss in humans caused by simultaneous long-term exposures to interacting environmental factors.
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PMID:Noise, impulse noise, and other physical factors: combined effects on hearing. 857 18

Plasminogen activator inhibitor (PAI-1), tissue type plasminogen activator (tPA) and von Willebrand factor (vWF) concentrations were measured by ELISA in the supernatant of the following cultures: endothelial cells from human umbilical vein (HUVEC); human colon cancer cells (HRT-18); and co-culture cells of HUVEC + HRT-18. No measurable amount of the three substances was found in the supernatant of HRT-18 cell culture. Compared to the value in the HUVEC supernatant, in the UVEC/HRT-18 co-cultures, tPA concentration was significantly lower (P = 0.0047), PAI-1 significantly higher (P = 0.026) and vWF also significantly higher (P = 0.0048). These data indicate that HRT-18 tumor cells do not produce tPA, PAI-1 and vWF; however, these tumor cells induce endothelial cells to change the production of these substances. As a consequence, the interaction between tumor and endothelial cells in vivo may lead to depression of fibrinolysis and enhancement of platelet adhesion.
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PMID:Expression of tissue-type plasminogen activator, plasminogen activator inhibitor and von Willebrand factor in the supernatant of endothelial cell cultures in response to the seeding of adenocarcinoma cell line HRT-18. 895 58

There is a significant association between cardiovascular disease and depression. Previous studies have documented changes in platelets in depression. It is unknown if depression causes functional changes in platelet surface receptors. Therefore, we analyzed (1) the surface expression of glycoprotein (GP)Ib and the integrin receptor alpha(IIb)beta(IIIa), receptors involved in platelet adhesion and aggregation, (2) CD62 (P-selectin) and CD63, integral granule proteins translocated during platelet activation, (3) platelet aggregation in response to ADP and (4) plasma levels of glycocalicin and von Willebrand factor (vWF), in depressed patients compared to healthy volunteers. Fifteen depressed patients with a Hamilton depression score of at least 22 and fifteen control subjects were studied. Platelets were assessed for surface expression levels of GPIb, alpha(IIb)beta(IIIa), CD62 and CD63 by flow cytometry. Genomic DNA was isolated to investigate a recently described polymorphism in the 5' untranslated region of the GPIbalpha gene. The number of GPIb receptors was significantly increased on the surface of platelets from patients with depression compared to control subjects. Surface expression of CD62 was also significantly increased in the depressed patients versus control subjects. There was no significant difference between depressed patients and healthy volunteers in the surface expression of alpha(IIb)beta(IIIa) or CD63, or in glycocalicin or vWF plasma concentration, or ADP-induced aggregation. There was no difference in allele frequency of the Kozak region polymorphism of the GPIbalpha gene, which can affect GPIb expression. The results of this study demonstrate that the number of GPIb receptors on platelets are increased in depression and suggest a novel risk factor for thrombosis in patients with depression.
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PMID:Depression is associated with an increase in the expression of the platelet adhesion receptor glycoprotein Ib. 1200 98

By promoting atherosclerosis and thrombosis, a blood-clotting diathesis could contribute to excess cardiovascular morbidity and mortality in patients with systemic hypertension and/or obstructive sleep apnoea. Since psychological states affect haemostatic activity, we wondered about the contribution of behavioural factors to a hypercoagulable state in subjects with increased risk of cardiovascular disease. To tease apart the potential additive nature of cardiovascular disease risk, we examined four patient groups - hypertensives and normotensives, with and without sleep apnoea. The procoagulant molecules thrombin-antithrombin III complex, fibrin D-dimer and von Willebrand factor antigen were measured in 88 subjects (mean age 47 years; range 32-64 years) who underwent full polysomnography. Subjects completed the Center for Epidemiological Studies - Depression (CES-D) Scale, the Cook-Medley (CM) Hostility Scale, and the Profile of Mood States (POMS). Sleep apnoea, hypertension status, age, body mass index and psychological variables (CES-D, CM Stress, and POMS Vigour-Activity) together explained 29% of the variance in D-dimer, a marker of fibrin turnover ( r (2)=0.29, P =0.001). CES-D, CM Stress and POMS Vigour-Activity explained 17% of this variance even after controlling for sleep apnoea, hypertension status, age and body mass index (Delta r (2)=0.17, P =0.001). Thrombin-antithrombin III complex and von Willebrand factor were not significantly related to psychological variables, but this may reflect limited statistical power. Thus psychological factors are independently associated with D-dimer and explain as much of its variance as do traditional correlates (hypertension, sleep apnoea, age and body mass index). These results may provide a rationale for linking behavioural aspects with cardiovascular events.
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PMID:Independent contribution of psychological factors to fibrin turnover in subjects with sleep apnoea and/or systemic hypertension. 1224 29

Bitiscetin, a platelet adhesion inducer isolated from venom of the snake Bitis arietans, activates the binding of the von Willebrand factor (VWF) A1 domain to glycoprotein Ib (GPIb) in vitro. This activation requires the formation of a bitiscetin-VWF A1 complex, suggesting an allosteric mechanism of action. Here, we report the crystal structure of bitiscetin-VWF A1 domain complex solved at 2.85 A. In the complex structure, helix alpha5 of VWF A1 domain lies on a concave depression on bitiscetin, and binding sites are located at both ends of the depression. The binding sites correspond well with those proposed previously based on alanine-scanning mutagenesis (Matsui, T., Hamako, J., Matsushita, T., Nakayama, T., Fujimura, Y., and Titani, K. (2002) Biochemistry 41, 7939-7946). Against our expectations, the structure of the VWF A1 domain bound to bitiscetin does not differ significantly from the structure of the free A1 domain. These results are similar to the case of botrocetin, another snake-derived inducer of platelet aggregation, although the binding modes of botrocetin and bitiscetin are different. The modeled structure of the ternary bitiscetin-VWF A1-GPIb complex suggests that an electropositive surface of bitiscetin may interact with a favorably positioned anionic region of GPIb. These results suggest that snake venom proteins induce VWF A1-GPIbalpha binding by interacting with both proteins, and not by causing conformational changes in VWF A1.
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PMID:Crystal structure of von Willebrand factor A1 domain complexed with snake venom, bitiscetin: insight into glycoprotein Ibalpha binding mechanism induced by snake venom proteins. 1285 90

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

Exaggerated procoagulant responses to acute mental stress may contribute to coronary thrombosis, and continuing low-grade systemic coagulation activation may link negative affect with the development of coronary artery disease. We investigated whether negative and positive affect and perceived social support would moderate stress procoagulant reactivity. Psychological functioning, exhaustion, negative affectivity, depression, anxiety, worrying, vigor, and social support were assessed in 27 apparently healthy men (mean age 47 +/- 8 years) who underwent the 13-min Trier Social Stress Test combining preparation, speech, and mental arithmetic. Plasma levels of von Willebrand factor antigen (VWF:Ag), fibrinogen, factor VII clotting activity (FVII:C), FVIII:C, FXII:C, and D-dimer were measured immediately before and after stress. Acute stress elicited significant increases in hemodynamic, cortisol, and coagulant activity (p values < 0.05). VWF:Ag reactivity showed inverse relationships with exhaustion (r = -0.63, p < 0.001), negative affectivity (r = -0.53, p = 0.005), and worrying (r = -0.53, p = 0.005). Exhaustion and negative affectivity emerged as independent predictors of VWF:Ag reactivity explaining 54% of its variance. Fibrinogen reactivity showed inverse relationships with negative affectivity (r = -0.59, p = 0.002) and anxiety (r = -0.54, p = 0.005); negative affectivity emerged as an independent predictor of fibrinogen reactivity explaining 35% of its variance. Psychological functioning and FVII:C reactivity were also correlated (r = -0.52, p = 0.006). Whereas FVIII:C reactivity correlated positively with vigorous mood (r = 0.48, p = 0.012), positive associations between social support and procoagulant reactivity did not reach significance. Negative affect was associated with attenuated procoagulant reactivity to stress and the opposite was observed for positive affect. Negative affect is not likely to enhance the acute procoagulant stress response in healthy men.
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PMID:Opposite effect of negative and positive affect on stress procoagulant reactivity. 1611 49

To characterize microvascular function, candidate risk pathways, and metabolic syndrome prevalence in women with cardiac syndrome X, 52 nondiabetic women with angiographically normal epicardial arteries but >1 mm of planar ST depression during exercise testing (patients) and 24 healthy controls of similar age were recruited. In addition to fasting blood samples and anthropometric measurements, forearm cutaneous microvascular function after iontophoresis of acetylcholine and sodium nitroprusside was assessed by laser Doppler imaging. Despite body mass index correction and a larger proportion on statin therapy, patients had high levels of insulin (p=0.016), triglycerides (p=0.018), intercellular adhesion molecule-1 (p=0.021), von Willebrand factor (p=0.005), and leptin (p=0.005) and lower levels of high-density lipoprotein cholesterol (p=0.042) compared with controls. Consistent with these data, 30% of patients but only 8% of controls fulfilled criteria for the metabolic syndrome as defined by the National Cholesterol Education Program (p=0.015). Endothelium-dependent and -independent microvascular functions were markedly impaired in patients (p<0.001), and the odds ratio for cardiac syndrome X was 7.38 (95% confidence interval 2.2 to 24.7) if the acetylcholine response was <8,710 flux units. In conclusion, women with cardiac syndrome X more commonly have metabolic syndrome and related adiposity, metabolic, and inflammatory derangements. They also have significantly impaired skin microvascular function as assessed by laser Doppler imaging, consistent with generalized vascular dysfunction, a finding with potential diagnostic implications.
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PMID:Microvascular function, metabolic syndrome, and novel risk factor status in women with cardiac syndrome X. 1676 22


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