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Buck, A A, 2592
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/374479Surname: BUCK
Given Name(s) or Initials: A A
Military Service Number or Last Known Location: 2592
Missing, Wounded and Prisoner of War Enquiry Card Index Number: 57595185854
Item: [2016.0049.06787] "Buck, A A, 2592
Chicago, Burlington & Quincy (CBQ) 2592
No full textA photograph print showing Chicago, Burlington & Quincy (CBQ) 2592, 4-4-2, St. Louis, MO
Astronomische nachrichten, n°s 2586-2592
No full textRadau Rodolphe. Astronomische nachrichten, n°s 2586-2592. In: Bulletin astronomique, tome 1, 1884. pp. 260-264
Majorique Bonclair. See 2592. Location: [Lowell], Massachusetts.
No full textTitle from NCLC caption card.Attribution to Hine based on provenance.In album: Mills.Hine no. 2597.Original reference to #2592; pencilled correction to #2593
2592. Concile de Lyon de 1245
No full text2592. Concile de Lyon de 1245. In: Molinier Auguste. Les Sources de l'histoire de France - Des origines aux guerres d'Italie (1494). III. Les Capétiens, 1180-1328. Paris : A. Picard et fils, 1903. p. 129
2592. Concile de Lyon de 1245
No full text2592. Concile de Lyon de 1245. In: Molinier Auguste. Les Sources de l'histoire de France - Des origines aux guerres d'Italie (1494). III. Les Capétiens, 1180-1328. Paris : A. Picard et fils, 1903. p. 129
PENGARUH EKSTRAK BIJI SRIKAYA (Annona squamosa L.) TERHADAP PERTUMBUHAN Candida albicans ATCC 2592
No full textCandida albicans dapat menyebabkan penyakit infeksi yang disebut kandidiasis. Pengobatan kandidiasis selama ini melibatkan agen antijamur yang tidak dapat di absorbsi oleh organ tubuh. Pengobatan dengan cara tersebut disamping mahal juga dapat menimbulkan efek toksik yang menonjol pada tubuh pasien. Berdasarkan hal tersebut maka telah dilakukan penelitian dengan tujuan untuk mengetahui macam hasil ekstraksi biji srikaya (Annona squamosa) yang mempunyai pengaruh penghambatan terhadap pertumbuhan C. albicans ATCC 2592, selain itu sebagai upaya pencarian bahan alami untuk pengobatan infeksi kandidiasis. Penelitian dilakukan dengan beberapa metode meliputi preparasi ekstrak biji srikaya, peremajaan biakan, pembuatan inokulum, pengujian macam ekstrak biji srikaya terhadap pertumbuhan C. albicans ATCC 2592 dan pengujian aktivitas ekstrak biji srikaya fasa minyak terhadap pertumbuhan C. albicans ATCC 2592. Basil pengujian macam ekstrak biji srikaya terhadap pertumbuhan C. albicans ATCC 2592 menunjukkan bahwa ekstrak biji srikaya fasa minyak 2,5% relatif tidak berpengaruh terhadap peningkatan pertumbuhan sel, tetapi lebih berpengaruh pada mempercepat fase kematian C albicans ATCC 2592 dibandingkan dengan ekstrak biji srikaya fasa endapan dan etanol 0,0475%. Basil pengujian aktivitas ekstrak biji srikaya (A. squamosa) fasa minyak dengan berbagai konsentrasi menunjukkan bahwa ekstrak biji srikaya (A. squamosa) fasa minyak 5% berpengaruh terhadap pertumbuhan C. albicans. ATCC 2592 dalam mempercepat fase stationer dibandingkan dengan konsentrasi 10%, 15% dan 20%
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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Abstract 2592: Helicobacter pylori-induced FGFR4 mediates nuclear accumulation of NRF2 in gastric tumorigenesis
No full textAbstract Background: Fibroblast growth factor receptor 4 (FGFR4) is a member of the transmembrane tyrosine kinase receptor family and has been linked to a variety of malignancies. NRF2 (Nuclear factor-erythroid 2-related factor) is a cytoprotective factor and a critical regulator in the antioxidant response pathway. In this study, we sought to uncover novel functions of FGFR4 and its role in regulating the antioxidant response in gastric carcinogenesis. Methods and Results: Using western blot and immunofluorescence, H. pylori infection in gastric cancer cell lines demonstrated high levels of reactive oxygen species and induction of both FGFR4 and NRF2. Using Flow cytometry, FGFR4 silencing resulted in decrease of NRF2 with a significant spike in ROS levels and an increase in DNA damage and cell death. FGFR4 knockdown showed a significant decrease in NRF2 transcriptional activity as measured by NRF2 ARE luciferase reporter assay and resulted in reduced mRNA levels of HO-1 (Heme Oxygenase-1), which is a classical target of NRF2. These results were confirmed by immunofluorescence showing a significant increase of nuclear accumulation of NRF2 after H. pylori infection which was abolished after FGFR4 knockdown. Similar results were found using recombinant protein FGF19, a FGFR4 ligand. C57/B6 wild-type mice were infected with the pylori strain (PMSS1). An increase in FGFR4, NRF2, and HO-1 was seen by immunofluorescence, Western blot, and quantitative real-time PCR in H. pylori-infected mice vs control mice. We observed a reduction in NRF2 in our in vitro and in vivo models using H3B-6527, a specific FGFR4 inhibitor. We also discovered an association between an increase in FGFR4 and P62 protein expressions and NRF2 protein stability. We detected a significant increase in FGFR4, NRF2, and HO1 in dysplastic and neoplastic gastric lesions using the TFF1-KO mouse model which was further aggravated by H. pylori infection. In terms of the mechanism, utilizing proximity ligation and immunoprecipitation assays, we found that FGFR4 binds to P62 to inhibit the interaction between NRF2 and KEAP1, allowing NRF2 to avoid degradation facilitating its translocation and accumulation in the nucleus. Conclusion: These findings revealed that FGFR4 has a unique functional role in promoting gastric carcinogenesis by mediating accumulation and activation of the NRF2 antioxidant response. The use of FGFR4 inhibitors is a viable treatment option that warrants further research in patients with gastric cancer. Citation Format: Nadeem S. Bhat, Mohammed Soutto, Xing Zhang, Zheng Chen, Ahmed Gomaa, Marwah Al-Mathkour, Selma Maacha, Heng Lu, Dunfa Peng, Zekuan Xu, Wael El-Rifai. Helicobacter pylori-induced FGFR4 mediates nuclear accumulation of NRF2 in gastric tumorigenesis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2592
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