| 1. |
- Armesto, N., et al.
(författare)
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Heavy-ion collisions at the LHC-Last call for predictions
- 2008
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Ingår i: Journal of Physics G. - : IOP Publishing. - 0954-3899 .- 1361-6471. ; 35:5, s. 054001-
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Forskningsöversikt (refereegranskat)abstract
- This writeup is a compilation of the predictions for the forthcoming Heavy Ion Program at the Large Hadron Collider, as presented at the CERN Theory Institute 'Heavy Ion Collisions at the LHC - Last Call for Predictions', held from 14th May to 10th June 2007.
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| 2. |
- Graslund, S, et al.
(författare)
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Protein production and purification
- 2008
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Ingår i: Nature methods. - : Springer Science and Business Media LLC. - 1548-7105 .- 1548-7091. ; 5:2, s. 135-146
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Tidskriftsartikel (refereegranskat)
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| 3. |
- Szatmari, Peter, et al.
(författare)
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Mapping autism risk loci using genetic linkage and chromosomal rearrangements.
- 2007
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 39:3, s. 319-328
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Tidskriftsartikel (refereegranskat)abstract
- Autism spectrum disorders (ASDs) are common, heritable neurodevelopmental conditions. The genetic architecture of ASDs is complex, requiring large samples to overcome heterogeneity. Here we broaden coverage and sample size relative to other studies of ASDs by using Affymetrix 10K SNP arrays and 1,168 families with at least two affected individuals, performing the largest linkage scan to date while also analyzing copy number variation in these families. Linkage and copy number variation analyses implicate chromosome 11p12-p13 and neurexins, respectively, among other candidate loci. Neurexins team with previously implicated neuroligins for glutamatergic synaptogenesis, highlighting glutamate-related genes as promising candidates for contributing to ASDs.
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| 4. |
- Amundadottir, Laufey, et al.
(författare)
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Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer.
- 2009
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 41, s. 986-990
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Tidskriftsartikel (refereegranskat)abstract
- We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based case-control study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 x 10(-8); multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12-1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B.
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| 5. |
- Ghavami, S., et al.
(författare)
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Apoptosis and cancer : mutations within caspase genes
- 2009
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Ingår i: Journal of Medical Genetics. - : B M J Group. - 0022-2593 .- 1468-6244. ; 46:8, s. 497-510
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Forskningsöversikt (refereegranskat)abstract
- The inactivation of programmed cell death has profound effects not only on the development but also on the overall integrity of multicellular organisms. Beside developmental abnormalities, it may lead to tumorigenesis, autoimmunity, and other serious health problems. Deregulated apoptosis may also be the leading cause of cancer therapy chemoresistance. Caspase family of cysteinyl-proteases plays the key role in the initiation and execution of programmed cell death. This review gives an overview of the role of caspases, their natural modulators like IAPs, FLIPs, and Smac/Diablo in apoptosis and upon inactivation, and also in cancer development. Besides describing the basic mechanisms governing programmed cell death, a large part of this review is dedicated to previous studies that were focused on screening tumours for mutations within caspase genes as well as their regulators. The last part of this review discusses several emerging treatments that involve modulation of caspases and their regulators. Thus, we also highlight caspase cascade modulating experimental anticancer drugs like cFLIP-antagonist CDDO-Me; cIAP1 antagonists OSU-03012 and ME-BS; and XIAP small molecule antagonists 1396-11, 1396-12, 1396-28, triptolide, AEG35156, survivin/Hsp90 antagonist shephedrin, and some of the direct activators of procaspase-3.
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| 6. |
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| 7. |
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| 8. |
- Pathmasiri, Wimal, et al.
(författare)
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Aryl ketones from Acronychia pedunculata with cyclooxygenase-2 inhibitory effects
- 2005
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Ingår i: Chemistry & biodiversity. - : Wiley. - 1612-1872 .- 1612-1880. ; 2:4, s. 463-469
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Tidskriftsartikel (refereegranskat)abstract
- 1-[2,4-Dihydroxy-6-methoxy-3,5-bis(3-methylbut-2-en-1-yl)phenyl]ethanone (1), and a new aryl ketone, named acrovestenol (2), were isolated as cyclooxygenase-2 (COX-2) inhibitory principles from a CH2Cl2 extract of the bark of Acronychia pedunculata by a bioassay-guided fractionation procedure. Compound 2 inhibited COX-2 with an IC50 value of 142.0+/-2.15 microM, compared to the COX-2 inhibitory reference compound NS-398 with an IC50 value of 11.3+/-1.12 microM. Compound 1 inhibited COX-2-catalyzed PG biosynthesis with 68% at a concentration of 500 microM. The structures were determined by UV, IR, and 1D- and 2D-NMR, including TOCSY, HSQC-DEPT, and HMBC, and MS investigations.
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| 9. |
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| 10. |
- Wallin, Åsa R., 1976-, et al.
(författare)
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Expression of PRL proteins at invasive margin of rectal cancers in relation to preoperative radiotherapy
- 2006
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Ingår i: International Journal of Radiation Oncology, Biology, Physics. - : Elsevier BV. - 0360-3016 .- 1879-355X. ; 65:2, s. 452-458
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: PRL-3 (phosphatase of regenerating liver) is involved in metastasis of colorectal cancer; however, its therapeutic implication in cancer patients has not been studied. We investigated the relationships of PRL expression to radiotherapy (RT) in rectal cancer patients.Methods and Materials: Phosphatase of regenerating liver expression was immunohistochemically examined in distant (n = 36) and adjacent (n = 82) normal mucosa, primary tumor (n = 125), biopsy specimens (n = 96), and lymph node metastasis (n = 30) from rectal cancer patients participating in a clinical trial of preoperative RT.Results: Phosphatase of regenerating liver expression was increased from the distant to adjacent mucosa and to the primary tumor (p < 0.05). PRL was highly expressed at the invasive margin in 28% of the primary tumors and 26% of the metastases. In the RT group, strong PRL expression at the invasive margin was related to distant recurrence (p = 0.006) and poor survival (p = 0.01), but not in the non-RT group. The survival significance remained even after adjusting for Dukes’ stage and differentiation (p = 0.02). Additional multivariate analyses showed that the correlation with prognostic significance of PRL differed between the RT and non-RT groups (p = 0.01).Conclusion: Phosphatase of regenerating liver expression (rather than PRL-3 alone) at the invasive margin predicted resistance to RT and unfavorable survival in rectal cancer patients with preoperative RT.
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| 11. |
- Zhou, X., et al.
(författare)
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Down-regulation of tumor necrosis factor-associated factor 6 is associated with progression of acute pancreatitis complicating lung injury in mice
- 2009
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Ingår i: Tohoku Journal of Experimental Medicine. - : Tohoku University Medical Press. - 0040-8727 .- 1349-3329. ; 217:4, s. 279-285
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Tidskriftsartikel (refereegranskat)abstract
- Acute lung injury is one of the critical complications of acute pancreatitis (AP). Tumor necrosis factor-associated factor 6 (TRAF6) is a key adaptor that regulates various inflammatory signaling pathways, including those mediated by Toll-like receptors (TLRs). This study was performed to investigate the potential role of TRAF6 in the pathogenesis of AP and pancreatitis-associated acute lung injury using a mouse model of caerulein-induced AP (CAP). CAP was induced by intraperitoneal injection of caerulein hourly for 7 times (50 µg/kg), and control mice were treated with saline of the same volume. Typical pancreatic and lung inflammation was observed in the early stage (1 h) of CAP, as judged by morphological changes. Likewise, in CAP mice, the pancreatic myeloperoxidase activity and serum levels of interleukin-6 add interleukin-10 were significantly increased after 2 h, peaked it 4h, and then decreased by 24 h. The expression of TRAF6 was then studied by real time-PCR, immunohistochemistry, and Western blot analysis. Compared with control group, TRAF6 mRNA level was decreased in CAP group within the first 12 h, and then significantly increased after 24 h, which was in accordance with the protein level detected by Western blot analysis and immunohistochemistry. Moreover, TRAF6 protein was expressed in both pancreatic acinar cells and lung bronchial epithelial cells. In conclusion, the down-regulation of TRAF6 was associated with increased inflammatory severity in the pancreas and lung, suggesting that TRAF6 is involved in the anti-inflammatory process during AP. TRAF6 may be a potential molecular target for treating AP.
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