Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Species
Language
Sex
Age
Showing 1 to 12 of 148 entries
Sorted by: Best Match Show Resources per page
Bone morphogenetic protein-4 and transforming growth factor-beta1 mechanisms in acute valvular response to supra-physiologic hemodynamic stresses.

World journal of cardiology

Sun L, Sucosky P.
PMID: 26131338
World J Cardiol. 2015 Jun 26;7(6):331-43. doi: 10.4330/wjc.v7.i6.331.

AIM: To explore ex vivo the role of bone morphogenetic protein-4 (BMP-4) and transforming growth factor-beta1 (TGF-β1) in acute valvular response to fluid shear stress (FSS) abnormalities.METHODS: Porcine valve leaflets were subjected ex vivo to physiologic FSS, supra-physiologic FSS...

Cite
Sun L, Sucosky P. Bone morphogenetic protein-4 and transforming growth factor-beta1 mechanisms in acute valvular response to supra-physiologic hemodynamic stresses. World J Cardiol. 2015;7(6):331-43doi: 10.4330/wjc.v7.i6.331.
Sun, L., & Sucosky, P. (2015). Bone morphogenetic protein-4 and transforming growth factor-beta1 mechanisms in acute valvular response to supra-physiologic hemodynamic stresses. World journal of cardiology, 7(6), 331-43. https://doi.org/10.4330/wjc.v7.i6.331
Sun, Ling, and Sucosky, Philippe. "Bone morphogenetic protein-4 and transforming growth factor-beta1 mechanisms in acute valvular response to supra-physiologic hemodynamic stresses." World journal of cardiology vol. 7,6 (2015): 331-43. doi: https://doi.org/10.4330/wjc.v7.i6.331
Sun L, Sucosky P. Bone morphogenetic protein-4 and transforming growth factor-beta1 mechanisms in acute valvular response to supra-physiologic hemodynamic stresses. World J Cardiol. 2015 Jun 26;7(6):331-43. doi: 10.4330/wjc.v7.i6.331. PMID: 26131338; PMCID: PMC4478568.
Copy Download .nbib Format: NLM
Correlation between PKB/Akt, GSK-3β expression and tubular epithelial-mesenchymal transition in renal allografts with chronic active antibody-mediated rejection.

Experimental and therapeutic medicine

Yan Q, Luo H, Wang B, Sui W, Zou G, Chen H, Zou H.
PMID: 28565830
Exp Ther Med. 2017 May;13(5):2217-2224. doi: 10.3892/etm.2017.4261. Epub 2017 Mar 24.

Chronic antibody-mediated rejection (ABMR) is a major cause of the transplant renal interstitial fibrosis and transplanted kidney epithelial cell transdifferentiation is one of the main mechanisms. The transforming growth factor (TGF)-β1/integrin-linked kinase (ILK) signaling pathway has a significant role...

Cite
Yan Q, Luo H, Wang B, et al. Correlation between PKB/Akt, GSK-3β expression and tubular epithelial-mesenchymal transition in renal allografts with chronic active antibody-mediated rejection. Exp Ther Med. 2017;13(5):2217-2224doi: 10.3892/etm.2017.4261.
Yan, Q., Luo, H., Wang, B., Sui, W., Zou, G., Chen, H., & Zou, H. (2017). Correlation between PKB/Akt, GSK-3β expression and tubular epithelial-mesenchymal transition in renal allografts with chronic active antibody-mediated rejection. Experimental and therapeutic medicine, 13(5), 2217-2224. https://doi.org/10.3892/etm.2017.4261
Yan, Qiang, et al. "Correlation between PKB/Akt, GSK-3β expression and tubular epithelial-mesenchymal transition in renal allografts with chronic active antibody-mediated rejection." Experimental and therapeutic medicine vol. 13,5 (2017): 2217-2224. doi: https://doi.org/10.3892/etm.2017.4261
Yan Q, Luo H, Wang B, Sui W, Zou G, Chen H, Zou H. Correlation between PKB/Akt, GSK-3β expression and tubular epithelial-mesenchymal transition in renal allografts with chronic active antibody-mediated rejection. Exp Ther Med. 2017 May;13(5):2217-2224. doi: 10.3892/etm.2017.4261. Epub 2017 Mar 24. PMID: 28565830; PMCID: PMC5443285.
Copy Download .nbib Format: NLM
The association of TGFB1 genetic polymorphisms with high myopia: a systematic review and meta-analysis.

International journal of clinical and experimental medicine

Meng B, Li SM, Yang Y, Yang ZR, Sun F, Kang MT, Sun YY, Ran AR, Wang JN, Yan R, BaI YW, Wang NL, Zhan SY.
PMID: 26884952
Int J Clin Exp Med. 2015 Nov 15;8(11):20355-67. eCollection 2015.

OBJECTIVE: The TGFB1 gene is among the most studied genes in high myopia due to its role in scleral remodeling. But reported findings of association on TGFB1 and high myopia are inconsistent. This present study is to evaluate the...

Cite
Meng B, Li SM, Yang Y, et al. The association of TGFB1 genetic polymorphisms with high myopia: a systematic review and meta-analysis. Int J Clin Exp Med. 2015;8(11):20355-67
Meng, B., Li, S. M., Yang, Y., Yang, Z. R., Sun, F., Kang, M. T., Sun, Y. Y., Ran, A. R., Wang, J. N., Yan, R., BaI, Y. W., Wang, N. L., & Zhan, S. Y. (2015). The association of TGFB1 genetic polymorphisms with high myopia: a systematic review and meta-analysis. International journal of clinical and experimental medicine, 8(11), 20355-67.
Meng, Bo, et al. "The association of TGFB1 genetic polymorphisms with high myopia: a systematic review and meta-analysis." International journal of clinical and experimental medicine vol. 8,11 (2015): 20355-67.
Meng B, Li SM, Yang Y, Yang ZR, Sun F, Kang MT, Sun YY, Ran AR, Wang JN, Yan R, BaI YW, Wang NL, Zhan SY. The association of TGFB1 genetic polymorphisms with high myopia: a systematic review and meta-analysis. Int J Clin Exp Med. 2015 Nov 15;8(11):20355-67. eCollection 2015. PMID: 26884952; PMCID: PMC4723797.
Copy Download .nbib Format: NLM
Angiotensin II stimulates the nuclear translocation of Smad2 and induces PAI-1 mRNA in rat hepatic stellate cells.

Hepatology research : the official journal of the Japan Society of Hepatology

Kamada Y, Tamura S, Kiso S, Fukui K, Doi Y, Ito N, Terui Y, Saito T, Watanabe H, Togashi H, Kawata S, Matsuzawa Y.
PMID: 12697251
Hepatol Res. 2003 Mar;25(3):296-305. doi: 10.1016/s1386-6346(02)00306-6.

It has recently been reported that angiotensin II (ANGII) stimulates gene expression of transforming growth factor-beta1 (TGF-beta1) and is involved in hepatic fibrosis. This effect is thought to be caused through ANGII type 1 receptor (ATR1). However, a role...

Cite
Kamada Y, Tamura S, Kiso S, et al. Angiotensin II stimulates the nuclear translocation of Smad2 and induces PAI-1 mRNA in rat hepatic stellate cells. Hepatol Res. 2003;25(3):296-305doi: 10.1016/s1386-6346(02)00306-6.
Kamada, Y., Tamura, S., Kiso, S., Fukui, K., Doi, Y., Ito, N., Terui, Y., Saito, T., Watanabe, H., Togashi, H., Kawata, S., & Matsuzawa, Y. (2003). Angiotensin II stimulates the nuclear translocation of Smad2 and induces PAI-1 mRNA in rat hepatic stellate cells. Hepatology research : the official journal of the Japan Society of Hepatology, 25(3), 296-305. https://doi.org/10.1016/s1386-6346(02)00306-6
Kamada, Yoshihiro, et al. "Angiotensin II stimulates the nuclear translocation of Smad2 and induces PAI-1 mRNA in rat hepatic stellate cells." Hepatology research : the official journal of the Japan Society of Hepatology vol. 25,3 (2003): 296-305. doi: https://doi.org/10.1016/s1386-6346(02)00306-6
Kamada Y, Tamura S, Kiso S, Fukui K, Doi Y, Ito N, Terui Y, Saito T, Watanabe H, Togashi H, Kawata S, Matsuzawa Y. Angiotensin II stimulates the nuclear translocation of Smad2 and induces PAI-1 mRNA in rat hepatic stellate cells. Hepatol Res. 2003 Mar;25(3):296-305. doi: 10.1016/s1386-6346(02)00306-6. PMID: 12697251.
Copy Download .nbib Format: NLM
Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model.

Hepatology research : the official journal of the Japan Society of Hepatology

Takahara T, Sugiyama K, Zhang LP, Ando O, Fujii M, Yata Y, Bo J, Xue F, Minemura M, Watanabe A.
PMID: 15036071
Hepatol Res. 2004 Mar;28(3):146-154. doi: 10.1016/j.hepres.2003.11.003.

Background/Aims: Interferon-alpha is used widely to treat viral hepatitis. Interferon-gamma modulates a system attacking infected cells and also has an anti-fibrotic effect. A treatment with interferon-alpha and -gamma has undergone trials in eliminating hepatitis C virus. We investigated effects...

Cite
Takahara T, Sugiyama K, Zhang LP, et al. Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model. Hepatol Res. 2004;28(3):146-154doi: 10.1016/j.hepres.2003.11.003.
Takahara, T., Sugiyama, K., Zhang, L. P., Ando, O., Fujii, M., Yata, Y., Bo, J., Xue, F., Minemura, M., & Watanabe, A. (2004). Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model. Hepatology research : the official journal of the Japan Society of Hepatology, 28(3), 146-154. https://doi.org/10.1016/j.hepres.2003.11.003
Takahara, Terumi, et al. "Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model." Hepatology research : the official journal of the Japan Society of Hepatology vol. 28,3 (2004): 146-154. doi: https://doi.org/10.1016/j.hepres.2003.11.003
Takahara T, Sugiyama K, Zhang LP, Ando O, Fujii M, Yata Y, Bo J, Xue F, Minemura M, Watanabe A. Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model. Hepatol Res. 2004 Mar;28(3):146-154. doi: 10.1016/j.hepres.2003.11.003. PMID: 15036071.
Copy Download .nbib Format: NLM
A role for interferon-beta in Guillain-Barré Syndrome?.

BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy

Créange A.
PMID: 18034551
BioDrugs. 2000 Jul;14(1):1-11. doi: 10.2165/00063030-200014010-00001.

Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating neuropathy that is associated with long-lasting morbidity and a substantial risk of mortality. The 2 reference treatments, plasma exchange and intravenous immunoglobulins (IVIg), do not change the functional prognosis for the...

Cite
Créange A. A role for interferon-beta in Guillain-Barré Syndrome?. BioDrugs. 2000;14(1):1-11doi: 10.2165/00063030-200014010-00001.
Créange, A. (2000). A role for interferon-beta in Guillain-Barré Syndrome?. BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy, 14(1), 1-11. https://doi.org/10.2165/00063030-200014010-00001
Créange, A. "A role for interferon-beta in Guillain-Barré Syndrome?." BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy vol. 14,1 (2000): 1-11. doi: https://doi.org/10.2165/00063030-200014010-00001
Créange A. A role for interferon-beta in Guillain-Barré Syndrome?. BioDrugs. 2000 Jul;14(1):1-11. doi: 10.2165/00063030-200014010-00001. PMID: 18034551.
Copy Download .nbib Format: NLM
Transforming growth factor beta stimulates rheumatoid synovial fibroblasts via the type II receptor.

Modern rheumatology

Bira Y, Tani K, Nishioka Y, Miyata J, Sato K, Hayashi A, Nakaya Y, Sone S.
PMID: 17029045
Mod Rheumatol. 2005;15(2):108-13. doi: 10.1007/s10165-004-0378-2.

Transforming growth factor (TGF)-beta regulates the function of fibroblasts, and has been shown to have a role in the pathogenesis of rheumatoid arthritis (RA) because several studies have demonstrated the presence of TGF-beta in the synovial tissue and synovial...

Cite
Bira Y, Tani K, Nishioka Y, et al. Transforming growth factor beta stimulates rheumatoid synovial fibroblasts via the type II receptor. Mod Rheumatol. 2005;15(2):108-13doi: 10.1007/s10165-004-0378-2.
Bira, Y., Tani, K., Nishioka, Y., Miyata, J., Sato, K., Hayashi, A., Nakaya, Y., & Sone, S. (2005). Transforming growth factor beta stimulates rheumatoid synovial fibroblasts via the type II receptor. Modern rheumatology, 15(2), 108-13. https://doi.org/10.1007/s10165-004-0378-2
Bira, Yanjmaa, et al. "Transforming growth factor beta stimulates rheumatoid synovial fibroblasts via the type II receptor." Modern rheumatology vol. 15,2 (2005): 108-13. doi: https://doi.org/10.1007/s10165-004-0378-2
Bira Y, Tani K, Nishioka Y, Miyata J, Sato K, Hayashi A, Nakaya Y, Sone S. Transforming growth factor beta stimulates rheumatoid synovial fibroblasts via the type II receptor. Mod Rheumatol. 2005;15(2):108-13. doi: 10.1007/s10165-004-0378-2. PMID: 17029045.
Copy Download .nbib Format: NLM
Effects of cytokines in burn blister fluids on fibroblast proliferation and their inhibition with the use of neutralizing antibodies.

Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society

Inoue M, Zhou LJ, Gunji H, Ono I, Kaneko F.
PMID: 17309693
Wound Repair Regen. 1996 Oct;4(4):426-32. doi: 10.1046/j.1524-475X.1996.40406.x.

Recent studies have shown that tissue exudates, such as burn blister fluid and donor site wound fluid, have promotive effects on wound healing. In the present study, results obtained with enzyme-linked immunosorbent assays showed that at least three cytokines,...

Cite
Inoue M, Zhou LJ, Gunji H, et al. Effects of cytokines in burn blister fluids on fibroblast proliferation and their inhibition with the use of neutralizing antibodies. Wound Repair Regen. 1996;4(4):426-32doi: 10.1046/j.1524-475X.1996.40406.x.
Inoue, M., Zhou, L. J., Gunji, H., Ono, I., & Kaneko, F. (1996). Effects of cytokines in burn blister fluids on fibroblast proliferation and their inhibition with the use of neutralizing antibodies. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society, 4(4), 426-32. https://doi.org/10.1046/j.1524-475X.1996.40406.x
Inoue, M, et al. "Effects of cytokines in burn blister fluids on fibroblast proliferation and their inhibition with the use of neutralizing antibodies." Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society vol. 4,4 (1996): 426-32. doi: https://doi.org/10.1046/j.1524-475X.1996.40406.x
Inoue M, Zhou LJ, Gunji H, Ono I, Kaneko F. Effects of cytokines in burn blister fluids on fibroblast proliferation and their inhibition with the use of neutralizing antibodies. Wound Repair Regen. 1996 Oct;4(4):426-32. doi: 10.1046/j.1524-475X.1996.40406.x. PMID: 17309693.
Copy Download .nbib Format: NLM
TGFbeta1 expression in colonic mucosa: modulation by dietary lipids.

Genes & nutrition

Biasi F, Mascia C, Poli G.
PMID: 18850178
Genes Nutr. 2007 Nov;2(2):233-43. doi: 10.1007/s12263-007-0053-2. Epub 2007 Sep 27.

Transforming growth factor beta1 (TGFbeta1) is fundamental to maintain the intestinal epithelial cell homeostasis through its control action on cell proliferation, differentiation and apoptosis. TGFbeta1 dysregulation has been observed in several chronic human diseases, including ulcerative colitis, Crohn's disease...

Cite
Biasi F, Mascia C, Poli G. TGFbeta1 expression in colonic mucosa: modulation by dietary lipids. Genes Nutr. 2007;2(2):233-43doi: 10.1007/s12263-007-0053-2.
Biasi, F., Mascia, C., & Poli, G. (2007). TGFbeta1 expression in colonic mucosa: modulation by dietary lipids. Genes & nutrition, 2(2), 233-43. https://doi.org/10.1007/s12263-007-0053-2
Biasi, Fiorella, et al. "TGFbeta1 expression in colonic mucosa: modulation by dietary lipids." Genes & nutrition vol. 2,2 (2007): 233-43. doi: https://doi.org/10.1007/s12263-007-0053-2
Biasi F, Mascia C, Poli G. TGFbeta1 expression in colonic mucosa: modulation by dietary lipids. Genes Nutr. 2007 Nov;2(2):233-43. doi: 10.1007/s12263-007-0053-2. Epub 2007 Sep 27. PMID: 18850178; PMCID: PMC2474948.
Copy Download .nbib Format: NLM
Proteomic Profiling of Mesenchymal Stem Cell Responses to Mechanical Strain and TGF-beta1.

Cellular and molecular bioengineering

Kurpinski K, Chu J, Wang D, Li S.
PMID: 20037637
Cell Mol Bioeng. 2009 Dec;2(4):606-614. doi: 10.1007/s12195-009-0090-6. Epub 2009 Oct 24.

Mesenchymal stem cells (MSCs) are a potential source of smooth muscle cells (SMCs) for constructing tissue-engineered vascular grafts. However, the details of how specific combinations of vascular microenvironmental factors regulate MSCs are not well understood. Previous studies have suggested...

Cite
Kurpinski K, Chu J, Wang D, et al. Proteomic Profiling of Mesenchymal Stem Cell Responses to Mechanical Strain and TGF-beta1. Cell Mol Bioeng. 2009;2(4):606-614doi: 10.1007/s12195-009-0090-6.
Kurpinski, K., Chu, J., Wang, D., & Li, S. (2009). Proteomic Profiling of Mesenchymal Stem Cell Responses to Mechanical Strain and TGF-beta1. Cellular and molecular bioengineering, 2(4), 606-614. https://doi.org/10.1007/s12195-009-0090-6
Kurpinski, Kyle, et al. "Proteomic Profiling of Mesenchymal Stem Cell Responses to Mechanical Strain and TGF-beta1." Cellular and molecular bioengineering vol. 2,4 (2009): 606-614. doi: https://doi.org/10.1007/s12195-009-0090-6
Kurpinski K, Chu J, Wang D, Li S. Proteomic Profiling of Mesenchymal Stem Cell Responses to Mechanical Strain and TGF-beta1. Cell Mol Bioeng. 2009 Dec;2(4):606-614. doi: 10.1007/s12195-009-0090-6. Epub 2009 Oct 24. PMID: 20037637; PMCID: PMC2792360.
Copy Download .nbib Format: NLM
Role of cytokines in myocardial ischemia and reperfusion.

Mediators of inflammation

Sharma HS, Das DK.
PMID: 18472818
Mediators Inflamm. 1997;6(3):175-83. doi: 10.1080/09629359791668.

Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has been paid to the possibility that the inflammation may result in deleterious complications for...

Cite
Sharma HS, Das DK. Role of cytokines in myocardial ischemia and reperfusion. Mediators Inflamm. 1997;6(3):175-83doi: 10.1080/09629359791668.
Sharma, H. S., & Das, D. K. (1997). Role of cytokines in myocardial ischemia and reperfusion. Mediators of inflammation, 6(3), 175-83. https://doi.org/10.1080/09629359791668
Sharma, H S, and Das, D K. "Role of cytokines in myocardial ischemia and reperfusion." Mediators of inflammation vol. 6,3 (1997): 175-83. doi: https://doi.org/10.1080/09629359791668
Sharma HS, Das DK. Role of cytokines in myocardial ischemia and reperfusion. Mediators Inflamm. 1997;6(3):175-83. doi: 10.1080/09629359791668. PMID: 18472818; PMCID: PMC2365828.
Copy Download .nbib Format: NLM
Human plasmacytoid dendritic cells from patients with chronic hepatitis B virus infection induce the generation of a higher proportion of CD4(+) and CD25(+) regulatory T cells compared with healthy patients.

Hepatology research : the official journal of the Japan Society of Hepatology

Hong J, Gong ZJ.
PMID: 18021229
Hepatol Res. 2008 Apr;38(4):362-73. doi: 10.1111/j.1872-034X.2007.00279.x. Epub 2007 Nov 16.

This study was undertaken to investigate whether plasmacytoid dendritic cells (PDC) are involved in the generation of a higher proportion of CD4(+) and CD25(+) regulatory T (Treg) cells in chronic hepatitis B virus (HBV) infection compared with healthy patients....

Cite
Hong J, Gong ZJ. Human plasmacytoid dendritic cells from patients with chronic hepatitis B virus infection induce the generation of a higher proportion of CD4(+) and CD25(+) regulatory T cells compared with healthy patients. Hepatol Res. 2007;38(4):362-73doi: 10.1111/j.1872-034X.2007.00279.x.
Hong, J., & Gong, Z. J. (2008). Human plasmacytoid dendritic cells from patients with chronic hepatitis B virus infection induce the generation of a higher proportion of CD4(+) and CD25(+) regulatory T cells compared with healthy patients. Hepatology research : the official journal of the Japan Society of Hepatology, 38(4), 362-73. https://doi.org/10.1111/j.1872-034X.2007.00279.x
Hong, Jun, and Gong, Zuo Jiong. "Human plasmacytoid dendritic cells from patients with chronic hepatitis B virus infection induce the generation of a higher proportion of CD4(+) and CD25(+) regulatory T cells compared with healthy patients." Hepatology research : the official journal of the Japan Society of Hepatology vol. 38,4 (2008): 362-73. doi: https://doi.org/10.1111/j.1872-034X.2007.00279.x
Hong J, Gong ZJ. Human plasmacytoid dendritic cells from patients with chronic hepatitis B virus infection induce the generation of a higher proportion of CD4(+) and CD25(+) regulatory T cells compared with healthy patients. Hepatol Res. 2008 Apr;38(4):362-73. doi: 10.1111/j.1872-034X.2007.00279.x. Epub 2007 Nov 16. PMID: 18021229.
Copy Download .nbib Format: NLM
Showing 1 to 12 of 148 entries