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Showing 1 to 12 of 17 entries
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Psychotropic drugs as inhibitors of glycerolipid biosynthesis and secretion in primary rat hepatocyte cultures.

Toxicology in vitro : an international journal published in association with BIBRA

Boelsterli UA, Bouis P, Donatsch P.
PMID: 20647077
Toxicol In Vitro. 1987;1(3):127-32. doi: 10.1016/0887-2333(87)90012-9.

Glycerolipid synthesis and secretion in rat hepatocyte monolayer cultures have been studied as possible endpoints in cytotoxicity assays. Ten psychotropic drugs of different structural classes were incubated with the hepatocytes at concentrations ranging from 10(-6)m to 5 x 10(-5)m...

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Boelsterli UA, Bouis P, Donatsch P. Psychotropic drugs as inhibitors of glycerolipid biosynthesis and secretion in primary rat hepatocyte cultures. Toxicol In Vitro. 1987;1(3):127-32doi: 10.1016/0887-2333(87)90012-9.
Boelsterli, U. A., Bouis, P., & Donatsch, P. (1987). Psychotropic drugs as inhibitors of glycerolipid biosynthesis and secretion in primary rat hepatocyte cultures. Toxicology in vitro : an international journal published in association with BIBRA, 1(3), 127-32. https://doi.org/10.1016/0887-2333(87)90012-9
Boelsterli, U A, et al. "Psychotropic drugs as inhibitors of glycerolipid biosynthesis and secretion in primary rat hepatocyte cultures." Toxicology in vitro : an international journal published in association with BIBRA vol. 1,3 (1987): 127-32. doi: https://doi.org/10.1016/0887-2333(87)90012-9
Boelsterli UA, Bouis P, Donatsch P. Psychotropic drugs as inhibitors of glycerolipid biosynthesis and secretion in primary rat hepatocyte cultures. Toxicol In Vitro. 1987;1(3):127-32. doi: 10.1016/0887-2333(87)90012-9. PMID: 20647077.
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Low adoption of pharmacogenetic testing: an exploration and explanation of the reasons in Australia.

Personalized medicine

Corkindale D, Ward H, McKinnon R.
PMID: 29788625
Per Med. 2007 May;4(2):191-199. doi: 10.2217/17410541.4.2.191.

The research reported here sought to identify and illuminate the reasons for the low adoption of pharmacogenetic tests in Australia. The research initially established possible reasons and propositions drawn from previous studies and surveys on the problem in Europe...

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Corkindale D, Ward H, McKinnon R. Low adoption of pharmacogenetic testing: an exploration and explanation of the reasons in Australia. Per Med. 2007;4(2):191-199doi: 10.2217/17410541.4.2.191.
Corkindale, D., Ward, H., & McKinnon, R. (2007). Low adoption of pharmacogenetic testing: an exploration and explanation of the reasons in Australia. Personalized medicine, 4(2), 191-199. https://doi.org/10.2217/17410541.4.2.191
Corkindale, David, et al. "Low adoption of pharmacogenetic testing: an exploration and explanation of the reasons in Australia." Personalized medicine vol. 4,2 (2007): 191-199. doi: https://doi.org/10.2217/17410541.4.2.191
Corkindale D, Ward H, McKinnon R. Low adoption of pharmacogenetic testing: an exploration and explanation of the reasons in Australia. Per Med. 2007 May;4(2):191-199. doi: 10.2217/17410541.4.2.191. PMID: 29788625.
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Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade.

Oncotarget

Flaig TW, Salzmann-Sullivan M, Su LJ, Zhang Z, Joshi M, Gijón MA, Kim J, Arcaroli JJ, Van Bokhoven A, Lucia MS, La Rosa FG, Schlaepfer IR.
PMID: 28915573
Oncotarget. 2017 Apr 21;8(34):56051-56065. doi: 10.18632/oncotarget.17359. eCollection 2017 Aug 22.

Prostate cancer (PCa) is the most common malignancy among Western men and the second leading-cause of cancer related deaths. For men who develop metastatic castration resistant PCa (mCRPC), survival is limited, making the identification of novel therapies for mCRPC...

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Flaig TW, Salzmann-Sullivan M, Su LJ, et al. Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade. Oncotarget. 2017;8(34):56051-56065doi: 10.18632/oncotarget.17359.
Flaig, T. W., Salzmann-Sullivan, M., Su, L. J., Zhang, Z., Joshi, M., Gijón, M. A., Kim, J., Arcaroli, J. J., Van Bokhoven, A., Lucia, M. S., La Rosa, F. G., & Schlaepfer, I. R. (2017). Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade. Oncotarget, 8(34), 56051-56065. https://doi.org/10.18632/oncotarget.17359
Flaig, Thomas W, et al. "Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade." Oncotarget vol. 8,34 (2017): 56051-56065. doi: https://doi.org/10.18632/oncotarget.17359
Flaig TW, Salzmann-Sullivan M, Su LJ, Zhang Z, Joshi M, Gijón MA, Kim J, Arcaroli JJ, Van Bokhoven A, Lucia MS, La Rosa FG, Schlaepfer IR. Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade. Oncotarget. 2017 Apr 21;8(34):56051-56065. doi: 10.18632/oncotarget.17359. eCollection 2017 Aug 22. PMID: 28915573; PMCID: PMC5593544.
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A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers.

Cancer & metabolism

Xu S, Catapang A, Braas D, Stiles L, Doh HM, Lee JT, Graeber TG, Damoiseaux R, Shirihai O, Herschman HR.
PMID: 29988332
Cancer Metab. 2018 Jun 28;6:7. doi: 10.1186/s40170-018-0181-8. eCollection 2018.

BACKGROUND: Precision medicine therapies require identification of unique molecular cancer characteristics. Hexokinase (HK) activity has been proposed as a therapeutic target; however, different hexokinase isoforms have not been well characterized as alternative targets. While HK2 is highly expressed in...

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Xu S, Catapang A, Braas D, et al. A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers. Cancer Metab. 2018;6:7doi: 10.1186/s40170-018-0181-8.
Xu, S., Catapang, A., Braas, D., Stiles, L., Doh, H. M., Lee, J. T., Graeber, T. G., Damoiseaux, R., Shirihai, O., & Herschman, H. R. (2018). A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers. Cancer & metabolism, 67. https://doi.org/10.1186/s40170-018-0181-8
Xu, Shili, et al. "A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers." Cancer & metabolism vol. 6 (2018): 7. doi: https://doi.org/10.1186/s40170-018-0181-8
Xu S, Catapang A, Braas D, Stiles L, Doh HM, Lee JT, Graeber TG, Damoiseaux R, Shirihai O, Herschman HR. A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers. Cancer Metab. 2018 Jun 28;6:7. doi: 10.1186/s40170-018-0181-8. eCollection 2018. PMID: 29988332; PMCID: PMC6022704.
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Krüppel-Like Factor 14 Deletion In Myeloid Cells Accelerates Atherosclerotic Lesion Development.

Cardiovascular research

Wang H, Guo Y, Lu H, Luo Y, Hu W, Liang W, Garcia-Barrio MT, Chang L, Schwendeman A, Zhang J, Chen YE.
PMID: 33538785
Cardiovasc Res. 2021 Feb 04; doi: 10.1093/cvr/cvab027. Epub 2021 Feb 04.

AIMS: Atherosclerosis is the dominant pathologic basis of many cardiovascular diseases. Large genome-wide association studies have identified that single nucleotide polymorphisms proximal to Krüppel-like factor 14 (KLF14), a member of the zinc finger family of transcription factors, are associated...

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Wang H, Guo Y, Lu H, et al. Krüppel-Like Factor 14 Deletion In Myeloid Cells Accelerates Atherosclerotic Lesion Development. Cardiovasc Res. 2021;doi: 10.1093/cvr/cvab027.
Wang, H., Guo, Y., Lu, H., Luo, Y., Hu, W., Liang, W., Garcia-Barrio, M. T., Chang, L., Schwendeman, A., Zhang, J., & Chen, Y. E. (2021). Krüppel-Like Factor 14 Deletion In Myeloid Cells Accelerates Atherosclerotic Lesion Development. Cardiovascular research, . https://doi.org/10.1093/cvr/cvab027
Wang, Huilun, et al. "Krüppel-Like Factor 14 Deletion In Myeloid Cells Accelerates Atherosclerotic Lesion Development." Cardiovascular research vol. (2021). doi: https://doi.org/10.1093/cvr/cvab027
Wang H, Guo Y, Lu H, Luo Y, Hu W, Liang W, Garcia-Barrio MT, Chang L, Schwendeman A, Zhang J, Chen YE. Krüppel-Like Factor 14 Deletion In Myeloid Cells Accelerates Atherosclerotic Lesion Development. Cardiovasc Res. 2021 Feb 04; doi: 10.1093/cvr/cvab027. Epub 2021 Feb 04. PMID: 33538785.
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Genomic testing as a tool to optimise drug therapy.

Australian prescriber

Somogyi AA, Phillips E.
PMID: 28798515
Aust Prescr. 2017 Jun;40(3):101-104. doi: 10.18773/austprescr.2017.027. Epub 2017 Jun 01.

No abstract available.

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Somogyi AA, Phillips E. Genomic testing as a tool to optimise drug therapy. Aust Prescr. 2017;40(3):101-104doi: 10.18773/austprescr.2017.027.
Somogyi, A. A., & Phillips, E. (2017). Genomic testing as a tool to optimise drug therapy. Australian prescriber, 40(3), 101-104. https://doi.org/10.18773/austprescr.2017.027
Somogyi, Andrew A, and Phillips, Elizabeth. "Genomic testing as a tool to optimise drug therapy." Australian prescriber vol. 40,3 (2017): 101-104. doi: https://doi.org/10.18773/austprescr.2017.027
Somogyi AA, Phillips E. Genomic testing as a tool to optimise drug therapy. Aust Prescr. 2017 Jun;40(3):101-104. doi: 10.18773/austprescr.2017.027. Epub 2017 Jun 01. PMID: 28798515; PMCID: PMC5478394.
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Nitroxyl: A Novel Strategy to Circumvent Diabetes Associated Impairments in Nitric Oxide Signaling.

Frontiers in pharmacology

Velagic A, Qin C, Woodman OL, Horowitz JD, Ritchie RH, Kemp-Harper BK.
PMID: 32508651
Front Pharmacol. 2020 May 19;11:727. doi: 10.3389/fphar.2020.00727. eCollection 2020.

Diabetes is associated with an increased mortality risk due to cardiovascular complications. Hyperglycemia-induced oxidative stress underlies these complications, leading to an impairment in endogenous nitric oxide (NO•) generation, together with reductions in NO• bioavailability and NO• responsiveness in the...

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Velagic A, Qin C, Woodman OL, et al. Nitroxyl: A Novel Strategy to Circumvent Diabetes Associated Impairments in Nitric Oxide Signaling. Front Pharmacol. 2020;11:727doi: 10.3389/fphar.2020.00727.
Velagic, A., Qin, C., Woodman, O. L., Horowitz, J. D., Ritchie, R. H., & Kemp-Harper, B. K. (2020). Nitroxyl: A Novel Strategy to Circumvent Diabetes Associated Impairments in Nitric Oxide Signaling. Frontiers in pharmacology, 11727. https://doi.org/10.3389/fphar.2020.00727
Velagic, Anida, et al. "Nitroxyl: A Novel Strategy to Circumvent Diabetes Associated Impairments in Nitric Oxide Signaling." Frontiers in pharmacology vol. 11 (2020): 727. doi: https://doi.org/10.3389/fphar.2020.00727
Velagic A, Qin C, Woodman OL, Horowitz JD, Ritchie RH, Kemp-Harper BK. Nitroxyl: A Novel Strategy to Circumvent Diabetes Associated Impairments in Nitric Oxide Signaling. Front Pharmacol. 2020 May 19;11:727. doi: 10.3389/fphar.2020.00727. eCollection 2020. PMID: 32508651; PMCID: PMC7248192.
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Management of the metabolic syndrome in cardiovascular disease.

Current treatment options in cardiovascular medicine

Chan WP, Sverdlov AL, Horowitz JD.
PMID: 18325305
Curr Treat Options Cardiovasc Med. 2008 Feb;10(1):27-38. doi: 10.1007/s11936-008-0004-2.

The main components of the metabolic syndrome (MS) are abdominal obesity, atherogenic dyslipidemia, raised blood pressure, insulin resistance with or without glucose intolerance, and proinflammatory and prothrombotic states. The clustering of these metabolic risk factors significantly increases the risk...

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Chan WP, Sverdlov AL, Horowitz JD. Management of the metabolic syndrome in cardiovascular disease. Curr Treat Options Cardiovasc Med. 2008;10(1):27-38doi: 10.1007/s11936-008-0004-2.
Chan, W. P., Sverdlov, A. L., & Horowitz, J. D. (2008). Management of the metabolic syndrome in cardiovascular disease. Current treatment options in cardiovascular medicine, 10(1), 27-38. https://doi.org/10.1007/s11936-008-0004-2
Chan, Wai Ping Alicia, et al. "Management of the metabolic syndrome in cardiovascular disease." Current treatment options in cardiovascular medicine vol. 10,1 (2008): 27-38. doi: https://doi.org/10.1007/s11936-008-0004-2
Chan WP, Sverdlov AL, Horowitz JD. Management of the metabolic syndrome in cardiovascular disease. Curr Treat Options Cardiovasc Med. 2008 Feb;10(1):27-38. doi: 10.1007/s11936-008-0004-2. PMID: 18325305.
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Plasma vs heart tissue concentration in humans - literature data analysis of drugs distribution.

Biopharmaceutics & drug disposition

Tylutki Z, Polak S.
PMID: 25765563
Biopharm Drug Dispos. 2015 Sep;36(6):337-351. doi: 10.1002/bdd.1944. Epub 2015 Apr 28.

Little is known about the uptake of drugs into the human heart, although it is of great importance nowadays, when science desires to predict tissue level behavior rather than to measure it. Although the drug concentration in cardiac tissue...

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Tylutki Z, Polak S. Plasma vs heart tissue concentration in humans - literature data analysis of drugs distribution. Biopharm Drug Dispos. 2015;36(6):337-351doi: 10.1002/bdd.1944.
Tylutki, Z., & Polak, S. (2015). Plasma vs heart tissue concentration in humans - literature data analysis of drugs distribution. Biopharmaceutics & drug disposition, 36(6), 337-351. https://doi.org/10.1002/bdd.1944
Tylutki, Zofia, and Polak, Sebastian. "Plasma vs heart tissue concentration in humans - literature data analysis of drugs distribution." Biopharmaceutics & drug disposition vol. 36,6 (2015): 337-351. doi: https://doi.org/10.1002/bdd.1944
Tylutki Z, Polak S. Plasma vs heart tissue concentration in humans - literature data analysis of drugs distribution. Biopharm Drug Dispos. 2015 Sep;36(6):337-351. doi: 10.1002/bdd.1944. Epub 2015 Apr 28. PMID: 25765563.
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Deranged Cardiac Metabolism and the Pathogenesis of Heart Failure.

Cardiac failure review

Fragasso G.
PMID: 28785448
Card Fail Rev. 2016 May;2(1):8-13. doi: 10.15420/cfr.2016:5:2.

Activation of the neuro-hormonal system is a pathophysiological consequence of heart failure. Neuro-hormonal activation promotes metabolic changes, such as insulin resistance, and determines an increased use of non-carbohydrate substrates for energy production. Fasting blood ketone bodies as well as...

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Fragasso G. Deranged Cardiac Metabolism and the Pathogenesis of Heart Failure. Card Fail Rev. 2016;2(1):8-13doi: 10.15420/cfr.2016:5:2.
Fragasso, G. (2016). Deranged Cardiac Metabolism and the Pathogenesis of Heart Failure. Cardiac failure review, 2(1), 8-13. https://doi.org/10.15420/cfr.2016:5:2
Fragasso, Gabriele. "Deranged Cardiac Metabolism and the Pathogenesis of Heart Failure." Cardiac failure review vol. 2,1 (2016): 8-13. doi: https://doi.org/10.15420/cfr.2016:5:2
Fragasso G. Deranged Cardiac Metabolism and the Pathogenesis of Heart Failure. Card Fail Rev. 2016 May;2(1):8-13. doi: 10.15420/cfr.2016:5:2. PMID: 28785448; PMCID: PMC5490933.
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The transcription factor KLF14 regulates macrophage glycolysis and immune function by inhibiting HK2 in sepsis.

Cellular & molecular immunology

Yuan Y, Fan G, Liu Y, Liu L, Zhang T, Liu P, Tu Q, Zhang X, Luo S, Yao L, Chen F, Li J.
PMID: 34983946
Cell Mol Immunol. 2022 Jan 04; doi: 10.1038/s41423-021-00806-5. Epub 2022 Jan 04.

Sepsis is a heterogeneous syndrome induced by a dysregulated host response to infection. Glycolysis plays a role in maintaining the immune function of macrophages, which is crucial for severely septic patients. However, how the pathways that link glycolysis and...

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Yuan Y, Fan G, Liu Y, et al. The transcription factor KLF14 regulates macrophage glycolysis and immune function by inhibiting HK2 in sepsis. Cell Mol Immunol. 2022;doi: 10.1038/s41423-021-00806-5.
Yuan, Y., Fan, G., Liu, Y., Liu, L., Zhang, T., Liu, P., Tu, Q., Zhang, X., Luo, S., Yao, L., Chen, F., & Li, J. (2022). The transcription factor KLF14 regulates macrophage glycolysis and immune function by inhibiting HK2 in sepsis. Cellular & molecular immunology, . https://doi.org/10.1038/s41423-021-00806-5
Yuan, Yuan, et al. "The transcription factor KLF14 regulates macrophage glycolysis and immune function by inhibiting HK2 in sepsis." Cellular & molecular immunology vol. (2022). doi: https://doi.org/10.1038/s41423-021-00806-5
Yuan Y, Fan G, Liu Y, Liu L, Zhang T, Liu P, Tu Q, Zhang X, Luo S, Yao L, Chen F, Li J. The transcription factor KLF14 regulates macrophage glycolysis and immune function by inhibiting HK2 in sepsis. Cell Mol Immunol. 2022 Jan 04; doi: 10.1038/s41423-021-00806-5. Epub 2022 Jan 04. PMID: 34983946.
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Targeting one-carbon metabolism requires mTOR inhibition: a new therapeutic approach in osteosarcoma.

Molecular & cellular oncology

Rathore R, Van Tine B.
PMID: 34027041
Mol Cell Oncol. 2021 Mar 25;8(3):1902250. doi: 10.1080/23723556.2021.1902250.

The rate-limiting enzyme of serine biosynthesis, 3-phosphoglycerate dehydrogenase (PHGDH), contributes to rapid growth and proliferation when it is overexpressed in cancer. We recently described the metabolic adaptations that occur upon PHGDH inhibition in osteosarcoma. PHGDH inhibition causes metabolite accumulation...

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Rathore R, Van Tine B. Targeting one-carbon metabolism requires mTOR inhibition: a new therapeutic approach in osteosarcoma. Mol Cell Oncol. 2021;8(3):1902250doi: 10.1080/23723556.2021.1902250.
Rathore, R., & Van Tine, B. (2021). Targeting one-carbon metabolism requires mTOR inhibition: a new therapeutic approach in osteosarcoma. Molecular & cellular oncology, 8(3), 1902250. https://doi.org/10.1080/23723556.2021.1902250
Rathore, Richa, and Van Tine, Brian. "Targeting one-carbon metabolism requires mTOR inhibition: a new therapeutic approach in osteosarcoma." Molecular & cellular oncology vol. 8,3 (2021): 1902250. doi: https://doi.org/10.1080/23723556.2021.1902250
Rathore R, Van Tine B. Targeting one-carbon metabolism requires mTOR inhibition: a new therapeutic approach in osteosarcoma. Mol Cell Oncol. 2021 Mar 25;8(3):1902250. doi: 10.1080/23723556.2021.1902250. PMID: 34027041; PMCID: PMC8128185.
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