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  • 1
    Online Resource
    Online Resource
    Design, synthesis and biological evaluation of novel 4-aminoquinazolines as dual target inhibitors of EGFR-PI3Kα
    Elsevier BV ; 2018
    In:  European Journal of Medicinal Chemistry Vol. 146 ( 2018-02), p. 460-470
    Details
    In: European Journal of Medicinal Chemistry, Elsevier BV, Vol. 146 ( 2018-02), p. 460-470
    Type of Medium: Online Resource
    ISSN: 0223-5234
    URL: Article
    DOI: 10.1016/j.ejmech.2018.01.081
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2005170-0
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Cytochrome P450 26A1 modulates natural killer cells in mouse early pregnancy
    Wiley ; 2017
    In:  Journal of Cellular and Molecular Medicine Vol. 21, No. 4 ( 2017-04), p. 697-710
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 21, No. 4 ( 2017-04), p. 697-710
    Abstract: Cytochrome P450 26A1 ( CYP 26A1) has a spatiotemporal expression pattern in the uterus, with a significant increase in mRNA and protein levels during peri‐implantation. Inhibiting the function or expression of CYP 26A1 can cause pregnancy failure, suggesting an important regulatory role of CYP 26A1 in the maintenance of pregnancy. However, little is known about the exact mechanism involved. In this study, using a pCR 3.1‐cyp26a1 plasmid immunization mouse model and a Cyp26a1‐ MO ( Cyp26a1 ‐specific antisense oligos) knockdown mouse model, we report that the number of Dolichos biflorus agglutinin ( DBA ) lectin‐positive uterine natural killer ( uNK ) cells was reduced in pCR 3.1‐cyp26a1 plasmid immunized and Cyp26a1‐ MO ‐treated mice. In contrast, the percentage of CD 3 − CD 49b + NK cells in the uteri from the treatment group was significantly higher than that of the control group in both models. Similarly, significantly up‐regulated expression of CD 49b (a pan‐ NK cell marker), interferon gamma, CCL 2, CCR 2 ( CCL 2 receptor) and CCL 3 were detected in the uteri of pCR 3.1‐cyp26a1‐ and Cyp26a1‐ MO ‐treated mice. Transcriptome analysis suggested that CYP 26A1 might regulate NK cells through chemokines. In conclusion, the present data suggest that silencing CYP 26A1 expression/function can decrease the number of uNK cells and significantly increase the percentage of CD 3 − CD 49b + NK cells in the uteri of pregnant mice. These findings provide a new line of evidence correlating the deleterious effects of blocking CYP 26A1 in pregnancy with the aberrant regulation of NK cells in the uterus.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2017.21.issue-4
    DOI: 10.1111/jcmm.13013
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2076114-4
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  • 3
    Online Resource
    Online Resource
    Spindle cell metaplastic carcinoma of breast: A clinicopathological and immunohistochemical analysis
    Wiley ; 2017
    In:  Asia-Pacific Journal of Clinical Oncology Vol. 13, No. 2 ( 2017-04)
    Details
    In: Asia-Pacific Journal of Clinical Oncology, Wiley, Vol. 13, No. 2 ( 2017-04)
    Abstract: To better characterize spindle cell metaplastic carcinoma ( SpCMC ) of breast, a rare variant of breast cancer that has been classified under the broad rubric of metaplastic carcinoma. Methods We presented herein 19 cases of metaplastic breast carcinoma with dominant spindle cell component. All cases were clinically of breast origin, showed more than 80% spindle morphology, 10 cases exhibited pure spindled morphology, 8 contained invasive ductal carcinoma ( IDC ) and 1 presented with ductal carcinoma in situ elements. Results Immunohistochemical studies showed evidence suggesting myoepithelial and epithelial differentiation as exhibited by immunoreactivity for at least one myoepithelial and epithelial markers in all pure spindle cell components. IDC group showed 21.7% of axillary lymph nodes metastasis rate, whereas the axillary lymph node metastasis rate of the SpCMC group was 1.3%, significantly lower than that of the IDC group ( P   〈  0.001). Immunohistochemical staining of IDC exhibited higher degrees of positivity for ER , PR and Her2 (90, 60 and 30%, respectively) when compared with the SpCMC group, which showed a positive degree of 5.2, 5.2 and 10.5% for ER , PR and Her2, respectively ( P   〈  0.001). Conclusion Based on this series, SpCMC is a rare variant of metaplastic breast carcinoma with the distinct histopathological and immunohistochemical features. The biological behaviors of SpCMC , like axillary lymph node status, were quite different from that of IDC , suggesting that it may act as an independent pathologic subtype. Immunohistochemical analysis of a panel of epithelial and myoepithelial markers could contribute to the pathologic diagnosis of SpCMC .
    Type of Medium: Online Resource
    ISSN: 1743-7555 , 1743-7563
    URL: Issue
    URL: Article
    DOI: 10.1111/ajco.2017.13.issue-2
    DOI: 10.1111/ajco.12322
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2187409-8
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  • 4
    Online Resource
    Online Resource
    Seminal plasma induces inflammation in the uterus through the γδ T/IL-17 pathway
    Springer Science and Business Media LLC ; 2016
    In:  Scientific Reports Vol. 6, No. 1 ( 2016-04-25)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 6, No. 1 ( 2016-04-25)
    Abstract: After insemination, a large number of leukocytes migrate into the uterus, which is accompanied by intense inflammation. However, the details of how seminal plasma interacts with the uterus are still not very clear. Here, we present that neutrophils migrate and accumulate around the uterine epithelium following insemination, which is accompanied by an increase in interleukin (IL) 17A levels. Additionally, we find that γδ T cells are the major source of IL-17A, and the seminal plasma could induce the γδ T cells to secret IL-17A. Blocking IL-17A could reduce the number of neutrophils in the uterus and prevent them from migrating to the epithelium by decreasing the chemokines CXCL1, CXCL2 and CXCL5. Blocking IL-17A did not affect the Th1/Th2 balance but actually diminished the inflammation in the uterus by reducing the expression of IL-1β and TNF-α. In summary, we found a new mechanism by which seminal plasma could influence the inflammation in the uterus through the γδ T/IL-17 pathway to regulate the expression of various chemokines and cytokines.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/srep25118
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2615211-3
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  • 5
    Online Resource
    Online Resource
    Clinical guideline on magnetically controlled capsule gastroscopy (2021 edition)
    Wiley ; 2023
    In:  Journal of Digestive Diseases Vol. 24, No. 2 ( 2023-02), p. 70-84
    Details
    In: Journal of Digestive Diseases, Wiley, Vol. 24, No. 2 ( 2023-02), p. 70-84
    Abstract: With the development and generalization of endoscopic technology and screening, clinical application of magnetically controlled capsule gastroscopy (MCCG) has been increasing. In recent years, various types of MCCG are used globally. Therefore, establishing relevant guidelines on MCCG is of great significance. The current guidelines containing 23 statements were established based on clinical evidence and expert opinions, mainly focus on aspects including definition and diagnostic accuracy, application population, technical optimization, inspection process, and quality control of MCCG. The level of evidence and strength of recommendations were evaluated. The guidelines are expected to guide the standardized application and scientific innovation of MCCG for the reference of clinicians.
    Type of Medium: Online Resource
    ISSN: 1751-2972 , 1751-2980
    URL: Issue
    URL: Article
    DOI: 10.1111/cdd.v24.2
    DOI: 10.1111/1751-2980.13173
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2317117-0
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  • 6
    Online Resource
    Online Resource
    Functional analyses of small secreted cysteine‐rich proteins identified candidate effectors in Verticillium dahliae
    Wiley ; 2020
    In:  Molecular Plant Pathology Vol. 21, No. 5 ( 2020-05), p. 667-685
    Details
    In: Molecular Plant Pathology, Wiley, Vol. 21, No. 5 ( 2020-05), p. 667-685
    Abstract: Secreted small cysteine‐rich proteins (SCPs) play a critical role in modulating host immunity in plant–pathogen interactions. Bioinformatic analyses showed that the fungal pathogen Verticillium dahliae encodes more than 100 VdSCPs, but their roles in host–pathogen interactions have not been fully characterized. Transient expression of 123 VdSCP‐encoding genes in Nicotiana benthamiana identified three candidate genes involved in host–pathogen interactions. The expression of these three proteins, VdSCP27, VdSCP113, and VdSCP126, in N. benthamiana resulted in cell death accompanied by a reactive oxygen species burst, callose deposition, and induction of defence genes. The three VdSCPs mainly localized to the periphery of the cell. BAK1 and SOBIR1 (associated with receptor‐like protein) were required for the immunity triggered by these three VdSCPs in N. benthamiana . Site‐directed mutagenesis showed that cysteine residues that form disulphide bonds are essential for the functioning of VdSCP126, but not VdSCP27 and VdSCP113. VdSCP27 , VdSCP113 , and VdSCP126 individually are not essential for V. dahliae infection of N. benthamiana and Gossypium hirsutum , although there was a significant reduction of virulence on N. benthamiana and G. hirsutum when inoculated with the VdSCP27 / VdSCP126 double deletion strain. These results illustrate that the SCPs play a critical role in the V. dahliae– plant interaction via an intrinsic virulence function and suppress immunity following infection.
    Type of Medium: Online Resource
    ISSN: 1464-6722 , 1364-3703
    URL: Issue
    URL: Article
    DOI: 10.1111/mpp.v21.5
    DOI: 10.1111/mpp.12921
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2020755-4
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Phenotype and Genotype Study of Chinese POMT2-Related α-Dystroglycanopathy
    Frontiers Media SA ; 2021
    In:  Frontiers in Genetics Vol. 12 ( 2021-8-3)
    Details
    In: Frontiers in Genetics, Frontiers Media SA, Vol. 12 ( 2021-8-3)
    Abstract: Alpha-dystroglycanopathy (α-DGP) is a subtype of muscular dystrophy caused by defects in the posttranslational glycosylation of α-dystroglycan (α-DG). Our study aimed to summarize the clinical and genetic features of POMT2 -related α-DGP in a cohort of patients in China. Methods Pedigrees, clinical data, and laboratory tests of patients diagnosed with POMT2 -related α-DGP were analyzed retrospectively. The pathogenicity of variants in POMT2 were predicted by bioinformatics software. The variants with uncertain significance were verified by further analysis. Results The 11 patients, comprising eight males and three females, were from nine non-consanguineous families. They exhibited different degrees of muscle weakness, ambulation, and intellectual impairment. Among them, three had a muscle-eye-brain disease (MEB)-like phenotype, five presented congenital muscular dystrophy with intellectual disability (CMD-ID), and three presented limb-girdle muscular dystrophy (LGMD). Overall, nine novel variants of POMT2 , including two non-sense, one frameshift and six missense variants, were identified. The pathogenicity of two missense variants, c.1891G & gt; C and c.874G & gt; C, was uncertain based on bioinformatics software prediction. In vitro minigene analysis showed that c.1891G & gt; C affects the splicing of POMT2 . Immunofluorescence staining with the IIH6C4 antibody of muscle biopsy from the patient carrying the c.874G & gt; C variant showed an apparent lack of expression. Conclusion This study summarizes the clinical and genetic characteristics of a cohort of POMT2 -related α-DGP patients in China for the first time, expanding the mutational spectrum of the disease. Further study of the pathogenicity of some missense variants based on enzyme activity detection is needed.
    Type of Medium: Online Resource
    ISSN: 1664-8021
    URL: Article
    DOI: 10.3389/fgene.2021.692479
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606823-0
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  • 8
    Online Resource
    Online Resource
    Uniparental disomy for chromosome 1 with POMGNT1 splice-site variant causes muscle-eye-brain disease
    Frontiers Media SA ; 2023
    In:  Frontiers in Genetics Vol. 14 ( 2023-6-5)
    Details
    In: Frontiers in Genetics, Frontiers Media SA, Vol. 14 ( 2023-6-5)
    Abstract: POMGNT1 , encoding protein O-mannose beta-1,2-N-acetylglucosaminyltransferase 1, is one of the genes responsible for dystroglycanopathy (DGP), which includes multiple phenotypes such as muscle-eye-brain disease (MEB), congenital muscular dystrophy with intellectual disability, and limb-girdle muscular dystrophy Here, we report a case of MEB that is the result of a homozygous variant of POMGNT1 that is revealed through uniparental disomy (UPD). An 8-month-old boy was admitted with mental and motor retardation, hypotonia, esotropia, early onset severe myopia, and structural brain abnormalities. A panel testing of genetic myopathy-related genes was used to identify a homozygous c.636C & gt;T (p.Phe212Phe) variant in exon 7 of POMGNT1 in the patient, a heterozygous c.636C & gt;T variant in the father, and the wild type in the mother. Quantitative polymerase chain reaction (q-PCR) revealed no abnormal copy numbers in exon 7. Trio-based whole-exome sequencing (trio-WES) revealed a possible paternal UPD on chromosome 1 of the patient. Chromosomal microarray analysis (CMA) revealed a 120,451 kb loss of heterozygosity (LOH) on 1p36.33-p11.2, encompassing POMGNT1 , and a 99,319 kb loss of heterozygosity on 1q21.2-q44, which indicated UPD. Moreover, RNA sequencing (RNA-seq) verified that the c.636C & gt;T variant was a splice-site variant, leading to skipping of exon 7 (p.Asp179Valfs*23). In conclusion, to the best of our knowledge, we present the first case of MEB caused by UPD, providing valuable insights into the genetic mechanisms underlying this condition.
    Type of Medium: Online Resource
    ISSN: 1664-8021
    URL: Article
    DOI: 10.3389/fgene.2023.1170089
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606823-0
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  • 9
    Online Resource
    Online Resource
    A new phenotype of syndromic retinitis pigmentosa with myopathy is caused by mutations in retinol dehydrogenase 11
    Wiley ; 2022
    In:  Clinical Genetics Vol. 101, No. 4 ( 2022-04), p. 448-453
    Details
    In: Clinical Genetics, Wiley, Vol. 101, No. 4 ( 2022-04), p. 448-453
    Abstract: Retinol dehydrogenase 11 (RDH11) is an 11‐cis‐retinol dehydrogenase that has a well‐characterized, albeit auxiliary role in the retinoid cycle. Diseases caused by mutations in the RDH11 gene are very rare, and only one affected family with eye and intelligence involvement has been reported. In the present study, we describe the clinical and genetic findings in a Chinese patient with retinitis pigmentosa (RP), juvenile cataracts, intellectual disability, and myopathy. Trio‐based whole‐exome sequencing and whole genomic copy number variation detection were performed in this family, and compound heterozygous mutations were identified in RDH11 of the patient: c.938T 〉 C (p.Leu313Pro) derived from the father and c.75‐3C 〉 A derived from the mother. Variant c.75‐3C 〉 A was confirmed to be a splice‐site mutation by cDNA sequencing. It caused exon 2 skipping, resulting in a frameshift mutation and premature translation termination (p.Lys26Serfs*38). Moreover, we found mislocalization of RDH11 protein in muscle cells of the patient by using immunofluorescence staining. This is the first case reported in the Chinese population harboring mutations in RDH11 and revealing a new phenotype of syndromic RP with myopathy.
    Type of Medium: Online Resource
    ISSN: 0009-9163 , 1399-0004
    URL: Issue
    URL: Article
    DOI: 10.1111/cge.v101.4
    DOI: 10.1111/cge.14108
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2004581-5
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  • 10
    Online Resource
    Online Resource
    Protective Effect of Nicotinamide Adenine Dinucleotide Phosphate on Renal Ischemia-Reperfusion Injury
    S. Karger AG ; 2018
    In:  Kidney and Blood Pressure Research Vol. 43, No. 3 ( 2018), p. 651-663
    Details
    In: Kidney and Blood Pressure Research, S. Karger AG, Vol. 43, No. 3 ( 2018), p. 651-663
    Abstract: 〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Renal ischemia-reperfusion injury (IRI) is a common consequence of acute kidney injury. Nicotinamide adenine dinucleotide phosphate (NADPH), which is derived from the pentose phosphate pathway, is essential for the proper functioning of essential redox and antioxidant defense systems. Previous studies have indicated that NADPH is responsible for protecting the brain from ischemic injury. The goal of this study was to analyze the protective function of NADPH in renal IRI. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 The IRI animal model was generated through a midline laparotomy surgery that clamped both sides of the renal pedicles for 40 min to induce renal ischemia. The 〈 i 〉 in vitro 〈 /i 〉 model was generated by removing oxygen and glucose from human kidney epithelial cells (HK-2 cells), followed by reoxygenation to imitate IRI. Renal function and histopathological changes were observed and evaluated. Additionally, malondialdehyde and glutathione levels were determined in renal tissue homogenate as indicators of oxidative stress. ROS production in cells was determined by DHE staining. Protein biomarker expression was evaluated by western blot, apoptosis was analyzed by TUNEL staining, and p65 nuclear translocation was visualized by immunofluorescence. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Our data indicated that NADPH safeguarded the kidneys from histological and functional damage, and significantly reduce cell injury along with preventing potential increases in blood urea nitrogen and creatinine levels. Furthermore, we observed that NADPH increased glutathione levels, while reducing levels of malondialdehyde and reactive oxygen species. Additionally, our results suggested that NADPH treatment may alleviate IRI-induced apoptosis and inflammation. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 NADPH treatment may protect against renal IRI and should be further developed as a new treatment for acute kidney injury.
    Type of Medium: Online Resource
    ISSN: 1420-4096 , 1423-0143
    URL: Article
    DOI: 10.1159/000489620
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482922-8
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