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  • 1.
    Danielsson Borssén, Åsa
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Kechagias, Stergios
    Department of Gastroenterology and Hepatology, Department of Medical and Health Sciences, Linköping University.
    Marschall, Hanns-Ulrich
    Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg.
    Bergquist, Annika
    Department of Medicine, Section of Hepatology and Gastroenterology, Karolinska Institutet.
    Rorsman, Fredrik
    Department of Medical Sciences, Section of Gastroenterology and Hepatology, Uppsala University.
    Weiland, Ola
    Division of Infectious Diseases, Department of Medicine, Karolinska Institutet.
    Verbaan, Hans
    Gastroenterology Division, Department of Clinical Sciences, Lund University.
    Nyhlin, Nils
    Department of Medicine, Section of Hepatology and Gastroenterology, Örebro University Hospital and Faculty of Medicine and Health, Örebro University.
    Nilsson, Emma
    Gastroenterology Division, Department of Clinical Sciences, Lund University.
    Werner, Mårten
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Histological improvement of liver fibrosis in well-treated patients with autoimmune hepatitis: a cohort study2017In: Medicine (Baltimore, Md.), ISSN 0025-7974, E-ISSN 1536-5964, Vol. 96, no 34, article id e7708Article in journal (Refereed)
    Abstract [en]

    Objectives Autoimmune hepatitis (AIH) is a chronic autoimmune liver disease that if left untreated may lead to the development of cirrhosis. Previous studies on AIH patients have suggested that fibrosis and even cirrhosis can be reversed by medical treatment. The aim of this study was to evaluate the efficacy of medical treatment for protection of developing fibrosis and cirrhosis.

    Methods Two hundred fifty-eight liver biopsies from 101 patients (72 women, 29 men) were analysed by a single pathologist and classified accordingly to the Ishak grading (inflammation) and staging (fibrosis) system. Liver histology was stratified according to the temporal changes of fibrosis stage (increased, decreased or stable), and groups were compared.

    Results Complete or partial response to medical treatment was 94.9%. Reduction of fibrosis stage from the first to the last biopsy was seen in 63 patients (62.4%). We found an association between a reduction in fibrosis stage and continuous glucocorticoid medication, as well as lowered scores of inflammation at last biopsy. Twenty-one patients had cirrhosis (Ishak stage 6) at least in one of the previous biopsies, but only five patients at the last biopsy.

    Conclusions Histological improvement is common in AIH patients that respond to medical treatment, and a reduction or stabilization of fibrosis stage occurs in about 2/3 of such patients.

  • 2.
    Hellman, Urban
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Mörner, Stellan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Henein, Michael
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Molecular & Clinical Sciences Research Institute, St. George University, London; Brunel University, Middlesex, UK.
    Genetic variants in cardiac calcification in Northern Sweden2019In: Medicine (Baltimore, Md.), ISSN 0025-7974, E-ISSN 1536-5964, Vol. 98, no 15, article id e15065Article in journal (Refereed)
    Abstract [en]

    Extensive coronary calcification without significant stenosis, described as calcific coronary artery disease (CCAD) may cause abnormal myocardial perfusion and hence generalized ischemia. There is a discrepancy in the expression pattern of CCAD compared to the well-known atherosclerotic disease which raises questions about the exact pathophysiology of coronary calcification and whether there is a genetic etiology for it.

    In this pilot study we studied 3 candidate genes, ectonucleotide pyrophosphatase/phosphodiesterase (ENPP1), ATP Binding Cassette Subfamily C Member 6 (ABCC6), and 5'-Nucleotidase Ecto (NT5E) involved in pyrophosphate (PPi) and inorganic phosphate (Pi) metabolism, which may predispose to coronary arterial or valvular calcification. We studied 70 patients with calcific cardiac disease; 65 with CCAD (age 43-83 years) and 5 with calcific aortic valve disease (CAVD) (age 76-82 years).

    Five DNA variants potentially affecting protein function were found in 6 patients. One variant is a known disease-causing mutation in the ABCC6 gene. Our findings support that disturbances in the PPi and Pi metabolism might influence the development of CCAD and CAVD. However, segregation in the families must first be performed to ascertain any damaging effect of these variants we have found.

    We report 4 new genetic variants potentially related to coronary calcification, through the disturbed Pi and PPi metabolism. The search for direct causative genetic variants in coronary artery and aortic valve calcification must be broadened with other genes particularly those involved with Pi and PPi metabolism.

  • 3. Miltenberger-Miltenyi, Gabriel
    et al.
    Conceicao, Vasco A.
    Gromicho, Marta
    Pronto-Laborinho, Ana Catarina
    Pinto, Susana
    Andersen, Peter M.
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience.
    De Carvalho, Mamede
    C9orf72 expansion is associated with accelerated decline of respiratory function and decreased survival in amyotrophic lateral sclerosis2019In: Medicine (Baltimore, Md.), ISSN 0025-7974, E-ISSN 1536-5964, Vol. 98, no 26Article in journal (Other academic)
  • 4.
    Stegmayr, Bernd G.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Sperker, Wolfgang
    Nilsson, Christina H.
    Degerman, Christina
    Persson, Sven-Erik
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Stenbaek, Jan
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Arnerlöv, Conny
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Few Outflow Problems With a Self-locating Catheter for Peritoneal Dialysis: A Randomized Trial2015In: Medicine (Baltimore, Md.), ISSN 0025-7974, E-ISSN 1536-5964, Vol. 94, no 48, article id e2083Article in journal (Refereed)
    Abstract [en]

    We developed a technique for direct start of peritoneal dialysis. Using a coiled or straight Tenckhoff catheter often results in obstruction of flow. A self-locating Wolfram catheter is on the market. It is not clarified if this results in a benefit.The primary aim of this study was to perform a randomized investigation to clarify if the use of a self-locating peritoneal dialysis (PD) catheter would result in different flow problems than a straight Tenckhoff catheter.A total of 61 insertions were made who were randomized and received either a straight Tenckhoff (n = 32) or a self-locating Wolfram catheter (n = 29). A previously described operation technique allowed immediate postoperative start of dialysis. Seven straight Tenckhoff catheters had to be changed into self-locating catheters, and none vice versa, due to flow problems (P = 0.011). An early leakage resulted in temporarily postponed PD in 4 patients. This study showed that using the present operation technique the self-locating PD-catheter causes fewer obstruction episodes than a straight Tenckhoff catheter. This facilitates immediate postoperative start of PD.

  • 5.
    Weidung, Bodil
    et al.
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine. Department of Public Health and Caring Sciences, Geriatric Medicine, Uppsala University, Uppsala.
    Toots, Annika
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine. Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Rehabilitation Medicine. Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Physiotherapy.
    Nordström, Peter
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Gustafson, Yngve
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine.
    Systolic blood pressure decline in very old individuals is explained by deteriorating health: Longitudinal changes from Umea85+/GERDA2017In: Medicine (Baltimore, Md.), ISSN 0025-7974, E-ISSN 1536-5964, Vol. 96, no 51, article id e9161Article in journal (Refereed)
    Abstract [en]

    Declining systolic blood pressure (SBP) is common in very old age and is associated with adverse events, such as dementia. Knowledge of factors associated with SBP changes could explain the etiology of this decline in SBP. This study investigated longitudinal changes in socioeconomic factors, medical conditions, drug prescriptions, and assessments and their associations with SBP changes among very old followed individuals.The study was based on data from the Umea85+/Gerontological Regional Database (GERDA) cohort study, which provided cross-sectional and longitudinal data on participants aged 85, 90, and 95 years from 2000 to 2015. Follow-up assessments were conducted after 5 years. The main outcome was a change in SBP. Factors associated with SBP changes were assessed using multivariate linear regression models.In the Umea85+/GERDA study, 454 surviving individuals underwent follow-up assessment after 5 years. Of these, 297 had SBP measured at baseline and follow-up. The mean changestandard deviation in SBP was -12 +/- 25mm Hg. SBP decline was associated independently with later investigation year (P=.009), higher baseline SBP (P<.001), baseline antidepressant prescription (P=.011), incident acute myocardial infarction during follow-up (P=.003), new diuretic prescription during follow-up (P=.044), and a decline in the Barthel Activities of Daily Living index at follow-up (P<.001).In conclusion, SBP declines among very old individuals. This decline seems to be associated with initial SBP level, investigation year, and health-related factors.

  • 6.
    Yu, Fang-Fang
    et al.
    Institute of Endemic Diseases, School of Public Health of Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi’an, China.
    Zhang, Yan-Xiang
    Department of Orthopedics, Baoji People’s Hospital, Baoji, China.
    Zhang, Lian-He
    Institute of Endemic Diseases, School of Public Health of Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi’an, China.
    Li, Wen-Rong
    Institute of Endemic Diseases, School of Public Health of Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi’an, China.
    Guo, Xiong
    Institute of Endemic Diseases, School of Public Health of Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi’an, China.
    Lammi, Mikko
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB). Institute of Endemic Diseases, School of Public Health of Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi’an, China.
    Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease2016In: Medicine (Baltimore, Md.), ISSN 0025-7974, E-ISSN 1536-5964, Vol. 95, no 52, article id e5669Article in journal (Refereed)
    Abstract [en]

    As environmental risk factors (ERFs) play an important role in the pathogenesis of Kashin-Beck disease (KBD), it is important to identify the interaction between ERFs and differentially expression genes (DEGs) in KBD. The environmental response genes (ERGs) were analyzed in cartilage of KBD in comparison to normal controls.We searched 5 English and 3 Chinese databases from inception to September 2015, to identify case-control studies that examined ERFs for KBD using integrative meta-analysis and systematic review. Total RNA was isolated from articular cartilage of KBD patients and healthy controls. Human whole genome microarray chip (Agilent) was used to analyze the amplified, labeled, and hybridized total RNA, and the validated microarray data were partially verified using real-time quantitative polymerase chain reaction (qRT-PCR). The ERGs were derived from the Comparative Toxicogenomics Database. The identified ERGs were subjected to KEGG pathway enrichment, biological process (BP), and interaction network analyses using the Database for Annotation, Visualization and Integrated Discovery (DAVID) v6.7, and STRING.The trace elements (selenium and iodine), vitamin E, and polluted grains (T-2 toxin/HT-2 toxin, deoxynivalenol, and nivalenol) were identified as the ERFs for KBD using meta-analysis and review. We identified 21 upregulated ERGs and 7 downregulated ERGs in cartilage with KBD compared with healthy controls, which involved in apoptosis, metabolism, and growth and development. KEGG pathway enrichment analysis found that 2 significant pathways were involved with PI3K-Akt signaling pathway and P53 signaling pathway, and gene ontology function analysis found 3 BPs involved with apoptosis, death, and cell death in KBD cartilage.According to previous results and our own research, we suggest that the trace element selenium and vitamin E induce PI3K-Akt signaling pathway and the mycotoxins (T-2 toxin/HT-2 toxin and DON) induce P53 signaling pathway, contributing to the development of KBD, and chondrocyte apoptosis and cell death.

1 - 6 of 6
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