| 1. |
- Scheffle, M., et al.
(författare)
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Low cost large area panel processing of MCM-D substrates and packages
- 2001
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Ingår i: Proceedings of IPACK’01. ; , s. -8
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Konferensbidrag (refereegranskat)abstract
- The paper describes the results of the EU research project LAP that had the target to develop and to demonstrate a low-cost high-density substrate manufacturing technology for 1st-level die assemblies. The cost target of 1€€/in2 had to be obtained by increasing toady’s 4x4in2 panel sizes to panels upto 24x24in2. The results focus on RF characterization (integrated antennas up to 83GHz, inductors up a Q value of 50), novel packaging strategies (integration of substrate and package), and cost achievements (approaching the cost target). The technology capabilities have been demonstrated with a 9:4 satellite switch operating up to 2.4GHz and readout electronics for physics experiments.
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| 2. |
- Kröger, A, et al.
(författare)
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The severity of human peri-implantitis lesions correlates with the level of submucosal microbial sysbiosis
- 2018
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Ingår i: Journal of Clinical Periodontology. - 0303-6979 .- 1600-051X. ; 45:12, s. 1498-1509
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To cross-sectionally analyze the submucosal microbiome of peri-implantitis (PI) lesions at different severity levels.MATERIALS AND METHODS: Microbial signatures of 45 submucosal plaque samples from untreated peri-implantitis lesions obtained from 30 non-smoking, systemically healthy subjects were assessed by 16s sequencing. Linear mixed models were used to identify taxa with differential abundance by probing depth, after correction for age, gender, and multiple samples per subject. Network analyses were performed to identify groups of taxa with mutual occurrence or exclusion. Subsequently, the effects of peri-implant probing depth on submucosal microbial dysbiosis was calculated using the microbial dysbiosis index.RESULTS: In total, we identified 337 different taxa in the submucosal microbiome of peri-implantitis. Total abundance of 12 taxa correlated significantly with increasing probing depth; a significant relationship with lower probing depth was found for 16 taxa. Network analysis identified two mutually exclusive complexes associated with shallow pockets and deeper pockets, respectively. Deeper peri-implant pockets were associated with significantly increased dysbiosis.CONCLUSION: Increases in peri-implant pocket depth are associated with substantial changes in the submucosal microbiome and increasing levels of dysbiosis. This article is protected by copyright. All rights reserved.
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| 3. |
- Kröger, A, et al.
(författare)
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The severity of human peri-implantitis lesions correlates with the level of submucosal microbial sysbiosis
- 2018
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Ingår i: Journal of Clinical Periodontology. - : Blackwell Munksgaard. - 0303-6979 .- 1600-051X. ; 45:12, s. 1498-1509
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To cross-sectionally analyze the submucosal microbiome of peri-implantitis (PI) lesions at different severity levels. MATERIALS AND METHODS: Microbial signatures of 45 submucosal plaque samples from untreated peri-implantitis lesions obtained from 30 non-smoking, systemically healthy subjects were assessed by 16s sequencing. Linear mixed models were used to identify taxa with differential abundance by probing depth, after correction for age, gender, and multiple samples per subject. Network analyses were performed to identify groups of taxa with mutual occurrence or exclusion. Subsequently, the effects of peri-implant probing depth on submucosal microbial dysbiosis was calculated using the microbial dysbiosis index. RESULTS: In total, we identified 337 different taxa in the submucosal microbiome of peri-implantitis. Total abundance of 12 taxa correlated significantly with increasing probing depth; a significant relationship with lower probing depth was found for 16 taxa. Network analysis identified twomutually exclusive complexes associated with shallow pockets and deeper pockets, respectively. Deeper peri-implant pockets were associated with significantly increased dysbiosis. CONCLUSION: Increases in peri-implant pocket depth are associated with substantial changes in the submucosal microbiome and increasing levels of dysbiosis. This article is protected by copyright. All rights reserved.
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| 4. |
- Zimmer, A. D., et al.
(författare)
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Sixteen novel mutations in PNPLA1 in patients with autosomal recessive congenital ichthyosis reveal the importance of an extended patatin domain in PNPLA1 that is essential for proper human skin barrier function
- 2017
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Ingår i: British Journal of Dermatology. - : John Wiley & Sons. - 0007-0963 .- 1365-2133. ; 177:2, s. 445-455
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Tidskriftsartikel (refereegranskat)abstract
- Background Autosomal recessive congenital ichthyosis (ARCI) is a genetically heterogeneous group of rare Mendelian skin disorders characterized by cornification and differentiation defects of keratinocytes. Mutations in nine genes including PNPLA1 are known to cause nonsyndromic forms of ARCI. To date, only 10 distinct pathogenic mutations in PNPLA1 have been reported. Objectives To identify new causative PNPLA1 mutations. Methods We screened genetically unresolved cases, including our ARCI collection, comprising more than 700 families. Screening for mutations was performed either by direct Sanger sequencing or in combination with a multigene panel, followed by sequence and mutation analysis. Results Here we report on 16 novel mutations present in patients from 17 families. While all previously reported mutations and most of our novel mutations are located within the core patatin domain, we report five novel PNPLA1 mutations that are downstream of this domain. Thus, as recently described for PNPLA2, we hypothesize that a region larger than the core domain is required for full enzymatic activity of PNPLA1 in human skin barrier formation. Conclusions We estimate the frequency of PNPLA1 mutations among patients with ARCI to be around 3%. Most of our patients were born as collodion babies and showed a relatively mild ichthyosis phenotype. In four unrelated patients we observed a cyclic scaling course, which seems to be a potential phenotypic variation in a small percentage of patients with PNPLA1 mutations. The variability of the clinical manifestations and the lack of typical clinical features are specific for patients with PNPLA1 mutations, and emphasize the importance of DNA sequencing for differential diagnosis of ARCIs.
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| 5. |
- Jönsson, D., et al.
(författare)
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Periodontal disease is associated with carotid plaque area: the Malmö Offspring Dental Study (MODS).
- 2020
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Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 287:3, s. 301-309
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Tidskriftsartikel (refereegranskat)abstract
- Background: Periodontal disease is associated with cardiovascular disease (CVD) but it is unknown if periodontal disease severity is associated with asymptomatic carotid plaque. The aim of the current population-based, observational study was to investigate if signs of periodontal disease are associated with the occurrence of carotid plaque and total plaque area (TPA). Methods: The Malmö Offspring Study (MOS) is a population-based study. MOS participants underwent a thorough cardiovascular phenotyping, including carotid ultrasonography. The Malmö Offspring Dental Study (MODS) invited participants of MOS for dental examination, including periodontal charting. Multivariable regression models were used to analyse the presence of carotid plaque and TPA in relation to periodontal parameters. Results: In all, 831 MODS participants were recruited, out of which 495 belonged to the children generation with mean age of 53 years, 63% had carotid plaque and 38% had moderate or severe periodontal disease. In models adjusted for CVD risk factors, the OR for having carotid plaque in subjects with vs without periodontal disease was 1.75 (95% CI: 1.11–2.78). In a linear model with TPA as dependent and number of periodontal pockets ≥ 4 mm as independent variable, the adjusted beta-coefficient was 0.34 mm2 (95% CI 0.16–0.52). Conclusion: Individuals within the highest quartile of periodontal pockets are expected to have 9 mm2 larger TPA compared to those without pockets. Our results suggest that intervention studies addressing periodontal disease could be useful for prevention of CVD.
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