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Showing 1 to 12 of 15 entries
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Nicotinic receptor contributions to smoking: insights from human studies and animal models.

Current addiction reports

Brunzell DH, Stafford AM, Dixon CI.
PMID: 26301171
Curr Addict Rep. 2015 Mar;2(1):33-46. doi: 10.1007/s40429-015-0042-2.

It is becoming increasingly evident that a variety of factors contribute to smoking behavior. Nicotine is a constituent of tobacco smoke that exerts its psychoactive effects via binding to nicotinic acetylcholine receptors (nAChRs) in brain. Human genetic studies have...

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Brunzell DH, Stafford AM, Dixon CI. Nicotinic receptor contributions to smoking: insights from human studies and animal models. Curr Addict Rep. 2015;2(1):33-46doi: 10.1007/s40429-015-0042-2.
Brunzell, D. H., Stafford, A. M., & Dixon, C. I. (2015). Nicotinic receptor contributions to smoking: insights from human studies and animal models. Current addiction reports, 2(1), 33-46. https://doi.org/10.1007/s40429-015-0042-2
Brunzell, Darlene H, et al. "Nicotinic receptor contributions to smoking: insights from human studies and animal models." Current addiction reports vol. 2,1 (2015): 33-46. doi: https://doi.org/10.1007/s40429-015-0042-2
Brunzell DH, Stafford AM, Dixon CI. Nicotinic receptor contributions to smoking: insights from human studies and animal models. Curr Addict Rep. 2015 Mar;2(1):33-46. doi: 10.1007/s40429-015-0042-2. PMID: 26301171; PMCID: PMC4540370.
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The polo-like kinase 1 inhibitor volasertib synergistically increases radiation efficacy in glioma stem cells.

Oncotarget

Dong J, Park SY, Nguyen N, Ezhilarasan R, Martinez-Ledesma E, Wu S, Henry V, Piao Y, Tiao N, Brunell D, Stephan C, Verhaak R, Sulman E, Balasubramaniyan V, de Groot JF.
PMID: 29535822
Oncotarget. 2018 Jan 08;9(12):10497-10509. doi: 10.18632/oncotarget.24041. eCollection 2018 Feb 13.

BACKGROUND: Despite the availability of hundreds of cancer drugs, there is insufficient data on the efficacy of these drugs on the extremely heterogeneous tumor cell populations of glioblastoma (GBM).RESULTS: The PKIS of 357 compounds was initially evaluated in 15...

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Dong J, Park SY, Nguyen N, et al. The polo-like kinase 1 inhibitor volasertib synergistically increases radiation efficacy in glioma stem cells. Oncotarget. 2018;9(12):10497-10509doi: 10.18632/oncotarget.24041.
Dong, J., Park, S. Y., Nguyen, N., Ezhilarasan, R., Martinez-Ledesma, E., Wu, S., Henry, V., Piao, Y., Tiao, N., Brunell, D., Stephan, C., Verhaak, R., Sulman, E., Balasubramaniyan, V., & de Groot, J. F. (2018). The polo-like kinase 1 inhibitor volasertib synergistically increases radiation efficacy in glioma stem cells. Oncotarget, 9(12), 10497-10509. https://doi.org/10.18632/oncotarget.24041
Dong, Jianwen, et al. "The polo-like kinase 1 inhibitor volasertib synergistically increases radiation efficacy in glioma stem cells." Oncotarget vol. 9,12 (2018): 10497-10509. doi: https://doi.org/10.18632/oncotarget.24041
Dong J, Park SY, Nguyen N, Ezhilarasan R, Martinez-Ledesma E, Wu S, Henry V, Piao Y, Tiao N, Brunell D, Stephan C, Verhaak R, Sulman E, Balasubramaniyan V, de Groot JF. The polo-like kinase 1 inhibitor volasertib synergistically increases radiation efficacy in glioma stem cells. Oncotarget. 2018 Jan 08;9(12):10497-10509. doi: 10.18632/oncotarget.24041. eCollection 2018 Feb 13. PMID: 29535822; PMCID: PMC5828226.
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Prehospital personnel's attitudes to pain management.

Scandinavian journal of pain

Castrèn M, Lindström V, Branzell JH, Niemi-Murola L.
PMID: 29911629
Scand J Pain. 2015 Jul 01;8(1):17-22. doi: 10.1016/j.sjpain.2015.02.003.

Objectives Pain is one of the most common reasons for patients to seek acute medical care. The management of pain is often inadequate both in the prehospital setting and in the emergency department. Our aim was to evaluate the...

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Castrèn M, Lindström V, Branzell JH, et al. Prehospital personnel's attitudes to pain management. Scand J Pain. 2015;8(1):17-22doi: 10.1016/j.sjpain.2015.02.003.
Castrèn, M., Lindström, V., Branzell, J. H., & Niemi-Murola, L. (2015). Prehospital personnel's attitudes to pain management. Scandinavian journal of pain, 8(1), 17-22. https://doi.org/10.1016/j.sjpain.2015.02.003
Castrèn, Maaret, et al. "Prehospital personnel's attitudes to pain management." Scandinavian journal of pain vol. 8,1 (2015): 17-22. doi: https://doi.org/10.1016/j.sjpain.2015.02.003
Castrèn M, Lindström V, Branzell JH, Niemi-Murola L. Prehospital personnel's attitudes to pain management. Scand J Pain. 2015 Jul 01;8(1):17-22. doi: 10.1016/j.sjpain.2015.02.003. PMID: 29911629.
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The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.

Biochemistry and biophysics reports

Kuiper BD, Keusch BJ, Dewdney TG, Chordia P, Ross K, Brunzelle JS, Kovari IA, MacArthur R, Salimnia H, Kovari LC.
PMID: 29124158
Biochem Biophys Rep. 2015 Jun 12;2:160-165. doi: 10.1016/j.bbrep.2015.06.003. eCollection 2015 Jul.

HIV-1 protease (PR) is a 99 amino acid protein responsible for proteolytic processing of the viral polyprotein - an essential step in the HIV-1 life cycle. Drug resistance mutations in PR that are selected during antiretroviral therapy lead to...

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Kuiper BD, Keusch BJ, Dewdney TG, et al. The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops. Biochem Biophys Rep. 2015;2:160-165doi: 10.1016/j.bbrep.2015.06.003.
Kuiper, B. D., Keusch, B. J., Dewdney, T. G., Chordia, P., Ross, K., Brunzelle, J. S., Kovari, I. A., MacArthur, R., Salimnia, H., & Kovari, L. C. (2015). The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops. Biochemistry and biophysics reports, 2160-165. https://doi.org/10.1016/j.bbrep.2015.06.003
Kuiper, Benjamin D, et al. "The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops." Biochemistry and biophysics reports vol. 2 (2015): 160-165. doi: https://doi.org/10.1016/j.bbrep.2015.06.003
Kuiper BD, Keusch BJ, Dewdney TG, Chordia P, Ross K, Brunzelle JS, Kovari IA, MacArthur R, Salimnia H, Kovari LC. The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops. Biochem Biophys Rep. 2015 Jun 12;2:160-165. doi: 10.1016/j.bbrep.2015.06.003. eCollection 2015 Jul. PMID: 29124158; PMCID: PMC5668655.
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Potential of essential fatty acid deficiency with extremely low fat diet in lipoprotein lipase deficiency during pregnancy: A case report.

BMC pregnancy and childbirth

Tsai EC, Brown JA, Veldee MY, Anderson GJ, Chait A, Brunzell JD.
PMID: 15610556
BMC Pregnancy Childbirth. 2004 Dec 20;4(1):27. doi: 10.1186/1471-2393-4-27.

BACKGROUND: Pregnancy in patients with lipoprotein lipase deficiency is associated with high risk of maternal pancreatitis and fetal death. A very low fat diet (< 10% of calories) is the primary treatment modality for the prevention of acute pancreatitis,...

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Tsai EC, Brown JA, Veldee MY, et al. Potential of essential fatty acid deficiency with extremely low fat diet in lipoprotein lipase deficiency during pregnancy: A case report. BMC Pregnancy Childbirth. 2004;4(1):27doi: 10.1186/1471-2393-4-27.
Tsai, E. C., Brown, J. A., Veldee, M. Y., Anderson, G. J., Chait, A., & Brunzell, J. D. (2004). Potential of essential fatty acid deficiency with extremely low fat diet in lipoprotein lipase deficiency during pregnancy: A case report. BMC pregnancy and childbirth, 4(1), 27. https://doi.org/10.1186/1471-2393-4-27
Tsai, Elaine C, et al. "Potential of essential fatty acid deficiency with extremely low fat diet in lipoprotein lipase deficiency during pregnancy: A case report." BMC pregnancy and childbirth vol. 4,1 (2004): 27. doi: https://doi.org/10.1186/1471-2393-4-27
Tsai EC, Brown JA, Veldee MY, Anderson GJ, Chait A, Brunzell JD. Potential of essential fatty acid deficiency with extremely low fat diet in lipoprotein lipase deficiency during pregnancy: A case report. BMC Pregnancy Childbirth. 2004 Dec 20;4(1):27. doi: 10.1186/1471-2393-4-27. PMID: 15610556; PMCID: PMC544881.
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Structural basis for recognition of diverse transcriptional repressors by the TOPLESS family of corepressors.

Science advances

Ke J, Ma H, Gu X, Thelen A, Brunzelle JS, Li J, Xu HE, Melcher K.
PMID: 26601214
Sci Adv. 2015 Jul 24;1(6):e1500107. doi: 10.1126/sciadv.1500107. eCollection 2015 Jul.

TOPLESS (TPL) and TOPLESS-related (TPR) proteins comprise a conserved family of plant transcriptional corepressors that are related to Tup1, Groucho, and TLE (transducin-like enhancer of split) corepressors in yeast, insects, and mammals. In plants, TPL/TPR corepressors regulate development, stress...

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Ke J, Ma H, Gu X, et al. Structural basis for recognition of diverse transcriptional repressors by the TOPLESS family of corepressors. Sci Adv. 2015;1(6):e1500107doi: 10.1126/sciadv.1500107.
Ke, J., Ma, H., Gu, X., Thelen, A., Brunzelle, J. S., Li, J., Xu, H. E., & Melcher, K. (2015). Structural basis for recognition of diverse transcriptional repressors by the TOPLESS family of corepressors. Science advances, 1(6), e1500107. https://doi.org/10.1126/sciadv.1500107
Ke, Jiyuan, et al. "Structural basis for recognition of diverse transcriptional repressors by the TOPLESS family of corepressors." Science advances vol. 1,6 (2015): e1500107. doi: https://doi.org/10.1126/sciadv.1500107
Ke J, Ma H, Gu X, Thelen A, Brunzelle JS, Li J, Xu HE, Melcher K. Structural basis for recognition of diverse transcriptional repressors by the TOPLESS family of corepressors. Sci Adv. 2015 Jul 24;1(6):e1500107. doi: 10.1126/sciadv.1500107. eCollection 2015 Jul. PMID: 26601214; PMCID: PMC4646777.
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The interaction of familial and secondary causes of hypertriglyceridemia: role in pancreatitis.

Journal of clinical lipidology

Brunzell JD, Schrott HG.
PMID: 23009776
J Clin Lipidol. 2012 Sep-Oct;6(5):409-12. doi: 10.1016/j.jacl.2012.06.005. Epub 2012 Jul 05.

No abstract available.

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Brunzell JD, Schrott HG. The interaction of familial and secondary causes of hypertriglyceridemia: role in pancreatitis. J Clin Lipidol. 2012;6(5):409-12doi: 10.1016/j.jacl.2012.06.005.
Brunzell, J. D., & Schrott, H. G. (2012). The interaction of familial and secondary causes of hypertriglyceridemia: role in pancreatitis. Journal of clinical lipidology, 6(5), 409-12. https://doi.org/10.1016/j.jacl.2012.06.005
Brunzell, John D, and Schrott, Helmut G. "The interaction of familial and secondary causes of hypertriglyceridemia: role in pancreatitis." Journal of clinical lipidology vol. 6,5 (2012): 409-12. doi: https://doi.org/10.1016/j.jacl.2012.06.005
Brunzell JD, Schrott HG. The interaction of familial and secondary causes of hypertriglyceridemia: role in pancreatitis. J Clin Lipidol. 2012 Sep-Oct;6(5):409-12. doi: 10.1016/j.jacl.2012.06.005. Epub 2012 Jul 05. PMID: 23009776.
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Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane.

The Biochemical journal

Zhou XE, Suino-Powell K, Schultz CR, Aleiwi B, Brunzelle JS, Lamp J, Vega IE, Ellsworth E, Bachmann AS, Melcher K.
PMID: 34796899
Biochem J. 2021 Dec 10;478(23):4137-4149. doi: 10.1042/BCJ20210647.

Ornithine decarboxylase (ODC) is the rate-limiting enzyme for the synthesis of polyamines (PAs). PAs are oncometabolites that are required for proliferation, and pharmaceutical ODC inhibition is pursued for the treatment of hyperproliferative diseases, including cancer and infectious diseases. The...

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Zhou XE, Suino-Powell K, Schultz CR, et al. Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane. Biochem J. 2021;478(23):4137-4149doi: 10.1042/BCJ20210647.
Zhou, X. E., Suino-Powell, K., Schultz, C. R., Aleiwi, B., Brunzelle, J. S., Lamp, J., Vega, I. E., Ellsworth, E., Bachmann, A. S., & Melcher, K. (2021). Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane. The Biochemical journal, 478(23), 4137-4149. https://doi.org/10.1042/BCJ20210647
Zhou, X Edward, et al. "Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane." The Biochemical journal vol. 478,23 (2021): 4137-4149. doi: https://doi.org/10.1042/BCJ20210647
Zhou XE, Suino-Powell K, Schultz CR, Aleiwi B, Brunzelle JS, Lamp J, Vega IE, Ellsworth E, Bachmann AS, Melcher K. Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane. Biochem J. 2021 Dec 10;478(23):4137-4149. doi: 10.1042/BCJ20210647. PMID: 34796899.
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Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane.

The Biochemical journal

Zhou XE, Suino-Powell K, Schultz CR, Aleiwi B, Brunzelle JS, Lamp J, Vega IE, Ellsworth E, Bachmann AS, Melcher K.
PMID: 34796899
Biochem J. 2021 Dec 10;478(23):4137-4149. doi: 10.1042/BCJ20210647.

Ornithine decarboxylase (ODC) is the rate-limiting enzyme for the synthesis of polyamines (PAs). PAs are oncometabolites that are required for proliferation, and pharmaceutical ODC inhibition is pursued for the treatment of hyperproliferative diseases, including cancer and infectious diseases. The...

Cite
Zhou XE, Suino-Powell K, Schultz CR, et al. Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane. Biochem J. 2021;478(23):4137-4149doi: 10.1042/BCJ20210647.
Zhou, X. E., Suino-Powell, K., Schultz, C. R., Aleiwi, B., Brunzelle, J. S., Lamp, J., Vega, I. E., Ellsworth, E., Bachmann, A. S., & Melcher, K. (2021). Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane. The Biochemical journal, 478(23), 4137-4149. https://doi.org/10.1042/BCJ20210647
Zhou, X Edward, et al. "Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane." The Biochemical journal vol. 478,23 (2021): 4137-4149. doi: https://doi.org/10.1042/BCJ20210647
Zhou XE, Suino-Powell K, Schultz CR, Aleiwi B, Brunzelle JS, Lamp J, Vega IE, Ellsworth E, Bachmann AS, Melcher K. Structural basis of binding and inhibition of ornithine decarboxylase by 1-amino-oxy-3-aminopropane. Biochem J. 2021 Dec 10;478(23):4137-4149. doi: 10.1042/BCJ20210647. PMID: 34796899.
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Xenotransplantation of pediatric low grade gliomas confirms the enrichment of .

Oncotarget

Kogiso M, Qi L, Lindsay H, Huang Y, Zhao X, Liu Z, Braun FK, Du Y, Zhang H, Bae G, Zhao S, Injac SG, Sobieski M, Brunell D, Mehta V, Tran D, Murray J, Baxter PA, Yuan XJ, Su JM, Adesina A, Perlaky L, Chintagumpala M, Parsons DW, Lau CC, Stephan CC, Lu X, Li XN.
PMID: 29152094
Oncotarget. 2017 Sep 08;8(50):87455-87471. doi: 10.18632/oncotarget.20713. eCollection 2017 Oct 20.

To identify cellular and molecular changes that driver pediatric low grade glioma (PLGG) progression, we analyzed putative cancer stem cells (CSCs) and evaluated key biological changes in a novel and progressive patient-derived orthotopic xenograft (PDOX) mouse model. Flow cytometric...

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Kogiso M, Qi L, Lindsay H, et al. Xenotransplantation of pediatric low grade gliomas confirms the enrichment of . Oncotarget. 2017;8(50):87455-87471doi: 10.18632/oncotarget.20713.
Kogiso, M., Qi, L., Lindsay, H., Huang, Y., Zhao, X., Liu, Z., Braun, F. K., Du, Y., Zhang, H., Bae, G., Zhao, S., Injac, S. G., Sobieski, M., Brunell, D., Mehta, V., Tran, D., Murray, J., Baxter, P. A., Yuan, X. J., Su, J. M., Adesina, A., Perlaky, L., Chintagumpala, M., Parsons, D. W., Lau, C. C., Stephan, C. C., Lu, X., & Li, X. N. (2017). Xenotransplantation of pediatric low grade gliomas confirms the enrichment of . Oncotarget, 8(50), 87455-87471. https://doi.org/10.18632/oncotarget.20713
Kogiso, Mari, et al. "Xenotransplantation of pediatric low grade gliomas confirms the enrichment of ." Oncotarget vol. 8,50 (2017): 87455-87471. doi: https://doi.org/10.18632/oncotarget.20713
Kogiso M, Qi L, Lindsay H, Huang Y, Zhao X, Liu Z, Braun FK, Du Y, Zhang H, Bae G, Zhao S, Injac SG, Sobieski M, Brunell D, Mehta V, Tran D, Murray J, Baxter PA, Yuan XJ, Su JM, Adesina A, Perlaky L, Chintagumpala M, Parsons DW, Lau CC, Stephan CC, Lu X, Li XN. Xenotransplantation of pediatric low grade gliomas confirms the enrichment of . Oncotarget. 2017 Sep 08;8(50):87455-87471. doi: 10.18632/oncotarget.20713. eCollection 2017 Oct 20. PMID: 29152094; PMCID: PMC5675646.
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Weight gain trajectories and obesity rates in intensive and conventional treatments of Type 1 diabetes from the DCCT compared to a control population without diabetes.

Diabetic medicine : a journal of the British Diabetic Association

Carlson NE, Horton KW, Hokanson JE, Cleary PA, Jacobs DR, Brunzell JD, Purnell JQ.
PMID: 35040196
Diabet Med. 2022 Jan 18;e14794. doi: 10.1111/dme.14794. Epub 2022 Jan 18.

AIM: Obesity is a significant health issue for participants with Type 1 diabetes undergoing intensive diabetes management. The temporal pattern and factors associated with weight gain after treatment initiation remain poorly understood including how weight gain in participants with...

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Carlson NE, Horton KW, Hokanson JE, et al. Weight gain trajectories and obesity rates in intensive and conventional treatments of Type 1 diabetes from the DCCT compared to a control population without diabetes. Diabet Med. 2022;e14794doi: 10.1111/dme.14794.
Carlson, N. E., Horton, K. W., Hokanson, J. E., Cleary, P. A., Jacobs, D. R., Brunzell, J. D., Purnell, J. Q. (2022). Weight gain trajectories and obesity rates in intensive and conventional treatments of Type 1 diabetes from the DCCT compared to a control population without diabetes. Diabetic medicine : a journal of the British Diabetic Association, e14794. https://doi.org/10.1111/dme.14794
Carlson, Nichole E, et al. "Weight gain trajectories and obesity rates in intensive and conventional treatments of Type 1 diabetes from the DCCT compared to a control population without diabetes." Diabetic medicine : a journal of the British Diabetic Association vol. (2022): e14794. doi: https://doi.org/10.1111/dme.14794
Carlson NE, Horton KW, Hokanson JE, Cleary PA, Jacobs DR, Brunzell JD, Purnell JQ. Weight gain trajectories and obesity rates in intensive and conventional treatments of Type 1 diabetes from the DCCT compared to a control population without diabetes. Diabet Med. 2022 Jan 18;e14794. doi: 10.1111/dme.14794. Epub 2022 Jan 18. PMID: 35040196.
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The role of the PGC1α Gly482Ser polymorphism in weight gain due to intensive diabetes therapy.

PPAR research

Deeb SS, Brunzell JD.
PMID: 19360113
PPAR Res. 2009;2009:649286. doi: 10.1155/2009/649286. Epub 2009 Apr 07.

The Diabetes Control and Complications Trial (DCCT) involved intensive diabetes therapy of subjects with type 1 diabetes mellitus (T1DM) for an average period of 6.5 years. A subset of these subjects gained excessive weight. We tested for association of...

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Deeb SS, Brunzell JD. The role of the PGC1α Gly482Ser polymorphism in weight gain due to intensive diabetes therapy. PPAR Res. 2009;2009:649286doi: 10.1155/2009/649286.
Deeb, S. S., & Brunzell, J. D. (2009). The role of the PGC1α Gly482Ser polymorphism in weight gain due to intensive diabetes therapy. PPAR research, 2009649286. https://doi.org/10.1155/2009/649286
Deeb, Samir S, and Brunzell, John D. "The role of the PGC1α Gly482Ser polymorphism in weight gain due to intensive diabetes therapy." PPAR research vol. 2009 (2009): 649286. doi: https://doi.org/10.1155/2009/649286
Deeb SS, Brunzell JD. The role of the PGC1α Gly482Ser polymorphism in weight gain due to intensive diabetes therapy. PPAR Res. 2009;2009:649286. doi: 10.1155/2009/649286. Epub 2009 Apr 07. PMID: 19360113; PMCID: PMC2666270.
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