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- Lohmander, L. Stefan, et al.
(author)
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Cartilage matrix metabolism in osteoarthritis : markers in synovial fluid, serum, and urine
- 1992
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In: Clinical Biochemistry. - 0009-9120. ; 25:3, s. 167-174
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Journal article (peer-reviewed)abstract
- Osteoarthritis is a major cause of disability and early retirement. Yet we lack the means to diagnose the disease in its early stages or to monitor the effects of treatment on the target tissue, the joint cartilage. Neither can we identify the disease mechanisms at the tissue or cell level. Current research focuses on the use of markers of cartilage matrix metabolism in body fluids as a means to diagnose and monitor osteoarthritis. Cartilage proteoglycan, collagen and glycoprotein fragments, as well as proteinases and their inhibitors, are being suggested for this purpose. Structural information on matrix molecule fragments released into body fluids may also help to identify the enzymes active in the destruction of the cartilage, a central issue in osteoarthritis.
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- Ahnström, Josefin, et al.
(author)
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Plasma concentrations of apolipoproteins A-I, B, and M in patients with abdominal aortic aneurysms.
- 2010
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In: Clinical Biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; 43:4-5, s. 407-410
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Journal article (peer-reviewed)abstract
- Objectives: Apolipoproteins play important roles in the development of atherosclerosis but their involvement in the pathogenesis of abdominal aortic aneurysm (AAA) is poorly understood. The aim was to investigate whether apoA-I, apoB and apoM are independently associated with AAA. Design and methods: Plasma apoA-I, apoB and apoM were measured in 343 patients with AAA and in 214 elderly apparently healthy control individuals from the background population. Results: AAA patients had lower apolipoprotein levels, as compared to healthy individuals; apoA-I, 1.62 vs. 2.08 g/l; apoB, 0.91 vs. 1.04 g/l; apoM, 0.72 vs. 0.91 mumol/l (p<0.0001 for all three). In multivariate analyses, apoA-I and apoB were associated with AAA, odds ratios (95% confidence intervals) being 0.53 (0.43-0.64) and 0.86 (0.75-0.998), respectively. Conclusions: ApoA-I, apoB and apoM levels were significantly lower in patients with AAA than in the control individuals, but only apoA-I and apoB were independently associated to AAA.
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| 8. |
- Ahnström, Josefin, et al.
(author)
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Plasma concentrations of apolipoproteins A-I, B, and M in patients with critical limb ischemia.
- 2010
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In: Clinical Biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; 43, s. 599-603
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Journal article (peer-reviewed)abstract
- OBJECTIVES: Apolipoproteins affect development of atherosclerosis, but their involvement in the pathogenesis of critical limb ischemia (CLI), a severe form of atherosclerosis, has not previously been examined. DESIGN AND METHODS: ApoA-I, apoB, and apoM were measured in plasma from 196 CLI subjects and 214 control individuals from the background population. RESULTS: Cases had lower levels of the apolipoproteins, as compared to controls; apoA-I, 1.23 vs. 2.08 g/L; apoB, 0.93 vs. 1.04 g/L; apoM, 0.75 vs. 0.91 mumol/L (p<0.0001 for all three). ApoA-I and apoM correlated negatively with inflammatory markers and positively to 1- and 3-year survival rates, whereas apoB did not. In multivariate analyses, apoA-I, but not apoB and apoM, was independently associated with CLI, the odds ratio being 0.015. CONCLUSIONS: In subjects with CLI, plasma concentrations of apoA-I, apoB and apoM were significantly lower than in control individuals, but only apoA-I was independently associated to CLI.
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- Apple, FS, et al.
(author)
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IFCC educational materials on selected analytical and clinical applications of high sensitivity cardiac troponin assays
- 2015
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In: Clinical Biochemistry. - : Elsevier BV. - 0009-9120 .- 1873-2933. ; 48:4-5, s. 201-203
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Journal article (peer-reviewed)abstract
- In 2011, the IFCC Task Force on Clinical Applications of Cardiac Bio-Markers (TF-CB) was formed, with the purpose of providing evidence based educational materials to assist all biomarker users, i.e. laboratorians, clinicians, researchers, in-vitro diagnostics and regulatory agencies, in better understanding important analytical and clinical aspects of established and novel cardiac biomarkers for use in clinical practice and research. The goal of the task force was to promulgate the same information conjointly through the in vitro diagnostic industry to the laboratory, emergency department and cardiologists. The initial undertaking of the TF-CB, which is comprised of laboratory medicine scientists, emergency medicine physicians and cardiologists, was to address two key issues pertaining to implementing high-sensitivity cardiac troponin (hs-cTn) assays in clinical practice: the 99th percentile upper reference limit (URL) and calculating serial change values in accord with the Universal Definition of AMI. The highlights of both concepts from IFCC statements are described.
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| 10. |
- Arkblad, Eva L, et al.
(author)
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Two cases of 5-fluorouracil toxicity linked with gene variants in the DPYD gene.
- 2010
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In: Clinical biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; 43:3, s. 331-4
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Journal article (peer-reviewed)abstract
- OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in endogenous pyrimidine catabolism and is responsible for the reduction of the pyrimidine analog 5-fluorouracil (5-FU). DPD deficiency is known to cause potentially lethal toxicity in patients receiving 5-FU. We here report a frequency analysis of one of the major splice-site mutations in the DPDY gene, and further two new DPYD gene variants. DESIGN AND METHODS: Restriction fragment length polymorphism (RFLP) and DNA sequence analysis were performed on genomic DNA and mRNA. RESULTS: In 400 patients that were diagnosed with cancer and were eligible for 5-FU treatment, 14 patients were found to be heterozygous for the splice-site mutation DPYD IVS14+1G>A, which corresponds to a population frequency of 3.5%. Two novel variants in the DPYD gene were identified. The first case was heterozygous for DPYD c.1796T>C (p.M599T). In the second case, we observed heterozygosity for the splice-site mutation DPYD IVS14+17A>G. CONCLUSIONS: We report two new DPYD gene variants, of which DPYD c.1796T>C is potentially pathogenic, whereas DPYD IVS14+17A>G is suggested as a variant without clinical significance.
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