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Randomized controlled trial of the NS5A inhibitor daclatasvir plus pegylated interferon and ribavirin for HCV genotype-4 (COMMAND-4).

Antiviral therapy

Hézode C, Alric L, Brown A, Hassanein T, Rizzetto M, Buti M, Bourlière M, Thabut D, Molina E, Rustgi V, Samuel D, McPhee F, Liu Z, Yin PD, Hughes E, Treitel M.
PMID: 26313445
Antivir Ther. 2015 Aug 27;21(3):195-205. doi: 10.3851/IMP2985. Epub 2015 Aug 27.

BACKGROUND: Treatment options for HCV genotype-4 (GT4) are limited. This Phase III study (COMMAND-4; AI444-042) evaluated the efficacy and safety of daclatasvir (DCV), a pan-genotypic HCV NS5A inhibitor, with pegylated interferon-α2a/ribavirin (PEG-IFN/RBV) in treatment-naive patients with HCV GT4 infection.METHODS:...

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Hézode C, Alric L, Brown A, et al. Randomized controlled trial of the NS5A inhibitor daclatasvir plus pegylated interferon and ribavirin for HCV genotype-4 (COMMAND-4). Antivir Ther. 2015;21(3):195-205doi: 10.3851/IMP2985.
Hézode, C., Alric, L., Brown, A., Hassanein, T., Rizzetto, M., Buti, M., Bourlière, M., Thabut, D., Molina, E., Rustgi, V., Samuel, D., McPhee, F., Liu, Z., Yin, P. D., Hughes, E., Treitel, M. (2015). Randomized controlled trial of the NS5A inhibitor daclatasvir plus pegylated interferon and ribavirin for HCV genotype-4 (COMMAND-4). Antiviral therapy, 21(3), 195-205. https://doi.org/10.3851/IMP2985
Hézode, Christophe, et al. "Randomized controlled trial of the NS5A inhibitor daclatasvir plus pegylated interferon and ribavirin for HCV genotype-4 (COMMAND-4)." Antiviral therapy vol. 21,3 (2015): 195-205. doi: https://doi.org/10.3851/IMP2985
Hézode C, Alric L, Brown A, Hassanein T, Rizzetto M, Buti M, Bourlière M, Thabut D, Molina E, Rustgi V, Samuel D, McPhee F, Liu Z, Yin PD, Hughes E, Treitel M. Randomized controlled trial of the NS5A inhibitor daclatasvir plus pegylated interferon and ribavirin for HCV genotype-4 (COMMAND-4). Antivir Ther. 2015 Aug 27;21(3):195-205. doi: 10.3851/IMP2985. Epub 2015 Aug 27. PMID: 26313445.
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Erratum: Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2.

Nature communications

Zhang H, Brainson CF, Koyama S, Redig AJ, Chen T, Li S, Gupta M, Garcia-de-Alba C, Paschini M, Herter-Sprie GS, Lu G, Zhang X, Marsh BP, Tuminello SJ, Xu C, Chen Z, Wang X, Akbay EA, Zheng M, Palakurthi S, Sholl LM, Rustgi AK, Kwiatkowski DJ, Alan Diehl J, Bass AJ, Sharpless NE, Dranoff G, Hammerman PS, Ji H, Bardeesy N, Saur D, Watanabe H, Kim CF, Wong KK.
PMID: 28598439
Nat Commun. 2017 Jun 09;8:15901. doi: 10.1038/ncomms15901.

This corrects the article DOI: 10.1038/ncomms14922.

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Zhang H, Brainson CF, Koyama S, et al. Erratum: Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2. Nat Commun. 2017;8:15901doi: 10.1038/ncomms15901.
Zhang, H., Brainson, C. F., Koyama, S., Redig, A. J., Chen, T., Li, S., Gupta, M., Garcia-de-Alba, C., Paschini, M., Herter-Sprie, G. S., Lu, G., Zhang, X., Marsh, B. P., Tuminello, S. J., Xu, C., Chen, Z., Wang, X., Akbay, E. A., Zheng, M., Palakurthi, S., Sholl, L. M., Rustgi, A. K., Kwiatkowski, D. J., Alan Diehl, J., Bass, A. J., Sharpless, N. E., Dranoff, G., Hammerman, P. S., Ji, H., Bardeesy, N., Saur, D., Watanabe, H., Kim, C. F., & Wong, K. K. (2017). Erratum: Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2. Nature communications, 815901. https://doi.org/10.1038/ncomms15901
Zhang, Haikuo, et al. "Erratum: Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2." Nature communications vol. 8 (2017): 15901. doi: https://doi.org/10.1038/ncomms15901
Zhang H, Brainson CF, Koyama S, Redig AJ, Chen T, Li S, Gupta M, Garcia-de-Alba C, Paschini M, Herter-Sprie GS, Lu G, Zhang X, Marsh BP, Tuminello SJ, Xu C, Chen Z, Wang X, Akbay EA, Zheng M, Palakurthi S, Sholl LM, Rustgi AK, Kwiatkowski DJ, Alan Diehl J, Bass AJ, Sharpless NE, Dranoff G, Hammerman PS, Ji H, Bardeesy N, Saur D, Watanabe H, Kim CF, Wong KK. Erratum: Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2. Nat Commun. 2017 Jun 09;8:15901. doi: 10.1038/ncomms15901. PMID: 28598439; PMCID: PMC5472705.
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Racial Disparities in Colorectal Cancer Survival: Is Elimination of Variation in Care the Cure?.

Journal of the National Cancer Institute

Doubeni CA, Rustgi A.
PMID: 26220735
J Natl Cancer Inst. 2015 Jul 28;107(10). doi: 10.1093/jnci/djv229. Print 2015 Oct.

No abstract available.

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Doubeni CA, Rustgi A. Racial Disparities in Colorectal Cancer Survival: Is Elimination of Variation in Care the Cure?. J Natl Cancer Inst. 2015;107(10)doi: 10.1093/jnci/djv229.
Doubeni, C. A., & Rustgi, A. (2015). Racial Disparities in Colorectal Cancer Survival: Is Elimination of Variation in Care the Cure?. Journal of the National Cancer Institute, 107(10), . https://doi.org/10.1093/jnci/djv229
Doubeni, Chyke A, and Rustgi, Anil. "Racial Disparities in Colorectal Cancer Survival: Is Elimination of Variation in Care the Cure?." Journal of the National Cancer Institute vol. 107,10 (2015). doi: https://doi.org/10.1093/jnci/djv229
Doubeni CA, Rustgi A. Racial Disparities in Colorectal Cancer Survival: Is Elimination of Variation in Care the Cure?. J Natl Cancer Inst. 2015 Jul 28;107(10). doi: 10.1093/jnci/djv229. Print 2015 Oct. PMID: 26220735.
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Periostin cooperates with mutant p53 to mediate invasion through the induction of STAT1 signaling in the esophageal tumor microenvironment.

Oncogenesis

Wong GS, Lee JS, Park YY, Klein-Szanto AJ, Waldron TJ, Cukierman E, Herlyn M, Gimotty P, Nakagawa H, Rustgi AK.
PMID: 23917221
Oncogenesis. 2013 Aug 05;2:e59. doi: 10.1038/oncsis.2013.17.

Periostin (POSTN), a matricellular protein, has been reported to be important in supporting tumor cell dissemination. However, the molecular mechanisms underlying POSTN function within the tumor microenvironment are poorly understood. In this study, we observe that the inducible knockdown...

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Wong GS, Lee JS, Park YY, et al. Periostin cooperates with mutant p53 to mediate invasion through the induction of STAT1 signaling in the esophageal tumor microenvironment. Oncogenesis. 2013;2:e59doi: 10.1038/oncsis.2013.17.
Wong, G. S., Lee, J. S., Park, Y. Y., Klein-Szanto, A. J., Waldron, T. J., Cukierman, E., Herlyn, M., Gimotty, P., Nakagawa, H., & Rustgi, A. K. (2013). Periostin cooperates with mutant p53 to mediate invasion through the induction of STAT1 signaling in the esophageal tumor microenvironment. Oncogenesis, 2e59. https://doi.org/10.1038/oncsis.2013.17
Wong, G S, et al. "Periostin cooperates with mutant p53 to mediate invasion through the induction of STAT1 signaling in the esophageal tumor microenvironment." Oncogenesis vol. 2 (2013): e59. doi: https://doi.org/10.1038/oncsis.2013.17
Wong GS, Lee JS, Park YY, Klein-Szanto AJ, Waldron TJ, Cukierman E, Herlyn M, Gimotty P, Nakagawa H, Rustgi AK. Periostin cooperates with mutant p53 to mediate invasion through the induction of STAT1 signaling in the esophageal tumor microenvironment. Oncogenesis. 2013 Aug 05;2:e59. doi: 10.1038/oncsis.2013.17. PMID: 23917221; PMCID: PMC3759121.
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IGFBP3 promotes esophageal cancer growth by suppressing oxidative stress in hypoxic tumor microenvironment.

American journal of cancer research

Natsuizaka M, Kinugasa H, Kagawa S, Whelan KA, Naganuma S, Subramanian H, Chang S, Nakagawa KJ, Rustgi NL, Kita Y, Natsugoe S, Basu D, Gimotty PA, Klein-Szanto AJ, Diehl JA, Nakagawa H.
PMID: 24482736
Am J Cancer Res. 2014 Jan 15;4(1):29-41. eCollection 2014.

Insulin-like growth factor binding protein 3 (IGFBP3), a hypoxia-inducible gene, regulates a variety of cellular processes including cell proliferation, senescence, apoptosis and epithelial-mesenchymal transition (EMT). IGFBP3 has been linked to the pathogenesis of cancers. Most previous studies focus upon...

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Natsuizaka M, Kinugasa H, Kagawa S, et al. IGFBP3 promotes esophageal cancer growth by suppressing oxidative stress in hypoxic tumor microenvironment. Am J Cancer Res. 2014;4(1):29-41
Natsuizaka, M., Kinugasa, H., Kagawa, S., Whelan, K. A., Naganuma, S., Subramanian, H., Chang, S., Nakagawa, K. J., Rustgi, N. L., Kita, Y., Natsugoe, S., Basu, D., Gimotty, P. A., Klein-Szanto, A. J., Diehl, J. A., & Nakagawa, H. (2014). IGFBP3 promotes esophageal cancer growth by suppressing oxidative stress in hypoxic tumor microenvironment. American journal of cancer research, 4(1), 29-41.
Natsuizaka, Mitsuteru, et al. "IGFBP3 promotes esophageal cancer growth by suppressing oxidative stress in hypoxic tumor microenvironment." American journal of cancer research vol. 4,1 (2014): 29-41.
Natsuizaka M, Kinugasa H, Kagawa S, Whelan KA, Naganuma S, Subramanian H, Chang S, Nakagawa KJ, Rustgi NL, Kita Y, Natsugoe S, Basu D, Gimotty PA, Klein-Szanto AJ, Diehl JA, Nakagawa H. IGFBP3 promotes esophageal cancer growth by suppressing oxidative stress in hypoxic tumor microenvironment. Am J Cancer Res. 2014 Jan 15;4(1):29-41. eCollection 2014. PMID: 24482736; PMCID: PMC3902230.
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Transport and magnetic properties of Fe(x)VSe(2) (x = 0-0.33).

Journal of physics. Condensed matter : an Institute of Physics journal

Yadav CS, Rastogi AK.
PMID: 21693857
J Phys Condens Matter. 2008 Nov 19;20(46):465219. doi: 10.1088/0953-8984/20/46/465219. Epub 2008 Oct 27.

We present the results of the effect of Fe intercalation on the structural, transport and magnetic properties of 1T-VSe(2). Intercalation of iron suppresses the charge density wave transition at 110 K in 1T-VSe(2). And for more than 10% Fe...

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Yadav CS, Rastogi AK. Transport and magnetic properties of Fe(x)VSe(2) (x = 0-0.33). J Phys Condens Matter. 2008;20(46):465219doi: 10.1088/0953-8984/20/46/465219.
Yadav, C. S., & Rastogi, A. K. (2008). Transport and magnetic properties of Fe(x)VSe(2) (x = 0-0.33). Journal of physics. Condensed matter : an Institute of Physics journal, 20(46), 465219. https://doi.org/10.1088/0953-8984/20/46/465219
Yadav, C S, and Rastogi, A K. "Transport and magnetic properties of Fe(x)VSe(2) (x = 0-0.33)." Journal of physics. Condensed matter : an Institute of Physics journal vol. 20,46 (2008): 465219. doi: https://doi.org/10.1088/0953-8984/20/46/465219
Yadav CS, Rastogi AK. Transport and magnetic properties of Fe(x)VSe(2) (x = 0-0.33). J Phys Condens Matter. 2008 Nov 19;20(46):465219. doi: 10.1088/0953-8984/20/46/465219. Epub 2008 Oct 27. PMID: 21693857.
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Energy levels of a hydrogenic impurity in GaAs/Ga1-xAlxAs multiple-quantum-well structures with narrow barriers in a magnetic field.

Physical review. B, Condensed matter

McCombe BD, Nguyen N, Ranganathan R, Rustgi ML, Zang JX.
PMID: 10007837
Phys Rev B Condens Matter. 1993 Nov 15;48(19):14226-14231. doi: 10.1103/physrevb.48.14226.

No abstract available.

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McCombe BD, Nguyen N, Ranganathan R, et al. Energy levels of a hydrogenic impurity in GaAs/Ga1-xAlxAs multiple-quantum-well structures with narrow barriers in a magnetic field. Phys Rev B Condens Matter. 1993;48(19):14226-14231doi: 10.1103/physrevb.48.14226.
McCombe, B. D., Nguyen, N., Ranganathan, R., Rustgi, M. L., & Zang, J. X. (1993). Energy levels of a hydrogenic impurity in GaAs/Ga1-xAlxAs multiple-quantum-well structures with narrow barriers in a magnetic field. Physical review. B, Condensed matter, 48(19), 14226-14231. https://doi.org/10.1103/physrevb.48.14226
McCombe, et al. "Energy levels of a hydrogenic impurity in GaAs/Ga1-xAlxAs multiple-quantum-well structures with narrow barriers in a magnetic field." Physical review. B, Condensed matter vol. 48,19 (1993): 14226-14231. doi: https://doi.org/10.1103/physrevb.48.14226
McCombe BD, Nguyen N, Ranganathan R, Rustgi ML, Zang JX. Energy levels of a hydrogenic impurity in GaAs/Ga1-xAlxAs multiple-quantum-well structures with narrow barriers in a magnetic field. Phys Rev B Condens Matter. 1993 Nov 15;48(19):14226-14231. doi: 10.1103/physrevb.48.14226. PMID: 10007837.
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Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition.

Nature medicine

Wong GS, Zhou J, Bin Liu J, Wu Z, Xu X, Li T, Xu D, Schumacher SE, Puschhof J, McFarland J, Zou C, Dulak A, Henderson L, Xu P, O'Day E, Rendak R, Liao WL, Cecchi F, Hembrough T, Schwartz S, Szeto C, Rustgi AK, Wong KK, Diehl JA, Jensen K, Graziano F, Ruzzo A, Fereshetian S, Mertins P, Carr SA, Beroukhim R, Nakamura K, Oki E, Watanabe M, Baba H, Imamura Y, Catenacci D, Bass AJ.
PMID: 30093730
Nat Med. 2018 Oct;24(10):1627. doi: 10.1038/s41591-018-0168-6.

In the Supplementary Information originally published with this article, a lane was missing in the β-actin blot in Supplementary Fig. 2. The lane has been added. The error has been corrected in the Supplementary Information associated with this article.

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Wong GS, Zhou J, Bin Liu J, et al. Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition. Nat Med. 2018;24(10):1627doi: 10.1038/s41591-018-0168-6.
Wong, G. S., Zhou, J., Bin Liu, J., Wu, Z., Xu, X., Li, T., Xu, D., Schumacher, S. E., Puschhof, J., McFarland, J., Zou, C., Dulak, A., Henderson, L., Xu, P., O'Day, E., Rendak, R., Liao, W. L., Cecchi, F., Hembrough, T., Schwartz, S., Szeto, C., Rustgi, A. K., Wong, K. K., Diehl, J. A., Jensen, K., Graziano, F., Ruzzo, A., Fereshetian, S., Mertins, P., Carr, S. A., Beroukhim, R., Nakamura, K., Oki, E., Watanabe, M., Baba, H., Imamura, Y., Catenacci, D., & Bass, A. J. (2018). Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition. Nature medicine, 24(10), 1627. https://doi.org/10.1038/s41591-018-0168-6
Wong, Gabrielle S, et al. "Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition." Nature medicine vol. 24,10 (2018): 1627. doi: https://doi.org/10.1038/s41591-018-0168-6
Wong GS, Zhou J, Bin Liu J, Wu Z, Xu X, Li T, Xu D, Schumacher SE, Puschhof J, McFarland J, Zou C, Dulak A, Henderson L, Xu P, O'Day E, Rendak R, Liao WL, Cecchi F, Hembrough T, Schwartz S, Szeto C, Rustgi AK, Wong KK, Diehl JA, Jensen K, Graziano F, Ruzzo A, Fereshetian S, Mertins P, Carr SA, Beroukhim R, Nakamura K, Oki E, Watanabe M, Baba H, Imamura Y, Catenacci D, Bass AJ. Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition. Nat Med. 2018 Oct;24(10):1627. doi: 10.1038/s41591-018-0168-6. PMID: 30093730.
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Pattern of Protein Expression in Developing Wheat Grains Identified through Proteomic Analysis.

Frontiers in plant science

Yang M, Gao X, Dong J, Gandhi N, Cai H, von Wettstein DH, Rustgi S, Wen S.
PMID: 28649254
Front Plant Sci. 2017 Jun 09;8:962. doi: 10.3389/fpls.2017.00962. eCollection 2017.

Grain development is one of the biological processes, which contributes to the final grain yield. To understand the molecular changes taking place during the early grain development, we profiled proteomes of two common wheat cultivars P271 and Chinese Spring...

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Yang M, Gao X, Dong J, et al. Pattern of Protein Expression in Developing Wheat Grains Identified through Proteomic Analysis. Front Plant Sci. 2017;8:962doi: 10.3389/fpls.2017.00962.
Yang, M., Gao, X., Dong, J., Gandhi, N., Cai, H., von Wettstein, D. H., Rustgi, S., & Wen, S. (2017). Pattern of Protein Expression in Developing Wheat Grains Identified through Proteomic Analysis. Frontiers in plant science, 8962. https://doi.org/10.3389/fpls.2017.00962
Yang, Mingming, et al. "Pattern of Protein Expression in Developing Wheat Grains Identified through Proteomic Analysis." Frontiers in plant science vol. 8 (2017): 962. doi: https://doi.org/10.3389/fpls.2017.00962
Yang M, Gao X, Dong J, Gandhi N, Cai H, von Wettstein DH, Rustgi S, Wen S. Pattern of Protein Expression in Developing Wheat Grains Identified through Proteomic Analysis. Front Plant Sci. 2017 Jun 09;8:962. doi: 10.3389/fpls.2017.00962. eCollection 2017. PMID: 28649254; PMCID: PMC5465268.
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Lectin-type oxidized LDL receptor-1 distinguishes population of human polymorphonuclear myeloid-derived suppressor cells in cancer patients.

Science immunology

Condamine T, Dominguez GA, Youn JI, Kossenkov AV, Mony S, Alicea-Torres K, Tcyganov E, Hashimoto A, Nefedova Y, Lin C, Partlova S, Garfall A, Vogl DT, Xu X, Knight SC, Malietzis G, Lee GH, Eruslanov E, Albelda SM, Wang X, Mehta JL, Bewtra M, Rustgi A, Hockstein N, Witt R, Masters G, Nam B, Smirnov D, Sepulveda MA, Gabrilovich DI.
PMID: 28417112
Sci Immunol. 2016 Aug;1(2). doi: 10.1126/sciimmunol.aaf8943. Epub 2016 Aug 05.

Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) are important regulators of immune responses in cancer and have been directly implicated in promotion of tumor progression. However, the heterogeneity of these cells and lack of distinct markers hampers the progress in understanding...

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Condamine T, Dominguez GA, Youn JI, et al. Lectin-type oxidized LDL receptor-1 distinguishes population of human polymorphonuclear myeloid-derived suppressor cells in cancer patients. Sci Immunol. 2016;1(2)doi: 10.1126/sciimmunol.aaf8943.
Condamine, T., Dominguez, G. A., Youn, J. I., Kossenkov, A. V., Mony, S., Alicea-Torres, K., Tcyganov, E., Hashimoto, A., Nefedova, Y., Lin, C., Partlova, S., Garfall, A., Vogl, D. T., Xu, X., Knight, S. C., Malietzis, G., Lee, G. H., Eruslanov, E., Albelda, S. M., Wang, X., Mehta, J. L., Bewtra, M., Rustgi, A., Hockstein, N., Witt, R., Masters, G., Nam, B., Smirnov, D., Sepulveda, M. A., & Gabrilovich, D. I. (2016). Lectin-type oxidized LDL receptor-1 distinguishes population of human polymorphonuclear myeloid-derived suppressor cells in cancer patients. Science immunology, 1(2), . https://doi.org/10.1126/sciimmunol.aaf8943
Condamine, Thomas, et al. "Lectin-type oxidized LDL receptor-1 distinguishes population of human polymorphonuclear myeloid-derived suppressor cells in cancer patients." Science immunology vol. 1,2 (2016). doi: https://doi.org/10.1126/sciimmunol.aaf8943
Condamine T, Dominguez GA, Youn JI, Kossenkov AV, Mony S, Alicea-Torres K, Tcyganov E, Hashimoto A, Nefedova Y, Lin C, Partlova S, Garfall A, Vogl DT, Xu X, Knight SC, Malietzis G, Lee GH, Eruslanov E, Albelda SM, Wang X, Mehta JL, Bewtra M, Rustgi A, Hockstein N, Witt R, Masters G, Nam B, Smirnov D, Sepulveda MA, Gabrilovich DI. Lectin-type oxidized LDL receptor-1 distinguishes population of human polymorphonuclear myeloid-derived suppressor cells in cancer patients. Sci Immunol. 2016 Aug;1(2). doi: 10.1126/sciimmunol.aaf8943. Epub 2016 Aug 05. PMID: 28417112; PMCID: PMC5391495.
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A Health Survey of Gastroenterologist Prescribing Practices of Adalimumab for Treatment of Crohn's Disease: Final Results.

Gastroenterology & hepatology

Zullow S, Flasar MH, Greenberg D, Tracy JK, Rustgi A, Cross RK.
PMID: 28845141
Gastroenterol Hepatol (N Y). 2014 Aug;10(8):503-509.

Adalimumab (Humira, AbbVie) has efficacy in treatment-naive and infliximab (Remicade, Janssen)-exposed patients with Crohn's disease (CD). An e-survey was sent to US gastroenterologists who were members of the American Gastroenterological Association. A total of 398 gastroenterologists (3%) completed the...

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Zullow S, Flasar MH, Greenberg D, et al. A Health Survey of Gastroenterologist Prescribing Practices of Adalimumab for Treatment of Crohn's Disease: Final Results. Gastroenterol Hepatol (N Y). 2014;10(8):503-509
Zullow, S., Flasar, M. H., Greenberg, D., Tracy, J. K., Rustgi, A., & Cross, R. K. (2014). A Health Survey of Gastroenterologist Prescribing Practices of Adalimumab for Treatment of Crohn's Disease: Final Results. Gastroenterology & hepatology, 10(8), 503-509.
Zullow, Samantha, et al. "A Health Survey of Gastroenterologist Prescribing Practices of Adalimumab for Treatment of Crohn's Disease: Final Results." Gastroenterology & hepatology vol. 10,8 (2014): 503-509.
Zullow S, Flasar MH, Greenberg D, Tracy JK, Rustgi A, Cross RK. A Health Survey of Gastroenterologist Prescribing Practices of Adalimumab for Treatment of Crohn's Disease: Final Results. Gastroenterol Hepatol (N Y). 2014 Aug;10(8):503-509. PMID: 28845141; PMCID: PMC5566191.
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Dense Electron-Hole Plasma Formation and Ultralong Charge Lifetime in Monolayer MoS.

Nano letters

Bataller AW, Younts RA, Rustagi A, Yu Y, Ardekani H, Kemper A, Cao L, Gundogdu K.
PMID: 30608697
Nano Lett. 2019 Feb 13;19(2):1104-1111. doi: 10.1021/acs.nanolett.8b04408. Epub 2019 Jan 14.

Many-body interactions in photoexcited semiconductors can bring about strongly interacting electronic states, culminating in the fully ionized matter of electron-hole plasma (EHP) and electron-hole liquid (EHL). These exotic phases exhibit unique electronic properties, such as metallic conductivity and metastable...

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Bataller AW, Younts RA, Rustagi A, et al. Dense Electron-Hole Plasma Formation and Ultralong Charge Lifetime in Monolayer MoS. Nano Lett. 2019;19(2):1104-1111doi: 10.1021/acs.nanolett.8b04408.
Bataller, A. W., Younts, R. A., Rustagi, A., Yu, Y., Ardekani, H., Kemper, A., Cao, L., & Gundogdu, K. (2019). Dense Electron-Hole Plasma Formation and Ultralong Charge Lifetime in Monolayer MoS. Nano letters, 19(2), 1104-1111. https://doi.org/10.1021/acs.nanolett.8b04408
Bataller, Alexander W, et al. "Dense Electron-Hole Plasma Formation and Ultralong Charge Lifetime in Monolayer MoS." Nano letters vol. 19,2 (2019): 1104-1111. doi: https://doi.org/10.1021/acs.nanolett.8b04408
Bataller AW, Younts RA, Rustagi A, Yu Y, Ardekani H, Kemper A, Cao L, Gundogdu K. Dense Electron-Hole Plasma Formation and Ultralong Charge Lifetime in Monolayer MoS. Nano Lett. 2019 Feb 13;19(2):1104-1111. doi: 10.1021/acs.nanolett.8b04408. Epub 2019 Jan 14. PMID: 30608697.
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