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- Broman, G, et al.
(författare)
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Older women's cardiovascular responses to deep-water running
- 2006
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Ingår i: Journal of aging and physical activity. - : Human Kinetics. - 1063-8652 .- 1543-267X. ; 14:1, s. 29-40
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the study was to examine submaximal and maximal physiological responses and perceived exertion during deep-water running with a vest compared with the responses during treadmill running in healthy elderly women. Eleven healthy women 70 ± 2 years old participated. On two different occasions they performed a graded maximal exercise test on a treadmill on land and a graded maximal exercise test in water wearing a vest. At maximal work the oxygen uptake was 29% lower (p < .05), the heart rate was 8% lower (p < .05), and the ventilation was 16% lower (p < .05) during deep-water running than during treadmill running. During submaximal absolute work the heart rate was higher during deep-water running than during treadmill running for the elderly women. The participants had lower maximal oxygen uptake, heart rate, ventilation, respiratory-exchange ratio, and rate of perceived exertion during maximal deep-water running with a vest than during maximal treadmill running. These responses were, however, higher during submaximal deep-water running than during treadmill running.
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- Gulez, N., et al.
(författare)
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Homozygosity For a Novel Mutation in the C1q C Chain Gene in a Turkish Family With Hereditary C1q Deficiency
- 2010
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Ingår i: Journal of Investigational Allergology & Clinical Immunology. - 1698-0808. ; 20:3, s. 255-258
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Tidskriftsartikel (refereegranskat)abstract
- Hereditary complete deficiency of complement component C1q is associated with a high prevalence of systemic lupus erythematosus and increased susceptibility to severe recurrent infections. An 11-year-old girl was screened for immunodeficiency due to a history of recurrent meningitis and pneumonia. Immunologic studies revealed absence of classic pathway hemolytic activity and undetectable levels of C1q. Exon-specific amplification of genomic DNA by polymerase chain reaction followed by direct sequence analysis revealed a novel homozygous missense mutation at codon 48 in the C1q C gene causing a glycine-to-arginine substitution affecting the collagen-like region of C1q. No changes were seen in the exons of the A and B chains. The mutation affected both the formation and the secretion of C1q variant molecules. We describe a novel mutation in the C1q C chain gene that leads to an interchange in amino acids resulting in absence of C1q in serum.
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- Martini, Paolo G. V., et al.
(författare)
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Recombinant human complement component C2 produced in a human cell line restores the classical complement pathway activity in-vitro: an alternative treatment for C2 deficiency diseases
- 2010
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Ingår i: BMC Immunology. - : Springer Science and Business Media LLC. - 1471-2172. ; 11
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Tidskriftsartikel (refereegranskat)abstract
- Background: Complement C2 deficiency is the most common genetically determined complete complement deficiency and is associated with a number of diseases. Most prominent are the associations with recurrent serious infections in young children and the development of systemic lupus erythematosus (SLE) in adults. The links with these diseases reflect the important role complement C2 plays in both innate immunity and immune tolerance. Infusions with normal fresh frozen plasma for the treatment of associated disease have demonstrated therapeutic effects but so far protein replacement therapy has not been evaluated. Results: Human complement C2 was cloned and expressed in a mammalian cell line. The purity of recombinant human C2 (rhC2) was greater than 95% and it was characterized for stability and activity. It was sensitive to C1s cleavage and restored classical complement pathway activity in C2-deficient serum both in a complement activation ELISA and a hemolytic assay. Furthermore, rhC2 could increase C3 fragment deposition on the human pathogen Streptococcus pneumoniae in C2-deficient serum to levels equal to those with normal serum. Conclusions: Taken together these data suggest that recombinant human C2 can restore classical complement pathway activity and may serve as a potential therapeutic for recurring bacterial infections or SLE in C2-deficient patients.
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