1,729,140 research outputs found
H-4073 and cisplatin combination treatment significantly inhibits tumor growth.
No full text<p>Animals bearing UM-SCC-74A, CAL27 and CAL27-CisR were treated with H-4073 (50 ppm) or cisplatin (CDDP, 5 mg/kg) alone or in combination. <b><i>A:</i></b> Representative photomicrographs of UM-SCC-74A tumors from untreated, cisplatin (CDDP), H-4073, or CDDP and H-4073-treated groups. <b><i>B:</i></b> Tumor growth curves for UM-SCC-74A tumors treated with cisplatin (CDDP), H-4073, or CDDP and H-4073. <b><i>C:</i></b> Tumor growth curves for CAL27 and CAL27-CisR tumors treated with cisplatin (CDDP), H-4073, or CDDP and H-4073. *, represents a significant difference (p<0.05) as compared to no treatment group and **, represents a significant difference (p<0.05) as compared to single treatment groups.</p
Turner, Robert Cecil, 2/4073
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete.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/428384Surname: Turner. Given Name(s) or Initials: Robert Cecil. Military Service Number or Last Known Location: 2/4073. Prisoner of War Enquiry Card Index Number: K 254. Division Enquiry: NSW. Rank: CPL/Mach Gnr. Unit: RAR Korea327140
Item: [2016.0049.60646] "Turner, Robert Cecil, 2/4073
H-4073 and cisplatin combination treatment significantly inhibits tumor angiogenesis.
No full text<p><b><i>A:</i></b> Representative photomicrographs of tumor blood vessel staining for untreated, cisplatin (CDDP) or H-4073 alone or combination groups for UM-SCC-74A tumors. <b><i>B:</i></b> Microvessel density in the tumor samples was calculated by counting 5 random fields (200×) and expressed as vessel density ± SE. <b><i>C:</i></b> UM-SCC-74A cells were treated with cisplatin or H-4073 alone or in combination. After 72 hours, culture supernatants were collected and assayed for VEGF levels. *, represents a significant difference (p<0.05) as compared to no treatment group and **, represents a significant difference (p<0.05) as compared to single treatment groups. <b><i>D:</i></b> Endothelial cells were treated with VEGF in the presence or absence of different concentrations of H-4073 for 30 minutes. ERK1/2, Akt and p38 phosphorylation was examined by Western blotting and equal protein loading was verified by stripping the blots and reprobing with GAPDH antibody.</p
4073. Antonio Morosini, chroniqueur du XVe siècle
No full text4073. Antonio Morosini, chroniqueur du XVe siècle. In: Molinier Auguste. Les Sources de l'histoire de France - Des origines aux guerres d'Italie (1494). IV. Les Valois, 1328-1461. Paris : A. Picard et fils, 1904. pp. 226-228
鉱物の結晶組織結晶構造および物性と生成条件
No full text研究課題/領域番号:X43050------4073, 研究期間(年度):1968出典：研究課題「鉱物の結晶組織結晶構造および物性と生成条件」課題番号 X43050------4073
（KAKEN：科学研究費助成事業データベース（国立情報学研究所））
（https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-X43050------4073/）を加工して作成金沢大学理学部research repor
H-4073 inhibits STAT3 activation and head and neck cancer cell proliferation in a dose dependent manner.
No full text<p><b><i>A:</i></b> HNSCC cell lines were treated with different concentrations of cisplatin (CDDP) and cell proliferation was assessed by MTT assay. <b><i>B:</i></b> Chemical structures of curcumin and H-4073. <b><i>C:</i></b> UM-SCC-74A cells were cultured in 10-cm culture dishes and treated with curcumin or H-4073 for 1 hour. Cellular uptake of curcumin and H-4073 was measured with a UV/Vis spectrophotometer. <b><i>D:</i></b> HNSCC cell lines were treated with different concentrations of H-4073 and cell proliferation was assessed by MTT assay. <b><i>E:</i></b> UM-SCC-74A cells were treated with different concentrations of H-4073 for 2 hours. STAT3, FAK, Akt and p38 phosphorylation was examined by Western blotting and equal protein loading was verified by stripping the blots and reprobing with GAPDH antibody.</p
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe 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
A novel curcumin analog (H-4073) enhances the therapeutic efficacy of cisplatin treatment in head and neck cancer.
No full textChemotherapy constitutes the standard modality of treatment for localized head and neck squamous cell carcinomas (HNSCC). However, many patients fail to respond and relapse after this treatments due to the acquisition of chemo-resistance. Therefore, there is an urgent need to develop novel drugs that could reverse the resistant phenotype. Curcumin, the constituent of the spice turmeric has been shown to have anti-inflammatory, anti-oxidant and anti-proliferative properties in several tumor types. However, use of curcumin has been limited due to its poor bio-absorption. Recently, a novel class of curcumin analogs, based on diarylidenylpiperidones (DAP), has been developed by incorporating a piperidone link to the beta-diketone structure and fluoro substitutions on the phenyl groups. In this study, we evaluated the effectiveness of H-4073, a parafluorinated variant of DAP, using both in vitro and in vivo head and neck cancer models. Our results demonstrate that H-4073 is a potent anti-tumor agent and it significantly inhibited cell proliferation in all the HNSCC cell lines tested in a dose-dependent manner. In addition, pretreatment of cisplatin-resistant HNSCC cell lines with H-4073 significantly reversed the chemo-resistance as observed by cell viability assay (MTT), apoptosis assay (Annexin V binding) and cleaved caspase-3 (Western blot). H-4073 mediated its anti-tumor effects by inhibiting JAK/STAT3, FAK, Akt and VEGF signaling pathways that play important roles in cell proliferation, migration, survival and angiogenesis. In the SCID mouse xenograft model, H-4073 significantly enhanced the anti-tumor and anti-angiogenesis effects of cisplatin, with no added systemic toxicity. Interestingly, H-4073 inhibited tumor angiogenesis by blocking VEGF production by tumor cells as well as directly inhibiting endothelial cell function. Taken together, our results suggest that H-4073 is a potent anti-tumor agent and it can be used to overcome chemotherapy resistance in HNSCC
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