Artykuły w czasopismach: „A-489”

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Hoffman, E. A., i E. L. Ritman. "Effect of body orientation on regional lung expansion in dog and sloth". Journal of Applied Physiology 59, nr 1 (1.07.1985): 283. http://dx.doi.org/10.1152/jappl.1985.59.1.283-u.

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Page 481: E. A. Hoffman and E. L. Ritman. “Effect of body orientation on regional lung expansion in dog and sloth.” Pages 484 (right-hand column, third paragraph, third line), 485 (Fig. 5 legend, ninth line), and 489 (left-hand column, first paragraph, fifth and sixth lines): substitute cm lung height for ml lung height.

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Diaz, Marta, Eva Valdivia, Manuel Martínez-Bueno, Matilde Fernández, Andrés Santos Soler-González, Hilario Ramírez-Rodrigo i Mercedes Maqueda. "Characterization of a New Operon, as-48EFGH, from the as-48 Gene Cluster Involved in Immunity to Enterocin AS-48". Applied and Environmental Microbiology 69, nr 2 (luty 2003): 1229–36. http://dx.doi.org/10.1128/aem.69.2.1229-1236.2003.

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ABSTRACT Enterocin AS-48 is a cyclic peptide produced by Enterococcus faecalis S-48 whose genetic determinants have been identified in the conjugative plasmid pMB2. A region of 7.8 kb, carrying the minimum information required for production of and immunity against AS-48, had been previously cloned and sequenced in pAM401 (pAM401-52). In this region, the as-48A structural gene and as-48B, as-48C, as-48C1 , as-48D, and as-48D1 genes and open reading frame 6 (ORF6) and ORF7 had been identified. The sequence analysis carried out in this work in the BglII B fragment (6.6-kb) from pMB2 cloned downstream from the last ORF identified (ORF7) revealed the existence of two new ORFs, as-48G and as-48H, necessary for full AS-48 expression. Thus, JH2-2 transformants obtained with the pAM401-81 plasmid became producers and resistant at the wild-type level. Tn5 disruption experiments in the last genes, as-48EFGH, were not able to reproduce these expression levels, confirming that expression of these genes is necessary to get the phenotype conferred by the wild-type pMB2 plasmid. The as-48EFGH operon encodes a new ABC transporter that could be involved in producer self-protection. On the basis of the observed similarities, As-48G would be the ATP-binding domain, the deduced amino acid sequences of As-48E and As48-H could be assigned as transmembrane subunits, and As-48F, with an N-terminal transmembrane segment and a coiled-coil domain, strongly resembles the structure of some known ABC transporter accessory proteins whose localization in the cell is discussed. This cluster of genes is expressed by two polycistronic mRNAs, T2 and T3, in JH2-2(pAM401-81) in coordinate expression. Our results also suggest that expression of T3 could be regulated, because in JH2-2(pAM401EH) transformants, T3 was not detected, suggesting that these genes do not by themselves confer immunity, in accordance with the requirement for the as-48D1 gene for immunity against AS-48.

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Zhang, Lie, Shuchuan Miao, Zhongxin Yang, Zongxi Li i Qun Zheng. "MiR-489 serves as a tumor inhibitor in pituitary prolactinoma targeting p21-activated kinase 3". Tropical Journal of Pharmaceutical Research 20, nr 3 (17.01.2022): 559–65. http://dx.doi.org/10.4314/tjpr.v20i3.17.

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Purpose: To evaluate the effect of microRNA-489 (miR-489) on pituitary prolactinoma and its mechanisms of action. Methods: MMQ and GH3 cells were transfected with miR-489, cell viability assessed with cell counting kit-8 (CCK-8), and clone spots was evaluated by colony formation assay. Transwell assay was applied to measure cell migration and invasion while TargetScan was employed to the presumed targets of miR-489, followed by luciferase reporter assays. was MiR-489 and p21-activated kinase 3 (PAK3) gene expression were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR. Protein levels of PAK3 were measured using western blots. Results: Transfection significantly increased miRNA-489 levels (p < 0.01). Cell viability, number of clone spots, as well as cell migration and invasion diminished in MMQ and GH3 cells following miR-489 transfection when compared to miR-NC mimic group (p < 0.01). The presumed binding site of miRNA- 489 was located in 3′-untranslated region (UTR) of PAK3, and miR-489 transfection repressed luciferase activity with the wild-type 3′-UTR (p < 0.05). In addition, miR-489 decreased PAK3 levels in MMQ and GH3 cells. Knockdown of PAK3 significantly suppressed cell viability, clone formation ability, as well as cell migration and invasion when compared to negative control (p < 0.01). Conclusion: MiR-489 overexpression suppresses pituitary prolactinoma by targeting PAK3, thus providing a potential therapeutic strategy for the management of pituitary prolactinoma.

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Li, Jing, Weixing Qu, Yazhou Jiang, Yi Sun, Yongyi Cheng, Tiejun Zou i Shuangkuan Du. "miR-489 Suppresses Proliferation and Invasion of Human Bladder Cancer Cells". Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 24, nr 6 (27.10.2016): 391–98. http://dx.doi.org/10.3727/096504016x14666990347518.

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MicroRNAs (miRNAs) have been shown to be involved in bladder cancer progression. miR-489 (also known as miR-489-3p) was recently reported to be a tumor suppressor in several cancers. However, its exact role and mechanism in the progression of bladder cancer are largely unknown. In this study, we explore the role of miR-489 in the proliferation and invasion of human bladder cancer cells. The miR-489 expression levels were detected in bladder cancer and normal adjacent tissues, as well as in human normal bladder epithelial cells and bladder cancer cell lines. The results showed that miR-489 was sharply reduced in bladder cancer tissues and cell lines. Then the miR-489 mimic or oligo anta-miR-489 was transfected into T24 and UMUC3 bladder cancer cell lines. The results showed that the miR-489 mimic greatly increased the miR-489 level and significantly decreased the proliferation and invasion of T24 and UMUC3 cells. In contrast, the anta-miR-489 had a completely opposite effect on miR-489 expression, cell proliferation, and cell invasion. Moreover, bioinformatics and luciferase reporter gene assays confirmed that miR-489 targeted the mRNA 3′-untranslated region (3′-UTR) region of Jagged1 (JAG1), a Notch ligand. In conclusion, miR-489 suppressed proliferation and invasion of human bladder cancer cells.

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Olave, Nelida, Charitharth V. Lal, Brian Halloran, Kusum Pandit, Alain C. Cuna, Ona M. Faye-Petersen, David R. Kelly i in. "Regulation of alveolar septation by microRNA-489". American Journal of Physiology-Lung Cellular and Molecular Physiology 310, nr 5 (1.03.2016): L476—L487. http://dx.doi.org/10.1152/ajplung.00145.2015.

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MicroRNAs (miRs) are small conserved RNA that regulate gene expression. Bioinformatic analysis of miRNA profiles during mouse lung development indicated a role for multiple miRNA, including miRNA-489. miR-489 increased on completion of alveolar septation [postnatal day 42 (P42)], associated with decreases in its conserved target genes insulin-like growth factor-1 ( Igf1) and tenascin C ( Tnc). We hypothesized that dysregulation of miR-489 and its target genes Igf1 and Tnc contribute to hyperoxia-induced abnormal lung development. C57BL/6 mice were exposed to normoxia (21%) or hyperoxia (85% O2) from P4 to P14, in combination with intranasal locked nucleic acid against miR-489 to inhibit miR-489, cytomegalovirus promoter (pCMV)-miR-489 to overexpress miR-489, or empty vector. Hyperoxia reduced miR-489 and increased Igf1 and Tnc. Locked nucleic acid against miR-489 improved lung development during hyperoxia and did not alter it during normoxia, whereas miR-489 overexpression inhibited lung development during normoxia. The 3′ untranslated region in vitro reporter studies confirmed Igf1 and Tnc as targets of miR-489. While miR-489 was of epithelial origin and present in exosomes, its targets Igf1 and Tnc were produced by fibroblasts. Infants with bronchopulmonary dysplasia (BPD) had reduced lung miR-489 and increased Igf1 and Tnc compared with normal preterm or term infants. These results suggest increased miR-489 is an inhibitor of alveolar septation. During hyperoxia or BPD, reduced miR-489 and increased Igf1 and Tnc may be inadequate attempts at compensation. Further inhibition of miR-489 may permit alveolar septation to proceed. The use of specific miRNA antagonists or agonists may be a therapeutic strategy for inhibited alveolarization, such as in BPD.

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Wijnsma, Uzume Z. "“And in the fourth year Egypt rebelled ...” The Chronology of and Sources for Egypt’s Second Revolt (ca. 487–484 BC)". Journal of Ancient History 7, nr 1 (26.05.2019): 32–61. http://dx.doi.org/10.1515/jah-2018-0023.

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Abstract Scholars continue to give different dates for Egypt’s second revolt against the Persians: Classicists generally date the revolt to 487–485 or 487/486–485/484 BC; Egyptologists and historians of the Achaemenid Empire generally date it to 486–485/484; while some scholars date it to 486/485–485/484. Such chronological differences may sound small, but they have important consequences for the way the rebellion is understood. The purpose of the present article is therefore twofold: first, it aims to clarify what we can and cannot know about the rebellion’s exact chronology. After a review of the relevant evidence, it will be argued that the best chronological framework for the rebellion remains the one provided by Herodotus’s Histories, which places the rebellion in ca. 487–484. Second, the article will show how this chronology influences our understanding of the geographical extent and social impact of the rebellion. The adoption of Herodotus’s chronological framework, for example, results in a larger number of Egyptian sources that can be connected to the period of revolt than was previously recognized. These sources, it will be argued, suggest that some people in the country remained loyal to the Persian regime while others were already fighting against it. Moreover, they indicate that the revolt reached Upper Egypt and that it may have affected the important city of Thebes.

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Nota, Jumpei, Tadahiko Saiki, Yoshihisa Okochi i Futoshi Watanabe. "A Study on 489 Cases of Epistaxis". Practica Oto-Rhino-Laryngologica 108, nr 3 (2015): 191–99. http://dx.doi.org/10.5631/jibirin.108.191.

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Nota, Jumpei, Tadahiko Saiki, Yoshihisa Okochi i Futoshi Watanabe. "A Study on 489 Cases of Epistaxis". Practica oto-rhino-laryngologica. Suppl. 144 (2015): 28–29. http://dx.doi.org/10.5631/jibirinsuppl.144.28.

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Yu, Suyun, Min Xue, Zhijun Yan, Bin Song, Haiping Hong i Xiwen Gao. "Correlation between TNF-α -308 and +489 Gene Polymorphism and Acute Exacerbation of Chronic Obstructive Pulmonary Diseases". BioMed Research International 2021 (1.03.2021): 1–8. http://dx.doi.org/10.1155/2021/6661281.

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Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is becoming a common respiratory disease, leading to increased morbidity and mortality worldwide. Tumor necrosis factor-alpha (TNF-α) is a powerful proinflammatory cytokine involved in the pathogenesis of AECOPD. Therefore, we proposed a close correlation between the TNF-α polymorphism [-308G/A (rs1800629), +489G/A (rs1800610)] and the disease progress of patients with AECOPD. Comparison of the TNF-α genotypes between the 198 AECOPD diagnosed patients groups and 195 healthy peoples suggested their significant differences of the three genotypes (AA, GA, GG) distribution for TNF-α -308 ( P < 0.05 ), but no differences of that for TNF-α +489. We found that patients with TNF-α -308 GA/AA genotypes showed smaller adjacent arterial diameter, thicker bronchial wall, higher bronchial artery ratio, higher bronchial wall grading, and higher frequency of acute exacerbations than those with TNF-α -308 GG genotype. Patients with TNF-α +489 GA/AA genotypes showed the same AECOPD properties as patients with TNF-α -308 except for the high frequency of acute exacerbations. Further experiment showed that the TNF-α -308 and+489 gene polymorphisms could affect the expression level of TNF-α in macrophages, suggesting the involvement of the macrophage population in disease regulation of AECOPD patients with TNF-α -308G/A and+489G/A genotype heterogeneity. In conclusion, the TNF-α -308 G/A genotype was related to AECOPD susceptibility and progress, while the TNF-α +489G/A genotype was related to AECOPD progress, but not AECOPD susceptibility.

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Wang, Bing, Wang-Xun Jin, Yun-Li Zhang, Ling Huang, Hai-Bin Ni i Dilong Fang. "Effects of miR-489 targeting on SOX4 gene on proliferation and apoptosis of human hepatocellular carcinoma cells". African Health Sciences 20, nr 3 (7.10.2020): 1292–98. http://dx.doi.org/10.4314/ahs.v20i3.34.

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Background: Hepatocellular carcinoma is one of the most common malignant tumors found all over the globe. Despite advances in surgery and chemotherapy, the five-year survival rate of patients with hepatocellular carcinoma is still low. It is known that the proliferation of hepatocellular carcinoma cells is closely related to the occurrence, development and prog- nosis of hepatocellular carcinoma. The present work investigates the expression of microRNA-489 (miR-489) in human hepatocellular carcinoma cells and its effect on the biological behavior of human hepatocellular carcinoma cells. Methods: The expression of miR-489 by fluorescence quantitative PCR detection in 30 patients with hepatoblastoma of liver cancer tissues and adjacent tissues was studied. Also, the determination of hepatoblastoma in four cell lines with differ- ent metastatic potential (HR8348, HCT116, HT29 and HEPG2) and the expression of miR-489 during miR-489 simulation process was studied. MTT assay, flow cytometry and Western blot analysis were performed to know the cell proliferation to detect the changes in cell cycle, apoptosis of cells, and SOX4 gene expression respectively. Results: RT-PCR results showed that the cells compared with pre-cancerous tissue, the expression level of miR-489 in hepatocellular carcinoma tissues than in adjacent tissue significantly decreased (P<0.05), and with liver cancer cell metastasis increased (P<0.05); analogue transfection constructed miR-489 overexpressing HEPG2 cell line by microRNA. MTT results showed that miR-489 can inhibit the proliferation of HEPG2 cells, the differences were statistically significant (P<0.05); flow cytometry results showed that miR-489 mimics was transfected into HEPG2 cells at 48 hours had no significant effect on cell cycle distribution (P > 0.05); but miR-489 expression could induce apoptosis, compared with the control group, the apoptosis of miR-489 mimics was significantly increased and the difference was statistically significant (P < 0.05). Conclusion: In conclusion, miR-489 can significantly inhibit the occurrence and development of hepatocellular carcinoma cells. The mechanism may be down regulated by the expression of SOX4 and inhibit cell proliferation. Further this study showed that the tumor cells SOX4 gene as a regulatory factor target the genes of miR-489 in hepatocellular carcinoma. Keywords: Hepatocellular carcinoma; mircroRNA-489; SOX4; apoptosis.

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Soung, Young Hwa, Heesung Chung, Cecilia Yan, Andrew Fesler, Hyungjin Kim, Eok-Soo Oh, Jingfang Ju i Jun Chung. "Therapeutic Potential of Chemically Modified miR-489 in Triple-Negative Breast Cancers". Cancers 12, nr 8 (7.08.2020): 2209. http://dx.doi.org/10.3390/cancers12082209.

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Triple-negative breast cancers (TNBCs) lack ER, PR and her2 receptors that are targets of common breast cancer therapies with poor prognosis due to their high rates of metastasis and chemoresistance. Based on our previous studies that epigenetic silencing of a potential metastasis suppressor, arrestin domain-containing 3 (ARRDC3), is linked to the aggressive nature of TNBCs, we identified a sub-group of tumor suppressing miRNAs whose expressions were significantly up-regulated by ARRDC3 over-expression in TNBC cells. Among these tumor suppressing miRs, we found that miR-489 is most anti-proliferative in TNBC cells. miR-489 also blocked DNA damaging responses (DDRs) in TNBC cells. To define the mechanism by which miR-489 inhibits TNBC cell functions, we screened the potential target genes of miR-489 and identified MDC-1 and SUZ-12 as novel target genes of miR-489 in TNBC cells. To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Our studies demonstrated that CMM489 shows superior effects over miR-489 or 5-FU in inhibition of TNBC cell proliferation and tumor progression, suggesting its therapeutic efficacy in TNBC models.

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Petersen, Peter J., C. Hal Jones, Aranapakam M. Venkatesan, Tarek S. Mansour, Steven J. Projan i Patricia A. Bradford. "Establishment of In Vitro Susceptibility Testing Methodologies and Comparative Activities of Piperacillin in Combination with the Penem β-Lactamase Inhibitor BLI-489". Antimicrobial Agents and Chemotherapy 53, nr 2 (10.11.2008): 370–84. http://dx.doi.org/10.1128/aac.01047-08.

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ABSTRACT The novel bicyclic penem inhibitor BLI-489 has demonstrated activity as an inhibitor of class A, C, and D β-lactamases. To determine the combination of piperacillin and BLI-489 to be used in susceptibility testing that would most accurately identify susceptible and resistant isolates, a predictor panel of β-lactamase-producing bacteria was utilized to determine the reliability of the combination of piperacillin-BLI-489 at a constant inhibitor concentration of 2 or 4 μg/ml and at ratios of 1:1, 2:1, 4:1, and 8:1. There were a number of strains that would be falsely reported as susceptible or intermediate if tested with the ratios of 1:1 and 2:1, whereas the constant concentration of 2 μg/ml of BLI-489 and the ratio of 8:1 had a tendency to overpredict resistance. Similar MICs were obtained with piperacillin-BLI-489 in a 4:1 ratio and when BLI-489 was held constant at 4 μg/ml. Based on these results, an in vitro testing methodology employing a constant concentration of 4 μg/ml BLI-489 was used to evaluate the combination of piperacillin-BLI-489 against a larger panel of recently identified clinical isolates. Approximately 55% of all of the enteric bacilli tested were nonsusceptible to piperacillin alone (MIC ≥ 32 μg/ml). However, 92% of these piperacillin nonsusceptible strains were inhibited by ≤16 μg/ml piperacillin-BLI-489; in contrast, only 66% were inhibited by ≤16 μg/ml piperacillin-tazobactam. The combination of piperacillin-BLI-489 also demonstrated improved activity compared to that of piperacillin-tazobactam against the problematic extended-spectrum β-lactamase- and AmpC-expressing strains.

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Rahman, Anisur, i Mark S. Lundstrom. "Erratum: A Compact Scattering Model for the Nanoscale Double-Gate MOSFET [Mar 02 481-489]". IEEE Transactions on Electron Devices 62, nr 7 (lipiec 2015): 2367. http://dx.doi.org/10.1109/ted.2015.2437276.

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Wall, J. V., I. J. Danziger, M. Pettini, R. S. Warwick i W. Wamsteker. "PKS 2005-489: A very bright BL Lac object in a nearby galaxy". Symposium - International Astronomical Union 119 (1986): 59–60. http://dx.doi.org/10.1017/s0074180900152271.

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The galaxy identified with the flat-spectrum radio source PKS 2005-489 has a bright stellar nucleus with V ⋍ 13 mag. Optical, UV and X-ray observations indicate variability and power-law continua in each of these wavebands, leading to the conclusion that PKS 2005-489 is one of the brightest BL Lac objects known.

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Soni, Mithil, Ozge Saatci, Gourab Gupta, Yogin Patel, Manikanda Raja Keerthi Raja, Jie Li, Xinfeng Liu i in. "miR-489 Confines Uncontrolled Estrogen Signaling through a Negative Feedback Mechanism and Regulates Tamoxifen Resistance in Breast Cancer". International Journal of Molecular Sciences 23, nr 15 (22.07.2022): 8086. http://dx.doi.org/10.3390/ijms23158086.

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Approximately 75% of diagnosed breast cancer tumors are estrogen-receptor-positive tumors and are associated with a better prognosis due to response to hormonal therapies. However, around 40% of patients relapse after hormonal therapies. Genomic analysis of gene expression profiles in primary breast cancers and tamoxifen-resistant cell lines suggested the potential role of miR-489 in the regulation of estrogen signaling and development of tamoxifen resistance. Our in vitro analysis showed that loss of miR-489 expression promoted tamoxifen resistance, while overexpression of miR-489 in tamoxifen-resistant cells restored tamoxifen sensitivity. Mechanistically, we found that miR-489 is an estrogen-regulated miRNA that negatively regulates estrogen receptor signaling by using at least the following two mechanisms: (i) modulation of the ER phosphorylation status by inhibiting MAPK and AKT kinase activities; (ii) regulation of nuclear-to-cytosol translocation of estrogen receptor α (ERα) by decreasing p38 expression and consequently ER phosphorylation. In addition, miR-489 can break the positive feed-forward loop between the estrogen-Erα axis and p38 MAPK in breast cancer cells, which is necessary for its function as a transcription factor. Overall, our study unveiled the underlying molecular mechanism by which miR-489 regulates an estrogen signaling pathway through a negative feedback loop and uncovered its role in both the development of and overcoming of tamoxifen resistance in breast cancers.

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Zheng, Bo, i Tao Chen. "MiR-489-3p inhibits cell proliferation, migration, and invasion, and induces apoptosis, by targeting the BDNF-mediated PI3K/AKT pathway in glioblastoma". Open Life Sciences 15, nr 1 (29.05.2020): 274–83. http://dx.doi.org/10.1515/biol-2020-0024.

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AbstractAmong astrocyte tumors, glioblastoma (GBM) is the most malignant glioma, highly aggressive and invasive, with extremely poor prognosis. Previous research has reported that microRNAs (miRNAs) participate in the progression of many cancers. Thus, this study aimed to explore the role and the underlying mechanisms of microRNA (miR)-489-3p in GBM progression. The expression of miR-489-3p and brain-derived neurotrophic factor (BDNF) mRNA was measured by quantitative real-time polymerase chain reaction. Western blot analysis was used to detect BDNF protein and the PI3K/AKT pathway-related protein. Cell proliferation, apoptosis, migration, and invasion were analyzed using CKK-8 assay, flow cytometry, and transwell assay, respectively. The interaction between BDNF and miR-489-3p was explored by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. MiR-489-3p was down-regulated and BDNF was up-regulated in GBM tissues and cells. MiR-489-3p re-expression or BDNF knockdown inhibited GBM cell proliferation, migration, and invasion, and promoted apoptosis. BDNF was a target of miR-489-3p, and BDNF up-regulation reversed the effects of miR-489-3p on GBM cells. The protein levels of p-AKT and p-PI3K were notably reduced in GBM cells by overexpression of miR-489-3p, but were rescued following BDNF up-regulation. Therefore, miR-489-3p inhibited proliferation, migration, and invasion, and induced apoptosis, by targeting the BDNF-mediated PI3K/AKT pathway in GBM, providing new strategies for clinical treatment of GBM.

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Dason, Ebernella Shirin, Madalina Maxim, Alexander Hartman, Qixuan Li, Salina Kanji, Tiantian Li, Charis Ng, Ella Huszti, Mara Sobel i Crystal Chan. "Pregnancy Outcomes With Donor Oocyte Embryos in Patients Diagnosed With Adenomyosis Using the Morphological Uterus Sonographic Assessment Criteria". Obstetrical & Gynecological Survey 78, nr 7 (lipiec 2023): 409–10. http://dx.doi.org/10.1097/01.ogx.0000947156.90590.45.

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(Abstracted from Fertil Steril 2023;119(3):484–489) Adenomyosis is a benign gynecologic condition that causes endometrial glands and stroma to be found in the myometrium. Although the criterion-standard diagnosis of adenomyosis remains histology after hysterectomy, ultrasound diagnosis has allowed earlier detection, but no standard definition of imaging-based diagnosis exists.

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Duncan, David R., i Bonnie H. Litwiller. "Turning Landslides into Cliff hangers: An Analysis of Presidential Election Returns". Mathematics Teacher 79, nr 8 (listopad 1986): 605–8. http://dx.doi.org/10.5951/mt.79.8.0605.

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The 1980 U.S. presidential election is widely perceived to have been a landslide. If one considers the electoral-vote totals (489 for Reagan; 49 for Carter), “landslide” seems an apt description. Popular-vote totals (43 899 248 for Reagan; 35 481 435 for Carter) depict a more competitive contest. The plurality (8 417 813) is still, however, substantial.

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Schenker, David J. "A Study in Choral Character: Aeschylus, Agamemnon 489-502". Transactions of the American Philological Association (1974-) 121 (1991): 63. http://dx.doi.org/10.2307/284443.

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Nguyen, Nancy, Teresa Worstell, Emily Griffin, Richard Beigi, Leonardo Pereira i Aaron Caughey. "489: Repeat antepartum GBS screening: a cost-effectiveness analysis". American Journal of Obstetrics and Gynecology 210, nr 1 (styczeń 2014): S244. http://dx.doi.org/10.1016/j.ajog.2013.10.522.

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Li, Wenhua, Yixin Zhang, Jian Wang, Qiang Li, Di Zhao, Bozan Tang, Shiwei Wang i Haifeng Shao. "MicroRNA-489 Promotes the Apoptosis of Cardiac Muscle Cells in Myocardial Ischemia-Reperfusion Based on Smart Healthcare". Journal of Healthcare Engineering 2022 (7.01.2022): 1–9. http://dx.doi.org/10.1155/2022/2538769.

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With the development of information technology, the concept of smart healthcare has gradually come to the fore. Smart healthcare uses a new generation of information technologies, such as the Internet of Things (loT), big data, cloud computing, and artificial intelligence, to transform the traditional medical system in an all-around way, making healthcare more efficient, more convenient, and more personalized. miRNAs can regulate the proliferation, differentiation, and apoptosis of human cells. Relevant studies have also shown that miRNAs may play a key role in the occurrence and development of myocardial ischemia-reperfusion injury (MIRI). This study aims to explore the effects of miR-489 in MIRI. In this study, miR-489 expression in a myocardial ischemia-reperfusion animal model and H9C2 cells induced by H/R was detected by qRT-PCR. The release of lactate dehydrogenase (LDH) and the activity of creatine kinase (CK) was detected after miR-489 knockdown in H9C2 cells induced by H/R. The apoptosis of H9C2 cells and animal models were determined by ELISA. The relationship between miR-489 and SPIN1 was verified by a double fluorescence reporter enzyme assay. The expression of the PI3K/AKT pathway-related proteins was detected by Western blot. Experimental results showed that miR-489 was highly expressed in cardiac muscle cells of the animal model and in H9C2 cells induced by H/R of the myocardial infarction group, which was positively associated with the apoptosis of cardiac muscle cells with ischemia-reperfusion. miR-489 knockdown can reduce the apoptosis of cardiac muscle cells caused by ischemia-reperfusion. In downstream targeting studies, it was found that miR-489 promotes the apoptosis of cardiac muscle cells after ischemia-reperfusion by targeting the inhibition of the SPIN1-mediated PI3K/AKT pathway. In conclusion, high expression of miR-489 is associated with increased apoptosis of cardiac muscle cells after ischemia-reperfusion, which can promote the apoptosis after ischemia-reperfusion by targeting the inhibition of the SPIN1-mediated PI3K/AKT pathway. Therefore, miR-489 can be one of the potential therapeutic targets for reducing the apoptosis of cardiac muscle cells after ischemia-reperfusion.

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Łakomy-Chłosta, Agnieszka, Agnieszka Franczyk-Cegła i Wanda A. Ciszewska. "Kronika". Z Badań nad Książką i Księgozbiorami Historycznymi 12 (24.12.2018): 477–96. http://dx.doi.org/10.33077/uw.25448730.zbkh.2018.23.

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Konferencja „Książka i biblioteki na przestrzeni wieków”, Katowice 23 V 2018 r. – sprawozdanie Agnieszka Łakomy-ChłostaInstytut Bibliotekoznawstwa i Informacji NaukowejUniwersytet Śląski w Katowicach, Katowice, Polskaa.lakomy@interia.plORCID 0000-0002-0024-0691 Z Badań nad Książką i Księgozbiorami Historycznymi 2018, t. 12, s. 477-481. ------------------------------------------------------------------------- Konferencja „Zbiory specjalne w bibliotekach polskich a problematyka cyfryzacji”, Książnica Pomorska im. St. Staszica w Szczecinie, 24-25 V 2018 r. – sprawozdanie Agnieszka Franczyk-CegłaDział Starych Druków Zakład Narodowy im. Ossolińskich, Wrocław, Polskaagnieszka.franczyk-cegla@znio.plORCID 0000-0002-1231-925X Z Badań nad Książką i Księgozbiorami Historycznymi 2018, t. 12, s. 481-486. ------------------------------------------------------------------------- Konferencja „Bibliotheca Universitatis: пам’ять – діалог – реінтерпретація”, Lwów, 26 X 2018 r. – sprawozdanie Agnieszka Franczyk-CegłaDział Starych Druków, Zakład Narodowy im. Ossolińskich, Wrocław, Polskaagnieszka.franczyk-cegla@znio.plORCID 0000-0002-1231-925X Z Badań nad Książką i Księgozbiorami Historycznymi 2018, t. 12, s. 486-489. ------------------------------------------------------------------------- Jubileuszowo o cenzurze –V Ogólnopolska Konferencja Naukowa „Niewygodne dla władzy. Ograniczanie wolności słowa”, 18–19 października 2018 r. Wanda A. CiszewskaInstytut Informacji Naukowej i BibliologiiUniwersytet Mikołaja Kopernika w Toruniu, Toruń, Polskatai@umk.plORCID 0000-0001-8716-9869 Z Badań nad Książką i Księgozbiorami Historycznymi 2018, t. 12, s. 490-496.

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Gupta, Gourab, Ryan Titus, Yogin Patel, Shakthika Sarvanan i Hexin Chen. "Abstract 3784: miR-489 induces apoptosis and immunogenic cell death through targeting FOXM1 in triple negative breast cancer cells". Cancer Research 83, nr 7_Supplement (4.04.2023): 3784. http://dx.doi.org/10.1158/1538-7445.am2023-3784.

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Abstract It has been well established that microRNAs (miRNAs) have an important role in cancer sustenance and progression. Our previous studies have established the role of miR-489 as a tumor suppressor miRNA in breast cancer. However, the multiple targets of this miRNA have diversified its mechanism from preventing tumor cell proliferation to promoting cell death pathways. In this study we have aimed to establish the role of miR-489 in cell cycle inhibition, leading to Endoplasmic Reticulum stress (ER stress) and ultimately immunogenic cell death (ICD). Firstly, we found that overexpression of miR-489 in triple negative breast cancer (TNBC) cell lines including MDA-MB-231, BT 549, drastically reduced cell proliferation using colony formation assay and real-time cell analysis. Furthermore, studies like GO analysis, sequence analysis and cell cycle analysis demonstrated that miR-489 induces cell cycle arrest and apoptosis in TNBC by directly targeting FOXM1 and regulating other kinases like CDK1. It was also shown for the first time that miR-489 overexpression induces ER stress and the release of damage associated molecular patterns (DAMPs), consistent with hallmarks of ICD like Calreticulin exposure on cellular surface and ATP release, triggering phagocytosis. It was also established that miR-489-induced apoptosis lead to the elevation of cleaved caspase 3, which was responsible for the activation of PANX1 and the consequent release of ATP. In conclusion, we tried to mechanistically understand the role of miR-489 in cell cycle arrest leading to cellular stress. Stress induced apoptosis and consequent ICD was also a possible outcome and it turned out miR-489 overexpression without any other ICD inducer was good enough to trigger the release of DAMPs and elucidate an immunogenic response. Citation Format: Gourab Gupta, Ryan Titus, Yogin Patel, Shakthika Sarvanan, Hexin Chen. miR-489 induces apoptosis and immunogenic cell death through targeting FOXM1 in triple negative breast cancer cells. [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 3784.

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Chen, Xiaoqiang, Chen Li, Wei Chen, Shuchun Lin, Xuehan Yi, Qin Lin, Hao Xu i Desheng Wang. "Metformin Inhibits the Development of Hypopharyngeal Squamous Cell Carcinoma through Circ_0003214-Mediated MiR-489-3p-ADAM10 Pathway". Journal of Oncology 2021 (13.07.2021): 1–13. http://dx.doi.org/10.1155/2021/2265475.

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Purpose. This study aims to explore the function of metformin in hypopharyngeal squamous cell carcinoma (HSCC) and the underlying mechanism. Methods. Cell viability, colony formation, cell apoptosis, and cell cycle were investigated using cell counting kit-8 assay, colony formation, and flow cytometry assay. Gene expression was detected by quantitative real-time polymerase chain reaction and western blot. The target relationship was validated by dual-luciferase reporter assay or RNA immunoprecipitation assay. An animal study was implemented to clarify the effect of metformin in vivo. Results. Metformin suppressed HSCC cell viability and colony formation ability and induced cell cycle arrest and apoptosis, and circ_0003214 overexpression weakened these effects. Circ_0003214 regulated A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression via targeting miR-489-3p. Besides, miR-489-3p restoration reversed the role of circ_0003214, and ADAM10 knockdown reversed miR-489-3p inhibition-mediated effect. Moreover, metformin blocked tumor growth via the circ_0003214-miR-489-3p-ADAM10 axis in vivo. Conclusion. Metformin inhibits HSCC progression through the circ_0003214/miR-489-3p/ADAM10 pathway.

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Pfeijffer, Ilja Leonard. "The date of Pindar's fifthNemeanand Bacchylides' thirteenth ode". Classical Quarterly 45, nr 2 (grudzień 1995): 318–32. http://dx.doi.org/10.1017/s0009838800043421.

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Just about every odd year in the early fifth century B.C. has been proposed as the date of the Nemean victory of Pytheas from Aegina, celebrated in Pindar's FifthNemeanand Bacchylides' thirteenth ode. Scholars have attempted to date both odes with the help ofIsthmian6 and 5, which celebrate victories of a member of the same family and the latter of which at 48ff. refers to Salamis as a recent event. Various interpretations of the victory catalogues inI.6 and 5 have led to various dates forN.5 and B. 13. The fullest analysis of the material is that by Severyns, who argues thatN.5 and B. 13 must be at least seven years earlier than I. 5. In his conclusion (pp. 50–51), however, he still suggests three possible dates forN.5 and B. 13: 487, 489, and 485 B.C., in what he considers to be the order of likelihood.

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Lunsford, Dale. "A Senior Level AIS Course Based On The AICPAs Top-Ten Technology Issues". Review of Business Information Systems (RBIS) 5, nr 4 (1.10.2001): 43–50. http://dx.doi.org/10.19030/rbis.v5i4.5367.

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In response to requests from accounting firms and companies that hire graduates of the Culverhouse School of Accountancy (CSA) at the University of Alabama (UA), the CSA was awarded a permanent increase in funding to enhance its Accounting Information Systems (AIS) course offerings. As a result of this, two new faculty were hired to teach AIS courses and a Collaborative Learning Lab (CLL) was constructed in the College of Commerce and Business Administration (CBA) computer center. Prior to this change, the AIS curriculum consisted of one undergraduate course and one graduate course in AIS. Two new courses were added to the curriculum, one each at the graduate and undergraduate levels. This past year I was responsible for the senior level AIS course, Accounting 489 (AC 489). Since there was no pre-specified list of topics to be covered in this course, I decided to use the American Institute of Certified Public Accountants (AICPA) top-ten technology issues list as a basis for the content of the course. This paper briefly describes the AIS curriculum at UA and then discusses challenges faced when defining AC 489, the structure of AC 489, and an evaluation of the course based on my experiences this past year.

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Keim, Garrett, Neethi Pinto, Jason Christie i Nadir Yehya. "489: READMISSION AFTER PEDIATRIC ACUTE RESPIRATORY FAILURE: A COMMON OCCURRENCE". Critical Care Medicine 50, nr 1 (16.12.2021): 235. http://dx.doi.org/10.1097/01.ccm.0000808280.13283.77.

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Kaplan, Atira H., Yuxi Chen i Matthew N. Bartels. "Poster 489 Rehabilitation After Pediatric Heart Transplant: A Case Report". PM&R 8, nr 9 (wrzesień 2016): S319. http://dx.doi.org/10.1016/j.pmrj.2016.07.407.

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Schwingel, P. A., H. P. Cotrim, B. C. R. Salles, C. E. R. Almeida, B. S. Nachef, C. A. B. Ferreira Filho i C. R. Santos Júnior. "489 ANDROGENIC-ANABOLIC STEROID USER AND A LARGE SPECTRUM DISEASE". Journal of Hepatology 54 (marzec 2011): S200. http://dx.doi.org/10.1016/s0168-8278(11)60491-1.

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Bertelsen, K. "489 A dose intensity study of carboplatin in ovarian cancer". European Journal of Cancer 31 (listopad 1995): S104—S105. http://dx.doi.org/10.1016/0959-8049(95)95743-p.

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Freitas, Ricardo Pacheco Mesquita de. "A NECESSIDADE DE INTERPRETAÇÃO RESTRITIVA DO ARTIGO 489, § 2º, DO NOVO CÓDIGO DE PROCESSO CIVIL". Revista de Doutrina Jurídica 109, nr 2 (21.09.2018): 123–36. http://dx.doi.org/10.22477/rdj.v109i2.167.

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O objetivo deste artigo é analisar a necessidade de se interpretar restritivamente o §2º do art. 489 da Lei 13.105/2015, tendo em vista que uma interpretação literal tem o condão de ameaçar o Estado de Direito e a Segurança Jurídica, ainda mais no presente contexto jurídico que vive o Brasil. Primeiro estabelece-se o conceito de norma jurídica e ressaltamos sua subdivisão em normas-princípio e normas-regra, enaltecendo a força normativa dos princípios. Em seguida, argumenta-se a inconveniência do §2º do art. 489 da Lei 13.105/2015 e os danos que podem ser causados por sua interpretação literal e por fim se delimitam as causas agravantes da insegurança jurídica no Brasil que podem ser potencializada por uma interpretação ampliativa do dispositivo analisado, chegando-se à conclusão, a partir da pesquisa realizada, que para resguardarmos o Estado de Direito e prestigiarmos a segurança jurídica, a palavra "normas" no art. 489, 2º do Novo CPC deve sempre ser interpretada, restritivamente, como sinônimo de princípios.

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Theiler, James, i Guen Grosklos. "Corrections to “Problematic Projection to the In-Sample Subspace for a Kernelized Anomaly Detector” [Apr 16 485-489]". IEEE Geoscience and Remote Sensing Letters 15, nr 2 (luty 2018): 307. http://dx.doi.org/10.1109/lgrs.2018.2790098.

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Zhang, Haoran, Wenqiu Wang, Junjie Lin, Junbo Qiao, Xinjun Wang, Bin Fang, Changkuan Chen, Yujiao Wang, Gaozan Zhu i Wenbo Liu. "Mechanism of LEF1-AS1 regulating HUVEC cells by targeting miR-489-3p/S100A11 axis". PeerJ 11 (1.11.2023): e16128. http://dx.doi.org/10.7717/peerj.16128.

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Background The venous malformation is the most common congenital vascular malformation and exhibits the characteristics of local invasion and lifelong progressive development. Long noncoding RNA (lncRNA) regulates endothelial cells, vascular smooth muscle cells, macrophages, vascular inflammation, and metabolism and also affects the development of venous malformations. This study aimed to elucidate the role of the lncRNA LEF1-AS1 in the development of venous malformations and examine the interaction among LEF1-AS1, miR-489-3p, and S100A11 in HUVEC cells. Methods Venous malformation tissues, corresponding normal venous tissues, and HUVEC cells were used. Agilent human lncRNA microarray gene chip was used to screen differential genes, RNA expression was detected using quantitative reverse transcription PCR, and protein expression was detected using Western blotting. The proliferation, migration, and angiogenesis of HUVEC cells were assessed using CCK8, transwell, and in vitro angiogenesis tests. Results A total of 1,651 lncRNAs were screened using gene chip analysis, of which 1015 were upregulated and 636 were downregulated. The lncRNA LEF1-AS1 was upregulated with an obvious difference multiple, and the fold-change value was 11.03273. The results of the analysis performed using the StarBase bioinformatics prediction website showed that LEF1-AS1 and miR-489-3p possessed complementary binding sites and that miR-489-3p and S100A11 also had complementary binding sites. The findings of tissue experiments revealed that the expressions of LEF1-AS1 and S100A11 were higher in tissues with venous malformations than in normal tissues, whereas the expression of miR-489-3p was lower in venous malformations than in normal tissues. Cell culture experiments indicated that LEF1-AS1 promoted the proliferation, migration, and angiogenesis of HUVEC cells. In these cells, LEF1-AS1 targeted miR-489-3p, which in turn targeted S100A11. LEF1-AS1 acted as a competitive endogenous RNA and promoted the expression of S100A11 by competitively binding to miR-489-3p and enhancing the proliferation, migration, and angiogenesis of HUVEC cells. Thus, LEF1-AS1 participated in the occurrence and development of venous malformation. Conclusions The expression of LEF1-AS1 was upregulated in venous malformations, and the expression of S100A11 was increased by the adsorption of miR-489-3p to venous endothelial cells, thus enhancing the proliferation, migration, and angiogenesis of HUVEC cells. In conclusion, LEF1-AS1 is involved in the occurrence and development of venous malformations by regulating the miR-489-3p/S100A11 axis, which provides valuable insights into the pathogenesis of this disease and opens new avenues for its treatment.

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Golubovskaya, Inna, Nadezhda Avalkina i William F. Sheridan. "New Insights Into the Role of the Maize ameiotic1 Locus". Genetics 147, nr 3 (1.11.1997): 1339–50. http://dx.doi.org/10.1093/genetics/147.3.1339.

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In maize the am1-1 mutant allele results in both the male and female meiocytes undergoing mitosis in place of the meiotic divisions. A second mutant allele am1-praI enables both the male and female meiocytes to proceed to the early zygotene stage of meiotic prophase I before being blocked. Here we report on three new alleles that allow all male meiocytes to undergo mitosis but in female meiocytes approximately one quarter (am1-2), one half (am1-485, or all (am1-489) of them are blocked at an abnormal interphase stage. Previous analysis has shown that am1-praI is dominant to am1-1 in male meiocytes. Cytological analysis of heteroallelic combinations in female meiocytes now indicates a dominance relationship of am1-praI > am1-1 > am1-2/am1-485 > am1-489. The evidence provided by the female phenotypes of the new mutant alleles suggest that, whereas the normal am1 allele is required for the meiocytes to proceed through meiosis, a partially functional allele may be required for their diversion into a mitotic division. The partial or complete blockage of mitosis in female meiocytes carrying the new am1 alleles rules out the possibility that the mitotic division of mutant meiocytes reflects a simple default pathway for cells that cannot initiate meiosis. This locus may have a dual function.

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Fu, Xiaomei, Jianfang Zhang, Xuanjie Huang, Zhifeng Mo, Ziyang Sang, Wenfei Duan i Wenfeng Huang. "Curcumin Antagonizes Glucose Fluctuation-Induced Renal Injury by Inhibiting Aerobic Glycolysis via the miR-489/LDHA Pathway". Mediators of Inflammation 2021 (18.08.2021): 1–25. http://dx.doi.org/10.1155/2021/6104529.

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It has been considered that glucose fluctuation (GF) plays a role in renal injury and is related to diabetic nephropathy (DN) development. But the mechanism is still unclear. Aerobic glycolysis has become a topical issue in DN in recent years. There is an internal connection between GF, aerobic glycolysis, and DN. Curcumin (Cur) is a principal curcuminoid of turmeric and possesses specific protective properties in kidney functions. Cur also participates in the regulation of aerobic glycolysis switch. In this study, we first measured the levels of aerobic glycolysis and evaluated Cur’s inhibitory ability in a cell model of HEK-293 under the condition of oscillating high glucose. The results indicated that GF exacerbated inflammation injury, oxidative stress, and apoptosis in HEK-293 cell, while Cur alleviated this cytotoxicity induced by GF. We found that GF increased aerobic glycolysis in HEK-293 cells and Cur presented a dose-dependent weakening effect to this exacerbation. Next, we built a panel of 17 miRNAs and 8 lncRNAs that were previously reported to mediate the Warburg effect. Our RT-qPCR results indicated that GF reduced the miR-489 content in the HEK-293 cell model and Cur could prevent this downregulation. Then, we planned to explore the character of miR-489 in Cur-triggered attenuation of the Warburg effect under GF condition. Our findings presented that Cur prevented GF-triggered aerobic glycolysis by upregulating miR-489 in HEK-293 cells. Next, we choose the miR-489/LDHA axis for further investigation. We confirmed that Cur prevented GF-triggered aerobic glycolysis via the miR-489/LDHA axis in HEK-293 cells. In conclusion, this study presented that Cur prevented GF-triggered renal injury by restraining aerobic glycolysis via the miR-489/LDHA axis in the HEK-293 cell model.

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Zhou, Lijun, Aiwu Li i Qiangye Zhang. "6 ′ -O-Galloylpaeoniflorin Exerts Inhibitory Bioactivities in Human Neuroblastoma Cells via Modulating AMPK/miR-489/XIAP Pathway". BioMed Research International 2022 (5.05.2022): 1–11. http://dx.doi.org/10.1155/2022/1327835.

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Although therapies against neuroblastoma (NBM) have advanced, the patients still suffer from poor prognoses due to distal metastasis or the occurrence of multidrug resistance. Accumulating evidence has proved that chemicals derived from natural products possess potent anti-NBM properties or can be used as adjuvants for chemotherapy. In the present study, we demonstrated that 6 ′ -O-galloylpaeoniflorin (GPF), a galloylated derivative of paeoniflorin isolated from the roots of Paeonia lactiflora Pall, exerted significant inhibitory effects on proliferation and invasion of SH-SY5Y cells (an NBM cell line) and enhanced the sensitivity of SH-SY5Y cells to cisplatin in vitro. Further studies showed that GPF treatment upregulated miR-489 in NBM cells via activating AMP-activated protein kinase (AMPK). We also demonstrated that similar to GPF treatment, miR-489 exhibited a significant anti-NBM capacity. Further studies showed that miR-489 directly targeted the X-linked inhibitor of apoptosis protein (XIAP). Overall, our results indicated that GPF possessed an evident anti-NBM capacity dependent on AMPK/miR-489/XIAP pathway, providing an emerging strategy for clinical treatment of NBM.

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Flick-Takács, Nikolett. "„Használati útmutató” a kutatói szemléletmód kialakításához a tudásalapú társadalmak pedagógusképzésében – Könyvismertetés". Gyermeknevelés 9, nr 2 (19.10.2021): 408–12. http://dx.doi.org/10.31074/gyntf.2021.2.408.412.

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Csíkos Csaba (2020). A neveléstudomány kutatásmódszertanának alapjai. Elte Eötvös Kiadó, p. 118, Budapest. ISBN 978-963-489-248-9https://www.eltereader.hu/media/2020/12/web_Csikos-Csaba_Bevezetes__.pdf

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Xia, Shaofeng, i Chenliang Wang. "Hsa_circ_0003220 Drives Chemoresistance of Human NSCLC Cells by Modulating miR-489-3p/IGF1". International Journal of Genomics 2023 (16.06.2023): 1–12. http://dx.doi.org/10.1155/2023/8845152.

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Circular RNAs (circRNAs) have been shown to have critical roles in developing cancer and treatment resistance in an increasing body of research. The aim was to look into the functions and processes of hsa_circ_0003220 in the non-small cell lung cancer (NSCLC) chemoresistance. The NSCLC cell lines H460 and A549 were employed in present work. hsa_circ_0003220, miR-489-3p, and insulin-like growth factors (IGF1) mRNA levels were assessed with a quantitative real time polymerase chain reaction (qRT-PCR). The cisplatin, docetaxel, and paclitaxel (PTX) resistances were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and the enzyme linked immunosorbent assay (ELISA) test measured IGF1 expression. In order to corroborate the miR-489-3p relation with hsa_circ_0003220 or IGF1, a dual-luciferase reporter method was applied. The level of hsa_circ_0003220 was raised in cells and tissues from PTX-resistant (PR) NSCLC. In PR NSCLC cells, hsa_circ_0003220 knockdown reduced chemoresistance. For the purpose of the mechanism study, hsa_circ_0003220 knockdown substantially reduced IGF1 expression via miR-489-3p sponging, reducing chemoresistance in PR NSCLC cells. By controlling the miR-489-3p/IGF1 axis, hsa_circ_0003220 knockdown helped NSCLC overcome chemoresistance, suggesting a potential circRNA-targeted therapy for the disease.

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da Empoli, Domenico. "A. Allocati (a cura di), Carteggio Loria–Graziani (1888–1943)". Journal of Public Finance and Public Choice 9, nr 2 (1.10.1991): 147–49. http://dx.doi.org/10.1332/251569298x15668907345324.

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Soung, Young Hwa, Jingfang Ju i Jun Chung. "The Sensitization of Triple-Negative Breast Cancers to Poly ADP Ribose Polymerase Inhibition Independent of BRCA1/2 Mutation Status by Chemically Modified microRNA-489". Cells 13, nr 1 (26.12.2023): 49. http://dx.doi.org/10.3390/cells13010049.

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Chemoresistance and inefficient therapeutic efficacies in triple-negative breast cancers (TNBCs) are among the major clinical problems in breast cancers. A potential new method to sensitize these tumors to current treatment options is, therefore, urgent and necessary. Our previous studies demonstrated that miR-489 serves as one of the top tumor-suppressing miRs and features downregulated expression in metastatic TNBCs and that the restoration of miR-489 expression in TNBCs effectively inhibits the metastatic potentials of TNBCs both in vitro and in vivo. The chemical modification of miR-489 (CMM489) through the replacement of uracil with 5-FU further enhances the therapeutic potential of miR-489. In the present study, we tested the effects of CMM489 in synergizing DNA damage response (DDR) inhibitors such as PARP inhibitors. CMM489 is particularly effective in sensitizing TNBC cell lines with inherent resistance to PARP inhibitors regardless of BRCA mutation status. One of the anti-cancer mechanisms through which CMM489 synergizes with PARP inhibitors is the blockade of homologous recombination (HR) in TNBC cells upon DNA damage. The results of this study highlight the potential use of CMM489 in combination treatments with PARP inhibitors in TNBCs.

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Rector, Travis A., i Eric S. Perlman. "A Search for Intraday Variability in the Blazar PKS 2005-489". Astronomical Journal 126, nr 1 (lipiec 2003): 47–52. http://dx.doi.org/10.1086/375644.

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Millar, P. J., H. Murai, B. L. Morris i J. S. Floras. "489 Activation by Human Heart Failure of a Sympathoexcitatory Cardiopulmonary Reflex". Canadian Journal of Cardiology 28, nr 5 (wrzesień 2012): S279. http://dx.doi.org/10.1016/j.cjca.2012.07.447.

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Kan, C., N. Silva, S. Golden, U. Rajala, M. Timonen, D. Stahl i K. Ismail. "A systematic review and meta-analysis of the association between depression and insulin resistance. Diabetes Care 2013;36:480-489". Diabetes Care 36, nr 5 (23.04.2013): 1429. http://dx.doi.org/10.2337/dc13-er05.

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Kim, JeongHwan, Eun Kyoung Kim, Min Jee Park, Ji Hye Park, Se-min Oh, Yujin Won, Nak-won Lee, Soo Kyung Lee, Hyelim Yi i Minjung Kim. "A Statistical Analysis of Forensic Autopsies Performed in the Jungbu Province of Korea in 2021". Korean Journal of Legal Medicine 47, nr 4 (30.11.2023): 110–21. http://dx.doi.org/10.7580/kjlm.2023.47.4.110.

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We analyzed 1,079 forensic autopsies conducted in 2021 by the National Forensic Service Daejeon Institute from the Jungbu province in the central part of South Korea, for their manner and cause of death. Among the manner of death (n=1,079), 45.3% (n=489) were categorised as unnatural, 39.5% (n=426) as natural, and 15.2% (n=164) were unknown. Among the unnatural deaths (n=489), 40.7% (n=199) were accidents, 36.8% (n=180) were suicides, 14.1% (n=69) were undetermined, and 8.4% (n=41) were homicides. The major causes of unnatural deaths (n=489) were by trauma, causing 34.4% (n=168), poisoning causing 26.8% (n=131), and asphyxia causing 17.2% (n=84). The major cause of death by trauma (n=168) was falling at 46.4% (n=78), and by asphyxia (n=84) was strangulation at 76.2% (n=64). Among natural deaths (n=426), heart disease was the major cause at 49.8% (n=212) followed by vascular disease at 16.7% (n=71). In future, a time-series statistical analysis on the manner and causes of death in Jungbu province may provide insight and allow for more advanced interpretations about both healthcare and public safety.

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Gomes Vieira, Guilherme. "A FUNDAMENTAÇÃO DE DECISÕES PROFERIDAS EM RECURSOS REPETITIVOS DA CORTE ESPECIAL DO SUPERIOR TRIBUNAL DE JUSTIÇA: UMA ANÁLISE DE 2016 A 2021". REVISTA BRASILEIRA DE DIREITO PROCESSUAL 30, nr 120 (2023): 1–28. http://dx.doi.org/10.52028/rbdpro.v30i120.210708df.

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O artigo 489, § 1º, do Código de Processo Civil estabeleceu hipóteses inéditas em que não se considera fundamentada determinada decisão judicial. A presente pesquisa objetiva investigar, de forma empírica, se o Superior Tribunal de Justiça observa essa novidade legislativa em determinadas deliberações jurisdicionais. Utilizando-se o repositório jurisprudencial deste órgão jurisdicional, foram analisados os acórdãos de Recursos Especiais Repetitivos julgados pela Corte Especial do Superior Tribunal de Justiça no quinquênio posterior à vigência do atual diploma processual civil. Adotaram-se os critérios de análise correspondentes às previsões normativas dos incisos do referido dispositivo legal. Os resultados indicam que um terço dos julgados investigados não observou, integralmente, o disposto no artigo 489, § 1º, do Código de Processo Civil.

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Rector, Travis, Eric Perlman, Rita Sambruna, Greg Madejski i Frederik Rantakyro. "Multifrequency Monitoring of the Blazar PKS 2005-489". Publications of the Astronomical Society of Australia 19, nr 1 (2002): 158–60. http://dx.doi.org/10.1071/as01115.

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AbstractWe present a multifrequency monitoring campaign of PKS 2005–489, a bright and highly variable blazar. Simultaneous observations were completed over a 13 day period in the X-ray with RXTE, in the optical at the CTIO 0.9 m telescope, at TeV energies with CANGAROO-II, and at submillimetre wavelengths with SEST. Previous multiwavelength monitoring campaigns of PKS 2005–489 and other blazars have found complex flux and spectral variability behaviour, with different modes and timescales from days to hours and shorter.PKS 2005–489 was observed in transition from a quiescent state into the early stages of a flare. A gradual increase in flux density was observed at optical and X-ray wavelengths during 19–27 August 2000, and a dramatic increase in X-ray emission was observed starting on 2 September 2000. Intraday and spectral variability were not detected during the campaign.

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Wall, J. V., I. J. Danziger, M. Pettini, R. S. Warwick i W. Wamsteker. "PKS 2005-489: a very bright BL Lac object in a nearby galaxy". Monthly Notices of the Royal Astronomical Society 219, nr 1 (1.03.1986): 23P—29P. http://dx.doi.org/10.1093/mnras/219.1.23p.

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Oliveira, Ademar P., Adriano C. Andrade, José Tavares Sobrinho i Nei Peixoto. "Avaliação de linhagens e cultivares de feijão-vagem de crescimento indeterminado, no município de Areia-PB". Horticultura Brasileira 19, nr 2 (lipiec 2001): 159–62. http://dx.doi.org/10.1590/s0102-05362001000200014.

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Avaliaram-se quinze linhagens (Hav 13, Hav 14, Hav 21, Hav 22, Hav 25, Hav 38, Hav 40, Hav 41, Hav 49, Hav 53, Hav 56, Hav 60, Hav 65, Hav 67 e Hav 68) e oito cultivares comerciais (Macarrão Favorito Ag 480, Macarrão Preferido Ag 482, Manteiga Maravilha Ag 481, Teresópolis Ag 484, Macarrão Bragança, Macarrão Trepador Topseed, Macarrão Trepador Hortivale e Macarrão Trepador Isla) de feijão-vagem de crescimento indeterminado. O ensaio foi conduzido na Universidade Federal da Paraíba, em Areia, no período de março a agosto de 1999 em Latossolo Vermelho-Amarelo. As linhagens Hav 22 (31,6 t/ha), Hav 38 (35,00t/ha), Hav 41 (31,5 t/ha), Hav 68 (30,5 t/ha), e as cultivares Macarrão Favorito Ag 480 (30,3 t/ha), Macarrão Preferido Ag 482 (39,1 t/ha) e Manteiga Maravilha Ag 481 (36,2 t/ha) destacaram-se por apresentarem alta produtividade, peso médio de vagens de acordo com a preferência do mercado local, e teor de fibra dentro dos padrões comerciais. A cultivar Teresópolis Ag 484 (58,5 t/ha), embora tenha apresentado alta produtividade, necessita de estudos de mercado, para que possa ser indicada para os produtores, uma vez que apresenta vagens grandes e achatadas.

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Trindade, André Karam, i João Carneiro Duarte Neto. "OS (DES)ACERTOS DO LEGISLADOR NA “POSITIVAÇÃO” DAS TEORIAS DE ROBERT ALEXY NO DIREITO PROCESSUAL CIVIL BRASILEIRO". Revista Eletrônica do Curso de Direito da UFSM 12, nr 3 (20.12.2017): 1044. http://dx.doi.org/10.5902/1981369429603.

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O presente artigo busca identificar a presença de elementos da teoria jurídica de Robert Alexy nos §§ 1º e 2º do artigo 489 do Código de Processo Civil. Para tanto, o estudo estrutura-se em duas partes. Na primeira, após introduzir a teoria da argumentação jurídica, analisa os dispositivos contidos no §1º do artigo 489 do Código de Processo Civil à luz da referida teoria, observando-se a harmonia entre o texto legal e alguma das formulações doutrinárias de Alexy. Na segunda, apresenta a teoria dos direitos fundamentais, com ênfase na distinção entre regras e princípios, na máxima da proporcionalidade e na técnica da ponderação, e examina o §2º do artigo 489 do Código de Processo Civil, verificando a total dissonância entre o texto legal e as bases teóricas de Alexy. Na conclusão, ao final, indicam-se os (des)acertos do legislador, apontando suas consequências para o direito brasileiro.

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Kalff, Anna, Kate Reed, Tiffany T. Khong, Sridurga Mithraprabhu, Malarmathy Ramachandran, John Reynolds, Krystal Bergin i in. "Roar: A Phase Ib Trial of Oral Azacitidine (CC-486) in Combination with Lenalidomide and Dexamethasone (Rd) for Patients with Relapsed and/or Refractory (R/R) Multiple Myeloma Who Have Failed a Prior Lenalidomide-Containing Regimen". Blood 128, nr 22 (2.12.2016): 2121. http://dx.doi.org/10.1182/blood.v128.22.2121.2121.

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Abstract Introduction Azacitidine (AZA) is a DNA methyltransferase inhibitor and cytotoxic agent with survival benefits in higher-risk MDS and AML. We have demonstrated that AZA rapidly induces apoptosis of MM cells, and induces synergistic killing when combined with lenalidomide (LEN). This, coupled with development of an oral AZA formulation (CC-486), provides rationale for pursuing this combination in MM. The cereblon [CBRN]-Ikaros/Aiolos-IRF4/c-MYC signalling pathway has been implicated in the mechanism of action of cytotoxicity for IMiD®compounds. This pathway, as well as immune markers (CD8, PD-1) may represent potential biomarkers for predicting outcomes/response to IMiD® compounds. Aims: In R/R myeloma patients who previously failed a LEN-containing regimen: to determine the maximum tolerated dose (MTD) of CC-486 in combination with Rd; to characterise safety/tolerability; to assess efficacy: overall response rate (ORR), progression free survival (PFS), overall survival (OS). To correlate pre-treatment MM protein expression (CRBN, Ikaros, Aiolos, IRF4, c-MYC), as well as whole marrow expression of CD8/PD-1 with response and survival (PFS/OS) in patients receiving CC-489 plus Rd. Methods: Phase Ib, single centre, 3 x 3 dose escalation study. LEN 25mg d1-21 and dexamethasone 40mg d1, 8, 15, 22 of 28 day cycle were combined with escalating doses of CC-489: initial dose 100mg for d1-14, increasing by either 7 days or 50mg/cohort, to a maximum of 200mg d1-21. Dose limiting toxicity (DLT) was assessed during cycle 1. Treatment continued until toxicity/progression. Single- and dual-IHC assays were performed on pre-treatment trephines (Single: CD8, PD-1; Dual: CD138 paired with CRBN, Aiolos, Ikaros, IRF4, c-MYC). In samples with >10% CD138, presence and sub-cellular localisation of each stain was documented, and given an H score: product of % of tumour positive and intensity of staining (0-3). Single CD8 and PD-1 IHC assays were reported as positive cells/mm2. Samples were grouped according to quartiles (Group1: lower quartile, Group2: mid-range, Group3: upper quartile) and analysis was performed using SAS statistical platform v9.4. Results: 22 patients commenced therapy (F=10, M=12), median age 67yrs (50-82yrs). Median prior lines of therapy: 5 (2-8), including 16 ASCT and 2 prior allogeneic transplant. All had failed LEN (R/R=18, primary refractory (PrimR)=4), 10/22 received and failed pomalidomide (POM) (R/R=4, PrimR=6). All had received bortezomib (R/R=10, PrimR=10), 18/22 were both bortezomib and LEN refractory. CC-486 dose reached was 200mg d1-21, with no DLTs observed at time of reporting. One patient died due to unrelated causes prior to end cycle 1, therefore was not evaluable for response. ORR (≥PR) was 43% (9/21): 8 PR, 1 VGPR. Of the remaining patients, 2 achieved MR, 5 SD, and 5 PD. (clinical benefit rate (≥MR) = 52%). Median time to best response in patients with ≥MR: 2.5m (1-3.7m). Responses were seen in cohorts: [100mg d1-14 (3PR=3), 100mg d1-21 (VGPR=1, PR=3), 150mg d1-21 (PR=2, MR=2)]. Median time on study: 3m; responders (≥MR): 6.3m (2.5-15m), non-responders: 1.7m (0.9-8m). Median PFS 3m, median OS 15m. One patient remains on study. 3/6 patients treated with LEN in prior 1-2 treatment lines responded (PR=2, VGPR=1), 1/6 had SD. 1/10 patients treated with POM in prior 1-2 treatment lines responded (PR), with 2 achieving MR and 3 SD. Patients with a lower expression of cMYC and IRF4 had superior PFS compared with patients with higher expression (cMYC: Group1 vs Group3 p=0.052; IRF4: Group1 vs Group2 p=0.04). Patients with lower numbers of CD8+ T-cells had better PFS than those with higher (p=0.069). There was no association between degree of expression of CBRN, Ikaros, Aiolos or PD-1 and survival (PFS/OS). As CRBN expression increased, patients were more likely to respond (≥PR) (p=0.07) and patients with low PD-1 expression were more likely to respond (≥ MR) (Group1 vs Group3 p=0.05). Conclusion CC-489 combined with Rd is well tolerated and effective with durable responses in a subset of heavily pre-treated R/R MM patients, including those who recently failed IMiD® compound therapy, suggesting that CC-489 may overcome drug resistance. IHC may have utility in identifying subsets of patients more likely to respond to CC-489 and Rd (CRBN, PD-1) and predict survival (cMYC, IRF4 and CD8). This trial has been expanded to include other sites and less heavily pre-treated patients. Disclosures Thakurta: Celgene: Employment, Equity Ownership. Wang:Celgene: Employment. Guzman:Celgene: Employment. Cuoto:Celgene: Employment. Ren:Celgene: Employment, Equity Ownership.

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