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  • Wiley  (9)
  • Wu, Xiaoying  (9)
  • 1
    In: PROTEOMICS, Wiley, Vol. 6, No. 2 ( 2006-01), p. 547-558
    Abstract: Few lung cancer‐specific molecular markers have been established in regard of “early‐stage” diagnosis and prognosis. In this study the proteome analysis of human lung squamous carcinoma (hLSC) was carried out using two strategies to explore the carcinogenic mechanisms and identify its molecular markers more directly and comprehensively. Comparative proteome analysis on 20 hLSC tissues and paired normal bronchial epithelial tissues revealed 76 differential proteins, among which 68 proteins were identified by PMF. The identified proteins fell into three categories: oncoproteins, cell cycle regulators and signaling molecules. To validate the identified differential proteins, the expressions levels of three differential proteins mdm2, c‐jun and EGFR were determined by immunohistochemical staining and immunoblots. The results verified proteome analysis results. Serological proteome analysis (SERPA) of ten hLSC tissues was performed to identify the tumor‐associated antigens. The results revealed 36 ± 8 differential proteins reactive with patients' autologous sera, of which 14 proteins were identified. Six of the 14 proteins, alpha enolase, pre‐B cell‐enhancing factor precursor, triosephosphate isomerase, phosphoglycerate mutase 1, fructose‐bisphosphate aldolase A, and guanine nucleotide‐binding protein beta subunit‐like protein, were also up‐regulated in hLSCs in the comparative proteomic study, which suggests potential application of these 6 hLSC‐associated antigens in diagnosis and therapy of hLSC.
    Type of Medium: Online Resource
    ISSN: 1615-9853 , 1615-9861
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2037674-1
    SSG: 12
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  • 2
    In: Clinical and Translational Medicine, Wiley, Vol. 13, No. 3 ( 2023-03)
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2697013-2
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  • 3
    In: European Journal of Immunology, Wiley, Vol. 51, No. 8 ( 2021-08), p. 2062-2073
    Abstract: MicroRNA‐147 (miR‐147) had been previously found induced in synoviocytes by inflammatory stimuli derived from T cells in experimental arthritis. This study was designed to verify whether loss of its function might alleviate inflammatory events in joints of experimental and rheumatoid arthritis (RA). Dark Agouti (DA) rats were injected intradermally with pristane to induce arthritis, and rno‐miR‐147 antagomir was locally administrated into individual ankle compared with negative control or rno‐miR‐155‐5p antagomir (potential positive control). Arthritis onset, macroscopic severity, and pathological changes were monitored. While in vitro, gain or loss function of hsa‐miR‐147b‐3p/hsa‐miR‐155‐5p and ZNF148 was achieved in human synovial fibroblast cell line SW982 and RA synovial fibroblasts (RASF). The expression of miRNAs and mRNAs was detected by using RT‐quantitative PCR, and protein expression was detected by using Western blotting. Anti‐miR‐147 therapy could alleviate the severity, especially for the synovitis and joint destruction in experimental arthritis. Gain of hsa‐miR‐147b‐3p/hsa‐miR‐155‐5p function in TNF‐α stimulated SW982 and RASF cells could upregulate, in contrast, loss of hsa‐miR‐147b‐3p/hsa‐miR‐155‐5p function could downregulate the gene expression of TNF‐α, IL‐6, MMP3 , and MMP13 . Hence, such alteration could participate in synovial inflammation and joint destruction. RNAi of ZNF148, a miR‐147's target, increased gene expression of TNF‐α, IL‐6, MMP3 , and MMP13 in SW982 and RASF cells. Also, mRNA sequencing data showed that hsa‐miR‐147b‐3p mimic and ZNF148 siRNA commonly regulated the gene expression of CCL3 and DEPTOR as well as some arthritis and inflammation‐related pathways. Taken together, miR‐147b‐3p contributes to synovial inflammation through repressing ZNF148 in RA and experimental arthritis.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1491907-2
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  • 4
    In: Journal of Diabetes, Wiley, Vol. 15, No. 4 ( 2023-04), p. 349-361
    Abstract: 目的: 探讨N6 ‐甲基腺苷(m 6 A)调节因子在2型糖尿病(T2DM)发病机制中的表达。我们进一步探索血清胰岛素样生长因子2 mRNA结合蛋白3 (IGF2BP3)水平与高危人群T2DM发病风险的关系。 方法: 从基因表达综合数据库获得基因表达数据集GSE25724, 使用R包ComplexHeatmap生成聚类热图。采用非配对T检验分析13个m 6 A RNA甲基化调控因子在非糖尿病对照者和T2DM受试者之间的差异表达。本研究为横断面研究, 共纳入393例研究对象, 其中新诊断T2DM患者131例, 年龄、性别相匹配的糖尿病前期患者131例, 健康对照者131例。采用限制性立方样条和logistic回归模型分析血清IGF2BP3浓度与T2DM的关系。 结果: 在T2DM患者胰岛中发现2个上调的m 6 A相关基因(IGF2BP2和IGF2BP3)和5个下调的m 6 A相关基因(METTL3、ALKBH1、YTHDF2、YTHDF3和HNRNPC)。校正BMI、腰围、舒张压、总胆固醇和三酰甘油后, 三次自然样条模型显示血清IGF2BP3水平与T2DM患病风险呈U型曲线关系。多因素logistic回归模型4显示, 当血清IGF2BP3水平低于0.62 ng/ml时, T2DM的发病风险逐渐增加[OR 3.03 (95% CI 1.23 ~ 7.47)]。 结论: T2DM患者存在7个m 6 A RNA甲基化基因的显著改变。中国成年人血清IGF2BP3水平与T2DM发病风险之间存在U型关联。本研究为进一步探讨m 6 A RNA甲基化尤其是血清IGF2BP3在T2DM风险评估中的作用提供了重要依据。
    Type of Medium: Online Resource
    ISSN: 1753-0393 , 1753-0407
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2485432-3
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  • 5
    In: Clinical and Translational Medicine, Wiley, Vol. 10, No. 4 ( 2020-08)
    Abstract: While there have been encouraging preliminary clinical results for immune checkpoint inhibitors (ICIs) in BTCs, it remains a challenge to identify the subset of patients who may benefit. In this study, we evaluated the efficacy of ICI treatment in patients with advanced BTCs, and explored potential biomarkers that are predictive of response. Methods The study enrolled 26 patients with advanced microsatellite stable BTCs (15 with gallbladder cancers [GCs] and 11 with intrahepatic cholangiocarcinoma [ICCs] ) who received ICI treatment. Targeted next‐generation sequencing (NGS) was performed on tumor tissue samples collected from 17 patients. Clinical and genomic characteristics were assessed for the correlation with clinical outcome. Results Analysis of the baseline clinical characteristics showed that performance score (PS) of 0 was associated with a better prognosis than PS of 1 (HR = 1.08 × 10 9 ; 95% CI, 0∼Inf; P  = .002). No significant correlations were found between clinical outcome and inflammation‐related indicators. NGS profiling of the available tumor tissues, revealed largely non‐overlapping somatic alterations between GCs and ICCs. Mutations in LRP1B (HR = 0.26; 95% CI, 0.06‐1.21; P  = .067), ERBB2 (HR = 0.15; 95% CI, 0.02‐1.19; P  = .04), or PKHD1 (HR  〈  0.01; 95% CI, 0‐Inf; P  = .04) showed strong association with increased progression‐free survival (PFS) benefit. Subsequent analysis showed that alterations in the RTK‐RAS pathway were associated with improved outcomes (HR = 0.12; 95% CI, 0.02‐0.63; P  = .003). Tumor mutation burden (TMB) was higher in patients with GC than those with ICC, and was associated with LRP1B mutations ( P  = .032). We found that patients with 19q amplification (19q Amp) and 9p deletion (9p Del) had poor PFS outcome (19q Amp, HR = 15.4; 95% CI, 2.7‐88.5; P   〈  .001; 9p Del; HR = 4.88 × 10 9 ; 95% CI, 0‐Inf; P   〈  .001), while those with chromosomal instability derived PFS benefit (HR = 0.24; 95% CI, 0.05‐1.17; P  = .057). Conclusion Our study identified several potential clinical and genomic features that may serve as biomarkers of clinical response to ICIs in advanced BTCs patients. A larger sample size is required for further verification.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2697013-2
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  • 6
    In: Pathology International, Wiley, Vol. 54, No. 10 ( 2004-10), p. 765-773
    Abstract: Processes involved in malignant transformation of the lung from preneoplasia are poorly understood. To better understand this process, two‐dimensional polyacrylamide gel electrophoresis (2‐D PAGE) profiles of proteins from the normal, metaplasia, dysplasia and carcinoma tissues of human bronchial epithelia were examined by differential proteomic analysis. The selected differential protein‐spots were identified by peptide mass fingerprint based on matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry and database searching. The average spots for normal epithelium, metaplasia, dysplasia and invasive carcinoma were 1189.50 ± 39.89, 1227.00 ± 37.90, 1273.00 ± 43.31 and 1326.00 ± 66.63, respectively. Well‐resolved, reproducible 2‐D PAGE patterns of the normal‐metaplasia‐dysplasia‐carcinoma tissues of bronchial epithelia were obtained. After matching, the number of spots of differential proteins between normal tissue and metaplasia, metaplasia and dysplasia, and dysplasia and invasive cancer tissues were 31.50 ± 7.67, 41.00 ± 9.07 and 56.00 ± 8.96, respectively. In total, 35 differential proteins, expressed only at the later stage of a two‐stage comparison, were identified, some of which are known to be involved in regulating the processes of proliferation, differentiation and signal transduction. Current data in this study, for the first time, provide the basis for identification of potential tumor markers of human lung squamous carcinoma and their involvement in the progression of malignant transformation of bronchial epithelium.
    Type of Medium: Online Resource
    ISSN: 1320-5463 , 1440-1827
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2004
    detail.hit.zdb_id: 2008574-6
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  • 7
    In: Child Development, Wiley, Vol. 83, No. 4 ( 2012-07), p. 1429-1443
    Type of Medium: Online Resource
    ISSN: 0009-3920
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 215602-7
    detail.hit.zdb_id: 2047406-4
    SSG: 5,2
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  • 8
    In: Acta Ophthalmologica, Wiley, Vol. 101, No. 5 ( 2023-08), p. 485-503
    Abstract: Post‐laser in situ keratomileusis (post‐LASIK) ectasia (PLE) is one of the most serious complications after refractive surgery, mainly manifested as progressive thinning and trembling thinning of the cornea, accompanied by increased myopia and astigmatism. The mechanisms behind mainly include genetic risk factors and external environmental factors such as eye rubbing and cornea surgery. In order to achieve the goal of reducing the incidence of ectasia, preoperative screening strategies need to be continuously improved, through the collection and assessment of genetic and environmental risk factors. Although previous preoperative screening methods did not have a uniform standard, the emergence of artificial intelligence (AI) can help us process a large amount of information and make rational use of the data. By using high‐fidelity finite element modelling, differences in preoperative and postoperative strain distributions can be observed, which can predict the risk of postoperative ectasia. In this review, we describe the incidence, aetiology, prevention and treatment of PLE for the purpose of comprehensive management. In terms of treatment, corneal collagen cross‐linking has been widely used to treat progressive keratoconus and other ectasia disease, either as a preventive measure during surgery or as a therapeutic modality after surgery to prevent progression of corneal dilation. Although the standard Dresden protocol has been identified as the gold standard treatment for corneal dilatation, a series of refinements, investigations and long‐term studies have been conducted in recent years. Thus, understanding the factors involved in delaying the onset and slowing progression of cornea ectasia will be key to reducing the incidence worldwide.
    Type of Medium: Online Resource
    ISSN: 1755-375X , 1755-3768
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2466981-7
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  • 9
    In: Cancer Medicine, Wiley, Vol. 7, No. 9 ( 2018-09), p. 4530-4541
    Abstract: Recently, an increasing number of studies have focused on the key function of long noncoding RNA s (lnc RNA s) in biological activity. Abnormal lnc RNA expression was found to relate to the development and pathogenesis of multiple cancers. Lnc RNA LINC 00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC 00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC 00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC 00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC 00152 and Myeloid cell leukemia‐1 ( MCL ‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC 00152, while MCL ‐1 was positively related to the LINC 00152 level. MiR‐125b could affect LINC 00152 levels as evaluated by qRT ‐ PCR . Finally, we affirmed that LINC 00152 mediated cell proliferation by affecting MCL ‐1 expression and MCL ‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ce RNA ) of miR‐125b. In summary, based on ce RNA theory, the combined research on miR‐125b and MCL ‐1, and taking LINC 00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer.
    Type of Medium: Online Resource
    ISSN: 2045-7634 , 2045-7634
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2659751-2
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