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  • 1
    Online Resource
    Online Resource
    Wiley ; 2015
    In:  European Journal of Oral Sciences Vol. 123, No. 2 ( 2015-04), p. 80-87
    In: European Journal of Oral Sciences, Wiley, Vol. 123, No. 2 ( 2015-04), p. 80-87
    Abstract: The purpose of this study was to determine the relationships among early childhood caries (ECC), root caries (RC), the quantity of Streptococcus mutans in saliva, and the concentrations of total and specific secretory IgA ( sIgA ). Saliva samples were collected from 70 children, 3–4 yr of age, with and without ECC, and from 43 adults, ≥60 yr of age, with and without RC. The decayed, missing, and filled teeth (dmft) and decayed, missing, and filled surfaces (dmfs) scores of each child, and the root decayed and filled teeth (RDFT) and root decayed and filled surfaces (RDFS) scores of each elderly subject, were determined. The S. mutans levels, total sIgA , and specific sIgA against two virulence antigens of S. mutans in saliva were analysed using quantitative real‐time PCR ( qPCR ) and ELISAs. The quantity of S. mutans was significantly higher in caries‐positive subjects within the two populations than in the caries‐free subjects; and a positive correlation was found between the quantity of S. mutans and the dmft, dmfs, RDFT, and RDFS scores. In addition, the salivary total sIgA was significantly higher in children with severe early childhood caries (SECC) and in the elderly subjects with RC. Moreover, although the S. mutans level was significantly higher, the concentrations of specific sIgA against S. mutans antigens were significantly lower in samples from elderly subjects than in samples from children. These results support the concept that S. mutans is positively associated with ECC and RC. Furthermore, the levels of S. mutans ‐specific antibodies in saliva are too low to prevent infection with cariogenic bacteria and to inhibit development of ECC and RC.
    Type of Medium: Online Resource
    ISSN: 0909-8836 , 1600-0722
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2025657-7
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  • 2
    In: Molecular Carcinogenesis, Wiley
    Abstract: Ovarian cancer (OC) is among the most common and deadly solid malignancies in women. Despite many advances in OC research, the incidence of OC continues to rise, and its pathogenesis remains largely unknown. Herein, we elucidated the function of hsa_circ_0061179 in OC. The levels of hsa_circ_0061179, miR‐143‐3p, TIMELESS, and DNA damage repair‐related proteins in OC or normal ovarian tissues and cells were measured using real‐time quantitative polymerase chain reaction and immunoblotting. The biological effects of hsa_circ_0061179 and miR‐143‐3p on proliferation, clone formation, DNA damage, and apoptosis of OC cells were detected by the cell counting kit‐8 assay, 5‐methylethyl‐2′‐deoxyuridine, flow cytometry, the comet assay, and immunofluorescence staining combined with the confocal microscopy. The interaction among hsa_circ_0061179, miR‐143‐3p, and TIMELESS was validated by the luciferase reporter assay. Mice tumor xenograft models were used to evaluate the influence of hsa_circ_0061179 on OC growth in vivo. We found that human OC biospecimens expressed higher levels of hsa_circ_0061179 and lower levels of miR‐143‐3p. Hsa_circ_0061179 was found to bind with miR‐143‐3p, which directly targets TIMELESS. Hsa_circ_0061179 knockdown or miR‐143‐3p overexpression suppressed the proliferation and clone formation of OC cells and increased DNA damage and apoptosis of OC cells via the miR‐143‐3p/TIMELESS axis. Furthermore, we demonstrated that METTL3 could direct the formation of has_circ_0061179 through a specific m6A modification site. YTHDC1 facilitated the cytoplasmic transfer of has_circ_0061179 by directly binding to the modified m6A site. Our findings suggest that hsa_circ_0061179 acts as the sponge of miR‐143‐3p to activate TIMELESS signaling and inhibits DNA damage and apoptosis in OC cells.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 2001984-1
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  • 3
    In: Asia-Pacific Journal of Clinical Oncology, Wiley
    Abstract: About 80% of hepatocellular carcinoma (HCC) patients are in advanced stages and ineligible for curative surgery. Palliative treatments just maintained limited survival, thus an effective downstaging therapy is badly needed. Here we report an initially unresectable patient who underwent radical hepatectomy after successful downstaging with selective internal radiation therapy (SIRT). A 34‐year‐old man was diagnosed with China Liver Cancer Staging (CNLC) IIIa HCC. Due to insufficient future liver remnant and vascular involvement, the patient was suggested to be unresectable. SIRT with yttrium‐90 resin microspheres was given. At three months post‐SIRT, a complete response was achieved. The tumor was downstaged to CNLC Ia stage. The patient underwent anatomical hepatectomy 5 months after SIRT. Histopathological examination of the resected specimen showed 4% viable tumor cells inside a necrotic mass. To our knowledge, this is the first case who underwent SIRT with yttrium‐90 resin microspheres in China mainland. The success of the downstaging in this case renders a possible cure to be achieved in an initially unresectable patient. In addition, the nearly complete tumor necrosis in the resected specimen indicates a good prognosis post‐surgery. This is the first case who underwent SIRT with yttrium‐90 resin microspheres in China mainland. SIRT followed by anatomical hepatectomy is a potentially curative strategy for unresectable HCC, which deserves a confirmative trial in the future.
    Type of Medium: Online Resource
    ISSN: 1743-7555 , 1743-7563
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2187409-8
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  • 4
    In: Journal of Cellular Physiology, Wiley, Vol. 235, No. 3 ( 2020-03), p. 1903-1914
    Abstract: Transforming growth factor β (TGF‐β) is part of the transforming growth factor β superfamily which is involved in many physiological processes and closely related to the carcinogenesis. Here, we discuss the TGF‐β structure, function, and its canonical Smads signaling pathway. Importantly, TGF‐β has been proved that it plays both tumor suppressor as well as an activator role in tumor progression. In an early stage, TGF‐β inhibits cell proliferation and is involved in cell apoptosis. In an advanced tumor, TGF‐β signaling pathway induces tumor invasion and metastasis through promoting angiogenesis, epithelial–mesenchymal transition, and immune escape. Furthermore, we are centered on updated research results into the inhibitors as drugs which have been studied in preclinical or clinical trials in tumor carcinogenesis to prevent the TGF‐β synthesis and block its signaling pathways such as antibodies, antisense molecules, and small‐molecule tyrosine kinase inhibitors. Thus, it is highlighting the crucial role of TGF‐β in tumor therapy and may provide opportunities for the new antitumor strategies in patients with cancer.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1478143-8
    SSG: 12
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  • 5
    In: Journal of Evidence-Based Medicine, Wiley, Vol. 13, No. 2 ( 2020-05), p. 91-92
    Type of Medium: Online Resource
    ISSN: 1756-5383 , 1756-5391
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2474496-7
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  • 6
    In: The Journal of Clinical Hypertension, Wiley, Vol. 25, No. 6 ( 2023-06), p. 573-581
    Abstract: The authors conducted an observational study to explore the association between body fat composition and the risk of hyperhomocysteinemia (HHcy) and their combined effect on the risk of developing cardiovascular disease (CVD). Adults aged 18–74 years from the Northwest China Natural Population Cohort: Ningxia Project (CNC‐NX) were recruited in this study. Association between body fat composition and HHcy was evaluated by logistic regression model. Restricted cubic spline was used to find nonlinear association. The impact of the interaction between HHcy and body fat composition on CVD was evaluated using the addition interaction model and mediation effect model. In total, 16 419 participants were included in this research. Body fat percentage, visceral fat level, and abdominal fat thickness were positively associated with overall HHcy ( p for trend  〈  .001). Adjusted odds ratios (ORs) in quarter 4 were 1.181 (95% CI: 1.062, 1.313), 1.202 (95% CI: 1.085, 1.332), and 1.168 (95% CI: 1.055, 1.293) for body fat percentage, visceral fat level, and abdominal fat thickness, respectively, compared with those in quarter 1. Subgroup analysis indicated age, estimated glomerular filtration rate (eGFR), total cholesterol (TC), low density lipoprotein cholesterol (LDL‐C), and CVD were the interaction factors of body fat percentage, visceral fat level, abdominal fat thickness with HHcy (all p for interaction  〈  .05). ORs of CVD were higher in participants with HHcy and high body fat. Body fat composition was positively associated with HHcy, indicating that reducing body, abdominal, and visceral fat content may lower the risk of HHcy and CVD.
    Type of Medium: Online Resource
    ISSN: 1524-6175 , 1751-7176
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2058690-5
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  • 7
    In: Advanced Functional Materials, Wiley, Vol. 31, No. 34 ( 2021-08)
    Abstract: Real‐time monitoring of wound healing remains a major challenge in clinical tissue regeneration, calling the need for the development of biomaterial‐guided on‐site monitoring wound healing technology. In this study, multifunctional double colorimetry‐integrated polyacrylamide‐quaternary ammonium chitosan‐carbon quantum dots (CQDs)‐phenol red hydrogels are presented, aiming to simultaneously detect the wound pH level, reduce bacterial infection, and promote wound healing. The hybridization of CQDs and pH indicator (phenol red) with the hydrogels enables their high responsiveness, reversibility, and accurate indication of pH variability to reflect the dynamic wound status in the context of both ultraviolet and visible light. Furthermore, these visual images can be collected by smartphones and converted into on‐site wound pH signals, allowing for a real‐time evaluation of the wound dynamic conditions in a remote approach. Notably, the hydrogels exhibit excellent hemostatic and adhesive properties, maintain sufficient wound moisture, and promote wound healing via their high antibacterial activity (against Staphylococcus Aureus , and Escherichia Coli ) and skin repair function. Overall, the resulting hydrogels have high potential as a novel smart and flexible wound dressing platform for theranostic skin regeneration.
    Type of Medium: Online Resource
    ISSN: 1616-301X , 1616-3028
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2029061-5
    detail.hit.zdb_id: 2039420-2
    SSG: 11
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  • 8
    In: Journal of Cellular Physiology, Wiley, Vol. 236, No. 5 ( 2021-05), p. 3466-3480
    Abstract: Leukemia is a severe malignancy of the hematopoietic system, which is characterized by uncontrolled proliferation and dedifferentiation of immature hematopoietic precursor cells in the lymphatic system and bone marrow. Leukemia is caused by alterations of the genetic and epigenetic regulation of processes underlying hematologic malignancies, including SUMO modification (SUMOylation). Small ubiquitin‐like modifier (SUMO) proteins covalently or noncovalently conjugate and modify a large number of target proteins via lysine residues. SUMOylation is a small ubiquitin‐like modification that is catalyzed by the SUMO‐specific activating enzyme E1, the binding enzyme E2, and the ligating enzyme E3. SUMO is covalently linked to substrate proteins to regulate the cellular localization of target proteins and the interaction of target proteins with other biological macromolecules. SUMOylation has emerged as a critical regulatory mechanism for subcellular localization, protein stability, protein–protein interactions, and biological function and thus regulates normal life activities. If the SUMOylation process of proteins is affected, it will cause a cellular reaction and ultimately lead to various diseases, including leukemia. There is growing evidence showing that a large number of proteins are SUMOylated and that SUMOylated proteins play an important role in the occurrence and development of various types of leukemia. Targeting the SUMOylation of proteins alone or in combination with current treatments might provide powerful targeted therapeutic strategies for the clinical treatment of leukemia.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1478143-8
    SSG: 12
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  • 9
    In: Journal of Diabetes, Wiley, Vol. 13, No. 12 ( 2021-12), p. 949-959
    Abstract: 妊娠高血糖会增加以后患糖尿病的风险。然而,与妊娠高血糖相关的未来心血管疾病(Cardiovascular diseases, CVD)的风险仍然不确定。本研究旨在探讨妊娠高血糖对中国老年女性后续心血管疾病风险的影响及其可能的影响因素。 方法 我们在中国2型糖尿病患者恶性肿瘤发生风险的流行病学(REACTION)研究的老年妇女中开展了一项病例对照研究。研究纳入82名妊娠高血糖女性及410名按年龄和研究中心匹配的对照女性。心血管疾病信息(包括冠心病、中风和心肌梗死)通过调查员辅助的标准化问卷收集。 结果 有妊娠高血糖的女性更容易发生糖尿病 [比值比(Odd ratio, OR),2.51; 95%可信区间(Confidence interval, CI),1.50‐4.18] 和CVD(OR,1.98; 95%CI,1.05‐3.74)。即使没有进展为 2 型糖尿病,妊娠高血糖也与 CVD 风险增加相关(OR,2.88;95%CI,1.18‐7.00)。然而,亚组分析表明,与没有妊娠期高血糖或高血压的女性相比,同时有妊娠期高血糖和高血压的女性患心血管疾病的风险更高(OR,3.98;95%CI,1.65‐9.58),而CVD风险在单纯有妊娠高血糖的女性中没有显著变化(OR,2.15;95%CI,0.71‐6.57)。分层分析表明,在超重/肥胖、缺乏体力活动或饮食不健康的人群中,妊娠高血糖会显著增加CVD风险。 结论 在中国老年女性中,妊娠期高血糖与晚年 CVD 风险增加有关。这种关联与是否发展为糖尿病无关,而可能会受到生活方式和高血压的影响。
    Type of Medium: Online Resource
    ISSN: 1753-0393 , 1753-0407
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2485432-3
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  • 10
    In: Journal of Medical Virology, Wiley, Vol. 95, No. 7 ( 2023-07)
    Abstract: Viral immune evasion is crucial to the pathogenesis of hepatitis B virus (HBV) infection. However, the role of HBV in the modulation of innate immune evasion is poorly understood. A liver‐specific histone acetyltransferase 1 ( Hat1 ) knockout (KO) mouse model and HAT1 KO cell line were established. Immunohistochemistry staining, Western blot analysis, Southern blot analysis, Northern blot analysis, immunofluorescence assays, enzyme‐linked immunosorbent assay, reverse transcription‐quantitative polymerase chain reaction, and chromatin immunoprecipitation assays were performed in the livers of mouse models, primary human hepatocytes, HepG2‐NTCP, and Huh7 and HepG2 cell lines. HBV‐elevated HAT1 increased the expression of miR‐181a‐5p targeting cyclic GMP‐AMP synthase (cGAS) messenger RNA 3′ untranslated regions through modulating acetylation of H4K5 and H4K12 in vitro and in vivo, leading to the inability of cGAS‐stimulator of interferon genes (STING) pathway and type I interferon (IFN‐I) signaling. Additionally, HBV‐elevated HAT1 promoted the expression of KPNA2 through modulating acetylation of H4K5 and H4K12 in the system, resulting in nuclear translocation of cGAS, HBx was responsible for the events by HAT1, suggesting that HBV‐elevated HAT1 controls the cGAS‐STING pathway and IFN‐I signaling to modulate viral innate immune evasion. HBV confers innate immune evasion through triggering HAT1/acetylation of H4K5/H4K12/miR‐181a‐5p or KPNA2/cGAS‐STING/IFN‐I signaling. Our finding provides new insights into the mechanism by which HBV drives viral innate immune evasion.
    Type of Medium: Online Resource
    ISSN: 0146-6615 , 1096-9071
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 752392-0
    detail.hit.zdb_id: 1475090-9
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