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Sökning: WFRF:(Andersson Björn)

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61.
  • Mårtensson, Carina, et al. (författare)
  • Knowledge of periodontitis and self-perceived oral health : a survey of periodontal specialist patients
  • 2013
  • Ingår i: Swedish Dental Journal. - : Swedish Dental Association. - 0347-9994. ; 37:1, s. 49-58
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to investigate changes in knowledge of periodontal disease among patients referred to periodontal specialist clinics. A further aim was to investigate the patients' self- perceived oral health before the treatment. Patients referred to five specialist clinics in periodontology for comprehensive periodontal treatment were consecutive sampled. The study was based on a questionnaire in a before and after design. The first questionnaire was sent to the patients before visiting the specialist clinic and the second was sent after six months. Four questions were analysed, two to measure knowledge about periodontitis and two to measure the patients self- perceived oral health. The first questionnaire was sent by post to 273 patients with a response rate of 31%. The second questionnaire was sent to 85 patients with a response rate of 73%. The results of the study showed a statistically significant improvement of correct answers on the knowledge questions after six months was found for scaling(p = 0.006), X-ray examination (p = 0.001) and increased space between the teeth (p = 0.001). The most frequent self-perceived trouble from the mouth was bleeding gum (70%) and sensitive teeth (51%). In conclusion knowledge of periodontitis improved after visiting the specialist clinic of periodontology. Many of the patients experienced some problems of the mouth.
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62.
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63.
  • Mårtensson, Carina, et al. (författare)
  • Patienters kunskap om parodontit granskas
  • 2009
  • Ingår i: Tandläkartidningen. - 0039-6982. ; 101:7, s. 64-65
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • En studie har påbörjats för att ge ökad insikt om patienters kunskap om parodontit före och efter parodontal behandling. Patienternas förväntningar inför och upplevelser av behandlingen ska också analyseras.
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64.
  • Mäkeläinen, Suvi, et al. (författare)
  • Deletion in the Bardet-Biedl Syndrome Gene TTC8 Results in a Syndromic Retinal Degeneration in Dogs
  • 2020
  • Ingår i: Genes. - : MDPI. - 2073-4425. ; 11:9
  • Tidskriftsartikel (refereegranskat)abstract
    • In golden retriever dogs, a 1 bp deletion in the canineTTC8gene has been shown to cause progressive retinal atrophy (PRA), the canine equivalent of retinitis pigmentosa. In humans,TTC8is also implicated in Bardet-Biedl syndrome (BBS). To investigate if the affected dogs only exhibit a non-syndromic PRA or develop a syndromic ciliopathy similar to human BBS, we recruited 10 affected dogs to the study. The progression of PRA for two of the dogs was followed for 2 years, and a rigorous clinical characterization allowed a careful comparison with primary and secondary characteristics of human BBS. In addition to PRA, the dogs showed a spectrum of clinical and morphological signs similar to primary and secondary characteristics of human BBS patients, such as obesity, renal anomalies, sperm defects, and anosmia. We used Oxford Nanopore long-read cDNA sequencing to characterize retinal full-lengthTTC8transcripts in affected and non-affected dogs, the results of which suggest that three isoforms are transcribed in the retina, and the 1 bp deletion is a loss-of-function mutation, resulting in a canine form of Bardet-Biedl syndrome with heterogeneous clinical signs.
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65.
  • Nordanstig, Joakim, et al. (författare)
  • Mortality with Paclitaxel-Coated Devices in Peripheral Artery Disease.
  • 2020
  • Ingår i: The New England journal of medicine. - : Massachusetts Medical Society. - 1533-4406 .- 0028-4793. ; 383, s. 2538-46
  • Tidskriftsartikel (refereegranskat)abstract
    • The results of a recent meta-analysis aroused concern about an increased risk of death associated with the use of paclitaxel-coated angioplasty balloons and stents in lower-limb endovascular interventions for symptomatic peripheral artery disease.We conducted an unplanned interim analysis of data from a multicenter, randomized, open-label, registry-based clinical trial. At the time of the analysis, 2289 patients had been randomly assigned to treatment with drug-coated devices (the drug-coated-device group, 1149 patients) or treatment with uncoated devices (the uncoated-device group, 1140 patients). Randomization was stratified according to disease severity on the basis of whether patients had chronic limb-threatening ischemia (1480 patients) or intermittent claudication (809 patients). The single end point for this interim analysis was all-cause mortality.No patients were lost to follow-up. Paclitaxel was used as the coating agent for all the drug-coated devices. During a mean follow-up of 2.49 years, 574 patients died, including 293 patients (25.5%) in the drug-coated-device group and 281 patients (24.6%) in the uncoated-device group (hazard ratio, 1.06; 95% confidence interval, 0.92 to 1.22). At 1 year, all-cause mortality was 10.2% (117 patients) in the drug-coated-device group and 9.9% (113 patients) in the uncoated-device group. During the entire follow-up period, there was no significant difference in the incidence of death between the treatment groups among patients with chronic limb-threatening ischemia (33.4% [249 patients] in the drug-coated-device group and 33.1% [243 patients] in the uncoated-device group) or among those with intermittent claudication (10.9% [44 patients] and 9.4% [38 patients], respectively).In this randomized trial in which patients with peripheral artery disease received treatment with paclitaxel-coated or uncoated endovascular devices, the results of an unplanned interim analysis of all-cause mortality did not show a difference between the groups in the incidence of death during 1 to 4 years of follow-up. (Funded by the Swedish Research Council and others; ClinicalTrials.gov number, NCT02051088.).
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66.
  • Näsström, Thomas, et al. (författare)
  • Synthetic NAC 71-82 Peptides Designed to Produce Fibrils with Different Protofilament Interface Contacts
  • 2021
  • Ingår i: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 22:17
  • Tidskriftsartikel (refereegranskat)abstract
    • Alpha-synucleinopathies are featured by fibrillar inclusions in brain cells. Although α-synuclein fibrils display structural diversity, the origin of this diversity is not fully understood. We used molecular dynamics simulations to design synthetic peptides, based on the NAC 71-82 amino acid fragment of α-synuclein, that govern protofilament contacts and generation of twisted fibrillar polymorphs. Four peptides with structures based on either single or double fragments and capped or non-capped ends were selected for further analysis. We determined the fibrillar yield and the structures from these peptides found in the solution after fibrillisation using protein concentration determination assay and circular dichroism spectroscopy. In addition, we characterised secondary structures formed by individual fibrillar complexes using laser-tweezers Raman spectroscopy. Results suggest less mature fibrils, based on the lower relative β-sheet content for double- than single-fragment peptide fibrils. We confirmed this structural difference by TEM analysis which revealed, in addition to short protofibrils, more elongated, twisted and rod-like fibril structures in non-capped and capped double-fragment peptide systems, respectively. Finally, time-correlated single-photon counting demonstrated a difference in the Thioflavin T fluorescence lifetime profiles upon fibril binding. It could be proposed that this difference originated from morphological differences in the fibril samples. Altogether, these results highlight the potential of using peptide models for the generation of fibrils that share morphological features relevant for disease, e.g., twisted and rod-like polymorphs.
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67.
  • Persson, Josefine, 1980, et al. (författare)
  • Stratification of COVID-19 patients based on quantitative immune-related gene expression in whole blood.
  • 2022
  • Ingår i: Molecular immunology. - : Elsevier BV. - 1872-9142 .- 0161-5890. ; 145, s. 17-26
  • Tidskriftsartikel (refereegranskat)abstract
    • The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes mild symptoms in the majority of infected individuals, yet in some cases it leads to a life-threatening condition. Determination of early predictive biomarkers enabling risk stratification for coronavirus disease 2019 (COVID-19) patients can inform treatment and intervention strategies. Herein, we analyzed whole blood samples obtained from individuals infected with SARS-CoV-2, varying from mild to critical symptoms, approximately one week after symptom onset. In order to identify blood-specific markers of disease severity status, a targeted expression analysis of 143 immune-related genes was carried out by dual-color reverse transcriptase multiplex ligation-dependent probe amplification (dcRT-MLPA). The clinically well-defined subgroups of COVID-19 patients were compared with healthy controls. The transcriptional profile of the critically ill patients clearly separated from that of healthy individuals. Moreover, the number of differentially expressed genes increased by severity of COVID-19. It was also found that critically ill patients can be distinguished by reduced peripheral blood expression of several genes, which most likely reflects the lower lymphocyte counts. There was a notable predominance of IFN-associated gene expression in all subgroups of COVID-19, which was most profound in critically ill patients. Interestingly, the gene encoding one of the main TNF-receptors, TNFRS1A, had selectively lower expression in mild COVID-19 cases. This report provides added value in understanding COVID-19 disease, and shows potential of determining early immune transcript signatures in the blood of patients with different disease severity. These results can guide further explorations to uncover mechanisms underlying immunity and immunopathology in COVID-19.
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68.
  • Rafter, Ingalill, et al. (författare)
  • Isoform-specific alanine aminotransferase measurement candistinguish hepatic from extrahepatic injury in humans
  • 2012
  • Ingår i: International Journal of Molecular Medicine. - : Spandidos Publications. - 1107-3756 .- 1791-244X. ; 30, s. 1241-1249
  • Tidskriftsartikel (refereegranskat)abstract
    • Serum alanine aminotransferase (ALT) is used asa clinical marker to detect hepatic damage and hepatoxicity.Two isoforms of ALT have been identified, ALT1 and ALT2,which have identical enzymatic capacities and are detectedsimultaneously in human serum/plasma using classical clinicalchemical assays. Differences exist in the expression patterns ofthe ALT1 and ALT2 proteins in different organs which suggestthat changes in the proportion of ALT1 and ALT2 in plasmamay arise and reflect damage to different human organs.However, this has not been previously studied due to the lackof a selective methodology that can quantify both ALT1 andALT2 isoforms in the total ALT activity normally measuredin clinical samples. To the best of our knowledge, our currentstudy reveals for the first time, that under 3 different conditionsof liver damage (non-alcoholic fatty liver disease, hepatitis Cand during liver surgery) the leakage of ALT1 activity intoplasma greatly exceeds that of ALT2, and that the measurementof ALT1 during liver damage is equal to the measurement oftotal ALT activity. By contrast, during skeletal muscle injury,induced in volunteers by physical exertion, the leakage ofALT2 exceeds that of ALT1 and the proportion of circulatingALT isoforms changes accordingly. The ALT isoform changesoccurring in plasma reflect previously demonstrated relativecontents of ALT1 and ALT2 activities in human liver and skeletalmuscle. These data suggest that assessing the percentagecontribution of ALT1 and ALT2 activities to total ALT activityin plasma may distinguish hepatic from extrahepatic injuryusing the same standard analytical platform.
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69.
  • Ragnarsdottir, Bryndis, et al. (författare)
  • Toll-like receptor 4 promoter polymorphisms: common TLR4 variants may protect against severe urinary tract infection.
  • 2010
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 5:5
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Polymorphisms affecting Toll-like receptor (TLR) structure appear to be rare, as would be expected due to their essential coordinator role in innate immunity. Here, we assess variation in TLR4 expression, rather than structure, as a mechanism to diversify innate immune responses. METHODOLOGY/PRINCIPAL FINDINGS: We sequenced the TLR4 promoter (4,3 kb) in Swedish blood donors. Since TLR4 plays a vital role in susceptibility to urinary tract infection (UTI), promoter sequences were obtained from children with mild or severe disease. We performed a case-control study of pediatric patients with asymptomatic bacteriuria (ABU) or those prone to recurrent acute pyelonephritis (APN). Promoter activity of the single SNPs or multiple allelic changes corresponding to the genotype patterns (GPs) was tested. We then conducted a replication study in an independent cohort of adult patients with a history of childhood APN. Last, in vivo effects of the different GPs were examined after therapeutic intravesical inoculation of 19 patients with Escherichia coli 83972. We identified in total eight TLR4 promoter sequence variants in the Swedish control population, forming 19 haplotypes and 29 genotype patterns, some with effects on promoter activity. Compared to symptomatic patients and healthy controls, ABU patients had fewer genotype patterns, and their promoter sequence variants reduced TLR4 expression in response to infection. The ABU associated GPs also reduced innate immune responses in patients who were subjected to therapeutic urinary E. coli tract inoculation. CONCLUSIONS: The results suggest that genetic variation in the TLR4 promoter may be an essential, largely overlooked mechanism to influence TLR4 expression and UTI susceptibility.
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70.
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