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2.
  • Klionsky, Daniel J., et al. (author)
  • Guidelines for the use and interpretation of assays for monitoring autophagy
  • 2012
  • In: Autophagy. - : Informa UK Limited. - 1554-8635 .- 1554-8627. ; 8:4, s. 445-544
  • Research review (peer-reviewed)abstract
    • In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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3.
  • Wang, Fang, et al. (author)
  • Emerging contaminants: A One Health perspective
  • 2024
  • In: Innovation. - 2666-6758. ; 5
  • Research review (peer-reviewed)abstract
    • Environmental pollution is escalating due to rapid global development that often prioritizes human needs over planetary health. Despite global efforts to mitigate legacy pollutants, the continuous introduction of new substances remains a major threat to both people and the planet. In response, global initiatives are focusing on risk assessment and regulation of emerging contaminants, as demonstrated by the ongoing efforts to establish the UN's Intergovernmental Science-Policy Panel on Chemicals, Waste, and Pollution Prevention. This review identifies the sources and impacts of emerging contaminants on planetary health, emphasizing the importance of adopting a One Health approach. Strategies for monitoring and addressing these pollutants are discussed, underscoring the need for robust and socially equitable environmental policies at both regional and international levels. Urgent actions are needed to transition toward sustainable pollution management practices to safeguard our planet for future generations.
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4.
  • Beal, Jacob, et al. (author)
  • Robust estimation of bacterial cell count from optical density
  • 2020
  • In: Communications Biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 3:1
  • Journal article (peer-reviewed)abstract
    • Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data.
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5.
  • Deng, Huan, et al. (author)
  • Altered Expression of the Hedgehog Pathway Proteins BMP2, BMP4, SHH, and IHH Involved in Knee Cartilage Damage of Patients With Osteoarthritis and Kashin-Beck Disease
  • 2022
  • In: Cartilage. - : Sage Publications. - 1947-6035 .- 1947-6043. ; 13:1
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: To investigate the expression of Hedgehog (HH) signaling pathway proteins in knee articular cartilage from Kashin-Beck disease (KBD) and osteoarthritis (OA) patients.METHODS: Knee articular cartilage samples were collected from normal (N), OA, and KBD adults (aged 38-60 years) and divided into 3 groups with 6 subjects in each group. The localization of the HH pathway proteins bone morphogenetic protein 2 (BMP2), bone morphogenetic protein 4 (BMP4), Sonic hedgehog (SHH), and Indian hedgehog (IHH) was observed with the microscope after immunohistochemical (IHC) staining. Positive staining cell rates of each proteins were compared.RESULTS: The strongest stainings of all proteins were observed in the middle zones of all 3 groups. The positive staining rates of BMP4 and IHH were significantly lower in the OA and KBD groups than those in the N group in all 3 zones. The positive staining rates of BMP2 and SHH tend to be lower in the OA and KBD groups than those in the N group in the deep zone, while higher in the OA and KBD groups than those in the N group in superficial and middle zones.CONCLUSIONS: Altered expression of the HH pathway proteins BMP2, BMP4, SHH, and IHH was found in OA and KBD articular cartilage. There seemed to be a compensatory effect between SHH and IHH in cartilage damage. Further studies on the pathogenesis of OA and KBD may be carried out from these aspects in the future.
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6.
  • Ferro, Ana, et al. (author)
  • Alcohol intake and gastric cancer : Meta-analyses of published data versus individual participant data pooled analyses (StoP Project)
  • 2018
  • In: Cancer Epidemiology. - : ELSEVIER SCI LTD. - 1877-7821 .- 1877-783X. ; 54, s. 125-132
  • Journal article (peer-reviewed)abstract
    • Background: Individual participant data pooled analyses allow access to non-published data and statistical reanalyses based on more homogeneous criteria than meta-analyses based on systematic reviews. We quantified the impact of publication-related biases and heterogeneity in data analysis and presentation in summary estimates of the association between alcohol drinking and gastric cancer.Methods: We compared estimates obtained from conventional meta-analyses, using only data available in published reports from studies that take part in the Stomach Cancer Pooling (StoP) Project, with individual participant data pooled analyses including the same studies.Results: A total of 22 studies from the StoP Project assessed the relation between alcohol intake and gastric cancer, 19 had specific data for levels of consumption and 18 according to cancer location; published reports addressing these associations were available from 18, 5 and 5 studies, respectively. The summary odds ratios [OR, (95%CI)] estimate obtained with published data for drinkers vs. non-drinkers was 10% higher than the one obtained with individual StoP data [18 vs. 22 studies: 1.21 (1.07-1.36) vs. 1.10 (0.99-1.23)] and more heterogeneous (1(2): 63.6% vs 54.4%). In general, published data yielded less precise summary estimates (standard errors up to 2.6 times higher). Funnel plot analysis suggested publication bias.Conclusion: Meta-analyses of the association between alcohol drinking and gastric cancer tended to overestimate the magnitude of the effects, possibly due to publication bias. Additionally, individual participant data pooled analyses yielded more precise estimates for different levels of exposure or cancer subtypes.
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7.
  • Ferro, Ana, et al. (author)
  • Tobacco smoking and gastric cancer: : meta-analyses of published data versus pooled analyses of individual participant data (StoP Project).
  • 2018
  • In: European Journal of Cancer Prevention. - 0959-8278 .- 1473-5709. ; 27:3, s. 197-204
  • Journal article (peer-reviewed)abstract
    • Tobacco smoking is one of the main risk factors for gastric cancer, but the magnitude of the association estimated by conventional systematic reviews and meta-analyses might be inaccurate, due to heterogeneous reporting of data and publication bias. We aimed to quantify the combined impact of publication-related biases, and heterogeneity in data analysis or presentation, in the summary estimates obtained from conventional meta-analyses. We compared results from individual participant data pooled-analyses, including the studies in the Stomach Cancer Pooling (StoP) Project, with conventional meta-analyses carried out using only data available in previously published reports from the same studies. From the 23 studies in the StoP Project, 20 had published reports with information on smoking and gastric cancer, but only six had specific data for gastric cardia cancer and seven had data on the daily number of cigarettes smoked. Compared to the results obtained with the StoP database, conventional meta-analyses overvalued the relation between ever smoking (summary odds ratios ranging from 7% higher for all studies to 22% higher for the risk of gastric cardia cancer) and yielded less precise summary estimates (SE ≤2.4 times higher). Additionally, funnel plot asymmetry and corresponding hypotheses tests were suggestive of publication bias. Conventional meta-analyses and individual participant data pooled-analyses reached similar conclusions on the direction of the association between smoking and gastric cancer. However, published data tended to overestimate the magnitude of the effects, possibly due to publication biases and limited the analyses by different levels of exposure or cancer subtypes.
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8.
  • Guo, Feilong, et al. (author)
  • How Early-Life Gut Microbiota Alteration Sets Trajectories for Health and Inflammatory Bowel Disease?
  • 2021
  • In: Frontiers in Nutrition. - : Frontiers Media S.A.. - 2296-861X. ; 8
  • Research review (peer-reviewed)abstract
    • Inflammatory bowel disease (IBD) is a recurrent chronic inflammatory condition of the intestine without any efficient therapeutic regimens. Gut microbiota, which plays an instrumental role in the development and maturation of the immune system, has been implicated in the pathogenesis of IBD. Emerging evidence has established that early-life events particularly maternal influences and antibiotic treatment are strongly correlated with the health or susceptibility to disease of an individual in later life. Thus, it is proposed that there is a critical period in infancy, during which the environmental exposures bestow a long-term pathophysiological imprint. This notion sheds new light on the development of novel approaches for the treatment, i.e., early interventions, more precisely, the prevention of many uncurable chronic inflammatory diseases like IBD. In this review, we have integrated current evidence to describe the feasibility of the "able-to-be-regulated microbiota," summarized the underlying mechanisms of the "microbiota-driven immune system education," explored the optimal intervention time window, and discussed the potential of designing early-probiotic treatment as a new prevention strategy for IBD.
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9.
  • Han, Jing, et al. (author)
  • Identification of N-glycoproteins of knee cartilage from adult osteoarthritis and Kashin-Beck disease based on quantitative glycoproteomics, compared with normal control cartilage
  • 2022
  • In: Cells. - : MDPI. - 2073-4409. ; 11:16, s. 2513-2513
  • Journal article (peer-reviewed)abstract
    • Glycoproteins are involved in the development of many diseases, while the type and content of N-glycoproteins in the cartilage of osteoarthritis (OA) and Kashin-Beck disease (KBD) are still unclear. This research aims to identify N-glycoproteins in knee cartilage patients with OA and KBD compared with normal control (N) adults. The cartilage samples were collected from gender- and age-matched OA (n = 9), KBD (n = 9) patients, and N (n = 9) adults. Glycoproteomics and label-free liquid chromatography-tandem mass spectrometry (LC-MS/MS) obtained N-glycoproteins of KBD and OA. A total of 594 N-glycoproteins and 1146 N-glycosylation peptides were identified. The identified data were further compared and analyzed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Protein-Protein Interactions (PPI). Pairwise comparison of the glycoproteins detected in the three groups showed that integrin beta-1 (ITGB1), collagen alpha-1 (II) chain (COL2A1), collagen alpha-1 (VII) chain (COL7A1), carbohydrate sulfotransferase 3 (CHST-3), carbohydrate sulfotransferase 4 (CHST-4), thrombospondin 2 (THBS2), bone morphogenetic protein 8A (BMP8A), tenascin-C (TNC), lysosome-associated membrane protein (LAMP2), and beta-glucuronidase (GUSB) were significantly differentially expressed. GO results suggested N-glycoproteins mainly belonged to protein metabolic process, single-multicellular and multicellular organism process, cell adhesion, biological adhesion, and multicellular organism development. KEGG and PPI results revealed that key N-glycoproteins were closely related to pathways for OA and KBD, such as phagosome, ECM-receptor interaction, lysosome, focal adhesion, protein digestion, and absorption. These results reflected glycoprotein expression for OA and KBD in the process of ECM degradation, material transport, cell-cell or cell-ECM interaction, and information transduction. These key significantly differentially expressed N-glycoproteins and pathways lead to the degeneration and degradation of the cartilage of OA and KBD mainly by disrupting the synthesis and catabolism of basic components of ECM and chondrocytes and interfering with the transfer of material or information. The key N-glycoproteins or pathways in this research are potential targets for pathological mechanisms and therapies of OA and KBD.
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10.
  • Huan, Tianxiao, et al. (author)
  • Genome-wide identification of DNA methylation QTLs in whole blood highlights pathways for cardiovascular disease
  • 2019
  • In: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10
  • Journal article (peer-reviewed)abstract
    • Identifying methylation quantitative trait loci (meQTLs) and integrating them with disease-associated variants from genome-wide association studies (GWAS) may illuminate functional mechanisms underlying genetic variant-disease associations. Here, we perform GWAS of >415 thousand CpG methylation sites in whole blood from 4170 individuals and map 4.7 million cis- and 630 thousand trans-meQTL variants targeting >120 thousand CpGs. Independent replication is performed in 1347 participants from two studies. By linking cis-meQTL variants with GWAS results for cardiovascular disease (CVD) traits, we identify 92 putatively causal CpGs for CVD traits by Mendelian randomization analysis. Further integrating gene expression data reveals evidence of cis CpG-transcript pairs causally linked to CVD. In addition, we identify 22 trans-meQTL hotspots each targeting more than 30 CpGs and find that trans-meQTL hotspots appear to act in cis on expression of nearby transcriptional regulatory genes. Our findings provide a powerful meQTL resource and shed light on DNA methylation involvement in human diseases.
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11.
  • Jin, Yi, et al. (author)
  • Self-aware distributed deep learning framework for heterogeneous IoT edge devices
  • 2021
  • In: Future generations computer systems. - : Elsevier BV. - 0167-739X .- 1872-7115. ; 125, s. 908-920
  • Journal article (peer-reviewed)abstract
    • Implementing artificial intelligence (AI) in the Internet of Things (IoT) involves a move from the cloud to the heterogeneous and low-power edge, following an urgent demand for deploying complex training tasks in a distributed and reliable manner. This work proposes a self-aware distributed deep learning (DDL) framework for IoT applications, which is applicable to heterogeneous edge devices aiming to improve adaptivity and amortize the training cost. The self-aware design including the dynamic self-organizing approach and the self-healing method enhances the system reliability and resilience. Three typical edge devices are adopted with cross-platform Docker deployment: Personal Computers (PC) for general computing devices, Raspberry Pi 4Bs (Rpi) for resource-constrained edge devices, and Jetson Nanos (Jts) for AI-enabled edge devices. Benchmarked with ResNet-32 on CIFAR-10, the training efficiency of tested distributed clusters is increased by 8.44x compared to the standalone Rpi. The cluster with 11 heterogeneous edge devices achieves a training efficiency of 200.4 images/s and an accuracy of 92.45%. Results prove that the self-organizing approach functions well with dynamic changes like devices being removed or added. The self-healing method is evaluated with various stabilities, cluster scales, and breakdown cases, testifying that the reliability can be largely enhanced for extensively distributed deployments. The proposed DDL framework shows excellent performance for training implementation with heterogeneous edge devices in IoT applications with high-degree scalability and reliability.
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12.
  • Kim, Jongho, et al. (author)
  • Remarkable conductivity enhancement in P-doped polythiophenes via rational engineering of polymer-dopant interactions
  • 2023
  • In: Materials Today Advances. - : Elsevier BV. - 2590-0498. ; 18
  • Journal article (peer-reviewed)abstract
    • Molecular doping is an effective approach to tune the charge density and optimize electrical performance of conjugated polymers. However, the introduction of dopants, on the other hand, may disturb the polymer microstructure and disrupt the charge transport path, often leading to a decrease of charge carrier mobility and deterioration of electrical conductivity of the doped films. Here we show that dopant-induced disorder can be overcome by rational engineering of polymer-dopant interactions, resulting in remarkable enhancement of electrical conductivity. Benchmark poly(3-hexylthiophene) (P3HT) and its analogous random polymers of 3-hexylthiophene and thiophene P[(3HT)1-x-stat-(T)x] were synthesized and doped by 2,3,5,6-tetrafluoro-7,7,8,8-tetracyanoquinodimethane (F4TCNQ). Remarkably, random P[(3HT)1-x-stat-(T)x] was doped to a far superior electrical conductivity, that in the case of x ≥ 0.24, the conductivity of P[(3HT)1-x-stat-(T)x] is over 100 times higher than that of the doped P3HT, despite both P3HT and P[(3HT)1-x-stat-(T)x] exhibit comparable charge carrier mobility in their pristine state and in spite of their practically identical redox properties. This result can be traced back to the formation of π-stacked polymer-dopant-polymer co-crystals exhibiting extremely short packing distances of 3.13–3.15 Å. The mechanism behind these performances is based on a new role played by the dopant molecules that we name “bridging-gluing”. The results are coherently verified by the combination of optical absorption spectroscopy, X-ray diffraction, density functional theory calculations, and molecular dynamics simulations.
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13.
  • Lei, Jian, et al. (author)
  • Altered expression of aggrecan, FAM20B, B3GALT6, and EXTL2 in patients with osteoarthritis and Kashin-Beck disease
  • 2021
  • In: Cartilage. - : Sage Publications. - 1947-6035 .- 1947-6043. ; 13:Suppl 1, s. 818S-828S
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: The objective of this study was to investigate the expression of enzymes involved in synthesis and modification of chondroitin sulfate (CS) in knee cartilage tissue of patients with osteoarthritis (OA) and Kashin-Beck disease (KBD).METHODS: The knee articular cartilage samples were obtained from 18 age- and gender-matched donors with 6 each in KBD, OA, and control groups. Hematoxylin and eosin (HE) staining, toluidine blue (TB) staining, and immunohistochemical (IHC) staining were performed to estimate the expression level and localization of aggrecan, along with FAM20B, GalT-II, and EXTL2, which are associated with CS synthesis and modification. Rank-based analyses of variance test was used for the multiple comparisons of discrepancy in the positive staining rate among the 3 groups.RESULTS: In HE and TB staining results, damaged morphology, decreased chondrocyte numbers and proteoglycans were observed in OA and KBD groups compared with the control group. In line with these trends, the positive staining rates of aggrecan were lower in KBD and OA groups than in the control group. Meanwhile, the positive staining rates of CS chain modifying enzymes FAM20B, GalT-II, and EXTL2 decreased in OA and KBD groups.CONCLUSIONS: In conclusion, it was demonstrated that altered expression of CS chain modifying enzymes in OA and KBD groups influenced the synthesis procession of CS and could contribute to the damage of cartilage. Further investigation of these enzymes can provide new theoretical and experimental targets for OA and KBD pathogenesis studies.
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14.
  • Lei, Jian, et al. (author)
  • Proteomic analysis of knee cartilage reveals potential signaling pathways in pathological mechanism of Kashin-Beck disease compared with osteoarthritis
  • 2020
  • In: Scientific Reports. - : Nature Publishing Group. - 2045-2322. ; 10
  • Journal article (peer-reviewed)abstract
    • The pathological mechanism of Kashin-Beck disease (KBD), an endemic osteoarthritic disease, remains to be poorly understood. This study was designed to identify signaling pathways and crucial proteins involved in the pathological mechanism of KBD compared with osteoarthritis (OA). The knee cartilage samples were collected from gender- and age-matched KBD (n = 9) and OA (n = 9) patients. After pre-processing, samples were labeled with Tamdem Mass Tags 6plex multiplex kit, and analyzed by liquid chromatography-tandem mass spectrometry. Proteomic results were analyzed with gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interactions (PPI). The differential abundance proteins from KBD and OA were validated using western blot analysis. As a result, A total number of 375 proteins were identified to have differential abundance between KBD and OA, of which 121 and 254 proteins were observed to be up-regulated or down-regulated in KBD group. GO analysis shows that the differential abundant proteins are associated with cell junction and signal transducer activity from extracellular to intracellular. KEGG pathways enrichment and PPI network indicate four major pathways, including extracellular matrix -receptor interaction, focal adhesion, phosphatidylinositol 3-kinase (PI3K)-Protein kinase B (Akt), and Ras signaling pathways were involved in the degeneration of cartilage. Moreover, integrins, laminins, NF-κB and other regulative molecules were found as crucial proteins. In conclusion, our results demonstrated that compared with OA, the differential abundance proteins and signaling pathways may contribute to the occurrence and development of joint damage in KBD. Further investigation of their regulative roles and interaction may provide new insights into the pathological mechanisms and therapeutic targets for KBD.
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15.
  • Li, Fang, et al. (author)
  • Lie Detection Using fNIRS Monitoring of Inhibition-Related Brain Regions Discriminates Infrequent but not Frequent Liars
  • 2018
  • In: Frontiers in Human Neuroscience. - : Frontiers Media S.A.. - 1662-5161. ; 12
  • Journal article (peer-reviewed)abstract
    • Functional near-infrared spectroscopy (fNIRS) was used to test whether monitoring inhibition-related brain regions is a feasible method for detecting both infrequent liars and frequent liars. Thirty-two participants were divided into two groups: the deceptive group (liars) and the non-deceptive group (ND group, innocents). All the participants were required to undergo a simulated interrogation by a computer. The participants from the deceptive group were instructed to tell a mix of lies and truths and those of the ND group were instructed always to tell the truth. Based on the number of deceptions, the participants of the deceptive group were further divided into a infrequently deceptive group (IFD group, infrequent liars) and a frequently deceptive group (FD group, frequent liars). The infrequent liars exhibited greater neural activities than the frequent liars and the innocents in the left middle frontal gyrus (MFG) when performing the deception detection tasks. While performing deception detection tasks, infrequent liars showed significantly greater neural activation in the left MFG than the baseline, but frequent liars and innocents did not exhibit this pattern of neural activation in any area of inhibition-related brain regions. The results of individual analysis showed an acceptable accuracy of detecting infrequent liars, but an unacceptable accuracy of detecting frequent liars. These results suggest that using fNIRS monitoring of inhibition-related brain regions is feasible for detecting infrequent liars, for whom deception may be more effortful and therefore more physiologically marked, but not frequent liars.
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16.
  • Liang, Yusen, et al. (author)
  • Migrating photon avalanche in different emitters at the nanoscale enables 46th-order optical nonlinearity
  • 2022
  • In: Nature Nanotechnology. - : Springer Nature. - 1748-3387 .- 1748-3395. ; 17:5, s. 524-530
  • Journal article (peer-reviewed)abstract
    • A photon avalanche (PA) effect that occurs in lanthanide-doped solids gives rise to a giant nonlinear response in the luminescence intensity to the excitation light intensity. As a result, much weaker lasers are needed to evoke such PAs than for other nonlinear optical processes. Photon avalanches are mostly restricted to bulk materials and conventionally rely on sophisticated excitation schemes, specific for each individual system. Here we show a universal strategy, based on a migrating photon avalanche (MPA) mechanism, to generate huge optical nonlinearities from various lanthanide emitters located in multilayer core/shell nanostructrues. The core of the MPA nanoparticle, composed of Yb3+ and Pr3+ ions, activates avalanche looping cycles, where PAs are synchronously achieved for both Yb3+ and Pr3+ ions under 852 nm laser excitation. These nanocrystals exhibit a 26th-order nonlinearity and a clear pumping threshold of 60 kW cm−2. In addition, we demonstrate that the avalanching Yb3+ ions can migrate their optical nonlinear response to other emitters (for example, Ho3+ and Tm3+) located in the outer shell layer, resulting in an even higher-order nonlinearity (up to the 46th for Tm3+) due to further cascading multiplicative effects. Our strategy therefore provides a facile route to achieve giant optical nonlinearity in different emitters. Finally, we also demonstrate applicability of MPA emitters to bioimaging, achieving a lateral resolution of ~62 nm using one low-power 852 nm continuous-wave laser beam.
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17.
  • Liang, Yannis Yan, et al. (author)
  • Association between sleep duration and metabolic syndrome : linear and nonlinear Mendelian randomization analyses
  • 2023
  • In: Journal of Translational Medicine. - : BioMed Central (BMC). - 1479-5876. ; 21:1
  • Journal article (peer-reviewed)abstract
    • Background Observational studies have found that both short and long sleep duration are associated with increased risk of metabolic syndrome (MetS). This study aimed to examine the associations of genetically determined sleep durations with MetS and its five components (i.e., central obesity, high blood pressure, dyslipidemia, hypertriglyceridemia, and hyperglycemia) among a group of elderly population.Methods In 335,727 participants of White British from the UK Biobank, linear Mendelian randomization (MR) methods were first employed to examine the causal association of genetically predicted continuous sleep duration with MetS and its each component. Nonlinear MR analyses were performed to determine the nonlinearity of these associations. The causal associations of short and long sleep duration with MetS and its components were further assessed by using genetic variants that associated with short (<= 6 h) and long sleep (>= 9 h) durations.Results Linear MR analyses demonstrated that genetically predicted 1-h longer sleep duration was associated with a 13% lower risk of MetS, a 30% lower risk of central obesity, and a 26% lower risk of hyperglycemia. Non-linear MR analyses provided evidence for non-linear associations of genetically predicted sleep duration with MetS and its five components (all P values < 0.008). Genetically predicted short sleep duration was moderately associated with MetS and its four components, including central obesity, dyslipidemia, hypertriglyceridemia, and hyperglycemia (all P values < 0.002), whereas genetically long sleep duration was not associated with MetS and any of its components.Conclusions Genetically predicted short sleep duration, but not genetically predicted long sleep duration, is a potentially causal risk factor for MetS.
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18.
  • Lin, Xialu, et al. (author)
  • Individual and combined toxicity of T-2 toxin and deoxynivalenol on human C-28/I2 and rat primary chondrocytes
  • 2019
  • In: Journal of Applied Toxicology. - : John Wiley & Sons. - 0260-437X .- 1099-1263. ; 39:2, s. 343-353
  • Journal article (peer-reviewed)abstract
    • Deoxynivalenol (DON) and T-2 toxin are prevalent mycotoxin contaminants in the food and feed stuffs worldwide, with non-negligible co-contamination and co-exposure conditions. Meanwhile, they are considerable risk factors for Kashin-Beck disease, a chronic endemic osteochondropathy. The aim of this study was to investigate the individual and combined cytotoxicity of DON and T-2 toxin on proliferating human C-28/I2 and newborn rat primary costal chondrocytes by MTT assay. Four molar concentration combination ratios of DON and T-2 toxin were used, 1:1 for R1 mixture, 10:1 for R10, 100:1 for R100 and 1000:1 for R1000. The toxicological interactions were quantified by the MixLow method. DON, T-2 toxin, and their mixtures all showed a clear dose-dependent toxicity for chondrocytes. The cytotoxicity of T-2 toxin was 285-fold higher than DON was in human chondrocytes, and 22-fold higher in the rat chondrocytes. The combination of DON and T-2 toxin was significantly synergistic at middle and high level concentrations of R10 mixtures in rat chondrocytes, but significantly antagonistic at the low concentrations of R100 mixtures in both cells and at the middle concentrations of R1000 mixtures in rat chondrocytes. These results indicated that the combined toxicity was influenced by the cell sensitivity for toxins, the difference between the combination ratio and equitoxic ratio, the concentrations and other factors.
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19.
  • Liu, C, et al. (author)
  • A DNA methylation biomarker of alcohol consumption.
  • 2018
  • In: Molecular Psychiatry. - : Springer Science and Business Media LLC. - 1359-4184 .- 1476-5578. ; 23, s. 422-433
  • Journal article (peer-reviewed)abstract
    • The lack of reliable measures of alcohol intake is a major obstacle to the diagnosis and treatment of alcohol-related diseases. Epigenetic modifications such as DNA methylation may provide novel biomarkers of alcohol use. To examine this possibility, we performed an epigenome-wide association study of methylation of cytosine-phosphate-guanine dinucleotide (CpG) sites in relation to alcohol intake in 13 population-based cohorts (ntotal=13 317; 54% women; mean age across cohorts 42-76 years) using whole blood (9643 European and 2423 African ancestries) or monocyte-derived DNA (588 European, 263 African and 400 Hispanic ancestry) samples. We performed meta-analysis and variable selection in whole-blood samples of people of European ancestry (n=6926) and identified 144 CpGs that provided substantial discrimination (area under the curve=0.90-0.99) for current heavy alcohol intake (⩾42 g per day in men and ⩾28 g per day in women) in four replication cohorts. The ancestry-stratified meta-analysis in whole blood identified 328 (9643 European ancestry samples) and 165 (2423 African ancestry samples) alcohol-related CpGs at Bonferroni-adjusted P<1 × 10(-7). Analysis of the monocyte-derived DNA (n=1251) identified 62 alcohol-related CpGs at P<1 × 10(-7). In whole-blood samples of people of European ancestry, we detected differential methylation in two neurotransmitter receptor genes, the γ-Aminobutyric acid-A receptor delta and γ-aminobutyric acid B receptor subunit 1; their differential methylation was associated with expression levels of a number of genes involved in immune function. In conclusion, we have identified a robust alcohol-related DNA methylation signature and shown the potential utility of DNA methylation as a clinically useful diagnostic test to detect current heavy alcohol consumption.
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20.
  • Liu, Huan, et al. (author)
  • Associations between selenium content in hair and Kashin-Beck Disease/Keshan Disease in children in Northwestern China : a prospective cohort study
  • 2018
  • In: Biological Trace Element Research. - : Springer. - 0163-4984 .- 1559-0720. ; 184:1, s. 16-23
  • Journal article (peer-reviewed)abstract
    • The objective of this study was to investigate the relationship between selenium content in hair and the incidence of Kashin-Beck disease (KBD) and Keshan disease (KD) in China. A prospective cohort study was conducted among children aged 5-12 years with different levels of low-selenium (group 1, Se ≤ 110 ng/g; group 2, 110 < Se ≤ 150 ng/g; and group 3, 150 < Se ≤ 200 ng/g) or selenium-supplemented (group 4, Se > 200 ng/g) exposure. A person-years approach was used to calculate the incidence and rate of positive clinical signs. Relative risk (RR), attributable risk, and etiologic fraction were used to determine the strength of association between selenium and disease incidence. Seven new KBD cases were diagnosed during 3-year follow-up. Positive clinical signs of KBD were found in 17.78 (95% confidence interval [CI] 14.27-21.29) cases per 100 person-years in group 1, 13.28 (9.82-16.74) in group 2, 12.95 (9.34-16.56) in group 3, and 8.18 (5.50-10.85) in group 4. Compared with group 4, the RR (95% CI) of groups 1, 2, and 3 were 2.17 (1.48-3.19), 1.62 (1.07-2.47), and 1.58 (1.03-2.43), respectively. Positive clinical signs of KD were 25.90 (18.62-33.18) cases per 100 person-years in group 1, 5.66 (1.26-10.06) in group 2, 4.60 (0.20-9.00) in group 3, and 14.62 (8.54-20.69) in group 4. Compared with group 4, the RR (95% CI) were 1.77 (1.07-2.93), 0.39 (0.16-0.93), and 0.31 (0.11-0.89), respectively. In children, the onset of KBD was negatively correlated with selenium content within a certain range. However, there may be a U-shaped association between selenium content and KD in children.
  •  
21.
  • Liu, Huan, et al. (author)
  • The first human induced pluripotent stem cell line of Kashin–Beck disease reveals involvement of heparan sulfate proteoglycan biosynthesis and PPAR pathway
  • 2022
  • In: The FEBS Journal. - : John Wiley & Sons. - 1742-464X .- 1742-4658. ; 289:1, s. 279-293
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: Kashin-Beck disease (KBD) is an endemic osteochondropathy. Due to a lack of suitable animal or cellular disease models, the research progress on KBD has been limited. Our goal was to establish the first disease-specific human induced pluripotent stem cells (hiPSCs) cellular disease model of KBD, and to explore its etiology and pathogenesis exploiting transcriptome sequencing.METHODS: HiPSCs were reprogrammed from dermal fibroblasts of two KBD and one healthy control donors via integration-free vectors. Subsequently, hiPSCs were differentiated into chondrocytes through three-week culture. Gene expression profiles in KBD, normal primary chondrocytes and hiPSC-derived chondrocytes were defined by RNA sequencing. A Venn diagram was constructed to show the number of shared differentially expressed genes (DEGs) between KBD and normal. Gene oncology and Kyoto Encyclopedia of Genes and Genomes annotations were performed, and six DEGs were further validated in other individuals by real-time quantitative reverse transcription PCR (RT-qPCR).RESULTS: KBD cellular disease models were successfully established by generation of hiPSC lines. Seventeen consistent and significant DEGs present in all compared groups (KBD and normal) were identified. RT-qPCR validation gave consistent results with the sequencing data. Glycosaminoglycan biosynthesis-heparan sulfate/heparin, PPAR signaling pathway and cell adhesion molecules (CAMs) pathways were identified to be significantly altered in KBD.CONCLUSION: Differentiated chondrocytes deriving from KBD-origin hiPSCs provide the first cellular disease model for etiological studies of KBD. This study also provides new sights into the pathogenesis and etiology of KBD and is likely to inform the development of targeted therapeutics for its treatment.
  •  
22.
  • Liu, Huan, et al. (author)
  • The potential of induced pluripotent stem cells as a tool to study skeletal dysplasias and cartilage-related pathologic conditions
  • 2017
  • In: Osteoarthritis and Cartilage. - : Elsevier. - 1063-4584 .- 1522-9653. ; 25:5, s. 616-624
  • Research review (peer-reviewed)abstract
    • The development of induced pluripotent stem cells (iPSCs) technology has opened up new horizons for development of new research tools especially for skeletal dysplasias, which often lack human disease models. Regenerative medicine and tissue engineering could be the next areas to benefit from refinement of iPSC methods to repair focal cartilage defects, while applications for osteoarthritis (OA) and drug screening have evolved rather slowly. Although the advances in iPSC research of skeletal dysplasias and repair of focal cartilage lesions are not directly relevant to OA, they can be considered to pave the way to future prospects and solutions to OA research, too. The same problems which face the present cell-based treatments of cartilage injuries concern also the iPSC-based ones. However, established iPSC lines, which have no genomic aberrations and which efficiently differentiate into extracellular matrix secreting chondrocytes, could be an invaluable cell source for cell transplantations in the future. The safety issues concerning the recipient risks of teratoma formation and immune response still have to be solved before the potential use of iPSCs in cartilage repair of focal cartilage defects and OA.
  •  
23.
  • Liu, Li, et al. (author)
  • Involvement of yes-associated protein 1 activation in the matrix degradation of human-induced-pluripotent-stem-cell-derived chondrocytes induced by T-2 toxin and deoxynivalenol alone and in combination
  • 2024
  • In: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 25:2
  • Journal article (peer-reviewed)abstract
    • T-2 toxin and deoxynivalenol (DON) are two prevalent mycotoxins that cause cartilage damage in Kashin-Beck disease (KBD). Cartilage extracellular matrix (ECM) degradation in chondrocytes is a significant pathological feature of KBD. It has been shown that the Hippo pathway is involved in cartilage ECM degradation. This study aimed to examine the effect of YAP, a major regulator of the Hippo pathway, on the ECM degradation in the hiPS-derived chondrocytes (hiPS-Ch) model of KBD. The hiPS-Ch injury models were established via treatment with T-2 toxin/DON alone or in combination. We found that T-2 toxin and DON inhibited the proliferation of hiPS-Ch in a dose-dependent manner; significantly increased the levels of YAP, SOX9, and MMP13; and decreased the levels of COL2A1 and ACAN (all p values < 0.05). Immunofluorescence revealed that YAP was primarily located in the nuclei of hiPS-Ch, and its expression level increased with toxin concentrations. The inhibition of YAP resulted in the dysregulated expression of chondrogenic markers (all p values < 0.05). These findings suggest that T-2 toxin and DON may inhibit the proliferation of, and induce the ECM degradation, of hiPS-Ch mediated by YAP, providing further insight into the cellular and molecular mechanisms contributing to cartilage damage caused by toxins.
  •  
24.
  • Loeb, Norman G., et al. (author)
  • New Generation of Climate Models Track Recent Unprecedented Changes in Earth's Radiation Budget Observed by CERES
  • 2020
  • In: Geophysical Research Letters. - 0094-8276 .- 1944-8007. ; 47:5
  • Journal article (peer-reviewed)abstract
    • We compare top-of-atmosphere (TOA) radiative fluxes observed by the Clouds and the Earth's Radiant Energy System (CERES) and simulated by seven general circulation models forced with observed sea-surface temperature (SST) and sea-ice boundary conditions. In response to increased SSTs along the equator and over the eastern Pacific (EP) following the so-called global warming hiatus of the early 21st century, simulated TOA flux changes are remarkably similar to CERES. Both show outgoing shortwave and longwave TOA flux changes that largely cancel over the west and central tropical Pacific, and large reductions in shortwave flux for EP low-cloud regions. A model's ability to represent changes in the relationship between global mean net TOA flux and surface temperature depends upon how well it represents shortwave flux changes in low-cloud regions, with most showing too little sensitivity to EP SST changes, suggesting a pattern effect that may be too weak compared to observations.
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25.
  • Lyu, Yizhen, et al. (author)
  • Identification of proteins and N-glycosylation sites of knee cartilage in Kashin-Beck Disease compared with osteoarthritis
  • 2022
  • In: International Journal of Biological Macromolecules. - : Elsevier. - 0141-8130 .- 1879-0003. ; 210, s. 128-138
  • Journal article (peer-reviewed)abstract
    • The aim of this study was to identify crucial proteins and N-glycosylated sites in the pathological mechanism of Kashin-Beck Disease (KBD) compared with osteoarthritis (OA). Nine KBD knee subjects and nine OA knee subjects were selected for the study. Quantitative proteomics and N-glycoproteomics data of KBD and OA were obtained by protein and N-glycoprotein enrichment and LC-MS/MS analysis. Differentially expressed proteins or N-glycosylation sites were examined with a comparative analysis between KBD and OA. Total 2205 proteins were identified in proteomic analysis, of which 375 were significantly different. Among these, 121 proteins were up-regulated and 254 were down-regulated. In N-glycoproteomic analysis, 278 different N-glycosylated sites that were related to 187 N-glycoproteins were identified. Proteins and their N-glycosylated sites are associated with KBD pathological process including ITGB1, LRP1, ANO6, COL1A1, MXRA5, DPP4, and CSPG4. CRLF1 and GLG1 are proposed to associate with both KBD and OA pathological processes. Key pathways in KBD vs. OA proteomic and N-glycoproteomic analysis contained extracellular matrix receptor interaction, focal adhesion, phagosome, protein digestion, and absorption. N-glycosylation may influence the pathological process by affecting the integrity of chondrocytes or cartilage. It regulated the intercellular signal transduction pathway, which contributes to cartilage destruction in KBD.
  •  
26.
  • Nan, Jun-hu, et al. (author)
  • Air-core characteristics in a swirling tunnel flow
  • 2022
  • In: Journal of Hydrodynamics. - : Springer Nature. - 1001-6058 .- 1000-4874 .- 1878-0342. ; 34:4, s. 634-646
  • Journal article (peer-reviewed)abstract
    • A cost-effective technique to dissipate the energy in hydropower systems is the formation of a swirling flow within a tunnel. In such flows, an air core with a significant cross section usually occurs. To reveal the air-core features in the horizontal tunnel of a high-head shaft spillway, laboratory tests, numerical modeling, and prototype observations are performed, to examine issues such as the formation of the air core, the interjacent air motion, the air-carrying capacity, and the scale effects. It is shown that the shape of the air core varies greatly in the axial and radial directions along the tunnel and that the center of the core deviates from the axis of the tunnel. The motion of the air within the core is caused by the combined action of the water entrainment on the inner surface of the swirling flow and the axial pressure difference in the air core. The aeration process can be divided into five processes with respect to the changes of the gate openings. A theoretical expression is established for the air-carrying capacity of the swirling flow. The vacuum degree is the similarity condition of the air-carrying capacity of the swirling flow between the model and prototype tests based on the Froude law of the similitude, and this similarity condition is verified by both the model and prototype results. This work provides a reference for the application of the swirling flows in horizontal hydropower tunnels.
  •  
27.
  • Petrache, C. M., et al. (author)
  • Highly deformed bands in Nd nuclei : New results and consistent interpretation within the cranked Nilsson-Strutinsky formalism
  • 2019
  • In: Physical Review C. - : American Physical Society (APS). - 2469-9985 .- 2469-9993. ; 100:5
  • Journal article (peer-reviewed)abstract
    • Three new highly-deformed (HD) bands are identified in Nd136 and the highly deformed band of Nd137 is extended at higher spin by four transitions, revealing a band crossing associated with the occupation of the second νi13/2 intruder orbital. Extended cranked Nilsson-Strutinsky calculations are performed for all HD bands observed in Nd134, Nd136, and Nd137, achieving for the first time a consistent interpretation of all HD bands in the Nd nuclei. The new interpretation has significant consequences, like the change of parity of the yrast HD bands of Nd134 and Nd136, and the involvement of two negative-parity neutron intruder orbitals in the configurations of most HD bands. The present experimental results and their theoretical interpretation represent an important step forward in the understanding of the second-minimum excitations in the Nd nuclei.
  •  
28.
  • Petrache, C. M., et al. (author)
  • Multiple chiral bands in 137 Nd
  • 2020
  • In: European Physical Journal A. - : Springer Nature. - 1434-6001 .- 1434-601X. ; 56:8
  • Journal article (peer-reviewed)abstract
    • Two new bands have been identified in 137Nd from a high-statistics JUROGAM II gamma-ray spectroscopy experiment. Constrained density functional theory and particle rotor model calculations are used to assign configurations and investigate the band properties, which are well described and understood. It is demonstrated that these two new bands can be interpreted as chiral partners of previously known three-quasiparticle positive- and negative-parity bands. The newly observed chiral doublet bands in 137Nd represent an important support to the existence of multiple chiral bands in nuclei. The present results constitute the missing stone in the series of Nd nuclei showing multiple chiral bands, which becomes the most extended sequence of odd–even and even-even nuclei presenting multiple chiral bands in the Segré chart.
  •  
29.
  • Petrache, C. M., et al. (author)
  • Signatures of enhanced octupole correlations at high spin in Nd 136
  • 2020
  • In: Physical Review C. - : American Physical Society (APS). - 2469-9985 .- 2469-9993. ; 102:1
  • Journal article (peer-reviewed)abstract
    • Experimental signatures of moderately enhanced octupole correlations at high spin in Nd136 are indicated for the first time. The extracted dipole moments of two negative-parity bands are only two times smaller than those of the lanthanide nuclei with N≈90 which present well-established octupole correlations. Calculations using the cranked quasiparticle random phase approximation and a model of quadrupole-octupole rotations with octupole vibrations reveal the structure of the bands and the enhanced octupole correlations at high spin in Nd136.
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30.
  • Praud, Delphine, et al. (author)
  • Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project.
  • 2018
  • In: European Journal of Cancer Prevention. - 0959-8278 .- 1473-5709. ; 27:2, s. 124-133
  • Journal article (peer-reviewed)abstract
    • Tobacco smoking is a known cause of gastric cancer, but several aspects of the association remain imprecisely quantified. We examined the relation between cigarette smoking and the risk of gastric cancer using a uniquely large dataset of 23 epidemiological studies within the 'Stomach cancer Pooling (StoP) Project', including 10 290 cases and 26 145 controls. We estimated summary odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) by pooling study-specific ORs using random-effects models. Compared with never smokers, the ORs were 1.20 (95% CI: 1.09-1.32) for ever, 1.12 (95% CI: 0.99-1.27) for former, and 1.25 (95% CI: 1.11-1.40) for current cigarette smokers. Among current smokers, the risk increased with number of cigarettes per day to reach an OR of 1.32 (95% CI: 1.10-1.58) for smokers of more than 20 cigarettes per day. The risk increased with duration of smoking, to reach an OR of 1.33 (95% CI: 1.14-1.54) for more than 40 years of smoking and decreased with increasing time since stopping cigarette smoking (P for trend<0.01) and became similar to that of never smokers 10 years after stopping. Risks were somewhat higher for cardia than noncardia gastric cancer. Risks were similar when considering only studies with information on Helicobacter pylori infection and comparing all cases to H. pylori+ controls only. This study provides the most precise estimate of the detrimental effect of cigarette smoking on the risk of gastric cancer on the basis of individual data, including the relationship with dose and duration, and the decrease in risk following stopping smoking.
  •  
31.
  • Rota, Matteo, et al. (author)
  • Alcohol consumption and gastric cancer risk-A pooled analysis within the StoP project consortium.
  • 2017
  • In: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 141:10, s. 1950-1962
  • Journal article (peer-reviewed)abstract
    • An association between heavy alcohol drinking and gastric cancer risk has been recently reported, but the issue is still open to discussion and quantification. We investigated the role of alcohol drinking on gastric cancer risk in the "Stomach cancer Pooling (StoP) Project," a consortium of epidemiological studies. A total of 9,669 cases and 25,336 controls from 20 studies from Europe, Asia and North America were included. We estimated summary odds-ratios (ORs) and the corresponding 95% confidence intervals (CIs) by pooling study-specific ORs using random-effects meta-regression models. Compared with abstainers, drinkers of up to 4 drinks/day of alcohol had no increase in gastric cancer risk, while the ORs were 1.26 (95% CI, 1.08-1.48) for heavy (>4 to 6 drinks/day) and 1.48 (95% CI 1.29-1.70) for very heavy (>6 drinks/day) drinkers. The risk for drinkers of >4 drinks/day was higher in never smokers (OR 1.87, 95% CI 1.35-2.58) as compared with current smokers (OR 1.14, 95% CI 0.93-1.40). Somewhat stronger associations emerged with heavy drinking in cardia (OR 1.61, 95% CI 1.11-2.34) than in non-cardia (OR 1.28, 95% CI 1.13-1.45) gastric cancers, and in intestinal-type (OR 1.54, 95% CI 1.20-1.97) than in diffuse-type (OR 1.29, 95% CI 1.05-1.58) cancers. The association was similar in strata of H. pylori infected (OR = 1.52, 95% CI 1.16-2.00) and noninfected subjects (OR = 1.69, 95% CI 0.95-3.01). Our collaborative pooled-analysis provides definite, more precise quantitative evidence than previously available of an association between heavy alcohol drinking and gastric cancer risk.
  •  
32.
  • Sampson, Joshua N., et al. (author)
  • Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
  • 2015
  • In: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 107:12
  • Journal article (peer-reviewed)abstract
    • Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
  •  
33.
  • Shao, Jun, et al. (author)
  • Photoluminescence probing of interface evolution with annealing in InGa(N)As/GaAs single quantum wells
  • 2015
  • In: Journal of Applied Physics. - : AIP Publishing. - 0021-8979 .- 1089-7550. ; 118:16, s. 165305-
  • Journal article (peer-reviewed)abstract
    • The effects of thermal annealing on the interfaces of InGa(N)As/GaAs single quantum wells(SQWs) are investigated by excitation-, temperature-, and magnetic field-dependent photoluminescence(PL). The annealing at 750 °C results in more significant blueshift and narrowing to the PLpeak than that at 600 °C. Each of the PL spectra can be reproduced with two PL components: (i)the low-energy component (LE) keeps energetically unchanged, while the high-energy component(HE) moves up with excitation and shows at higher energy for the In0.375Ga0.625As/GaAs butcrosses over with the LE at a medium excitation power for the In0.375Ga0.625N0.012As0.988/GaAsSQWs. The HE is broader than the corresponding LE, the annealing at 750 °C narrows the LE andHE and shrinks their energetic separation; (ii) the PL components are excitonic, and the InGaNAsshows slightly enhanced excitonic effects relative to the InGaAs SQW; (iii) no typical S-shape evolutionof PL energy with temperature is detectable, and similar blueshift and narrowing are identifiedfor the same annealing. The phenomena are mainly from the interfacial processes. Annealingimproves the intralayer quality, enhances the interfacial In-Ga interdiffusion, and reduces the interfacialfluctuation. The interfacial interdiffusion does not change obviously by the small N contentand hence similar PL-component narrowing and blueshift are observed for the SQWs after a nominallyidentical annealing. Comparison with previous studies is made and the PL measurementsunder different conditions are shown to be effective for probing the interfacial evolution in QWs.
  •  
34.
  • Wang, Sen, et al. (author)
  • Roles of glycoprotein glycosylation in the pathogenesis of an endemic osteoarthritis, Kashin–Beck disease, and effectiveness evaluation of sodium hyaluronate treatment
  • 2020
  • In: Turkish Journal of Medical Sciences. - : TÜBİTAK (the Scientific and Technological Research Council of Turkey). - 1300-0144 .- 1303-6165. ; 50:4, s. 1028-1037
  • Journal article (peer-reviewed)abstract
    • Background/aim: We aimed to explore the roles of glycoprotein glycosylation in the pathogenesis of Kashin–Beck disease (KBD), and evaluated the effectiveness of sodium hyaluronate treatment.Materials and methods: Blood and saliva were collected from KBD patients before and after the injection of sodium hyaluronate. Normal healthy subjects were included as controls. Saliva and serum lectin microarrays and saliva and serum microarray verifications were used to screen and confirm the differences in lectin levels among the three groups.Results: In saliva lectin microarray, bindings to Sophora japonica agglutinin (SJA), Griffonia (Bandeiraea) simplicifolia lectin I (GSL-I), Euonymus europaeus lectin (EEL), Maackia amurensis lectin II (MAL-II), Sambucus nigra lectin (SNA), Hippeastrum hybrid lectin (HHL), and Aleuria aurantia lectin (AAL) were higher in the untreated KBD patients than in the control group. Increased levels of HHL, MAL-II, and GSL-I in the untreated KBD patients discriminated them in particular from the treated ones. Jacalin was lower in the untreated KBD patients compared to the treated KBD and control groups. In serum lectin microarray, HHL and peanut agglutinin (PNA) were increased in the untreated KBD group in comparison to the control one. AAL, Phaseolus vulgaris agglutinin (E+L) (PHA- E+L), and Psophocarpus tetragonolobus lectin I (PTL-I) were lower in the untreated KBD patients compared to the treated KBD and control groups. Hyaluronate treatment appeared to normalize SNA, AAL, and MAL-II levels in saliva, and HHL, PNA, AAL, PTL-I, and PHA-E+L levels in serum. Saliva reversed microarray verification confirmed significant differences between the groups in SNA and Jacalin, in particular for GSL-I levels, while serum reversed microarray verification indicated that HHL, PNA, and AAL levels returned to normal levels after the hyaluronate treatment. Lectin blot confirmed significant differences in HHL, AAL, and Jacalin in saliva, and HHL, PNA, PHA-E+L, and AAL in serum.Conclusion: HHL in saliva and serum may be a valuable diagnostic biomarker of KBD, and it may be used as follow-up for the hyaluronate treatment.
  •  
35.
  • Wang, Sen, et al. (author)
  • The importance of Se-related genes in the chondrocyte of Kashin-Beck disease revealed by whole genomic microarray and network analysis
  • 2019
  • In: Biological Trace Element Research. - : Springer. - 0163-4984 .- 1559-0720. ; 187:2, s. 367-375
  • Journal article (peer-reviewed)abstract
    • Kashin-Beck disease (KBD) is an endemic, chronic, and degenerative osteoarthropathy. Selenium (Se) deficiency plays important role in the pathogenesis of KBD. We aimed to screen Se-related gene from chondrocytes of patients with KBD. Whole-genome oligonucleotide microarrays were used to detect differentially expressed genes. qRT-PCR was used to confirm the microarray results. Comparative Toxicogenomics Database (CTD) was used to screen Se-related genes from differentially expressed genes. Gene Ontology (GO) classifications and network analysis of Se-related genes were constituted by STRING online system. Three hundred ninety-nine differentially expressed genes were obtained from microarray. Among them, 54 Se-related genes were identified by CTD. The qRT-PCR validation showed that four genes expressed similarly with the ones in the microarray transcriptional profiles. The Se-related genes were categorized into 6 cellular components, 8 molecular functions, 44 biological processes, 10 pathways, and 1 network by STRING. The Se-related gene insulin-like growth factor binding protein 2 (IGFBP2), insulin-like growth factor binding protein 3 (IGFBP3), interleukin 6 (IL6), BCL2, apoptosis regulator (BCL2), and BCL2-associated X, apoptosis regulator (BAX), which involved in many molecular functions, biological processes, and apoptosis pathway may play important roles in the pathogenesis of KBD.
  •  
36.
  • Wu, Cuiyan, et al. (author)
  • Long noncoding RNA expression profile reveals lncRNAs signature associated with extracellular matrix degradation in kashin-beck disease
  • 2017
  • In: Scientific Reports. - : Nature Publishing Group. - 2045-2322. ; 7
  • Journal article (peer-reviewed)abstract
    • Kashin-Beck disease (KBD) is a deformative, endemic osteochondropathy involving degeneration and necrosis of growth plates and articular cartilage. The pathogenesis of KBD is related to gene expression and regulation mechanisms, but long noncoding RNAs (lncRNAs) in KBD have not been investigated. In this study, we identified 316 up-regulated and 631 down-regulated lncRNAs (≥ 2-fold change) in KBD chondrocytes using microarray analysis, of which more than three-quarters were intergenic lncRNAs and antisense lncRNAs. We also identified 232 up-regulated and 427 down-regulated mRNAs (≥ 2-fold change). A lncRNA-mRNA correlation analysis combined 343 lncRNAs and 292 mRNAs to form 509 coding-noncoding gene co-expression networks (CNC networks). Eleven lncRNAs were predicted to have cis-regulated target genes, including NAV2 (neuron navigator 2), TOX (thymocyte selection-associated high mobility group box), LAMA4 (laminin, alpha 4), and DEPTOR (DEP domain containing mTOR-interacting protein). The differentially expressed mRNAs in KBD significantly contribute to biological events associated with the extracellular matrix. Meanwhile, 34 mRNAs and 55 co-expressed lncRNAs constituted a network that influences the extracellular matrix. In the network, FBLN1 and LAMA 4 were the core genes with the highest significance. These novel findings indicate that lncRNAs may play a role in extracellular matrix destruction in KBD.
  •  
37.
  • Xiao, Xiang, et al. (author)
  • Chondroitin Sulfate and Hyaluronic Acid Perfusion for Interstitial Cystitis/Bladder Pain Syndrome : A Systematic Review and Meta-Analysis
  • 2021
  • In: Science Insights. - : Insights Publisher. - 2372-8191 .- 2329-5856. ; 39:4, s. 361-373
  • Research review (peer-reviewed)abstract
    • Currently, no suitable delivery methods are available for the drugs to interstitial cystitis/ bladder pain syndrome (IC/BPS). Herein we systematically evaluated the therapeutic effects of intravesical infusion of hyaluronic acid (HA) and chondroitin sulfate (CS) in patients with IC/BPS. This study includes randomized controlled trials (RCT) and self-controlled studies of IC/BPS patients treated with HA, CS, or both. English databases like PubMed, Cochrane Library, Embase, and Medline were searched until up to January 31, 2021. Information was extracted based on the inclusion and exclusion criteria, and then meta-analysis was performed. Sixteen studies including 491 patients were included and analyzed. The responsive rate of treatment was 91.24%. In 3 RCTs, the analogue scale (VAS) for pain on fix-effect model was [mean difference, MD -0.57 (95%CI, -1.55, -0.41)]. A significant improvement on random-effect model was [MD -2.78 (95%CI, -3.48, -2.07)] in 13 self-controlled studies. Outcomes on O’Leary-Sant Interstitial Cystitis Symptom Index, Problem Index, frequency, urgency, and bladder capacity were also significantly improved. Subgroup analysis showed significant difference between HA, CS, and the combination, and the perfusion of HA was more effective (Z = 29.97, P < 0.01). Also, different follow-up times after last treatment showed significant difference (Z = 7.69, P < 0.01). It can be beneficial for IC/BPS patients who have not responded to conventional treatments.
  •  
38.
  • Xu, Huan, et al. (author)
  • Nanostructured Phase Morphology of a Biobased Copolymer for Tough and UV-Resistant Polylactide
  • 2021
  • In: ACS Applied Polymer Materials. - : American Chemical Society (ACS). - 2637-6105. ; 3:4, s. 1973-1982
  • Journal article (peer-reviewed)abstract
    • Despite technological feasibility and industrial scalability in toughening polylactide (PLA) by direct blending, avoiding the sacrifice of mechanical strength or full renewability remains a challenge. Here, low-molecular-weight poly(ethylene 2,5-furandicarboxylate)-block-polylactide (PEF-b-PLA) was synthesized to yield a fully biobased copolymer with expected partial miscibility with PLA. The ability of PEF-b-PLA to toughen PLA at 10 wt % (PLA10) and 20 wt % (PLA20) loadings was then evaluated. To understand the achieved properties, the formation of a nanostructured dispersion phase due to favorable interfacial adhesion arising from the miscibility of the PLA block with the PLA matrix was investigated. The morphological features, together with comparable strength inherited from the PEF blocks, afforded an unusual combination of toughness and strength for the PLA blends. Compared to the poor tensile toughness of a pure PLA film (1.77 MJ/m(3)), a striking increase of 839 and 912% was achieved for PLA10 and PLA20, respectively. More importantly, both pure PLA and the blends were characterized by comparable yield strength (similar to 30 MPa). This was accompanied by excellent UV-shielding imparted by the functional groups on the PEF blocks, which would improve the prospects of realizing PLA-based functional packing materials. The proposed design of copolymers, with good industrial feasibility, should be useful to guide the toughening approaches for PLA and probably other degradable polyester blends by profound morphology control.
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39.
  • Yang, Lei, et al. (author)
  • Field synopsis and meta-analyses of genetic epidemiological evidence for Kashin-Beck disease, an endemic osteoarthropathy in China
  • 2016
  • In: Molecular Genetics and Genomics. - : Springer Berlin/Heidelberg. - 1617-4615 .- 1617-4623. ; 291:5, s. 1823-1833
  • Journal article (peer-reviewed)abstract
    • Kashin-Beck disease (KBD) is a chronic degenerative osteoarthropathy with unclear etiology. To provide current evidence supporting a genetic predisposition for KBD, we conducted a systematic review and meta-analysis of published literature on the genetic epidemiology of KBD. The PubMed, China National Knowledge Infrastructure and Wan Fang Data were searched up to August 2015 for articles published in English and Chinese. Genome-wide and exome sequencing, linkage, and case-control association studies for any genetic variants associated with KBD were included. Meta-analysis was performed for all single nucleotide polymorphisms (SNPs) that were evaluated in two or more studies. The effect size was summarized as odds ratios (ORs) with 95 % confidence intervals (CIs) by fixed and random effects models. A total of 24 articles were systematically reviewed. Eleven short tandem repeats on chromosomes 2, 11 and 12, 34 SNPs in 12 genes, as well as copy number variant 452 were identified as KBD susceptibility factors in individual studies. The meta-analysis of the GPX1 rs1050450, DIO2 rs225014, TrxR2 rs5748469 and HLA-DRB1 rs7745040 failed to reveal any associations with KBD. However, the meta-analysis of HLA-DRB1 rs9275295 allele A was associated with KBD (OR = 1.737, 95 % CI: 1.002-3.012). In addition, seven haplotypes in GPX1, GPX4, HLA-DRB1 and GDF5 genes also showed significant associations with KBD. In conclusions, our study could identify a number of genetic markers associated with KBD. However, the evidence does not currently support a strong association between the specific variants and KBD because of the limited number of studies, and in the future, more rigorous studies are needed to confirm KBD's links with these variants.
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40.
  • Yang, Lei, et al. (author)
  • The potential biochemical markers of Kashin-Beck disease : a meta-analysis
  • 2016
  • In: Biomarkers. - : Taylor & Francis. - 1354-750X .- 1366-5804. ; 21:7, s. 633-638
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: The objective of this study is to explore the cytokines in serum, synovial fluid as potential biomarkers of Kashin-Beck disease (KBD) and to further understand the role of these cytokines in the pathogenesis of KBD.METHODS: A systematic electronic database search was performed from inception up to 15 March 2015. Meta-analysis was performed for cytokines more than one repetition in studies with available data. The effect size was summarized as standardized mean difference (SMD) with 95% confidence intervals (CIs) by a random effect model.RESULTS: A total of 18 articles were included. The pooled standardized mean differences showed the serum levels of tumor necrosis factor alpha (2.72, 95% CI: 1.8 5-3.59), interleukin-1 beta (1.21, 95% CI: 0.6 1-1.80), and nitric oxide (2.60, 95% CI: 1.5 2-3.68) were significantly higher in adult KBD patients compared with that in healthy controls.CONCLUSIONS: There was explicit evidence showing that the tumor necrosis factor alpha, interleukin-1 beta and nitric oxide were closely related to the presence of KBD, and these cytokines played a vital role in the pathogenesis of KBD.
  •  
41.
  • Yang, Shangchen, et al. (author)
  • Genomic investigation of the Chinese alligator reveals wild-extinct genetic diversity and genomic consequences of their continuous decline
  • 2023
  • In: Molecular Ecology Resources. - : Wiley. - 1755-098X .- 1755-0998. ; 23:1, s. 294-311
  • Journal article (peer-reviewed)abstract
    • Critically endangered species are usually restricted to small and isolated populations. High inbreeding without gene flow among populations further aggravates their threatened condition and reduces the likelihood of their long-term survival. Chinese alligator (Alligator sinensis) is one of the most endangered crocodiles in the world and has experienced a continuous decline over the past c. 1 million years. In order to identify the genetic status of the remaining populations and aid conservation efforts, we assembled the first high-quality chromosome-level genome of Chinese alligator and explored the genomic characteristics of three extant breeding populations. Our analyses revealed the existence of at least three genetically distinct populations, comprising two breeding populations in China (Changxing and Xuancheng) and one breeding population in an American wildlife refuge. The American population does not belong to the last two populations of its native range (Xuancheng and Changxing), thus representing genetic diversity extinct in the wild and provides future opportunities for genetic rescue. Moreover, the effective population size of these three populations has been continuously declining over the past 20 ka. Consistent with this decline, the species shows extremely low genetic diversity, a large proportion of long runs of homozygous fragments, and mutational load across the genome. Finally, to provide genomic insights for future breeding management and conservation, we assessed the feasibility of mixing extant populations based on the likelihood of introducing new deleterious alleles and signatures of local adaptation. Overall, this study provides a valuable genomic resource and important genomic insights into the ecology, evolution, and conservation of critically endangered alligators. 
  •  
42.
  • Yao, Zhen, et al. (author)
  • A highly efficient transcriptome-based biosynthesis of non-ethanol chemicals in Crabtree negative Saccharomyces cerevisiae
  • 2023
  • In: Biotechnology for Biofuels and Bioproducts. - : Springer Science and Business Media LLC. - 2731-3654. ; 16:1
  • Journal article (peer-reviewed)abstract
    • Background: Owing to the Crabtree effect, Saccharomyces cerevisiae produces a large amount of ethanol in the presence of oxygen and excess glucose, leading to a loss of carbon for the biosynthesis of non-ethanol chemicals. In the present study, the potential of a newly constructed Crabtree negative S. cerevisiae, as a chassis cell, was explored for the biosynthesis of various non-ethanol compounds. Results: To understand the metabolic characteristics of Crabtree negative S. cerevisiae sZJD-28, its transcriptional profile was compared with that of Crabtree positive S. cerevisiae CEN.PK113-11C. The reporter GO term analysis showed that, in sZJD-28, genes associated with translational processes were down-regulated, while those related to carbon metabolism were significantly up-regulated. To verify a potential increase in carbon metabolism for the Crabtree negative strain, the production of non-ethanol chemicals, derived from different metabolic nodes, was then undertaken for both sZJD-28 and CEN.PK113-11C. At the pyruvate node, production of 2,3-butanediol and lactate in sZJD-28-based strains was remarkably higher than that of CEN.PK113-11C-based ones, representing 16.8- and 1.65-fold increase in titer, as well as 4.5-fold and 0.65-fold increase in specific titer (mg/L/OD), respectively. Similarly, for shikimate derived p-coumaric acid, the titer of sZJD-28-based strain was 0.68-fold higher than for CEN.PK113-11C-based one, with a 0.98-fold increase in specific titer. While farnesene and lycopene, two acetoacetyl-CoA derivatives, showed 0.21- and 1.88-fold increases in titer, respectively. From malonyl-CoA, the titer of 3-hydroxypropionate and fatty acids in sZJD-28-based strains were 0.19- and 0.76-fold higher than that of CEN.PK113-11C-based ones, respectively. In fact, yields of products also improved by the same fold due to the absence of residual glucose. Fed-batch fermentation further showed that the titer of free fatty acids in sZJD-28-based strain 28-FFA-E reached 6295.6 mg/L with a highest reported specific titer of 247.7 mg/L/OD in S. cerevisiae. Conclusions: Compared with CEN.PK113-11C, the Crabtree negative sZJD-28 strain displayed a significantly different transcriptional profile and obvious advantages in the biosynthesis of non-ethanol chemicals due to redirected carbon and energy sources towards metabolite biosynthesis. The findings, therefore, suggest that a Crabtree negative S. cerevisiae strain could be a promising chassis cell for the biosynthesis of various chemicals.
  •  
43.
  • Yu, Fang Fang, et al. (author)
  • Comparison of T-2 Toxin and HT-2 Toxin Distributed in the Skeletal System with That in Other Tissues of Rats by Acute Toxicity Test
  • 2017
  • In: Biomedical and environmental sciences. - 0895-3988 .- 2214-0190. ; 30:11, s. 851-854
  • Journal article (peer-reviewed)abstract
    • Twelve healthy rats were divided into the T-2 toxin group receiving gavage of 1 mg/kg T-2 toxin and the control group receiving gavage of normal saline. Total relative concentrations of T-2 toxin and HT-2 toxin in the skeletal system (thighbone, knee joints, and costal cartilage) were significantly higher than those in the heart, liver, and kidneys (P < 0.05). The relative concentrations of T-2 toxin and HT-2 toxin in the skeletal system (thighbone and costal cartilage) were also significantly higher than those in the heart, liver, and kidneys. The rats administered T-2 toxin showed rapid metabolism compared with that in rats administered HT-2 toxin, and the metabolic conversion rates in the different tissues were 68.20%-90.70%.
  •  
44.
  • Yu, Fang-Fang, et al. (author)
  • Selenium promotes metabolic conversion of T-2 toxin to HT-2 toxin in cultured human chondrocytes
  • 2017
  • In: Journal of Trace Elements in Medicine and Biology. - : Elsevier. - 0946-672X .- 1878-3252. ; 44, s. 218-224
  • Journal article (peer-reviewed)abstract
    • To explore the metabolism of T-2 toxin in human chondrocytes (HCs) and determine the impact of selenium supplementation. For determination of cytotoxicity using the MTT assay, optical density values were read with an automatic enzyme-linked immunosorbent assay reader at 510nm. Cell survival was calculated and the cytotoxicity estimated. To identify the metabolites of T-2 toxin, the medium supernatants and C28/I2 cells were analyzed by high-performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS) separately. For HPLC-MS/MS, the mobile phase A was water and phase B was 98% methanol. The gradient for the elution was: 0-0.5min, 50% of B; 0.5-2.0min, 100% of B; 2.0-3.5min, 100% of B; 3.6-6min, 50% of B. T-2 toxin increased the toxicity to C28/I2 cells significantly in a dose- and time-dependent manner (viability range 91.5-22.0%). Supplementation with selenium (100ng/mL) could increase the cell viability after the 24h incubation. The concentration of T-2 toxin in the cell medium decreased from 20 to 6.67±1.02ng/mL, and the concentration of HT-2 toxin increased from 0 to 6.88±1.23ng/mL during the 48h incubation, whereas the relative concentration of T-2 toxin in cells increased from 0 to 12.80±1.84ng/g. Supplementary selenium in the HCs cultures reduced the cytotoxicity induced by T-2 toxin significantly, and was associated with rapid conversion of T-2 toxin in the culture medium to HT-2 toxin. T-2 toxin was more toxic to HCs than HT-2 toxin at equivalent concentrations. HT-2 toxin was a detectable metabolite of T-2 toxin in cultured HCs, and selenium enhanced the metabolic conversion of T-2 toxin, reducing its cytotoxicity to HCs.
  •  
45.
  • Zhang, Yanan, et al. (author)
  • Dysregulation of Cells Cycle and Apoptosis in Human Induced Pluripotent Stem Cells Chondrocytes Through p53 Pathway by HT-2 Toxin : An in vitro Study
  • 2021
  • In: Frontiers in Genetics. - : Frontiers Media S.A.. - 1664-8021. ; 12
  • Journal article (peer-reviewed)abstract
    • Kashin–Beck disease (KBD) mainly damages growth plate of adolescents and is susceptible to both gene and gene–environmental risk factors. HT-2 toxin, which is a primary metabolite of T-2 toxin, was regarded as one of the environmental risk factors of KBD. We used successfully generated KBD human induced pluripotent stem cells (hiPSCs) and control hiPSCs, which carry different genetic information. They have potential significance in exploring the effects of HT-2 toxin on hiPSC chondrocytes and interactive genes with HT-2 toxin for the purpose of providing a cellular disease model for KBD. In this study, we gave HT-2 toxin treatment to differentiating hiPSC chondrocytes in order to investigate the different responses of KBD hiPSC chondrocytes and control hiPSC chondrocytes to HT-2 toxin. The morphology of HT-2 toxin-treated hiPSC chondrocytes investigated by transmission electron microscope clearly showed that the ultrastructure of organelles was damaged and type II collagen expression in hiPSC chondrocytes was downregulated by HT-2 treatment. Moreover, dysregulation of cell cycle was observed; and p53, p21, and CKD6 gene expressions were dysregulated in hiPSC chondrocytes after T-2 toxin treatment. Flow cytometry also demonstrated that there were significantly increased amounts of late apoptotic cells in KBD hiPSC chondrocytes and that the mRNA expression level of Fas was upregulated. In addition, KBD hiPSC chondrocytes presented stronger responses to HT-2 toxin than control hiPSC chondrocytes. These findings confirmed that HT-2 is an environmental risk factor of KBD and that p53 pathway interacted with HT-2 toxin, causing damaged ultrastructure of organelles, accelerating cell cycle in G1 phase, and increasing late apoptosis in KBD hiPSC chondrocytes.
  •  
46.
  • Zhu, Huilin, et al. (author)
  • Reduced interhemispheric functional connectivity of children with autism spectrum disorder : evidence from functional near infrared spectroscopy studies
  • 2014
  • In: Biomedical Optics Express. - 2156-7085. ; 5:4, s. 1262-1274
  • Journal article (peer-reviewed)abstract
    • Autism spectrum disorder (ASD) is a neuro-developmental disorder, which has been associated with atypical neural synchronization. In this study, functional near infrared spectroscopy (fNIRS) was used to study the differences in functional connectivity in bilateral inferior frontal cortices (IFC) and bilateral temporal cortices (TC) between ASD and typically developing (TD) children between 8 and 11 years of age. As the first report of fNIRS study on the resting state functional connectivity (RSFC) in children with ASD, ten children with ASD and ten TD children were recruited in this study for 8 minute resting state measurement. Compared to TD children, children with ASD showed reduced interhemispheric connectivity in TC. Children with ASD also showed significantly lower local connectivity in bilateral temporal cortices. In contrast to TD children, children with ASD did not show typical patterns of symmetry in functional connectivity in temporal cortex. These results support the feasibility of using the fNIRS method to assess atypical functional connectivity of cortical responses of ASD and its potential application in diagnosis.
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