| 21. |
- Davi, F., et al.
(author)
-
Technical design report for the endcap disc DIRC
- 2022
-
In: Journal of Physics G. - : Institute of Physics Publishing (IOPP). - 0954-3899 .- 1361-6471. ; 49:12
-
Journal article (peer-reviewed)abstract
- PANDA (anti-proton annihiliation at Darmstadt) is planned to be one of the four main experiments at the future international accelerator complex FAIR (Facility for Antiproton and Ion Research) in Darmstadt, Germany. It is going to address fundamental questions of hadron physics and quantum chromodynamics using cooled antiproton beams with a high intensity and and momenta between 1.5 and 15 GeV/c. PANDA is designed to reach a maximum luminosity of 2 × 1032 cm−2 s. Most of the physics programs require an excellent particle identification (PID). The PID of hadronic states at the forward endcap of the target spectrometer will be done by a fast and compact Cherenkov detector that uses the detection of internally reflected Cherenkov light (DIRC) principle. It is designed to cover the polar angle range from 5° to 22° and to provide a separation power for the separation of charged pions and kaons up to 3 standard deviations (s.d.) for particle momenta up to 4 GeV/c in order to cover the important particle phase space. This document describes the technical design and the expected performance of the novel PANDA disc DIRC detector that has not been used in any other high energy physics experiment before. The performance has been studied with Monte-Carlo simulations and various beam tests at DESY and CERN. The final design meets all PANDA requirements and guarantees sufficient safety margins.
|
|
| 22. |
|
|
| 23. |
- Gu, Fangyi, et al.
(author)
-
Eighteen insulin-like growth factor pathway genes, circulating levels of IGF-I and its binding protein, and risk of prostate and breast cancer
- 2010
-
In: Cancer Epidemiology, Biomarkers and Prevention. - : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 19:11, s. 2877-2887
-
Journal article (peer-reviewed)abstract
- Background: Circulating levels of insulin-like growth factor I (IGF-I) and its main binding protein, IGF binding protein 3 (IGFBP-3), have been associated with risk of several types of cancer. Heritable factors explain up to 60% of the variation in IGF-I and IGFBP-3 in studies of adult twins.Methods: We systematically examined common genetic variation in 18 genes in the IGF signaling pathway for associations with circulating levels of IGF-I and IGFBP-3. A total of 302 single nucleotide polymorphisms (SNP) were genotyped in >5,500 Caucasian men and 5,500 Caucasian women from the Breast and Prostate Cancer Cohort Consortium.Results: After adjusting for multiple testing, SNPs in the IGF1 and SSTR5 genes were significantly associated with circulating IGF-I (P < 2.1 × 10−4); SNPs in the IGFBP3 and IGFALS genes were significantly associated with circulating IGFBP-3. Multi-SNP models explained R2 = 0.62% of the variation in circulating IGF-I and 3.9% of the variation in circulating IGFBP-3. We saw no significant association between these multi-SNP predictors of circulating IGF-I or IGFBP-3 and risk of prostate or breast cancers.Conclusion: Common genetic variation in the IGF1 and SSTR5 genes seems to influence circulating IGF-I levels, and variation in IGFBP3 and IGFALS seems to influence circulating IGFBP-3. However, these variants explain only a small percentage of the variation in circulating IGF-I and IGFBP-3 in Caucasian men and women.Impact: Further studies are needed to explore contributions from other genetic factors such as rare variants in these genes and variation outside of these genes.
|
|
| 24. |
- Guthold, Regina, et al.
(author)
-
Global and regional levels and trends of child and adolescent morbidity from 2000 to 2016 : an analysis of years lost due to disability (YLDs)
- 2021
-
In: BMJ Global Health. - : BMJ Publishing Group Ltd. - 2059-7908. ; 6:3
-
Journal article (peer-reviewed)abstract
- Introduction Non-fatal health loss makes a substantial contribution to the total disease burden among children and adolescents. An analysis of these morbidity patterns is essential to plan interventions that improve the health and well-being of children and adolescents. Our objective was to describe current levels and trends in the non-fatal disease burden from 2000 to 2016 among children and adolescents aged 0-19 years. Methods We used years lost due to disability (YLD) estimates in WHO's Global Health Estimates to describe the non-fatal disease burden from 2000 to 2016 for the age groups 0-27 days, 28 days-11 months, 1-4 years, 5-9 years, 10-14 years and 15-19 years globally and by modified WHO region. To describe causes of YLDs, we used 18 broad cause groups and 54 specific cause categories. Results In 2016, the total number of YLDs globally among those aged 0-19 years was about 130 million, or 51 per 1000 population, ranging from 30 among neonates aged 0-27 days to 67 among older adolescents aged 15-19 years. Global progress since 2000 in reducing the non-fatal disease burden has been limited (53 per 1000 in 2000 for children and adolescents aged 0-19 years). The most important causes of YLDs included iron-deficiency anaemia and skin diseases for both sexes, across age groups and regions. For young children under 5 years of age, congenital anomalies, protein-energy malnutrition and diarrhoeal diseases were important causes of YLDs, while childhood behavioural disorders, asthma, anxiety disorders and depressive disorders were important causes for older children and adolescents. We found important variations between sexes and between regions, particularly among adolescents, that need to be addressed context-specifically. Conclusion The disappointingly slow progress in reducing the global non-fatal disease burden among children and adolescents contrasts starkly with the major reductions in mortality over the first 17 years of this century. More effective action is needed to reduce the non-fatal disease burden among children and adolescents, with interventions tailored for each age group, sex and world region.
|
|
| 25. |
- Haycock, Philip C., et al.
(author)
-
Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases A Mendelian Randomization Study
- 2017
-
In: JAMA Oncology. - : American Medical Association. - 2374-2437 .- 2374-2445. ; 3:5, s. 636-651
-
Journal article (peer-reviewed)abstract
- IMPORTANCE: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. OBJECTIVE: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. DATA SOURCES: Genomewide association studies (GWAS) published up to January 15, 2015. STUDY SELECTION: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. DATA EXTRACTION AND SYNTHESIS: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. MAIN OUTCOMES AND MEASURES: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. RESULTS: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [ 95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [ 95% CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [ 95% CI, 0.49-0.81]), celiac disease (OR, 0.42 [ 95% CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [ 95% CI, 0.05-0.15]). CONCLUSIONS AND RELEVANCE: It is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases.
|
|
| 26. |
- Hendrickson, Sara J., et al.
(author)
-
Plasma Carotenoid- and Retinol-Weighted Multi-SNP Scores and Risk of Breast Cancer in the National Cancer Institute Breast and Prostate Cancer Cohort Consortium
- 2013
-
In: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia, PA, USA : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 22:5, s. 927-936
-
Journal article (peer-reviewed)abstract
- Background: Dietary and circulating carotenoids have been inversely associated with breast cancer risk, but observed associations may be due to confounding. Single-nucleotide polymorphisms (SNPs) in beta-carotene 15,15'-monooxygenase 1 (BCMO1), a gene encoding the enzyme involved in the first step of synthesizing vitamin A from dietary carotenoids, have been associated with circulating carotenoid concentrations and may serve as unconfounded surrogates for those biomarkers. We determined associations between variants in BCMO1 and breast cancer risk in a large cohort consortium. Methods: We used unconditional logistic regression to test four SNPs in BCMO1 for associations with breast cancer risk in 9,226 cases and 10,420 controls from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3). We also tested weighted multi-SNP scores composed of the two SNPs with strong, confirmed associations with circulating carotenoid concentrations. Results: Neither the individual SNPs nor the weighted multi-SNP scores were associated with breast cancer risk [OR (95% confidence interval) comparing extreme quintiles of weighted multi-SNP scores = 1.04 (0.94-1.16) for beta-carotene, 1.08 (0.98-1.20) for alpha-carotene, 1.04 (0.94-1.16) for beta-cryptoxanthin, 0.95 (0.87-1.05) for lutein/zeaxanthin, and 0.92 (0.83-1.02) for retinol]. Furthermore, no associations were observed when stratifying by estrogen receptor status, but power was limited. Conclusions: Our results do not support an association between SNPs associated with circulating carotenoid concentrations and breast cancer risk. Impact: Future studies will need additional genetic surrogates and/or sample sizes at least three times larger to contribute evidence of a causal link between carotenoids and breast cancer. (C) 2013 AACR.
|
|
| 27. |
- Jaghult, Susanna, et al.
(author)
-
Stress as a trigger for relapses in IBD : A case-crossover study
- 2013
-
In: Gastroenterology Research. - : Elmer Press, Inc.. - 1918-2805 .- 1918-2813. ; 6:1, s. 10-16
-
Journal article (peer-reviewed)abstract
- Background: It is important to identify factors that influence the risk of relapses in inflammatory bowel disease. Few studies have been conducted and with limited methodology. This prospective case-crossover study, aims to examine whether perceived stress has a short-term acute effect, namely whether it acts as a trigger, on the risk of relapse in inflammatory bowel disease.Methods: Sixty patients with inflammatory bowel disease and in remission were included. The case-crossover design was employed, which is an epidemiological design developed to study triggers for acute events and diseases. To collect information regarding symptoms and potential trigger factors, such as perceived stress, a structured diary was constructed. The participants were instructed to fill in the diary daily during six months. Fifty patients completed the study.Results: The analysis showed an effect for high level of perceived stress. Being exposed to “quite a lot” of stress, yield an increase in risk for relapse during the forthcoming day (OR = 4.8, 95% CI 1.09 - 21.10). No statistically increased risk for lower levels of perceived stress was found, although elevated effect estimates were found for “some” stress.Conclusion: This study supports earlier findings regarding perceived stress as an important factor in triggering relapses in IBD. However, this is the first case-crossover study performed to explore the trigger risk of stress in this population. Further investigations with larger patient samples are needed to confirm the findings.
|
|
| 28. |
- Johansson, Anna, et al.
(author)
-
Long-term soil organic carbon changes after cropland conversion to grazed grassland in Southern Sweden
- 2024
-
In: Soil use and management. - 0266-0032 .- 1475-2743. ; 40:1
-
Journal article (peer-reviewed)abstract
- There is growing awareness of the potential value of agricultural land for climate change mitigation. In Sweden, cropland areas have decreased by approximately 30% over recent decades, creating opportunities for these former croplands to be managed for climate change mitigation by increasing soil organic carbon (SOC) stocks. One potential land-use change is conversion of cropland to grazed grasslands, but the long-term effect of such change in management is not well understood and likely varies with soil type and site-specific conditions. Through sampling of mineral and peatland soils within a 75-year chronosequence of land converted from crop production to grazed grassland, we assessed how time since conversion, catenary position, and soil depth affected SOC storage. The SOC stocks calculated at an equivalent soil or ash mass increased through time since conversion in mineral soils at all topographic positions, at a rate of ~0.65% year−1. Soils at low topographic positions gained the most carbon. Peat SOC stock gains after conversion were large, but only marginally significant and only when calculated at an equivalent ash mass. We conclude that the conversion of mineral soil to grazed grassland promotes SOC accumulation at our sites, but climate change mitigation potential would need to be evaluated through a full greenhouse gas balance.
|
|
| 29. |
- Johansson Lindgren, Jessica, et al.
(author)
-
Anfall av gåshud visade sig vara anti-LGI-1-encefalit
- 2020
-
In: Läkartidningen. - 0023-7205. ; 117
-
Journal article (peer-reviewed)abstract
- Anti-LGI-1 encephalitis is a type of autoimmune encephalopathy, where antibodies react against the cell surface protein leucine-rich glioma inactivated protein 1 (LGI-1). It presents with a subacute confusion, changes in behaviour, short-term memory deficits and seizures. A piloerectile semiology is common, which has been described as reflecting insular ictal activity. Patients may have temporal lobe abnormalities on brain MRI and EEG. More than half of the patients with limbic encephalitis associated with anti-LGI1 antibodies have hyponatremia. The diagnosis of anti-LGI-1 encephalitis can be made by the detection of antibodies against LGI-1 in serum and/or cerebrospinal fluid. Prompt diagnosis and treatment are important to avoid long-term disability. This case report describes a man with episodes of goose bumps and mild confusion caused by anti-LGI-1 encephalitis.
|
|
| 30. |
- Johansson, Unn-Britt, et al.
(author)
-
A morning dose of insulin glargine prevents nocturnal ketosis after postprandial interruption of continuous subcutaneous insulin infusion with insulin lispro
- 2007
-
In: Diabetes & Metabolism. - : Elsevier BV. - 1262-3636 .- 1878-1780. ; 33:6, s. 469-71
-
Journal article (peer-reviewed)abstract
- AIM: The aim of this crossover trial was to evaluate the potential of partial substitution of basal insulin with glargine, administered once daily in the morning, to protect against nocturnal ketosis after postprandial interruption of continuous subcutaneous insulin infusion (CSII). METHODS: Seven patients with type 1 diabetes received 4 weeks of treatment with insulin lispro, administered by CSII, and 4 weeks of treatment with CSII and a partial basal replacement dose of insulin glargine administered in the morning. On day 28 of each treatment phase, patients were admitted to the research unit where dinner was served and their usual dinner insulin bolus dose given, after which CSII was discontinued at 7 pm. Plasma (p) beta-hydroxybutyrate and p glucose were measured every hour for 12 h thereafter. RESULTS: Plasma beta-hydroxybutyrate at 7 pm was 0.16+/-0.05 and 0.13+/-0.07 mmol/l with and without glargine, respectively, and increased to 0.17+/-0.10 and 0.60+/-0.3 mmol/l within 6 h (P=0.02). Plasma glucose increased without glargine, from 8.6+/-2.9 to 21.1+/-3.0 mmol/l (P=0.003), but did not rise significantly following glargine (13.6+/-4.7 vs. 12.6+/-5.6 mmol/l; P=0.65). CONCLUSIONS: Partial replacement with a morning dose of insulin glargine protects against the development of ketosis for as much as 12 h after postprandial interruption of CSII. This treatment strategy could, therefore, be useful for patients who are prone to ketosis but, for other reasons, are deemed suitable for CSII.
|
|
