This study explored the possible beneficial effects of singing on well-being during a singing lesson. Eight amateur (2m, 6f, age 28-53 yrs) and eight professional (4m, 4f, age 26-49 yrs) singers who had been attending singing lessons for at least six months were included. Continuous ECG was recorded and computerized spectral analysis was performed. Serum concentrations of TNF-alpha, prolactin, cortisol, and oxytocin were measured before and 30 min after the lesson. Five visual analogue scales (VAS, sad-joyful, anxious-calm, worried-elated, listless-energetic, and tense-relaxed) were scored before and after the lesson. In addition, a semi-structured interview was performed. Heart rate variability analyses showed significant changes over time in the two groups for total power, and low and high frequency power. Power increased during singing in professionals, whereas there were no changes in amateurs. This indicates an ability to retain more "heart-brain connection." i.e., more cardio-physiological fitness for singing in professional singers, compared to amateur singers. Serum concentration of TNF-alpha increased in professionals after the singing lesson, whereas the concentration in amateurs decreased. Serum concentrations of prolactin and cortisol increased after the lesson in the group of men and vice versa for women. Oxytocin concentrations increased significantly in both groups after the singing lesson. Amateurs reported increasing joy and elatedness (VAS), whereas professionals did not. However, both groups felt more energetic and relaxed after the singing lesson. The interviews showed that the professionals were clearly achievement-oriented, with focus on singing technique, vocal apparatus and body during the lesson. The amateurs used the singing lessons as a means of self-actualization and self-expression as a way to release emotional tensions. In summary, in this study, singing during a singing lesson seemed to promote more well-being and less arousal for amateurs compared to professional singers, who seemed to experience less well-being and more arousal.
The effects of age and gender on heart rate variability as measured by spectral and time domain analysis of 24 h ECG recordings were evaluated in 101 healthy subjects, 49 men and 52 women (20-69 years of age). In the frequency domain, total power, very low-frequency power, low-frequency power and high-frequency power were negatively correlated to age (P < 0.001 for all variables). Total power decreased by 30% between 20-29 and 60-69 years of age. In the time domain, SDNN-index, the mean of the standard deviations of all normal R-R intervals for all 5 min segments of a 24 h ECG recording, was negatively correlated to age (P < 0.001). Total power, very low-frequency power, low-frequency power and the low-frequency/high-frequency ratio were lower in women (P < 0.05, P < 0.05, P < 0.01 and P < 0.01), although the absolute differences were much smaller than for age. There was a pronounced circadian variation; at night total power increased in all age groups (P < 0.01). The results show that age, and to a lesser degree gender, are important determinants of heart rate variability in healthy subjects. Heart rate variability is a valuable tool for risk stratification in cardiovascular disease, but the physiological effects of ageing, with diminishing heart rate variability in older age groups, must also be taken into account.
These findings suggest heart rate variability to be a mediating mechanism that could explain at least part of the reported associations between social isolation, suppressed anger, and health outcomes.
A human thioredoxin cDNA was modified to optimize Escherichia coli expression and subcloned into the plasmid pACA, a vector for T7 RNA polymerase-directed expression. The substitution of structural (noncatalytic) half-cystines in human thioredoxin (hTrx) was made by site-directed mutagenesis. The recombinant wild-type (wt) hTrx and its mutant C61S, C72S, and C61S/C72S were expressed and purified to homogeneity. Characterization of the wt and mutant hTrx was done with respect to redox activity with thioredoxin reductase (TR), tryptophan fluorescence, and effects of incubation with GS-Se-SG, which is believed to be the major metabolite of inorganic selenium compounds in mammalian tissues. The Km and kcat of wild-type hTrx for human placenta thioredoxin reductase (HP-TR) at pH 7.0 were 2.0 microM and 2800 min-1, respectively. The mutant proteins C61S, C72S, and C61S/C72S had Km and kcat values similar to those of the wt thioredoxin. Tryptophan fluorescence measurements showed that the wt and mutant proteins had similar stability to a denaturing agent. Incubation of fully reduced thioredoxin with 0.1 molar equivalent of GS-Se-SG resulted in continued oxidation of SH groups. After 3.5 h only 0.5 of initially 4.6 SH groups/thioredoxin remained. With the oxidized protein, a pronounced lag phase in thioredoxin reductase-dependent insulin disulfide reduction was present. Disulfide-linked dimers of the protein were present. The results clearly showed that noncatalytic cysteine residues in hTrx were oxidized accompanied by dimerization and inactivation. The activities of the mutant proteins C72S and C61S/C72S were unchanged after 3 h of incubation with GS-Se-SG. No dimer appeared of the C72S thioredoxin.(ABSTRACT TRUNCATED AT 250 WORDS)
Using a Cybex II, eight healthy male subjects performed isokinetic knee extensions at two different speeds (30 and 180 deg/sec) and two different positions of the resistance pad (proximal and distal). A sagittal plane, biomechanical model was used for calculating the magnitude of the tibiofemoral joint compressive and shear forces. The magnitude of isokinetic knee extending moments was found to be significantly lower with the resistance pad placed proximally on the leg instead of distally. The tibiofemoral compressive force was of the same magnitude as the patellar tendon force, with a maximum of 6300 N or close to 9 times body weight (BW). The tibiofemoral shear force changed direction from being negative (tibia tends to move posteriorly in relation to femur) to a positive magnitude of about 700 N or close to 1 BW, indicating that high forces arise in the ACL when the knee is extended more than 60 degrees. The anteriorly directed shear force was lowered considerably by locating the resistance pad to a proximal position on the leg. This model may be used when it is desirable to control stress on the ACL, e.g., in the rehabilitative period after ACL repairs or reconstructions.
HLA class II molecules are constitutively expressed on human B lymphocytes and are induced on human T lymphocytes after activation, through which signal transduction via these molecules has been extensively described. We have observed cell death of as many as 60% after stimulation of lymphocytes via HLA class II DR molecules, but not via DP or DQ. Propidium iodide fluorescence, DNA fragmentation and morphology of the dead cells were examined. The reported cell death was very rapid, and independent of Fc receptors and of complement. A morphologically distinct sub-population of activated B cells was sensitive to HLA-DR mediated death, while resting B lymphocytes from the same donor did not die as a result of HLA class II mediated stimulation. Death via HLA-DR was distinguishable from necrosis. Cytoskeletal integrity, serine/threonine phosphatase activity and endonucleases were required for the pathway leading to HLA-DR mediated death. The 'ladder' pattern of DNA fragmentation which typically characterizes apoptosis was not observed, despite the observation of cell and nuclear shrinkage normally associated with apoptosis. These data suggest that HLA class II mediated death is a means of rapidly removing either T or B lymphocytes which have already served their role in the immune response, thereby avoiding the inflammatory responses associated with necrosis and concentrating the ligands for new TCR and/or CD4 interactions.
Purpose. Both heart rate variability (HRV) and inflammatory markers are carrying prognostic information in coronary heart disease (CHD), however, we know of no studies examining their relation in CHD. The aim of this study, therefore, was to assess the association between HRV and inflammatory activity, as reflected by the levels of interleukin-6 (IL-6), IL-1 receptor antagonist (IL-1ra) and C-reactive protein (CRP). Subjects and methods. Consecutive women patients who survived hospitalization for acute myocardial infarction, and/or underwent a percutaneous transluminal coronary angioplasty or a coronary artery bypass grafting were included and evaluated in a stable condition 1 year after the index events. An ambulatory 24-h ECG was recorded during normal activities. SDNN index (mean of the standard deviations of all normal to normal intervals for all 5-min segments of the entire recording) and the following frequency domain parameters were assessed: total power, high frequency (HF) power, low frequency (LF) power and very low frequency (VLF) power. Levels of high-sensitivity CRP were measured by nephelometry, IL-6 and IL-1ra concentrations were determined by enzyme immunoassay.Results. Levels of IL-6 showed an inverse relation with HRV measures even after controlling for potential confounding factors. The P-values were 0.02, 0.04, 0.01, 0.03, 0.18 for the multivariate association with SDDN index, total power, VLF power, LF power and HF power respectively. In contrast, the inverse relationship between HRV measures and CRP or IL-1ra levels were weak and nonsignificant. Correlation coefficients for the relationship between IL-6 and HRV measures were both uni-and multivariately higher than for the relationship between HRV measures and any other factors evaluated in this study. Conclusion. Concentration of IL-6 showed a negative, independent association with HRV in women with CHD. Thus, increased inflammatory activity, as reflected by IL-6 levels, may represent a new auxiliary mechanism linking decreased HRV to poor prognosis in CHD.
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