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  • 1
    Online Resource
    Online Resource
    A dual‐label time‐resolved fluorescence immunoassay for the simultaneous determination of carcinoembryonic antigen and squamous cell carcinoma antigen
    Wiley ; 2018
    In:  Biotechnology and Applied Biochemistry Vol. 65, No. 6 ( 2018-11), p. 816-821
    Details
    In: Biotechnology and Applied Biochemistry, Wiley, Vol. 65, No. 6 ( 2018-11), p. 816-821
    Abstract: Among women worldwide, cervical cancer is the second‐most common cancer, and cervical smears and DNA detection have low sensitivity or are too expensive. The concentrations of carcinoembryonic antigen (CEA) and squamous cell carcinoma (SCC) in the serum were detected using a sandwich immunoassay. The CEA and SCC in the serum were captured by anti‐CEA and anti‐SCC antibodies. After combining other anti‐CEA‐ and anti‐SCC‐labeled antibodies with europium (III) (Eu 3+ ) and samarium (III) (Sm 3+ ) chelates, CEA and SCC were detected with time‐resolved fluorometry (TRF). The linear correlation coefficients ( R 2 ) of the CEA and SCC standard curves were 0.9997 and 0.9997, respectively. The minimum detection level for CEA was 1.15 ng/mL (the linear dynamic range was 3.24–543.67 ng/mL), and the average recovery was 100.83%. The sensitivity for SCC detection was 0.54 ng/mL (the linear dynamic range was 2.47–96.58 ng/mL), and the average recovery was 101.02%. High R 2 between the results of commercial assays and this method were obtained ( R 2  = 0.9983 for CEA, R 2   = 0.9878 for SCC). These findings indicated that the dual‐label TRFIA invented in this study has high sensitivity, accuracy, and specificity in clinical analysis, which indicates that this method could be used for the early diagnosis and follow‐up surveillance of cervical cancer.
    Type of Medium: Online Resource
    ISSN: 0885-4513 , 1470-8744
    URL: Issue
    URL: Article
    DOI: 10.1002/bab.2018.65.issue-6
    DOI: 10.1002/bab.1663
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1496341-3
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  • 2
    Online Resource
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    Circular RNA microarray expression profile in 3,4‐benzopyrene/angiotensin II‐induced abdominal aortic aneurysm in mice
    Wiley ; 2019
    In:  Journal of Cellular Biochemistry Vol. 120, No. 6 ( 2019-06), p. 10484-10494
    Details
    In: Journal of Cellular Biochemistry, Wiley, Vol. 120, No. 6 ( 2019-06), p. 10484-10494
    Abstract: Abdominal aortic aneurysm (AAA) is an unpredictable but lethal disease that poses a therapeutic dilemma. Circular RNAs (circRNAs), whose functional roles as transcriptional regulators and microRNA (miRNA) sponges have been shown in former studies, are potential biomarkers for many diseases. AAA in male C57BL/6 J mice was induced by coadministration of angiotensin II (Ang II) and 3,4‐benzopyrene (BaP). The circRNA expression profiling was performed using two samples from the control group and two samples from the AAA group. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to confirm the reliability of the microarray results. Among the 14 236 detected circRNAs, 413 showed obvious expression changes (fold change ≥ 2; P   〈  0.05) between the BaP/Ang II‐induced AAA group and control group. Of the 413 that showed significant changes, 271 were upregulated, while the other 142 were downregulated. The expression levels of 10 circRNAs were validated by qRT‐PCR. The interactions of the differentially expressed circRNAs with miRNAs were predicted. Immunofluorescence showed prominent vascular smooth muscle cell apoptosis in abdominal aortic tissues in the BaP/Ang II group. Furthermore, a circRNA‐miRNA coexpression network based on six apoptosis‐related circRNAs was built. The genes regulated by the network mapped to several pathways, including apoptosis, the IL‐17 signaling pathway, and vascular endothelial growth factor signaling pathway, all of which are related to AAA formation. This study performed circRNA expression profiling in AAA and the results specifically predicted the regulatory role of circRNAs in AAA pathogenesis.
    Type of Medium: Online Resource
    ISSN: 0730-2312 , 1097-4644
    URL: Issue
    URL: Article
    DOI: 10.1002/jcb.v120.6
    DOI: 10.1002/jcb.28333
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1479976-5
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  • 3
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    The neutrophil-lymphocyte ratio: A promising predictor of mortality in coronary care unit patients — A cohort study
    Elsevier BV ; 2019
    In:  International Immunopharmacology Vol. 74 ( 2019-09), p. 105692-
    Details
    In: International Immunopharmacology, Elsevier BV, Vol. 74 ( 2019-09), p. 105692-
    Type of Medium: Online Resource
    ISSN: 1567-5769
    URL: Article
    DOI: 10.1016/j.intimp.2019.105692
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 2049924-3
    SSG: 15,3
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  • 4
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    Retracted : EphB3‐targeted regulation of miR‐149 in the migration and invasion of human colonic carcinoma HCT 116 and SW 620 cells
    Wiley ; 2017
    In:  Cancer Science Vol. 108, No. 3 ( 2017-03), p. 408-418
    Details
    In: Cancer Science, Wiley, Vol. 108, No. 3 ( 2017-03), p. 408-418
    Abstract: micro RNA s play key roles during various crucial cell processes such as proliferation, migration, invasion and apoptosis. Also, micro RNA s have been shown to possess oncogenic and tumor‐suppressive functions in human cancers. Here, we describe the regulation and function of miR‐149 in colorectal cancer cell lines. miR‐149 expression patterns were detected in human colorectal cell lines and tissue samples, and then focused on its role in regulation of cell growth, migration, invasion, and its target gene identification. Furthermore, the function of the target gene of miR‐149 was analyzed in vitro and in vivo . miR‐149 expression was downregulated in human colorectal cancer HCT 116 and SW 620 cell lines compared to the normal colon epithelial NCM 460 cell line using quantitative real‐time polymerase chain reaction methods. Further studies indicated that introduction of miR‐149 was able to suppress cell migration and invasion. Then, EphB3 was identified as a direct target gene of miR‐149 in colorectal cancer cells. Moreover, experiments in vitro showed that knockdown expression of EphB3 could suppress cell proliferation and invasion, and ectopic expression of EphB3 restored the phenotypes of CRC cell lines transfected with miR149. In addition, silencing of EphB3 significantly affected cycle progression distribution and increased apoptosis in CRC cell lines. Finally, in vivo results demonstrated that knockdown of EphB3 by si RNA inhibited tumor growth. In conclusion,the important role of miR‐149 in colorectal cancer progression suggesting that miR‐149 may serve as a therapeutic target for colorectal cancer treatment.
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Issue
    URL: Article
    DOI: 10.1111/cas.2017.108.issue-3
    DOI: 10.1111/cas.13161
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2115647-5
    detail.hit.zdb_id: 2111204-6
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  • 5
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    Yes‐associated protein regulates glutamate homeostasis through promoting the expression of excitatory amino acid transporter‐2 in astrocytes via β‐catenin signaling
    Wiley ; 2023
    In:  Glia Vol. 71, No. 5 ( 2023-05), p. 1197-1216
    Details
    In: Glia, Wiley, Vol. 71, No. 5 ( 2023-05), p. 1197-1216
    Abstract: The homeostasis of glutamate is mainly regulated by the excitatory amino acid transporters (EAATs), especially by EAAT2 in astrocytes. Excessive glutamate in the synaptic cleft caused by dysfunction or dysregulation of EAAT2 can lead to excitotoxicity, neuronal death and cognitive dysfunction. However, it remains unclear about the detailed regulation mechanism of expression and function of astrocytic EAAT2. In this study, first, we found increased neuronal death and impairment of cognitive function in YAP GFAP ‐CKO mice (conditionally knock out Yes‐associated protein [YAP] in astrocytes), and identified EAAT2 as a downstream target of YAP through RNA sequencing. Second, the expression of EAAT2 was decreased in cultured YAP −/− astrocytes and the hippocampus of YAP GFAP ‐CKO mice, and glutamate uptake was reduced in YAP −/− astrocytes, but increased in YAP‐upregulated astrocytes. Third, further investigation of the mechanism showed that the mRNA and protein levels of β‐catenin were decreased in YAP −/− astrocytes and increased in YAP‐upregulated astrocytes. Wnt3a activated YAP signaling and up‐regulated EAAT2 through β‐catenin. Furthermore, over‐expression or activation of β‐catenin partially restored the downregulation of EAAT2, the impairment of glutamate uptake, neuronal death and cognitive decline that caused by YAP deletion. Finally, activation of EAAT2 also rescued neuronal death and cognitive decline in YAP GFAP ‐CKO mice. Taken together, our study identifies an unrecognized role of YAP signaling in the regulation of glutamate homeostasis through the β‐catenin/EAAT2 pathway in astrocytes, which may provide novel insights into the pathogenesis of brain diseases that closely related to the dysfunction or dysregulation of EAAT2, and promote the development of clinical strategy.
    Type of Medium: Online Resource
    ISSN: 0894-1491 , 1098-1136
    URL: Issue
    URL: Article
    DOI: 10.1002/glia.v71.5
    DOI: 10.1002/glia.24332
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 1474828-9
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  • 6
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    Data_Sheet_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Psychiatry Vol. 13 ( 2022-9-29)
    Details
    In: Frontiers in Psychiatry, Frontiers Media SA, Vol. 13 ( 2022-9-29)
    Abstract: Previous studies suggest that alcohol dependence is associated with depression, however, the effect of alcohol dependence varies from individual to individual, which may be due to different genetic backgrounds. The interactions between alcohol dependence and different gene polymorphisms may finally shape the onset of depression. Neuropeptide Y (NPY), which can maintain homeostasis from high-stress stimulation, may protect individuals from the onset of depression. Here, we explored whether the NPY rs16147:T & gt; C has an association with depression in individuals with alcohol dependence during the period of alcohol dependence withdrawal. Methods A total of 455 males with alcohol dependence were recruited. The scale of Michigan Alcoholism Screening Test (MAST) and Self-Depression Scale (SDS) were respectively used to analyze the condition of alcohol dependence and depression. Genomic DNA was extracted from each blood sample and NPY polymorphisms were genotyped. The interaction between NPY rs16147:T & gt; C and alcohol dependence on depression was first analyzed. Then, region of significance analysis was used to confirm which model provided the best fit for the interaction (diathesis-stress or differential susceptibility). Finally, by using internal replication analyses, the accuracy and robustness of the interaction results were improved. Results Alcohol dependence was positively correlated with depression. CC homozygotes of NPY rs16147:T & gt; C exhibited less depression when exposed to low alcohol dependence, but more depression when exposed to high alcohol dependence. Individuals with the T allele showed the opposite result. Conclusion NPY rs16147:T & gt; C might be correlated with susceptibility for depression in males during alcohol dependence withdrawal. The findings support the differential susceptibility model.
    Type of Medium: Online Resource
    ISSN: 1664-0640
    URL: Article
    URL: Article
    DOI: 10.3389/fpsyt.2022.1012850
    DOI: 10.3389/fpsyt.2022.1012850.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2564218-2
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  • 7
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    The Interaction Between Genetic Variant ZNF804A rs1344706 and Alcohol Withdrawal on Impulsivity: Evidence for the Diathesis-Stress Model
    Frontiers Media SA ; 2022
    In:  Frontiers in Psychiatry Vol. 12 ( 2022-1-3)
    Details
    In: Frontiers in Psychiatry, Frontiers Media SA, Vol. 12 ( 2022-1-3)
    Abstract: Objective: Alcohol use disorder (AUD) is the most common substance use disorder, which may relate to increased impulsivity. A more detailed understanding of the potential moderating factor on association between AUD and impulsivity is likely to have far-reaching effects. This study aims to examine whether the interaction between a genetic variant ZNF804A rs1344706 and alcohol use is related to impulsivity in Chinese Han adult males diagnosed with AUD. Methods: A total of 455 Chinese Han adult males diagnosed with AUD were included in this study. Impulsivity was assessed using Barratt Impulsiveness Scale. Alcohol dependence was measured by Michigan Alcoholism Screening Test. Genomic DNA was extracted from peripheral blood of participants and genotyped. Results: Hierarchical multiple regression yielded a significant interaction between ZNF804A rs1344706 and alcohol use (β = 0.20, p = 0.0237). Then, A region of significance (RoS) test was performed to interpret the interaction effect. Re-parameterized regression models revealed that the interaction between ZNF804A rs1344706 and alcohol problem severity fit to the weak diathesis-stress model ( R 2 = 0.15, p & lt; 0.0010), indicating that the T allele carriers are more susceptible to alcohol problem severity, jointly contributing to impulsivity. Conclusions: This study, which analyzed a specific gene-environment interaction, demonstrated that carriers of the T allele of ZNF804A rs1344706 may be more susceptible to alcohol problem severity, correlated with higher levels of impulsivity during withdrawal.
    Type of Medium: Online Resource
    ISSN: 1664-0640
    URL: Article
    DOI: 10.3389/fpsyt.2021.761237
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2564218-2
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  • 8
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    Online Resource
    RNA sequencing revealing the role of AMP-activated protein kinase signaling in mice myocardial ischemia reperfusion injury
    Elsevier BV ; 2019
    In:  Gene Vol. 703 ( 2019-06), p. 91-101
    Details
    In: Gene, Elsevier BV, Vol. 703 ( 2019-06), p. 91-101
    Type of Medium: Online Resource
    ISSN: 0378-1119
    URL: Article
    DOI: 10.1016/j.gene.2019.04.010
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 1491012-3
    SSG: 12
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  • 9
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    SARM1 deletion in parvalbumin neurons is associated with autism-like behaviors in mice
    Springer Science and Business Media LLC ; 2022
    In:  Cell Death & Disease Vol. 13, No. 7 ( 2022-07-22)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 13, No. 7 ( 2022-07-22)
    Abstract: Autism spectrum disorder (ASD), a group of neurodevelopmental disorder diseases, is characterized by social deficits, communication difficulties, and repetitive behaviors. Sterile alpha and TIR motif-containing 1 protein (SARM1) is known as an autism-associated protein and is enriched in brain tissue. Moreover, SARM1 knockdown mice exhibit autism-like behaviors. However, its specific mechanism in ASD pathogenesis remains unclear. Here we generated parvalbumin-positive interneurons (PVI)-specific conditional SARM1 knockout (SARM1 PV -CKO) mice. SARM1 PV -CKO male mice showed autism-like behaviors, such as mild social interaction deficits and repetitive behaviors. Moreover, we found that the expression level of parvalbumin was reduced in SARM1 PV -CKO male mice, together with upregulated apoptosis-related proteins and more cleaved-caspase-3-positive PVIs, suggesting that knocking out SARM1 may cause a reduction in the number of PVIs due to apoptosis. Furthermore, the expression of c-fos was shown to increase in SARM1 PV -CKO male mice, in combination with upregulation of excitatory postsynaptic proteins such as PSD-95 or neuroligin-1, indicating enhanced excitatory synaptic input in mutant mice. This notion was further supported by the partial rescue of autism-like behavior deficits by the administration of GABA receptor agonists in SARM1 PV -CKO male mice. In conclusion, our findings suggest that SARM1 deficiency in PVIs may be involved in the pathogenesis of ASD.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-022-05083-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2541626-1
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  • 10
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    SARM1 promotes the neuroinflammation and demyelination through IGFBP2 / NF‐κB pathway in experimental autoimmune encephalomyelitis mice
    Wiley ; 2023
    In:  Acta Physiologica Vol. 238, No. 2 ( 2023-06)
    Details
    In: Acta Physiologica, Wiley, Vol. 238, No. 2 ( 2023-06)
    Abstract: Multiple sclerosis (MS) is an autoimmune disease, and its typical characteristics are neuroinflammation and the demyelination of neurons in the central nervous system (CNS). Sterile alpha and TIR motif containing 1 (SARM1) is an essential factor mediating axonal degeneration and SARM1 deletion reduces the neuroinflammation in spinal cord injury. This study aimed to explore the roles of SARM1 and its underlying mechanisms in MS. Methods Experimental autoimmune encephalomyelitis (EAE, a model of MS) model was established. Immunostaining, western blot, electron microscope, and HE staining were used to examine the pathological manifestations such as inflammation, demyelination, and neuronal death in SARM1 f/f EAE mice and SARM1 Nestin ‐CKO EAE mice. In addition, RNA‐seq, real‐time PCR and double‐immunostaining were used to examine the underlying mechanism of SARM1 in EAE mice. Results SARM1 was upregulated in neurons of the spinal cords of EAE mice. SARM1 knockout in CNS ameliorated EAE with less neuroinflammation, demyelination, and dead neurons. Mechanically, SARM1 knockout resulted in the reduction of insulin‐like growth factor (IGF)‐binding protein 2 (IGFBP2) in neurons of EAE mice, which might inhibit the neuroinflammation through inhibiting NF‐κB signaling. Finally, activation of NF‐κB partially aggravated the neuroinflammation and demyelination deficits of SARM1 Nestin ‐CKO EAE mice. Conclusions These results identified the unknown role of SARM1 in the promotion of neuroinflammation and demyelination and revealed a novel drug target pathway of SARM1/IGFBP2/NF‐κB for MS.
    Type of Medium: Online Resource
    ISSN: 1748-1708 , 1748-1716
    URL: Issue
    URL: Article
    DOI: 10.1111/apha.v238.2
    DOI: 10.1111/apha.13974
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2617148-X
    detail.hit.zdb_id: 2219379-0
    SSG: 12
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