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- Dick, FD, et al.
(författare)
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Environmental risk factors for Parkinson's disease and parkinsonism : The Geoparkinson study
- 2007
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Ingår i: Occupational and Environmental Medicine. - : BMJ. - 1351-0711 .- 1470-7926. ; 64:10, s. 666-672
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To investigate the associations between Parkinson's disease and other degenerative parkinsonian syndromes and environmental factors in five European countries. Methods: A case-control study of 959 prevalent cases of parkinsonism (767 with Parkinson's disease) and 1989 controls in Scotland, Italy, Sweden, Romania and Malta was carried out. Cases were defined using the United Kingdom Parkinson's Disease Society Brain Bank criteria, and those with drug-induced or vascular parkinsonism or dementia were excluded. Subjects completed an interviewer-administered questionnaire about lifetime occupational and hobby exposure to solvents, pesticides, iron, copper and manganese. Lifetime and average annual exposures were estimated blind to disease status using a job-exposure matrix modified by subjective exposure modelling. Results were analysed using multiple logistic regression, adjusting for age, sex, country, tobacco use, ever knocked unconscious and family history of Parkinson's disease. Results: Adjusted logistic regression analyses showed significantly increased odds ratios for Parkinson's disease/parkinsonism with an exposure-response relationship for pesticides (low vs no exposure, odds ratio (OR) =1.13, 95% Cl 0.82 to 1.57, high vs no exposure, OR =1.41, 95% Cl 1.06 to 1.88) and ever knocked unconscious (once vs never, OR= 1.35, 95% Cl 1.09 to 1.68, more than once vs never, OR = 2.53, 95% Cl 1.78 to 3.59). Hypnotic, anxiolytic or antidepressant drug use for more than 1 year and a family history of Parkinson's disease showed significantly increased odds ratios. Tobacco use was protective (OR = 0.50, 95% Cl 0.42 to 0.60). Analyses confined to subjects with Parkinson's disease gave similar results. Conclusions: The association of pesticide exposure with Parkinson's disease suggests a causative role. Repeated traumatic loss of consciousness is associated with increased risk.
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| 2. |
- Dick, FD, et al.
(författare)
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Gene-environment interactions in parkinsonism and Parkinson's disease : The Geoparkinson study
- 2007
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Ingår i: Occupational and Environmental Medicine. - : BMJ. - 1351-0711 .- 1470-7926. ; 64:10, s. 673-680
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: To investigate associations of Parkinson's disease (PD) and parkinsonian syndromes with polymorphic genes that influence metabolism of either foreign chemical substances or dopamine and to seek evidence of gene-environment interaction effects that modify risk. Methods: A case-control study of 959 prevalent cases of parkinsonism (767 with PD) and 1989 controls across five European centres. Occupational hygienists estimated the average annual intensity of exposure to solvents, pesticides and metals, (iron, copper, manganese), blind to disease status. CYP2D6, PON1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, CYP1B1, MAO-A, MAO-B, SOD 2, EPHX, DATl, DRD2 and NAT2 were genotyped. Results were analysed using multiple logistic regression adjusting for key confounders. Results: There was a modest but significant association between MAO-A polymorphism in males and disease risk (G vs T, OR 1.30, 95% C1 1.02 to 1.66, adjusted). The majority of gene-environment analyses did not show significant interaction effects. There were possible interaction effects between GSTM1 null genotype and solvent exposure (which were stronger when limited to PD cases only). Conclusions: Many small studies have reported associations between genetic polymorphisms and PD. Fewer have examined gene-environment interactions. This large study was sufficiently powered to examine these aspects. GSTM1 null subjects heavily exposed to solvents appear to be at increased risk of PD. There was insufficient evidence that the other gene-environment combinations investigated modified disease risk, suggesting they contribute little to the burden of PD.
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| 7. |
- Borgström, Magnus, et al.
(författare)
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Precursor evaluation for in situ InP nanowire doping
- 2008
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Ingår i: Nanotechnology. - : IOP Publishing. - 0957-4484 .- 1361-6528. ; 19:44
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Tidskriftsartikel (refereegranskat)abstract
- The use of tetraethyltin (TESn) and dimethylzinc (DMZn) as in situ n- and p-dopant precursors during particle-assisted growth of InP nanowires is reported. Gate voltage dependent transport measurements demonstrate that the nanowires can be predictably synthesized as either n- or p-type. These doped nanowires can be characterized based on their electric field response and we find that n- type doping scales over a range from 10(17) to 10(19) cm(-3) with increasing input TESn dopant molar fraction. On the other hand, the p-type doping using DMZn saturates at low levels, probably related to a strong increase in nanowire growth rate with increasing DMZn molar fractions. By optimizing growth conditions with respect to tapering, axial pn-junctions exhibiting rectifying behavior were fabricated. The pn-junctions can be operated as light emitting diodes.
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| 9. |
- Delbro, Dick, et al.
(författare)
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Is acetylcholine an autocrine/paracrine growth factor via the nicotinic α-receptor subtype in the human colon cancer cell line HT-29?
- 2009
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Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999 .- 1879-0712. ; 609:1-3, s. 27-33
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Tidskriftsartikel (refereegranskat)abstract
- We used immunochemistry to demonstrate expression of acetylcholine's nicotinic 7-receptor subtype inhuman colon cancer cell line HT-29. Moreover, RT-PCR and immunochemistry showed that cholineacetyltransferase and acetylcholine esterase, the enzymes responsible for acetylcholine synthesis anddegradation, respectively, localise in HT-29 cells. Bromoacetylcholine bromide, an inhibitor of cholineacetyltransferase, significantly attenuated basal cell growth. Our findings suggest that acetylcholine mightserve as an autocrine/paracrineor speculatively, even intracrinesignalling molecule in cell line HT-29, thuscontributing to carcinogenesis/cancer progression
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| 10. |
- Delbro, Dick, et al.
(författare)
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The influence of opioids on urokinase plasminogen activator on protein and mRNA level in MCF-7 breast cancer cell line
- 2009
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Ingår i: Chemical Biology and Drug Design. - 1747-0277 .- 1747-0285. ; 74:4, s. 390-396
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Tidskriftsartikel (refereegranskat)abstract
- Urokinase plasminogen activator plays a key role intumor-associated processes, increasing cancer cellinvasion and metastasis, and is therefore used as amarker in cancer prognosis. In this study, we havedetermined the effect of mu-opioid receptor agonistsand antagonists on the urokinase plasminogen activatorsecretion in MCF-7 cell line. It was shown thatmu-opioid receptor agonists, such as morphine andendomorphins, greatly stimulate urokinase plasminogenactivator secretion, while naloxone andMOR-selective antagonists elicit the oppositeeffect. The same tendency was observed also onthe urokinase plasminogen activator mRNA level.However, neither agonists nor antagonists had anyeffect on proliferation of MCF-7 cells. The findingsreported in this study may be useful in designingfurther experiments aimed at elucidating the roleof the opioid system in cancer cells
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