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Sökning: L773:0025 7974 > Umeå universitet

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1.
  • Abdelrahim, Nada Abdelghani, et al. (författare)
  • Viral meningitis in Sudanese children : differentiation, etiology and review of literature
  • 2022
  • Ingår i: Medicine. - : Lippincott Williams & Wilkins. - 0025-7974 .- 1536-5964. ; 101:46
  • Forskningsöversikt (refereegranskat)abstract
    • Diagnosis of viral meningitis (VM) is uncommon practice in Sudan and there is no local viral etiological map. We therefore intended to differentiate VM using standardized clinical codes and determine the involvement of herpes simplex virus types-1 and 2 (HSV-1/2), varicella zoster virus, non-polio human enteroviruses (HEVs), and human parechoviruses in meningeal infections in children in Sudan. This is a cross-sectional hospital-based study. Viral meningitis was differentiated in 503 suspected febrile attendee of Omdurman Hospital for Children following the criteria listed in the Clinical Case Definition for Aseptic/Viral Meningitis. Patients were children age 0 to 15 years. Viral nucleic acids (DNA/RNA) were extracted from cerebrospinal fluid (CSF) specimens using QIAamp® UltraSens Virus Technology. Complementary DNA was prepared from viral RNA using GoScriptTM Reverse Transcription System. Viral nucleic acids were amplified and detected using quantitative TaqMan® Real-Time and conventional polymerase chain reactions (PCRs). Hospital diagnosis of VM was assigned to 0%, when clinical codes were applied; we considered 3.2% as having VM among the total study population and as 40% among those with proven infectious meningitis. Two (0.4%) out of total 503 CSF specimens were positive for HSV-1; Ct values were 37.05 and 39.10 and virus copies were 652/PCR run (261 × 103/mL CSF) and 123/PCR run (49.3 × 103/mL CSF), respectively. Other 2 (0.4%) CSF specimens were positive for non-polio HEVs; Ct values were 37.70 and 38.30, and the approximate virus copies were 5E2/PCR run (~2E5/mL CSF) and 2E2/PCR run (~8E4/mL CSF), respectively. No genetic materials were detected for HSV-2, varicella zoster virus, and human parechoviruses. The diagnosis of VM was never assigned by the hospital despite fulfilling the clinical case definition. Virus detection rate was 10% among cases with proven infectious meningitis. Detected viruses were HSV-1 and non-polio HEVs. Positive virus PCRs in CSFs with normal cellular counts were seen.
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2.
  • Danielsson Borssén, Åsa, 1977-, et al. (författare)
  • Histological improvement of liver fibrosis in well-treated patients with autoimmune hepatitis : A cohort study
  • 2017
  • Ingår i: Medicine. - : Lippincott Williams & Wilkins. - 0025-7974 .- 1536-5964. ; 96:34
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.A total of 258 liver biopsies from 101 patients (72 women, 29 men) were analyzed by a single pathologist and classified according 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.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 the 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 5 patients at the last biopsy.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.
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3.
  • Hellman, Urban, 1966-, et al. (författare)
  • Genetic variants in cardiac calcification in Northern Sweden
  • 2019
  • Ingår i: Medicine. - : Wolters Kluwer. - 0025-7974 .- 1536-5964. ; 98:15
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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4.
  • Ljungman, Lisa, 1981-, et al. (författare)
  • Study protocol for the Fex-Can Childhood project An observational study and a randomized controlled trial focusing on sexual dysfunction and fertility-related distress in young adult survivors of childhood cancer
  • 2020
  • Ingår i: Medicine. - : Ovid Technologies (Wolters Kluwer Health). - 0025-7974 .- 1536-5964. ; 99:28
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: This study protocol describes the Fex-Can Childhood project, comprising two studies: The Fex-Can Childhood observational study (OS) and the Fex-Can Childhood randomized controlled trial (RCT). The Fex-Can Childhood OS aims to determine the prevalence and predictors of sexual dysfunction and fertility-related distress in young adult childhood cancer survivors (aged 19-40) compared to an age matched comparison group; the Fex-Can Childhood RCT will evaluate the effect of a web-based psycho-educational intervention (Fex-Can intervention) on sexual dysfunction and fertility-related distress. Methods: The Fex-Can Childhood OS will have a population-based cross-sectional design. All individuals treated for childhood cancer in Sweden at the age of 0 to 17 years (current age 19-40) will be identified through the National Quality Registry for Childhood Cancer. Established self-reported instruments will be used to measure sexual function, fertility-related distress, body image, anxiety and depression, and health-related quality of life. Self-efficacy related to sexual function and fertility, and fertility-related knowledge, will be assessed by study-specific measures. Clinical variables will be collected from the registry. Results will be compared to an age-matched comparison group from the general population. Participants in the Fex-Can Childhood OS who report a high level of sexual dysfunction and/or fertility-related distress will be invited to participate in the RCT. The Fex-Can intervention comprises two programs: The Fex-Can Sex and the Fex-Can Fertility targeting sexual dysfunction and fertility-related distress, respectively. The control condition will be a wait-list. Sexual function and fertility-related distress will be the primary outcomes. The secondary outcomes include body image, anxiety and depression, health-related quality of life and self-efficacy related to sexual function and fertility. Post- and follow-up assessments will be conducted directly after end of intervention (primary end point), at 3 months and 6 months after end of intervention. Additionally, a process-evaluation including study-specific items and a qualitative interview will be conducted. Discussion: The Fex-Can Childhood project will advance knowledge in the areas of sexual function and fertility-related distress among young adult survivors of childhood cancer. If the Fex-Can intervention proves to be efficacious, steps will be taken to implement it in the follow-up care provided to this population.
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6.
  • Stegmayr, Bernd G., et al. (författare)
  • Few Outflow Problems With a Self-locating Catheter for Peritoneal Dialysis : A Randomized Trial
  • 2015
  • Ingår i: Medicine. - 0025-7974 .- 1536-5964. ; 94:48
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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7.
  • Weidung, Bodil, et al. (författare)
  • Systolic blood pressure decline in very old individuals is explained by deteriorating health : Longitudinal changes from Umea85+/GERDA
  • 2017
  • Ingår i: Medicine. - : Lippincott Williams & Wilkins. - 0025-7974 .- 1536-5964. ; 96:51
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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8.
  • Yu, Fang-Fang, et al. (författare)
  • Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease
  • 2016
  • Ingår i: Medicine. - : Wolters Kluwer. - 0025-7974 .- 1536-5964. ; 95:52
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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9.
  • Zhang, Feng'e, et al. (författare)
  • Cell cycle-related lncRNAs and mRNAs in osteoarthritis chondrocytes in a Northwest Chinese Han Population
  • 2020
  • Ingår i: Medicine. - : Lippincott Williams & Wilkins. - 0025-7974 .- 1536-5964. ; 99:24
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: A group of differentially expressed long non-coding RNAs (lncRNAs) have been shown to play key roles in osteoarthritis (OA), although they represented only a small proportion of lncRNAs that may be biologically and physiologically relevant. Since our knowledge of regulatory functions of non-coding RNAs is still limited, it is important to gain better understanding of their relation to the pathogenesis of OA.Methods: We performed mRNA and lncRNA microarray analysis to detect differentially expressed RNAs in chondrocytes from three OA patients compared with four healthy controls. Then, enrichment analysis of the differentially expressed mRNAs was carried out to define disease molecular networks, pathways and gene ontology (GO) function. Furthermore, target gene prediction based on the co-expression network was performed to reveal the potential relationships between lncRNAs and mRNAs, contributing an exploration of a role of lncRNAs in OA mechanism. Quantitative RT-PCR analyses were used to demonstrate the reliability of the experimental results.Findings: Altogether 990 lncRNAs (666 up-regulated and 324 down-regulated) and 546 mRNAs (419 up-regulated and 127 down-regulated) were differentially expressed in OA samples compared with the normal ones. The enrichment analysis revealed a set of genes involved in cell cycle. In total, 854 pairs of mRNA and lncRNA were highly linked, and further target prediction appointed 12 genes specifically for their corresponding lncRNAs. The lncRNAs lncRNA-CTD-2184D3.4, ENST00000564198.1, and ENST00000520562.1 were predicted to regulate SPC24, GALM, and ZNF345 mRNA expressions in OA.Interpretation: This study uncovered several novel genes potentially important in pathogenesis of OA, and forecast the potential function of lnc-CTD-2184D3.4, especially for the cell cycle in the chondrocytes. These findings may promote additional aspects in studies of OA.
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