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Sökning: WFRF:(Han C) > Linköpings universitet

  • Resultat 1-10 av 17
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2.
  • Asbun, H.J., et al. (författare)
  • The Miami International Evidence-based Guidelines on Minimally Invasive Pancreas Resection
  • 2020
  • Ingår i: Annals of Surgery. - : Lippincott Williams and Wilkins. - 0003-4932 .- 1528-1140. ; 271:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The aim of this study was to develop and externally validate the first evidence-based guidelines on minimally invasive pancreas resection (MIPR) before and during the International Evidence-based Guidelines on Minimally Invasive Pancreas Resection (IG-MIPR) meeting in Miami (March 2019).Summary Background Data: MIPR has seen rapid development in the past decade. Promising outcomes have been reported by early adopters from high-volume centers. Subsequently, multicenter series as well as randomized controlled trials were reported; however, guidelines for clinical practice were lacking. Methods: The Scottisch Intercollegiate Guidelines Network (SIGN) methodology was used, incorporating these 4 items: systematic reviews using PubMed, Embase, and Cochrane databases to answer clinical questions, whenever possible in PICO style, the GRADE approach for assessment of the quality of evidence, the Delphi method for establishing consensus on the developed recommendations, and the AGREE-II instrument for the assessment of guideline quality and external validation. The current guidelines are cosponsored by the International Hepato-Pancreato-Biliary Association, the Americas Hepato-Pancreato-Biliary Association, the Asian-Pacific Hepato-Pancreato-Biliary Association, the European-African Hepato-Pancreato-Biliary Association, the European Association for Endoscopic Surgery, Pancreas Club, the Society of American Gastrointestinal and Endoscopic Surgery, the Society for Surgery of the Alimentary Tract, and the Society of Surgical Oncology. Results: After screening 16,069 titles, 694 studies were reviewed, and 291 were included. The final 28 recommendations covered 6 topics; laparoscopic and robotic distal pancreatectomy, central pancreatectomy, pancreatoduodenectomy, as well as patient selection, training, learning curve, and minimal annual center volume required to obtain optimal outcomes and patient safety.Conclusion: The IG-MIPR using SIGN methodology give guidance to surgeons, hospital administrators, patients, and medical societies on the use and outcome of MIPR as well as the approach to be taken regarding this challenging type of surgery. © 2019 Wolters Kluwer Health, Inc. All rights reserved.
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3.
  • Hoshino, Ayuko, et al. (författare)
  • Extracellular Vesicle and Particle Biomarkers Define Multiple Human Cancers
  • 2020
  • Ingår i: Cell. - : CELL PRESS. - 0092-8674 .- 1097-4172. ; 182:4, s. 1044-
  • Tidskriftsartikel (refereegranskat)abstract
    • There is an unmet clinical need for improved tissue and liquid biopsy tools for cancer detection. We investigated the proteomic profile of extracellular vesicles and particles (EVPs) in 426 human samples from tissue explants (TEs), plasma, and other bodily fluids. Among traditional exosome markers, CD9, HSPA8, ALIX, and HSP90AB1 represent pan-EVP markers, while ACTB, MSN, and RAP1B are novel pan-EVP markers. To confirm that EVPs are ideal diagnostic tools, we analyzed proteomes of TE- (n =151) and plasma-derived (n =120) EVPs. Comparison of TE EVPs identified proteins (e.g., VCAN, TNC, and THBS2) that distinguish tumors from normal tissues with 90% sensitivity/94% specificity. Machine-learning classification of plasma-derived EVP cargo, including immunoglobulins, revealed 95% sensitivity/90% specificity in detecting cancer Finally, we defined a panel of tumor-type-specific EVP proteins in TEs and plasma, which can classify tumors of unknown primary origin. Thus, EVP proteins can serve as reliable biomarkers for cancer detection and determining cancer type.
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4.
  • Kurilshikov, Alexander, et al. (författare)
  • Large-scale association analyses identify host factors influencing human gut microbiome composition
  • 2021
  • Ingår i: Nature Genetics. - : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 53:2, s. 156-165
  • Tidskriftsartikel (refereegranskat)abstract
    • To study the effect of host genetics on gut microbiome composition, the MiBioGen consortium curated and analyzed genome-wide genotypes and 16S fecal microbiome data from 18,340 individuals (24 cohorts). Microbial composition showed high variability across cohorts: only 9 of 410 genera were detected in more than 95% of samples. A genome-wide association study of host genetic variation regarding microbial taxa identified 31 loci affecting the microbiome at a genome-wide significant (P < 5 x 10(-8)) threshold. One locus, the lactase (LCT) gene locus, reached study-wide significance (genome-wide association study signal: P = 1.28 x 10(-20)), and it showed an age-dependent association with Bifidobacterium abundance. Other associations were suggestive (1.95 x 10(-10) < P < 5 x 10(-8)) but enriched for taxa showing high heritability and for genes expressed in the intestine and brain. A phenome-wide association study and Mendelian randomization identified enrichment of microbiome trait loci in the metabolic, nutrition and environment domains and suggested the microbiome might have causal effects in ulcerative colitis and rheumatoid arthritis.
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5.
  • Roberts, Jason D., et al. (författare)
  • Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy
  • 2019
  • Ingår i: Journal of Clinical Investigation. - : AMER SOC CLINICAL INVESTIGATION INC. - 0021-9738 .- 1558-8238. ; 129:8, s. 3171-3184
  • Tidskriftsartikel (refereegranskat)abstract
    • Arrhythmogenic cardiomyopathy (ACM) is an inherited arrhythmia syndrome characterized by severe structural and electrical cardiac phenotypes, including myocardial fibrofatty replacement and sudden cardiac death. Clinical management of ACM is largely palliative, owing to an absence of therapies that target its underlying pathophysiology, which stems partially from our limited insight into the condition. Following identification of deceased ACM probands possessing ANK2 rare variants and evidence of ankyrin-B loss of function on cardiac tissue analysis, an ANK2 mouse model was found to develop dramatic structural abnormalities reflective of human ACM, including biventricular dilation, reduced ejection fraction, cardiac fibrosis, and premature death. Desmosomal structure and function appeared preserved in diseased human and murine specimens in the presence of markedly abnormal beta-catenin expression and patterning, leading to identification of a previously unknown interaction between ankyrin-B and beta-catenin. A pharmacological activator of the WNT/beta-catenin pathway, SB-216763, successfully prevented and partially reversed the murine ACM phenotypes. Our findings introduce what we believe to be a new pathway for ACM, a role of ankyrin-B in cardiac structure and signaling, a molecular link between ankyrin-B and beta-catenin, and evidence for targeted activation of the WNT/beta-catenin pathway as a potential treatment for this disease.
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6.
  • Abou Ghayda, Ramy, et al. (författare)
  • The global case fatality rate of coronavirus disease 2019 by continents and national income: A meta-analysis
  • 2022
  • Ingår i: Journal of Medical Virology. - : WILEY. - 0146-6615 .- 1096-9071. ; 94:6, s. 2402-2413
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study is to provide a more accurate representation of COVID-19s case fatality rate (CFR) by performing meta-analyses by continents and income, and by comparing the result with pooled estimates. We used multiple worldwide data sources on COVID-19 for every country reporting COVID-19 cases. On the basis of data, we performed random and fixed meta-analyses for CFR of COVID-19 by continents and income according to each individual calendar date. CFR was estimated based on the different geographical regions and levels of income using three models: pooled estimates, fixed- and random-model. In Asia, all three types of CFR initially remained approximately between 2.0% and 3.0%. In the case of pooled estimates and the fixed model results, CFR increased to 4.0%, by then gradually decreasing, while in the case of random-model, CFR remained under 2.0%. Similarly, in Europe, initially, the two types of CFR peaked at 9.0% and 10.0%, respectively. The random-model results showed an increase near 5.0%. In high-income countries, pooled estimates and fixed-model showed gradually increasing trends with a final pooled estimates and random-model reached about 8.0% and 4.0%, respectively. In middle-income, the pooled estimates and fixed-model have gradually increased reaching up to 4.5%. in low-income countries, CFRs remained similar between 1.5% and 3.0%. Our study emphasizes that COVID-19 CFR is not a fixed or static value. Rather, it is a dynamic estimate that changes with time, population, socioeconomic factors, and the mitigatory efforts of individual countries.
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7.
  • Wang, Gang, et al. (författare)
  • Tumour extracellular vesicles and particles induce liver metabolic dysfunction
  • 2023
  • Ingår i: Nature. - : NATURE PORTFOLIO. - 0028-0836 .- 1476-4687. ; 618:7964, s. 374-382
  • Tidskriftsartikel (refereegranskat)abstract
    • Cancer alters the function of multiple organs beyond those targeted by metastasis(1,2). Here we show that inflammation, fatty liver and dysregulated metabolism are hallmarks of systemically affected livers in mouse models and in patients with extrahepatic metastasis. We identified tumour-derived extracellular vesicles and particles (EVPs) as crucial mediators of cancer-induced hepatic reprogramming, which could be reversed by reducing tumour EVP secretion via depletion of Rab27a. All EVP subpopulations, exosomes and principally exomeres, could dysregulate hepatic function. The fatty acid cargo of tumour EVPs-particularly palmitic acid-induced secretion of tumour necrosis factor (TNF) by Kupffer cells, generating a pro-inflammatory microenvironment, suppressing fatty acid metabolism and oxidative phosphorylation, and promoting fatty liver formation. Notably, Kupffer cell ablation or TNF blockade markedly decreased tumour-induced fatty liver generation. Tumour implantation or pre-treatment with tumour EVPs diminished cytochrome P450 gene expression and attenuated drug metabolism in a TNF-dependent manner. We also observed fatty liver and decreased cytochrome P450 expression at diagnosis in tumour-free livers of patients with pancreatic cancer who later developed extrahepatic metastasis, highlighting the clinical relevance of our findings. Notably, tumour EVP education enhanced side effects of chemotherapy, including bone marrow suppression and cardiotoxicity, suggesting that metabolic reprogramming of the liver by tumour-derived EVPs may limit chemotherapy tolerance in patients with cancer. Our results reveal how tumour-derived EVPs dysregulate hepatic function and their targetable potential, alongside TNF inhibition, for preventing fatty liver formation and enhancing the efficacy of chemotherapy.
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8.
  • Wang, X., et al. (författare)
  • Involvement of the MKK6-p38? cascade in ?-radiation-induced cell cycle arrest
  • 2000
  • Ingår i: Molecular and Cellular Biology. - 0270-7306 .- 1098-5549. ; 20:13, s. 4543-4552
  • Tidskriftsartikel (refereegranskat)abstract
    • The p38 group of kinases belongs to the mitogen-activated protein (MAP) kinase superfamily with structural and functional characteristics distinguishable from those of the ERK, JNK (SAPK), and BMK (ERK5) kinases. Although there is a high degree of similarity among members of the p38 group in terms of structure and activation, each member appears to have a unique function. Here we show that activation of p38-? (also known as ERK6 or SAPK3), but not the other p38 isoforms, is required for ?-irradiation- induced G2 arrest. Activation of the MKK6-p38? cascade is sufficient to induce G2 arrest in cells, and expression of dominant negative alleles of MKK6 or p38? allows cells to escape the DNA damage-induce G2 delay. Activation of p38? is dependent on ATM and leads to activation of Cds1 (also known as Chk2). These data suggest a model in which activation of ATM by ? irradiation leads to the activation of MKK6, p38?, and Cds1 and that activation of both MKK6 and p38? is essential for the proper regulation of the G2 checkpoint in mammalian cells.
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9.
  • Weiffenbach, Julia E., et al. (författare)
  • Unraveling the mechanisms and implications of a stronger mid-Pliocene Atlantic Meridional Overturning Circulation (AMOC) in PlioMIP2
  • 2023
  • Ingår i: Climate of the Past. - : COPERNICUS GESELLSCHAFT MBH. - 1814-9324 .- 1814-9332. ; 19:1, s. 61-85
  • Tidskriftsartikel (refereegranskat)abstract
    • The mid-Pliocene warm period (3.264-3.025 Ma) is the most recent geological period in which the atmospheric CO2 concentration was approximately equal to the concentration we measure today (ca. 400 ppm). Sea surface temperature (SST) proxies indicate above-average warming over the North Atlantic in the mid-Pliocene with respect to the pre-industrial period, which may be linked to an intensified Atlantic Meridional Overturning Circulation (AMOC). Earlier results from the Pliocene Model Intercomparison Project Phase 2 (PlioMIP2) show that the ensemble simulates a stronger AMOC in the mid-Pliocene than in the pre-industrial. However, no consistent relationship between the stronger mid-Pliocene AMOC and either the Atlantic northward ocean heat transport (OHT) or average North Atlantic SSTs has been found. In this study, we look further into the drivers and consequences of a stronger AMOC in mid-Pliocene compared to pre-industrial simulations in PlioMIP2. We find that all model simulations with a closed Bering Strait and Canadian Archipelago show reduced freshwater transport from the Arctic Ocean into the North Atlantic. This contributes to an increase in salinity in the subpolar North Atlantic and Labrador Sea that can be linked to the stronger AMOC in the mid-Pliocene. To investigate the dynamics behind the ensembles variable response of the total Atlantic OHT to the stronger AMOC, we separate the Atlantic OHT into two components associated with either the overturning circulation or the wind-driven gyre circulation. While the ensemble mean of the overturning component is increased significantly in magnitude in the mid-Pliocene, it is partly compensated by a reduction in the gyre component in the northern subtropical gyre region. This indicates that the lack of relationship between the total OHT and AMOC is due to changes in OHT by the subtropical gyre. The overturning and gyre components should therefore be considered separately to gain a more complete understanding of the OHT response to a stronger mid-Pliocene AMOC. In addition, we show that the AMOC exerts a stronger influence on North Atlantic SSTs in the mid-Pliocene than in the pre-industrial, providing a possible explanation for the improved agreement of the PlioMIP2 ensemble mean SSTs with reconstructions in the North Atlantic.
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10.
  • Zhou, Han-yu, et al. (författare)
  • Multisensory temporal binding window in autism spectrum disorders and schizophrenia spectrum disorders: A systematic review and meta-analysis
  • 2018
  • Ingår i: Neuroscience and Biobehavioral Reviews. - : Elsevier. - 0149-7634 .- 1873-7528. ; 86, s. 66-76
  • Tidskriftsartikel (refereegranskat)abstract
    • Multisensory temporal integration could be compromised in both autism spectrum disorders (ASD) and schizophrenia spectrum disorders (SSD) and may play an important role in perceptual and cognitive impairment in these two disorders. This review aimed to quantitatively compare the sensory temporal acuity between healthy controls and the two clinical groups (ASD and SSD). Impairment of sensory temporal integration was robust and comparable in both patients with SSD (Hedges’ g = 0.91, 95%CI[0.62–1.19]; Z = 6.21, p < .001) and ASD (Hedges’ g = 0.85, (95%CI[0.54–1.15]; Z = 5.39, p < .001). By further separating studies into unisensory and multisensory (bimodal: audiovisual) ones, subgroup analysis indicated heterogeneous and unstable effects for unisensory temporal binding in the ASD group, but a more consistent and severe impairment in multisensory temporal integration represented by an enlarged temporal binding window in both clinical groups. Such multisensory dysfunction is associated with symptoms like hallucinations and impaired social communications. Future studies focusing on improving multisensory temporal functions may have important implications for the amelioration of schizophrenia and autistic symptoms.
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