| 1. |
- Blennow, Kaj, 1958, et al.
(author)
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No association between the alpha2-macroglobulin (A2M) deletion and Alzheimer's disease, and no change in A2M mRNA, protein, or protein expression.
- 2000
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In: Journal of neural transmission (Vienna, Austria : 1996). - : Springer Science and Business Media LLC. - 0300-9564 .- 1435-1463. ; 107:8-9, s. 1065-79
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Journal article (peer-reviewed)abstract
- A polymorphism consisting of a deletion near the 5' splice site of exon 18 on the alpha2-macroglobulin (A2M) gene (A2M-2) has been suggested to be associated with Alzheimer's disease (AD) in family-based studies. We studied the A2M-2 allele together with the ApoE alleles in a large series on patients with AD (n = 449) and age-matched controls (n = 349). Neuropathologically confirmed diagnoses were available in 199 cases (94 AD and 107 control cases). We found no increase in A2M-2 genotype or allele frequencies in AD (27.5% and 14.6%) versus controls (26.4% and 14.9%). In contrast, a marked increase (p < 0.0001) in ApoE epsilon4 genotype or allele frequencies was found in AD (66.6% and 41.2%) as compared with controls (29.8% and 16.5%), suggesting sufficient statistical power in our sample. No relation was found between the A2M-2 and the ApoE epsilon4 allele. No change in A2M exon 17-18 mRNA size or sequence or A2M protein size was found in cases carrying the A2M-2 deletion, suggesting that there is no biological consequences of the A2M intronic deletion. No change in A2M protein level in cerebrospinal fluid was found in AD, suggesting that the A2M-2 allele does not effect the A2M protein expression in the brain. The lack of an association between the A2M-2 allele and AD in the present study, and the lack of abnormalities in the A2M mRNA or protein suggest that the A2M-2 allele is not associated with AD.
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| 2. |
- Amer-Wåhlin, Isis, et al.
(author)
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Brain-specific NSE and S-100 proteins in umbilical blood after normal delivery
- 2001
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In: Clinica Chimica Acta. - 0009-8981. ; 304:1-2, s. 57-63
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Journal article (peer-reviewed)abstract
- BACKGROUND: To determine normal blood levels of brain-specific proteins S-100 and neuron specific enolase (NSE) in healthy newborns and their mothers following uncomplicated birth. METHODS: Umbilical artery and vein blood and maternal venous blood was collected at 112 consecutive uncomplicated deliveries. Venous blood samples were taken from 18 of the neonates 3 days after birth. S-100 and NSE were analyzed quantitatively by double antibody immunoluminometric assay (Sangtec Medical AB, Sweden). RESULTS: Compared with adults, healthy neonates had higher levels of both S-100 and NSE. For S-100, median levels (range) were 1.10 microg/l (0.38-5.50 microg/l and 0.98 microg/l (0.43-2.70 microg/l) in umbilical artery and vein, respectively. For NSE, median levels (range) in umbilical artery blood and vein were 27 microg/l (10-140 microg/l) and 10.75 microg/l (8.80->/=200 microg/l) respectively. The maternal venous blood levels of both S-100 and NSE were significantly lower than in their infants. At 3 days of life, neonatal venous levels of the proteins were still high: S-100, 0.48-9.70 microg/l; NSE, 17->/=200 microg/l. In contrast to adults, haemolysis affected the S-100 levels in umbilical blood significantly. CONCLUSION: Concentrations of both S-100 and NSE in blood are greater in newborns after normal birth than in healthy adults. The higher levels in umbilical artery blood than in umbilical vein blood are consistent with a fetal origin of these proteins. High levels in venous blood at 3 days of life suggest that the high levels at birth are not related to the birth process but reflect a high activity of these proteins during fetal development.
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| 3. |
- Andersson, Anders, et al.
(author)
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Hyperhomocysteinemia and changed plasma thiol redox status in chronic obstructive pulmonary disease
- 2001
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In: Clinical Chemistry and Laboratory Medicine. - 1434-6621. ; 39:3, s. 229-233
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Journal article (peer-reviewed)abstract
- Reduced and total homocysteine, cysteine, glutathione and cysteinylglycine in plasma were investigated in 19 patients with chronic obstructive pulmonary disease and in 29 healthy subjects. The purpose was to examine the influence of pro-oxidant activity caused by the lung disease on the metabolism of homocysteine and other plasma thiols. We observed a decreased concentration of reduced glutathione and a decreased ratio of reduced/total glutathione in the patients compared to the healthy individuals, which supports the hypothesis of an association between free radicals and pathogenesis in some lung diseases. We also observed an increased total plasma homocysteine. The influence of a possible extracellular pro-oxidant activity on the concentration of total plasma homocysteine is discussed.
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| 4. |
- Andersson, Anders S, et al.
(author)
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Vitamin supplementation normalizes total plasma homocysteine concentration but not plasma homocysteine redox status in patients with acute coronary syndromes and hyperhomocysteinemia.
- 2002
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In: Clinical Chemistry and Laboratory Medicine. - 1434-6621. ; 40:6, s. 554-558
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Journal article (peer-reviewed)abstract
- Despite the growing evidence that elevated total homocysteine (tHcy) in plasma is a cardiovascular risk factor, the mechanism underlying the vascular injury is still unknown. Studies are difficult due to the fact that little is known about the formation of different homocysteine species in vivo. In the present study we have investigated the different fractions of tHcy in 21 patients with acute coronary syndromes and elevated concentration of plasma tHcy. A subgroup of the patients (n=16) was investigated before and after a 3 months study period with or without vitamin supplementation (folic acid 5 mg, pyridoxine 40 mg and cyanocobalamin 1 mg once daily). A major finding is that these patients had a lowered ratio (0.95%) between the concentration of reduced homocysteine (HcyH) and tHcy compared to controls (1.38%). A low ratio HcyH/tHcy in plasma in combination with elevated plasma tHcy concentrations might reflect increased oxidative activity or decreased reducing capacity in plasma from the patients. Another main finding in the present study is that, although vitamin supplementation of these patients normalized plasma tHcy, the ratio between HcyH and tHcy did not normalize. Since substantial evidence indicates that progression of arteriosclerosis is related to enhanced oxidant activity, the premature vascular disease associated with increased plasma tHcy concentration might be due to increased oxidative activity and the elevated plasma tHcy concentration may only reflect the increased oxidative stress.
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| 5. |
- Carlson, Joyce, et al.
(author)
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In Memoriam, Carl-Bertil Laurell
- 2001
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In: Clinical Chemistry and Laboratory Medicine. - 1434-6621. ; 39:11, s. 1019-1019
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Journal article (peer-reviewed)
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| 9. |
- Jeppsson, Jan-Olof, et al.
(author)
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Approved IFCC reference method for the measurement of HbA1c in human blood.
- 2002
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In: Clinical Chemistry and Laboratory Medicine. - 1434-6621. ; 40:1, s. 78-89
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Journal article (peer-reviewed)abstract
- HbA1C is the stable glucose adduct to the N-terminal group of the beta-chain of HbA0. The measurement of HbA1c in human blood is most important for the long-term control of the glycaemic state in diabetic patients. Because there was no internationally agreed reference method the IFCC Working Group on HbA1c Standardization developed a reference method which is here described. In a first step haemoglobin is cleaved into peptides by the enzyme endoproteinase Glu-C, and in a second step the glycated and non-glycated N-terminal hexapeptides of the beta-chain obtained are separated and quantified by HPLC and electrospray ionisation mass spectrometry or in a two-dimensional approach using HPLC and capillary electrophoresis with UV-detection. Both principles give identical results. HbA1c is measured as ratio between the glycated and non-glycated hexapeptides. Calibrators consisting of mixtures of highly purified HbA1c and HbA0 are used. The analytical performance of the reference method has been evaluated by an international network of reference laboratories comprising laboratories from Europe, Japan and the USA. The intercomparison studies of the network showed excellent results with intra-laboratory CVs of 0.5 to 2% and inter-laboratory CVs of 1.4 to 2.3%. Possible interferences have been carefully investigated. Due to the higher specificity of the reference method the results are lower than those generated with most of the present commercial methods which currently are calibrated with unspecific designated comparison methods. The new reference method has been approved by the member societies of the International Federation of Clinical Chemistry and Laboratory Medicine and will be the basis for the future uniform standardization of HbA1c routine assays worldwide.
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| 10. |
- Jonasson, Torfi, et al.
(author)
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Renal function exerts only a minor influence on high plasma homocysteine concentrations in patients with acute coronary syndromes.
- 2002
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In: Clinical Chemistry and Laboratory Medicine. - 1434-6621. ; 40:2, s. 137-142
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Journal article (peer-reviewed)abstract
- It has been suggested that hyperhomocysteinemia observed in patients with occlusive vascular disease is caused by reduced renal function secondary to renovascular disease. We have therefore used serum cystatin C, a new sensitive marker for glomerular filtration, in 59 patients with acute coronary syndromes and high plasma homocysteine (tHcy) concentration to measure renal function. Samples were also obtained from 34 patients with low-normal plasma tHcy and 50 control subjects. The patients with low-normal plasma tHcy concentration showed decreased concentrations of serum cystatin C and serum creatinine and increased concentrations of blood folate and serum cobalamin compared to the controls and to the patients with high plasma tHcy. There was a large overlap in cystatin C concentrations between patients with high and low-normal plasma tHcy. None of the parameters investigated except plasma tHcy were significantly different in the group of patients with high plasma tHcy concentration compared to the control group. In order to further demonstrate the importance of renal impairment, a subgroup of the patients with high plasma tHcy was supplemented daily with folic acid 5 mg, pyridoxine 40 mg and cyancobalamin 1 mg for 3 months. Vitamin therapy reduced plasma tHcy from 18.3+/-4.6 pmol/l to 9.6+/-2.2 pmol/l (p<0.0001). However, vitamin treatment did not strengthen the correlation between cystatin C and plasma tHcy concentrations. These findings do not support the hypothesis that subtle renal dysfunction is an important cause of high plasma tHcy concentration in patients with acute coronary syndromes.
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