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| 2. |
- Graham, J, et al.
(författare)
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Genetic effects on age-dependent onset and islet cell autoantibody markers in type 1 diabetes
- 2002
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Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 51:5, s. 1346-1355
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Tidskriftsartikel (refereegranskat)abstract
- Age-dependent associations between type 1 diabetes risk genes HLA, INS VNTR, and CTLA-4 and autoantibodies to GAD65 (GADAs), ICA512/IA-2, insulin, and islet cells were determined by logistic regression analysis in 971 incident patients with type 1 diabetes and 702 control subjects aged 0–34 years. GADAs were associated with HLA-DQ2 in young but not in older patients (P = 0.009). Autoantibodies to insulin were negatively associated with age (P < 0.0001) but positively associated with DQ8 (P = 0.03) and with INS VNTR (P = 0.04), supporting possible immune tolerance induction. ICA512/IA-2 were negatively associated with age (P < 0.0001) and with DQ2 (P < 0.0001) but positively associated with DQ8 (P = 0.04). Males were more likely than females to be negative for GADA (P < 0.0001), autoantibodies to islet cells (P = 0.04), and all four autoantibody markers (P = 0.004). The CTLA-4 3′ end microsatellite marker was not associated with any of the autoantibodies. We conclude that age and genetic factors such as HLA-DQ and INS VNTR need to be combined with islet autoantibody markers when evaluating the risk for type 1 diabetes development.
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| 3. |
- Johar, Dina, et al.
(författare)
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Inflammatory response, reactive oxygen species, programmed (necrotic-like and apoptotic) cell death and cancer
- 2004
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Ingår i: Roczniki Akademii Medycznej w Bialymstoku (1995). ; 49, s. 31-39
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Forskningsöversikt (refereegranskat)abstract
- In this short review we attempt to establish and/or strengthen connections between clinical, inflammatory manifestation of cancer, inflammatory processes driven by lipoxy-metabolites and their contribution to immortalized phenotype and apoptosis inhibition. Particularly the resemblance between symptoms of inflammation and signs associated with cancer chemotherapy and/or cytokine therapy is illustrated. In this context the role of apoptosis and necrosis in inflammation as well as the role of RedOx processes and lipid-oxidizing enzymes particularly cyclooxygenase-2 (COX-2) and also to lesser extend the 5-lipooxygenase (5-LOX) is highlighted. The multitude of biological effects of reactive oxygen species is shortly summarized and some aspects of it are being discussed in greater detail. Apoptotic cell death is discussed in the context of the "resolve-phase" of an inflammatory response. The disturbance of apoptosis is mainly deliberated in the framework of insufficient removal of immuno-effector cells that may cause autoimmunity. The role of COX-2 in apoptosis resistance is being highlighted mainly in the context of malignant transformation. The mechanism of cell death (apoptotic or necrotic) and its influence on the immune system and potential benefits of necrotic cell death induction during cancer chemotherapy is indicated.
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| 5. |
- Rehm, J., et al.
(författare)
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Alcohol
- 2004
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Ingår i: Comparative quantification of health risks. - Geneva : World Health Organization. - 9241580313 ; , s. 959-1108
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Rehm, J., et al.
(författare)
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Alcohol as a risk factor for global burden of disease
- 2003
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Ingår i: European Addiction Research. - : S. Karger AG. - 1022-6877 .- 1421-9891. ; 9:4, s. 157-164
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Tidskriftsartikel (refereegranskat)abstract
- AIM:To make quantitative estimates of the burden of disease attributable to alcohol in the year 2000 on a global basis.DESIGN:Secondary data analysis.MEASUREMENTS:Two dimensions of alcohol exposure were included: average volume of alcohol consumption and patterns of drinking. There were also two main outcome measures: mortality, i.e. the number of deaths, and disability-adjusted life years (DALYs), i.e. the number of years of life lost to premature mortality or to disability. All estimates were prepared separately by sex, age group and WHO region.FINDINGS:Alcohol causes a considerable disease burden: 3.2% of the global deaths and 4.0% of the global DALYs in the year 2000 could be attributed to this exposure. There were marked differences by sex and region for both outcomes. In addition, there were differences by disease category and type of outcome; in particular, unintentional injuries contributed most to alcohol-attributable mortality burden while neuropsychiatric diseases contributed most to alcohol-attributable disease burden.DISCUSSION/CONCLUSIONS:The underlying assumptions are discussed and reasons are given as to why the estimates should still be considered conservative despite the considerable burden attributable to alcohol globally.
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