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Insulin-like Growth Factor-1 (IGF-1) is a Costimulator of the Expansion of Lineage Committed Cells Derived from Peripheral Blood Mobilized CD34(+) Cells in Multiple Myeloma Patients.

Hematology (Amsterdam, Netherlands)

Frostad S, Bjerknes R, Hervig T, Nesthus I, Olweus J, Bruserud Ø.
PMID: 27420550
Hematology. 1999;4(3):217-29. doi: 10.1080/10245332.1999.11746445.

The effect of insulin-like growth factor-1 (IGF-1) on highly enriched human apheresis CD34(+) progenitor cells was investigated in vitro. The progenitor cells were mobilized by treatment with cyclophosphamide + granulocyte-colony stimulating factor (G-CSF) in patients with multiple myeloma. CD34(+)...

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Frostad S, Bjerknes R, Hervig T, et al. Insulin-like Growth Factor-1 (IGF-1) is a Costimulator of the Expansion of Lineage Committed Cells Derived from Peripheral Blood Mobilized CD34(+) Cells in Multiple Myeloma Patients. Hematology. 1999;4(3):217-29doi: 10.1080/10245332.1999.11746445.
Frostad, S., Bjerknes, R., Hervig, T., Nesthus, I., Olweus, J., & Bruserud, �. �. (1999). Insulin-like Growth Factor-1 (IGF-1) is a Costimulator of the Expansion of Lineage Committed Cells Derived from Peripheral Blood Mobilized CD34(+) Cells in Multiple Myeloma Patients. Hematology (Amsterdam, Netherlands), 4(3), 217-29. https://doi.org/10.1080/10245332.1999.11746445
Frostad, S, et al. "Insulin-like Growth Factor-1 (IGF-1) is a Costimulator of the Expansion of Lineage Committed Cells Derived from Peripheral Blood Mobilized CD34(+) Cells in Multiple Myeloma Patients." Hematology (Amsterdam, Netherlands) vol. 4,3 (1999): 217-29. doi: https://doi.org/10.1080/10245332.1999.11746445
Frostad S, Bjerknes R, Hervig T, Nesthus I, Olweus J, Bruserud Ø. Insulin-like Growth Factor-1 (IGF-1) is a Costimulator of the Expansion of Lineage Committed Cells Derived from Peripheral Blood Mobilized CD34(+) Cells in Multiple Myeloma Patients. Hematology. 1999;4(3):217-29. doi: 10.1080/10245332.1999.11746445. PMID: 27420550.
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SVP-B5 peptide from .

Experimental and therapeutic medicine

Wang Y, Xing B, Li T, Wang C, Zhou M, Liu Y, Fan L, Hu L, Peng X, Xiang Y, Wang H, Kong T, Dong W, Guo Q.
PMID: 29201218
Exp Ther Med. 2017 Nov;14(5):5081-5086. doi: 10.3892/etm.2017.5152. Epub 2017 Sep 20.

Previous studies have demonstrated the radioprotective efficacy of scorpion venom peptide, fraction II (SVPII) from the venom of

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Wang Y, Xing B, Li T, et al. SVP-B5 peptide from . Exp Ther Med. 2017;14(5):5081-5086doi: 10.3892/etm.2017.5152.
Wang, Y., Xing, B., Li, T., Wang, C., Zhou, M., Liu, Y., Fan, L., Hu, L., Peng, X., Xiang, Y., Wang, H., Kong, T., Dong, W., & Guo, Q. (2017). SVP-B5 peptide from . Experimental and therapeutic medicine, 14(5), 5081-5086. https://doi.org/10.3892/etm.2017.5152
Wang, Yan, et al. "SVP-B5 peptide from ." Experimental and therapeutic medicine vol. 14,5 (2017): 5081-5086. doi: https://doi.org/10.3892/etm.2017.5152
Wang Y, Xing B, Li T, Wang C, Zhou M, Liu Y, Fan L, Hu L, Peng X, Xiang Y, Wang H, Kong T, Dong W, Guo Q. SVP-B5 peptide from . Exp Ther Med. 2017 Nov;14(5):5081-5086. doi: 10.3892/etm.2017.5152. Epub 2017 Sep 20. PMID: 29201218; PMCID: PMC5704312.
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Peripheral blood monocytes can differentiate into efficient insulin-producing cells in vitro.

Hippokratia

Kyventidis A, Tzimagiorgis G, Didangelos T.
PMID: 27688700
Hippokratia. 2015 Oct-Dec;19(4):344-51.

BACKGROUND: Recent studies provide evidence that peripheral blood monocytes have the ability to differentiate into mesenchymal-like cells. The ability of cultured monocytes to differentiate and produce insulin in vitro is analysed in the present study.METHODS: Peripheral blood monocytes were...

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Kyventidis A, Tzimagiorgis G, Didangelos T. Peripheral blood monocytes can differentiate into efficient insulin-producing cells in vitro. Hippokratia. 2015;19(4):344-51
Kyventidis, A., Tzimagiorgis, G., & Didangelos, T. (2015). Peripheral blood monocytes can differentiate into efficient insulin-producing cells in vitro. Hippokratia, 19(4), 344-51.
Kyventidis, A, et al. "Peripheral blood monocytes can differentiate into efficient insulin-producing cells in vitro." Hippokratia vol. 19,4 (2015): 344-51.
Kyventidis A, Tzimagiorgis G, Didangelos T. Peripheral blood monocytes can differentiate into efficient insulin-producing cells in vitro. Hippokratia. 2015 Oct-Dec;19(4):344-51. PMID: 27688700; PMCID: PMC5033146.
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The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide.

Cellular and molecular gastroenterology and hepatology

Rong B, Wu Q, Reiter RJ, Sun C.
PMID: 34242820
Cell Mol Gastroenterol Hepatol. 2021;12(5):1643-1667. doi: 10.1016/j.jcmgh.2021.06.024. Epub 2021 Jul 06.

BACKGROUND & AIMS: Gut microbiota have been reported to be sensitive to circadian rhythms and host lipometabolism, respectively. Although melatonin-mediated beneficial efforts on many physiological sites have been revealed, the regulatory actions of oral melatonin on the communication between...

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Rong B, Wu Q, Reiter RJ, et al. The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide. Cell Mol Gastroenterol Hepatol. 2021;12(5):1643-1667doi: 10.1016/j.jcmgh.2021.06.024.
Rong, B., Wu, Q., Reiter, R. J., & Sun, C. (2021). The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide. Cellular and molecular gastroenterology and hepatology, 12(5), 1643-1667. https://doi.org/10.1016/j.jcmgh.2021.06.024
Rong, Bohan, et al. "The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide." Cellular and molecular gastroenterology and hepatology vol. 12,5 (2021): 1643-1667. doi: https://doi.org/10.1016/j.jcmgh.2021.06.024
Rong B, Wu Q, Reiter RJ, Sun C. The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide. Cell Mol Gastroenterol Hepatol. 2021;12(5):1643-1667. doi: 10.1016/j.jcmgh.2021.06.024. Epub 2021 Jul 06. PMID: 34242820; PMCID: PMC8536535.
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The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling.

International journal of molecular sciences

Wen TH, Tsai KW, Wu YJ, Liao MT, Lu KC, Hu WC.
PMID: 34948112
Int J Mol Sci. 2021 Dec 10;22(24). doi: 10.3390/ijms222413310.

The human host immune responses to parasitic infections are complex. They can be categorized into four immunological pathways mounted against four types of parasitic infections. For intracellular protozoa, the eradicable host immunological pathway is TH1 immunity involving macrophages (M1),...

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Wen TH, Tsai KW, Wu YJ, et al. The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling. Int J Mol Sci. 2021;22(24)doi: 10.3390/ijms222413310.
Wen, T. H., Tsai, K. W., Wu, Y. J., Liao, M. T., Lu, K. C., & Hu, W. C. (2021). The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling. International journal of molecular sciences, 22(24), . https://doi.org/10.3390/ijms222413310
Wen, Tsung-Han, et al. "The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling." International journal of molecular sciences vol. 22,24 (2021). doi: https://doi.org/10.3390/ijms222413310
Wen TH, Tsai KW, Wu YJ, Liao MT, Lu KC, Hu WC. The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling. Int J Mol Sci. 2021 Dec 10;22(24). doi: 10.3390/ijms222413310. PMID: 34948112; PMCID: PMC8705408.
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The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling.

International journal of molecular sciences

Wen TH, Tsai KW, Wu YJ, Liao MT, Lu KC, Hu WC.
PMID: 34948112
Int J Mol Sci. 2021 Dec 10;22(24). doi: 10.3390/ijms222413310.

The human host immune responses to parasitic infections are complex. They can be categorized into four immunological pathways mounted against four types of parasitic infections. For intracellular protozoa, the eradicable host immunological pathway is TH1 immunity involving macrophages (M1),...

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Wen TH, Tsai KW, Wu YJ, et al. The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling. Int J Mol Sci. 2021;22(24)doi: 10.3390/ijms222413310.
Wen, T. H., Tsai, K. W., Wu, Y. J., Liao, M. T., Lu, K. C., & Hu, W. C. (2021). The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling. International journal of molecular sciences, 22(24), . https://doi.org/10.3390/ijms222413310
Wen, Tsung-Han, et al. "The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling." International journal of molecular sciences vol. 22,24 (2021). doi: https://doi.org/10.3390/ijms222413310
Wen TH, Tsai KW, Wu YJ, Liao MT, Lu KC, Hu WC. The Framework for Human Host Immune Responses to Four Types of Parasitic Infections and Relevant Key JAK/STAT Signaling. Int J Mol Sci. 2021 Dec 10;22(24). doi: 10.3390/ijms222413310. PMID: 34948112.
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Utility of the Ba/F3 cell system for exploring on-target mechanisms of resistance to targeted therapies for lung cancer.

Cancer science

Koga T, Suda K, Mitsudomi T.
PMID: 34997674
Cancer Sci. 2022 Jan 07; doi: 10.1111/cas.15263. Epub 2022 Jan 07.

Molecularly targeted therapies are the standard of care for front-line treatment of metastatic non-small cell lung cancers (NSCLCs) harboring driver gene mutations. However, despite the initial dramatic responses, the emergence of acquired resistance is inevitable. Acquisition of secondary mutations...

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Koga T, Suda K, Mitsudomi T. Utility of the Ba/F3 cell system for exploring on-target mechanisms of resistance to targeted therapies for lung cancer. Cancer Sci. 2022;doi: 10.1111/cas.15263.
Koga, T., Suda, K., & Mitsudomi, T. (2022). Utility of the Ba/F3 cell system for exploring on-target mechanisms of resistance to targeted therapies for lung cancer. Cancer science, . https://doi.org/10.1111/cas.15263
Koga, Takamasa, et al. "Utility of the Ba/F3 cell system for exploring on-target mechanisms of resistance to targeted therapies for lung cancer." Cancer science vol. (2022). doi: https://doi.org/10.1111/cas.15263
Koga T, Suda K, Mitsudomi T. Utility of the Ba/F3 cell system for exploring on-target mechanisms of resistance to targeted therapies for lung cancer. Cancer Sci. 2022 Jan 07; doi: 10.1111/cas.15263. Epub 2022 Jan 07. PMID: 34997674.
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The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide.

Cellular and molecular gastroenterology and hepatology

Rong B, Wu Q, Reiter RJ, Sun C.
PMID: 34242820
Cell Mol Gastroenterol Hepatol. 2021;12(5):1643-1667. doi: 10.1016/j.jcmgh.2021.06.024. Epub 2021 Jul 06.

BACKGROUND & AIMS: Gut microbiota have been reported to be sensitive to circadian rhythms and host lipometabolism, respectively. Although melatonin-mediated beneficial efforts on many physiological sites have been revealed, the regulatory actions of oral melatonin on the communication between...

Cite
Rong B, Wu Q, Reiter RJ, et al. The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide. Cell Mol Gastroenterol Hepatol. 2021;12(5):1643-1667doi: 10.1016/j.jcmgh.2021.06.024.
Rong, B., Wu, Q., Reiter, R. J., & Sun, C. (2021). The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide. Cellular and molecular gastroenterology and hepatology, 12(5), 1643-1667. https://doi.org/10.1016/j.jcmgh.2021.06.024
Rong, Bohan, et al. "The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide." Cellular and molecular gastroenterology and hepatology vol. 12,5 (2021): 1643-1667. doi: https://doi.org/10.1016/j.jcmgh.2021.06.024
Rong B, Wu Q, Reiter RJ, Sun C. The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide. Cell Mol Gastroenterol Hepatol. 2021;12(5):1643-1667. doi: 10.1016/j.jcmgh.2021.06.024. Epub 2021 Jul 06. PMID: 34242820; PMCID: PMC8536535.
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Macrophages Derived From Human Induced Pluripotent Stem Cells: The Diversity of Protocols, Future Prospects, and Outstanding Questions.

Frontiers in cell and developmental biology

Lyadova I, Gerasimova T, Nenasheva T.
PMID: 34150747
Front Cell Dev Biol. 2021 Jun 02;9:640703. doi: 10.3389/fcell.2021.640703. eCollection 2021.

Macrophages (Mφ) derived from induced pluripotent stem cells (iMphs) represent a novel and promising model for studying human Mφ function and differentiation and developing new therapeutic strategies based on or oriented at Mφs. iMphs have several advantages over the...

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Lyadova I, Gerasimova T, Nenasheva T. Macrophages Derived From Human Induced Pluripotent Stem Cells: The Diversity of Protocols, Future Prospects, and Outstanding Questions. Front Cell Dev Biol. 2021;9:640703doi: 10.3389/fcell.2021.640703.
Lyadova, I., Gerasimova, T., & Nenasheva, T. (2021). Macrophages Derived From Human Induced Pluripotent Stem Cells: The Diversity of Protocols, Future Prospects, and Outstanding Questions. Frontiers in cell and developmental biology, 9640703. https://doi.org/10.3389/fcell.2021.640703
Lyadova, Irina, et al. "Macrophages Derived From Human Induced Pluripotent Stem Cells: The Diversity of Protocols, Future Prospects, and Outstanding Questions." Frontiers in cell and developmental biology vol. 9 (2021): 640703. doi: https://doi.org/10.3389/fcell.2021.640703
Lyadova I, Gerasimova T, Nenasheva T. Macrophages Derived From Human Induced Pluripotent Stem Cells: The Diversity of Protocols, Future Prospects, and Outstanding Questions. Front Cell Dev Biol. 2021 Jun 02;9:640703. doi: 10.3389/fcell.2021.640703. eCollection 2021. PMID: 34150747; PMCID: PMC8207294.
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IL-3 in the development and function of basophils.

Seminars in immunology

Varricchi G, Poto R, Marone G, Schroeder JT.
PMID: 34756806
Semin Immunol. 2021 Oct 29;101510. doi: 10.1016/j.smim.2021.101510. Epub 2021 Oct 29.

The β common chain (βc) cytokine family includes granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3) and IL-5, all of which use βc as key signaling receptor subunit. GM-CSF, IL-3 and IL-5 have specific roles as hematopoietic growth factors. IL-3 binds...

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Varricchi G, Poto R, Marone G, et al. IL-3 in the development and function of basophils. Semin Immunol. 2021;101510doi: 10.1016/j.smim.2021.101510.
Varricchi, G., Poto, R., Marone, G., & Schroeder, J. T. (2021). IL-3 in the development and function of basophils. Seminars in immunology, 101510. https://doi.org/10.1016/j.smim.2021.101510
Varricchi, Gilda, et al. "IL-3 in the development and function of basophils." Seminars in immunology vol. (2021): 101510. doi: https://doi.org/10.1016/j.smim.2021.101510
Varricchi G, Poto R, Marone G, Schroeder JT. IL-3 in the development and function of basophils. Semin Immunol. 2021 Oct 29;101510. doi: 10.1016/j.smim.2021.101510. Epub 2021 Oct 29. PMID: 34756806.
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IgE-Dependent Histamine-Releasing Factor: A Unique Cytokine.

International archives of allergy and immunology

Langdon J, MacDonald SM.
PMID: 34167235
Int Arch Allergy Immunol. 1992;99(2):316-318. doi: 10.1159/000236272. Epub 2009 Sep 02.

Numerous cytokines have been reported to influence basophil histamine release. The IgE-dependent histamine-releasing factor (HRF), interleukin-3 and mononuclear cell chemotactic activating factor (MCAF) are among the direct agonists of basophil histamine release. Kinetic experiments distinguish these three agonists with...

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Langdon J, MacDonald SM. IgE-Dependent Histamine-Releasing Factor: A Unique Cytokine. Int Arch Allergy Immunol. 2009;99(2):316-318doi: 10.1159/000236272.
Langdon, J., & MacDonald, S. M. (1992). IgE-Dependent Histamine-Releasing Factor: A Unique Cytokine. International archives of allergy and immunology, 99(2), 316-318. https://doi.org/10.1159/000236272
Langdon, Jacqueline, and MacDonald, Susan M. "IgE-Dependent Histamine-Releasing Factor: A Unique Cytokine." International archives of allergy and immunology vol. 99,2 (1992): 316-318. doi: https://doi.org/10.1159/000236272
Langdon J, MacDonald SM. IgE-Dependent Histamine-Releasing Factor: A Unique Cytokine. Int Arch Allergy Immunol. 1992;99(2):316-318. doi: 10.1159/000236272. Epub 2009 Sep 02. PMID: 34167235.
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Specific cellular signal-transduction responses to in vivo combination therapy with ATRA, valproic acid and theophylline in acute myeloid leukemia.

Blood cancer journal

Skavland J, Jørgensen KM, Hadziavdic K, Hovland R, Jonassen I, Bruserud O, Gjertsen BT.
PMID: 22829110
Blood Cancer J. 2011 Feb;1(2):e4. doi: 10.1038/bcj.2011.2. Epub 2011 Feb 11.

Acute myeloid leukemia (AML) frequently comprises mutations in genes that cause perturbation in intracellular signaling pathways, thereby altering normal responses to growth factors and cytokines. Such oncogenic cellular signal transduction may be therapeutic if targeted directly or through epigenetic...

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Skavland J, Jørgensen KM, Hadziavdic K, et al. Specific cellular signal-transduction responses to in vivo combination therapy with ATRA, valproic acid and theophylline in acute myeloid leukemia. Blood Cancer J. 2011;1(2):e4doi: 10.1038/bcj.2011.2.
Skavland, J., Jørgensen, K. M., Hadziavdic, K., Hovland, R., Jonassen, I., Bruserud, O., & Gjertsen, B. T. (2011). Specific cellular signal-transduction responses to in vivo combination therapy with ATRA, valproic acid and theophylline in acute myeloid leukemia. Blood cancer journal, 1(2), e4. https://doi.org/10.1038/bcj.2011.2
Skavland, J, et al. "Specific cellular signal-transduction responses to in vivo combination therapy with ATRA, valproic acid and theophylline in acute myeloid leukemia." Blood cancer journal vol. 1,2 (2011): e4. doi: https://doi.org/10.1038/bcj.2011.2
Skavland J, Jørgensen KM, Hadziavdic K, Hovland R, Jonassen I, Bruserud O, Gjertsen BT. Specific cellular signal-transduction responses to in vivo combination therapy with ATRA, valproic acid and theophylline in acute myeloid leukemia. Blood Cancer J. 2011 Feb;1(2):e4. doi: 10.1038/bcj.2011.2. Epub 2011 Feb 11. PMID: 22829110; PMCID: PMC3255270.
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