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      1. Author :
        Head, Trajen; Dau, Peter; Duffort, Stephanie; Daftarian, Pirouz; Joshi, Pratibha M.; Vazquez-Padron, Roberto; Deo, Sapna K.; Daunert, Sylvia
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Cell Death Dis
      6. Products :
      7. Volume :
        8
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI ex vivo
      12. Abstract :
        The process of controlled cellular death known as apoptosis has an important central role not only in normal homeostatic maintenance of tissues, but also in numerous diseases such as cancer, neurodegenerative, autoimmune, and cardiovascular diseases. As a result, new technologies with the capability to selectively detect apoptotic cells represent a central focus of research for the study of these conditions. We have developed a new biosensor for the detection of apoptotic cells, incorporating the targeted selectivity for apoptotic cells from Annexin V with the sensitivity of bioluminescence signal generation from a serum-stable mutant of Renilla luciferase (RLuc8). Our data presents a complete characterization of the structural and biochemical properties of this new Annexin-Renilla fusion protein (ArFP) construct, as well as a validation of its ability to detect apoptosis in vitro. Moreover, this work represents the first report of a bioluminescent Annexin V apoptosis sensor utilized in vivo. With this new construct, we examine apoptosis within disease-relevant animal models of surgery-induced ischemia/reperfusion, corneal injury, and retinal cell death as a model of age-related macular degeneration. In each of these experiments, we demonstrate successful application of the ArFP construct for detection and bioluminescence imaging of apoptosis within each disease or treatment model. ArFP represents an important new tool in the continuously growing kit of technologies for apoptosis detection, and our results from both in vitro and in vivo experiments suggest a diverse range of potential clinically relevant applications including cancer therapeutic screening and efficacy analysis, atherosclerosis and cardiovascular disease detection, and the monitoring of any number of other conditions in which apoptosis has a central role.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520691/pdf/cddis2017141a.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13933
      15. Serial :
        14052
      1. Author :
        Ham, Song-Hee; Min, Kyoung Ah; Shin, Meong Cheol
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Acta Pharmacol Sin
      6. Products :
      7. Volume :
        38
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        gelonin; toxin; F3 peptide; selective tumor targeting; glioblastoma; IVIS; IVIS FLI in ex vivo
      12. Abstract :
        Therapeutically potent macromolecular drugs have shown great promise for overcoming the limitations of small-molecule anti-cancer drugs. But tumor cell-selective intracellular delivery of the macromolecules remains a major hurdle for their successful clinical application. To overcome this challenge, we engineered a novel genetic fusion protein (F3-Gel) that composed of F3 peptide, a tumor-homing peptide, and gelonin, a plant-derived ribosome-inactivating protein (RIP), and then evaluated its anti-cancer activity in vitro and in vivo. The F3-Gel-encoding gene was synthesized by genetic recombination, and F3-Gel was successfully expressed in E coli. The anti-cancer activity of the produced F3-Gel was evaluated by various in vitro assays, which revealed that F3-Gel maintained equipotent protein synthesis inhibition activity (IC50=11 pmol/L) as unmodified gelonin (IC50=10 pmol/L). Furthermore, F3-Gel displayed enhanced cellular uptake into cancer cells (U87 MG, HeLa, LnCaP and 9L) than noncancerous cells (293 HEK and SVGp12). Compared with gelonin, F3-Gel exerted significantly higher cytotoxicity against these cancer cells. F3-Gel displayed significantly greater inhibition of protein translation in U87 MG cells: F3-Gel (0.5 μmol/L) was able to reduce the protein level to less than 50%, while gelonin (1 μmol/L) did not affect the intracellular protein level. In a U87 MG xenograft tumor-bearing mouse model, F3-Gel was accumulated in the tumor site at much higher levels and maintained for a prolonged time compared with gelonin. Administration of F3-Gel (0.5, 0.75 mol/kg, iv) caused 36% and 66%, respectively, inhibition of tumor growth in U87 MG xenograft mice, suggesting that it is a promising candidate drug for cancer treatment. Furthermore, this study demonstrates that fusion of F3 peptide to a potent macromolecule could provides an effective method for targeting tumors and eventually could improve their druggability.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520187/pdf/aps201720a.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13705
      15. Serial :
        14057
      1. Author :
        Shenouda, Mira M.; Gillgrass, Amy; Nham, Tina; Hogg, Richard; Lee, Amanda J.; Chew, Marianne V.; Shafaei, Mahsa; Aarts, Craig; Lee, Dean A.; Hassell, John; Bane, Anita; Dhesy-Thind, Sukhbinder; Ashkar, Ali A.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Breast Cancer Research
      6. Products :
      7. Volume :
        19
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Immunotherapy; PDX; NK cell expansion; NK cell therapy; IVIS; IVIS BLI in vivo
      12. Abstract :
        Background: Natural killer (NK) cells play a critical role in cancer immunosurveillance. Recent developments in NK cell ex-vivo expansion makes it possible to generate millions of activated NK cells from a small volume of peripheral blood. We tested the functionality of ex vivo expanded NK cells in vitro against breast cancer cell lines and in vivo using a xenograft mouse model. The study aim was to assess functionality and phenotype of expanded NK cells from breast cancer patients against breast cancer cell lines and autologous primary tumours. Methods: We used a well-established NK cell co-culture system to expand NK cells ex vivo from healthy donors and breast cancer patients and examined their surface marker expression. Moreover, we tested the ability of expanded NK cells to lyse the triple negative breast cancer and HER2-positive breast cancer cell lines MDA-MB-231 and MDA-MB-453, respectively. We also tested their ability to prevent tumour growth in vivo using a xenograft mouse model. Finally, we tested the cytotoxicity of expanded NK cells against autologous and allogeneic primary breast cancer tumours in vitro. Results: After 3 weeks of culture we observed over 1000-fold expansion of NK cells isolated from either breast cancer patients or healthy donors. We also showed that the phenotype of expanded NK cells is comparable between those from healthy donors and cancer patients. Moreover, our results confirm the ability of ex vivo expanded NK cells to lyse tumour cell lines in vitro. While the cell lines examined had differential sensitivity to NK cell killing we found this was correlated with level of major histocompatibility complex (MHC) class I expression. In our in vivo model, NK cells prevented tumour establishment and growth in immunocompromised mice. Finally, we showed that NK cells expanded from the peripheral blood of breast cancer patients show high cytotoxicity against allogeneic and autologous patient-derived tumour cells in vitro. Conclusion: NK cells from breast cancer patients can be expanded similarly to those from healthy donors, have a high cytotoxic ability against breast cancer cell lines and patient-derived tumour cells, and can be compatible with current cancer treatments to restore NK cell function in cancer patients.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5493877/pdf/13058_2017_Article_867.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 14060
      15. Serial :
        13758
      1. Author :
        Li, Jia-Kuan; Chen, Cheng; Liu, Jia-Yi; Shi, Jia-Zi; Liu, Shu-Peng; Liu, Bing; Wu, Deng-Shuang; Fang, Zi-Yu; Bao, Yi; Jiang, Ming-Ming; Yuan, Ji-Hang; Qu, Le; Wang, Lin-Hui
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Molecular Cancer
      6. Products :
      7. Volume :
        16
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Clear cell renal cell carcinoma; Long noncoding RNA; Metastasis; MAPK signaling; IVIS; IVIS BLI in vivo
      12. Abstract :
        Background: Recent evidences showed that long noncoding RNAs (lncRNAs) are frequently dysregulated and play important roles in various cancers. Clear cell renal cell carcinoma (ccRCC) is one of the leading cause of cancer-related death, largely due to the metastasis of ccRCC. However, the clinical significances and roles of lncRNAs in metastatic ccRCC are still unknown. Methods: lncRNA expression microarray analysis was performed to search the dysregulated lncRNA in metastatic ccRCC. quantitative real-time PCR was performed to measure the expression of lncRNAs in human ccRCC samples. Gain-of-function and loss-of-function experiments were performed to investigate the biological roles of lncRNAs on ccRCC cell proliferation, migration, invasion and in vivo metastasis. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and western blot were performed to explore the molecular mechanisms underlying the functions of lncRNAs. Results: The microarray analysis identified a novel lncRNA termed metastatic renal cell carcinoma-associated transcript 1 (MRCCAT1), which is highly expressed in metastatic ccRCC tissues and associated with the metastatic properties of ccRCC. Multivariate Cox regression analysis revealed that MRCCAT1 is an independent prognostic factor for ccRCC patients. Overexpression of MRCCAT1 promotes ccRCC cells proliferation, migration, and invasion. Depletion of MRCCAT1 inhibites ccRCC cells proliferation, migration, and invasion in vitro, and ccRCC metastasis in vivo. Mechanistically, MRCCAT1 represses NPR3 transcription by recruiting PRC2 to NPR3 promoter, and subsequently activates p38-MAPK signaling pathway. Conclusions: MRCCAT1 is a critical lncRNA that promotes ccRCC metastasis via inhibiting NPR3 and activating p38-MAPK signaling. Our results imply that MRCCAT1 could serve as a prognostic biomarker and therapeutic target for ccRCC.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490088/pdf/12943_2017_Article_681.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 14052
      15. Serial :
        13945
      1. Author :
        Duran, George E.; Wang, Yan C.; Moisan, Francois; Francisco, E. Brian; Sikic, Branimir I.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Br J Cancer
      6. Products :
      7. Volume :
        116
      8. Issue :
        10
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        non-MDR; drug resistance; taxanes; EMT; ovarian cancer; tubulin polymerisation; IVIS; IVIS BLI in vivo
      12. Abstract :
        Background: ABCB1 expression is uncommon in ovarian cancers in the clinical setting so we investigated non-MDR mechanisms of resistance to taxanes. Methods: We established eight taxane-resistant variants from the human ovarian carcinoma cell lines A2780/1A9, ES-2, MES-OV and OVCAR-3 by selection with paclitaxel or docetaxel, with counter-selection by the transport inhibitor valspodar. Results: Non-MDR taxane resistance was associated with reduced intracellular taxane content compared to parental controls, and cross-resistance to other microtubule stabilising drugs. Collateral sensitivity to depolymerising agents (vinca alkaloids and colchicine) was observed with increased intracellular vinblastine. These variants exhibited marked decreases in basal tubulin polymer and in tubulin polymerisation in response to taxane exposure. TUBB3 content was increased in 6 of the 8 variants. We profiled gene expression of the parental lines and resistant variants, and identified a transcriptomic signature with two highly significant networks built around FN1 and CDKN1A that are associated with cell adhesion, cell-to-cell signalling, and cell cycle regulation. miR-200 family members miR-200b and miR-200c were downregulated in resistant cells, associated with epithelial to mesenchymal transition (EMT), with increased VIM, FN1, MMP2 and/or MMP9. Conclusions: These alterations may serve as biomarkers for predicting taxane effectiveness in ovarian cancer and should be considered as therapeutic targets.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482726/pdf/bjc2017102a.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13665
      15. Serial :
        14111
      1. Author :
        Barash, NR; Nosala, Christopher; Pham, Jonathan K; McInally, Shane G; Gourguechon, Stephane; McCarthy-Sinclair, Brendan; Dawson, Scott C
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        mSphere
      6. Products :
      7. Volume :
        2
      8. Issue :
        3
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Giardia; bioluminescence; encystation; parasite; pathogenesis; IVIS; IVIS BLI in vivo
      12. Abstract :
        Giardia lamblia is a highly prevalent yet understudied protistan parasite causing significant diarrheal disease worldwide. Hosts ingest Giardia cysts from contaminated sources. In the gastrointestinal tract, cysts excyst to become motile trophozoites, colonizing and attaching to the gut epithelium. Trophozoites later differentiate into infectious cysts that are excreted and contaminate the environment. Due to the limited accessibility of the gut, the temporospatial dynamics of giardiasis in the host are largely inferred from laboratory culture and thus may not mirror Giardia physiology in the host. Here, we have developed bioluminescent imaging (BLI) to directly interrogate and quantify the in vivo temporospatial dynamics of Giardia infection, thereby providing an improved murine model to evaluate anti-Giardia drugs. Using BLI, we determined that parasites primarily colonize the proximal small intestine nonuniformly in high-density foci. By imaging encystation-specific bioreporters, we show that encystation initiates shortly after inoculation and continues throughout the duration of infection. Encystation also initiates in high-density foci in the proximal small intestine, and high density contributes to the initiation of encystation in laboratory culture. We suggest that these high-density in vivo foci of colonizing and encysting Giardia likely result in localized disruption to the epithelium. This more accurate visualization of giardiasis redefines the dynamics of the in vivo Giardia life cycle, paving the way for future mechanistic studies of density-dependent parasitic processes in the host.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5480036/pdf/mSphere.00343-16.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 14129
      15. Serial :
        14204
      1. Author :
        Liu, Aibin; Zhu, Jinrong; Wu, Geyan; Cao, Lixue; Tan, Zhanyao; Zhang, Shuxia; Jiang, Lili; Wu, Jueheng; Li, Mengfeng; Song, Libing; Li, Jun
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Molecular Cancer
      6. Products :
      7. Volume :
        16
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        miR-455-3p; Chemoresistance; Esophageal squamous cell carcinoma; OncomiR; IVIS; IVIS BLI
      12. Abstract :
        Background: The plasticity of cancer stem cells (CSCs)/tumor-initiating cells (T-ICs) suggests that multiple CSC/T-IC subpopulations exist within a tumor and that multiple oncogenic pathways collaborate to maintain the CSC/T-IC state. Here, we aimed to identify potential therapeutic targets that concomitantly regulate multiple T-IC subpopulations and CSC/T-IC-associated pathways. Methods: A chemoresistant patient-derived xenograft (PDX) model of human esophageal squamous cell carcinoma (ESCC) was employed to identify microRNAs that contribute to ESCC aggressiveness. The oncogenic effects of microRNA-455-3p (miR-455-3p) on ESCC chemoresistance and tumorigenesis were examined by in vivo and in vitro chemoresistance, tumorsphere formation, side-population, and in vivo limiting dilution assays. The roles of miR-455-3p in activation of the Wnt/β-catenin and transforming growth factor-β (TGF-β)/Smad pathways were determined by luciferase and RNA immunoprecipitation assays. Results: We found that miR-455-3p played essential roles in ESCC chemoresistance and tumorigenesis. Treatment with a miR-455-3p antagomir dramatically chemosensitized ESCC cells and reduced the subpopulations of CD90+ and CD271+ T-ICs via deactivation of multiple stemness-associated pathways, including Wnt/β-catenin and TGF-β signaling. Importantly, miR-455-3p exhibited aberrant upregulation in various human cancer types, and was significantly associated with decreased overall survival of cancer patients. Conclusions: Our results demonstrate that miR-455-3p functions as an oncomiR in ESCC progression and may provide a potential therapeutic target to achieve better clinical outcomes in cancer patients.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479030/pdf/12943_2017_Article_669.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 14019
      15. Serial :
        13926
      1. Author :
        Gay, Fabien; Aguera, Karine; Sénéchal, Karine; Tainturier, Angie; Berlier, Willy; Maucort-Boulch, Delphine; Honnorat, Jérôme; Horand, Françoise; Godfrin, Yann; Bourgeaux, Vanessa
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Cancer Medicine
      6. Products :
      7. Volume :
        6
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Erymet; methionine-dependent cancers; methionine gamma-lyase; pyridoxal 5′-phosphate; red blood cells; IVIS; IVIS BLI in vivo
      12. Abstract :
        Erymet is a new therapy resulting from the encapsulation of a methionine gamma-lyase (MGL; EC number 4.4.1.11) in red blood cells (RBC). The aim of this study was to evaluate erymet potential efficacy in methionine (Met)-dependent cancers. We produced a highly purified MGL using a cGMP process, determined the pharmacokinetics/pharmacodynamics (PK/PD) properties of erymet in mice, and assessed its efficacy on tumor growth prevention. Cytotoxicity of purified MGL was tested in six cancer cell lines. CD1 mice were injected with single erymet product supplemented or not with vitamin B6 vitamer pyridoxine (PN; a precursor of PLP cofactor). NMRI nude mice were xenografted in the flank with U-87 MG-luc2 glioblastoma cells for tumor growth study following five intravenous (IV) injections of erymet with daily PN oral administration. Endpoints included efficacy and event-free survival (EFS). Finally, a repeated dose toxicity study of erymet combined with PN cofactor was conducted in CD1 mice. Recombinant MGL was cytotoxic on 4/6 cell lines tested. MGL half-life was increased from <24 h to 9–12 days when encapsulated in RBC. Conversion of PN into PLP by RBC was demonstrated. Combined erymet + PN treatment led to a sustained Met depletion in plasma for several days with a 85% reduction of tumor volume after 45 days following cells implantation, and a significant EFS prolongation for treated mice. Repeated injections in mice exhibited a very good tolerability with only minor impact on clinical state (piloerection, lean aspect) and a slight decrease in hemoglobin and triglyceride concentrations. This study demonstrated that encapsulation of methioninase inside erythrocyte greatly enhanced pharmacokinetics properties of the enzyme and is efficacy against tumor growth. The perspective on these results is the clinical evaluation of the erymet product in patients with Met starvation-sensitive tumors.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5463067/pdf/CAM4-6-1437.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13914
      15. Serial :
        14078
      1. Author :
        Nguyen, Tri; Parker, Rebecca; Hawkins, Elisa; Holkova, Beata; Yazbeck, Victor; Kolluri, Akhil; Kmieciak, Maciej; Rahmani, Mohamed; Grant, Steven
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Oncotarget
      6. Products :
      7. Volume :
        8
      8. Issue :
        19
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        non-Hodgkin’s lymphoma,; volasertib,; belinostat; IVIS; IVIS BLI in vivo
      12. Abstract :
        Interactions between the polo-like kinase 1 (PLK1) inhibitor volasertib and the histone deacetylase inhibitor (HDACI) belinostat were examined in diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL) cells in vitro and in vivo. Exposure of DLBCL cells to very low concentrations of volasertib in combination with belinostat synergistically increased cell death (apoptosis). Similar interactions occurred in GC-, ABC-, double-hit DLBCL cells, MCL cells, bortezomib-resistant cells and primary lymphoma cells. Co-exposure to volasertib/belinostat induced a marked increase in M-phase arrest, phospho-histone H3, mitotic errors, cell death in M-phase, and DNA damage. Belinostat diminished c-Myc mRNA and protein expression, an effect significantly enhanced by volasertib co-exposure. c-Myc knock-down increased DNA damage and cell death in response to volasertib, arguing that c-Myc down-regulation plays a functional role in the lethality of this regimen. Notably, PLK1 knock-down in DLBCL cells significantly increased belinostat-induced M-phase accumulation, phospho-histone H3, γH2AX, and cell death. Co-administration of volasertib and belinostat dramatically reduced tumor growth in an ABC-DLBCL flank model (U2932) and a systemic double-hit lymphoma model (OCI-Ly18), accompanied by a pronounced increase in survival without significant weight loss or other toxicities. Together, these findings indicate that PLK1/HDAC inhibition warrants attention as a therapeutic strategy in NHL.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458223/pdf/oncotarget-08-31478.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13491
      15. Serial :
        13854
      1. Author :
        Al-Jameel, Waseem; Gou, Xiaojun; Forootan, Shiva S; Al Fayi, Majed Saad; Rudland, Philip S; Forootan, Farzad S; Zhang, Jiacheng; Cornford, Philip A; Hussain, Syed A; Ke, Youqiang
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Oncotarget
      6. Products :
      7. Volume :
        8
      8. Issue :
        19
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        SBFI26; FABP5; CRPC; PPARγ; metastasis; IVIS; IVIS BLI in vitro
      12. Abstract :
        Castration resistant-prostate cancer is largely impervious to feather hormonal therapy and hence the outlook for patients is grim. Here we use an approach to attach the recently discovered Achilles heel. The experimental treatment established in this study is based on the recent discovery that it is the FABP5-PPARγ-VEGF signalling axis, rather than the androgen receptor pathway, played a dominant role in promoting the malignant progression of castration resistant prostate cancer cells. Treatments have been established in mice by suppressing the biological activity of FABP5 using a chemical inhibitor SBFI26. The inhibitor significantly suppressed the proliferation, migration, invasiveness and colony formation of PC3-M cells in vitro. It also produced a highly significant suppression of both the metastases and the primary tumours developed from cancer cells implanted orthotopically into the prostate glands of the mice. The inhibitor SBFI26 interferes with the FABP5-PPARγ- signalling pathway at the initial stage of the signal transduction by binding competitively to FABP5 to inhibit cellular fatty acid uptake. This avoids the fatty-acid stimulation of PPARγ and prevents it activating the down-stream regulated cancer-promoting genes. This entirely novel experimental approach to treating castration- resistant prostate cancer is completely different from current treatments that are based on androgen-blockade therapy.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458187/pdf/oncotarget-08-31041.pdf
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13573
      15. Serial :
        14226
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