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- Bergström, Gunnar, Professor, et al.
(författare)
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Reliability and factor structure of the Multidimensional Pain Inventory--Swedish Language Version (MPI-S).
- 1998
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Ingår i: Pain. - : LWW. - 0304-3959 .- 1872-6623. ; 75:1, s. 101-10
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Tidskriftsartikel (refereegranskat)abstract
- The psychological assessment of chronic pain is often accomplished using questionnaires such as the (West Haven-Yale) Multidimensional Pain Inventory ((WHY)MPI) which is constructed to capture the multidimensionality of chronic pain. The (WHY)MPI theoretically originates from behavioural and cognitive behavioural theories of pain. It is divided into three parts and measures psychosocial and behavioural consequences of pain. This questionnaire has displayed satisfactory psychometric properties and translations of the original English version into German and Dutch have been demonstrated to be reliable and valid. The aim of this study was to test the reliability and factor structure of a Swedish translation of the (WHY)MPI, the MPI-S, and also to test the generalisability of the factor structure found for the (WHY)MPI. We performed analyses of internal consistency using Cronbach's alpha, and carried out a confirmatory factor analysis (CFA) employing LISREL-8 on a population of 682 patients suffering from chronic musculoskeletal pain. Test-retest analysis was accomplished on a sub-sample of 54 individuals taken from the aforementioned population. For sections 1 and 2 of the MPI-S the overall reliability and stability were good, and after the exclusion of four items, the factor structure was similar to other versions of the MPI. For section 3, despite removal of five questions, the proposed factor structure could not be replicated. This part of the inventory is designed to measure the extent of different types of activities, and our results suggest that this section may only be used for assessing general activity level. We conclude that, with a few adjustments, the analyses yielded satisfactory results for sections 1 and 2 of the MPI-S regarding its factor structure, reliability and generalisability. For section 3 the hypothesised factor structure could not be confirmed.
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- Jensen-Urstad, K, et al.
(författare)
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Heart rate variability in healthy subjects is related to age and gender.
- 1997
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772 .- 1365-201X. ; 160:3, s. 235-41
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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- LI, L, et al.
(författare)
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Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice
- 1995
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 92:20, s. 9235-9239
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Tidskriftsartikel (refereegranskat)abstract
- Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exocytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination. The organization of synaptic vesicles at presynaptic terminals of synapsin I-deficient mice was markedly altered: densely packed vesicles were only present in a narrow rim at active zones, whereas the majority of vesicles were dispersed throughout the terminal area. This was in contrast to the organized vesicle clusters present in terminals of wild-type animals. Release of glutamate from nerve endings, induced by K+,4-aminopyridine, or a Ca2+ ionophore, was markedly decreased in synapsin I mutant mice. The recovery of synaptic transmission after depletion of neurotransmitter by high-frequency stimulation was greatly delayed. Finally, synapsin I-deficient mice exhibited a strikingly increased response to electrical stimulation, as measured by electrographic and behavioral seizures. These results provide strong support for the hypothesis that synapsin I plays a key role in the regulation of nerve terminal function in mature synapses.
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- Wallin, H, et al.
(författare)
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Altered aromatic amine metabolism in epileptic patients treated with phenobarbital
- 1995
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Ingår i: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. - 1055-9965. ; 4:7, s. 3-771
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Tidskriftsartikel (refereegranskat)abstract
- The fate of carcinogens differs among individuals who have different activities of drug-metabolizing enzymes that are important in activating and detoxifying carcinogens. A drug that profoundly alters the metabolism of the drugs and carcinogens is the anticonvulsive agent phenobarbital. To investigate why epileptic patients appear to have a low risk of cancer of the urinary bladder, and on the basis of the observation that levels of aromatic amine-hemoglobin adducts are strongly associated with various risk factors for cancer at that site, we determined aromatic amine-hemoglobin adducts in 62 epileptic patients as a surrogate measure of the reaction of carcinogenic metabolites with DNA in target tissue. Although adducts were detected in all subjects, the levels were proportional to daily tobacco consumption. When the subjects were stratified into groups smoking 20 g tobacco/day or more, smoking <20 g/day, and not smoking, an effect of medication was detected. Epileptic patients treated chronically with phenobarbital or primidone, which is effectively metabolized to phenobarbital, were found to have lower levels of 4-aminobiphenyl adducts than patients on the other treatment (P = 0.02; ANOVA). In nonsmokers, no effect of medication could be demonstrated above background variation; however, an increasing effect was seen with tobacco consumption with only one-half the increase in adducts per g of tobacco smoked as epileptic patients on other treatment. The difference in the increases (slopes of regression lines) was highly significant statistically. This reduction in the level of hemoglobin-aromatic amine adducts is probably due to induction of detoxification enzymes in the patients treated with phenobarbital.
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