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Imatinib treatment reduces brain injury in a murine model of traumatic brain injury.

Frontiers in cellular neuroscience

Su EJ, Fredriksson L, Kanzawa M, Moore S, Folestad E, Stevenson TK, Nilsson I, Sashindranath M, Schielke GP, Warnock M, Ragsdale M, Mann K, Lawrence AL, Medcalf RL, Eriksson U, Murphy GG, Lawrence DA.
PMID: 26500491
Front Cell Neurosci. 2015 Oct 07;9:385. doi: 10.3389/fncel.2015.00385. eCollection 2015.

Current therapies for Traumatic brain injury (TBI) focus on stabilizing individuals and on preventing further damage from the secondary consequences of TBI. A major complication of TBI is cerebral edema, which can be caused by the loss of blood...

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Su EJ, Fredriksson L, Kanzawa M, et al. Imatinib treatment reduces brain injury in a murine model of traumatic brain injury. Front Cell Neurosci. 2015;9:385doi: 10.3389/fncel.2015.00385.
Su, E. J., Fredriksson, L., Kanzawa, M., Moore, S., Folestad, E., Stevenson, T. K., Nilsson, I., Sashindranath, M., Schielke, G. P., Warnock, M., Ragsdale, M., Mann, K., Lawrence, A. L., Medcalf, R. L., Eriksson, U., Murphy, G. G., & Lawrence, D. A. (2015). Imatinib treatment reduces brain injury in a murine model of traumatic brain injury. Frontiers in cellular neuroscience, 9385. https://doi.org/10.3389/fncel.2015.00385
Su, Enming J, et al. "Imatinib treatment reduces brain injury in a murine model of traumatic brain injury." Frontiers in cellular neuroscience vol. 9 (2015): 385. doi: https://doi.org/10.3389/fncel.2015.00385
Su EJ, Fredriksson L, Kanzawa M, Moore S, Folestad E, Stevenson TK, Nilsson I, Sashindranath M, Schielke GP, Warnock M, Ragsdale M, Mann K, Lawrence AL, Medcalf RL, Eriksson U, Murphy GG, Lawrence DA. Imatinib treatment reduces brain injury in a murine model of traumatic brain injury. Front Cell Neurosci. 2015 Oct 07;9:385. doi: 10.3389/fncel.2015.00385. eCollection 2015. PMID: 26500491; PMCID: PMC4596067.
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Metabolic network motifs can provide novel insights into evolution: The evolutionary origin of Eukaryotic organelles as a case study.

Computational biology and chemistry

Shellman ER, Chen Y, Lin X, Burant CF, Schnell S.
PMID: 25462333
Comput Biol Chem. 2014 Dec;53:242-250. doi: 10.1016/j.compbiolchem.2014.09.006. Epub 2014 Sep 21.

Phylogenetic trees are typically constructed using genetic and genomic data, and provide robust evolutionary relationships of species from the genomic point of view. We present an application of network motif mining and analysis of metabolic pathways that when used...

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Shellman ER, Chen Y, Lin X, et al. Metabolic network motifs can provide novel insights into evolution: The evolutionary origin of Eukaryotic organelles as a case study. Comput Biol Chem. 2014;53:242-250doi: 10.1016/j.compbiolchem.2014.09.006.
Shellman, E. R., Chen, Y., Lin, X., Burant, C. F., & Schnell, S. (2014). Metabolic network motifs can provide novel insights into evolution: The evolutionary origin of Eukaryotic organelles as a case study. Computational biology and chemistry, 53242-250. https://doi.org/10.1016/j.compbiolchem.2014.09.006
Shellman, Erin R, et al. "Metabolic network motifs can provide novel insights into evolution: The evolutionary origin of Eukaryotic organelles as a case study." Computational biology and chemistry vol. 53 (2014): 242-250. doi: https://doi.org/10.1016/j.compbiolchem.2014.09.006
Shellman ER, Chen Y, Lin X, Burant CF, Schnell S. Metabolic network motifs can provide novel insights into evolution: The evolutionary origin of Eukaryotic organelles as a case study. Comput Biol Chem. 2014 Dec;53:242-250. doi: 10.1016/j.compbiolchem.2014.09.006. Epub 2014 Sep 21. PMID: 25462333; PMCID: PMC4254655.
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Identification of a neurovascular signaling pathway regulating seizures in mice.

Annals of clinical and translational neurology

Fredriksson L, Stevenson TK, Su EJ, Ragsdale M, Moore S, Craciun S, Schielke GP, Murphy GG, Lawrence DA.
PMID: 26273685
Ann Clin Transl Neurol. 2015 Jul;2(7):722-38. doi: 10.1002/acn3.209. Epub 2015 May 01.

OBJECTIVE: A growing body of evidence suggests that increased blood-brain barrier (BBB) permeability can contribute to the development of seizures. The protease tissue plasminogen activator (tPA) has been shown to promote BBB permeability and susceptibility to seizures. In this...

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Fredriksson L, Stevenson TK, Su EJ, et al. Identification of a neurovascular signaling pathway regulating seizures in mice. Ann Clin Transl Neurol. 2015;2(7):722-38doi: 10.1002/acn3.209.
Fredriksson, L., Stevenson, T. K., Su, E. J., Ragsdale, M., Moore, S., Craciun, S., Schielke, G. P., Murphy, G. G., & Lawrence, D. A. (2015). Identification of a neurovascular signaling pathway regulating seizures in mice. Annals of clinical and translational neurology, 2(7), 722-38. https://doi.org/10.1002/acn3.209
Fredriksson, Linda, et al. "Identification of a neurovascular signaling pathway regulating seizures in mice." Annals of clinical and translational neurology vol. 2,7 (2015): 722-38. doi: https://doi.org/10.1002/acn3.209
Fredriksson L, Stevenson TK, Su EJ, Ragsdale M, Moore S, Craciun S, Schielke GP, Murphy GG, Lawrence DA. Identification of a neurovascular signaling pathway regulating seizures in mice. Ann Clin Transl Neurol. 2015 Jul;2(7):722-38. doi: 10.1002/acn3.209. Epub 2015 May 01. PMID: 26273685; PMCID: PMC4531055.
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Diet-induced obesity promotes myelopoiesis in hematopoietic stem cells.

Molecular metabolism

Singer K, DelProposto J, Morris DL, Zamarron B, Mergian T, Maley N, Cho KW, Geletka L, Subbaiah P, Muir L, Martinez-Santibanez G, Lumeng CN.
PMID: 25161889
Mol Metab. 2014 Jul 10;3(6):664-75. doi: 10.1016/j.molmet.2014.06.005. eCollection 2014 Sep.

Obesity is associated with an activated macrophage phenotype in multiple tissues that contributes to tissue inflammation and metabolic disease. To evaluate the mechanisms by which obesity potentiates myeloid activation, we evaluated the hypothesis that obesity activates myeloid cell production...

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Singer K, DelProposto J, Morris DL, et al. Diet-induced obesity promotes myelopoiesis in hematopoietic stem cells. Mol Metab. 2014;3(6):664-75doi: 10.1016/j.molmet.2014.06.005.
Singer, K., DelProposto, J., Morris, D. L., Zamarron, B., Mergian, T., Maley, N., Cho, K. W., Geletka, L., Subbaiah, P., Muir, L., Martinez-Santibanez, G., & Lumeng, C. N. (2014). Diet-induced obesity promotes myelopoiesis in hematopoietic stem cells. Molecular metabolism, 3(6), 664-75. https://doi.org/10.1016/j.molmet.2014.06.005
Singer, Kanakadurga, et al. "Diet-induced obesity promotes myelopoiesis in hematopoietic stem cells." Molecular metabolism vol. 3,6 (2014): 664-75. doi: https://doi.org/10.1016/j.molmet.2014.06.005
Singer K, DelProposto J, Morris DL, Zamarron B, Mergian T, Maley N, Cho KW, Geletka L, Subbaiah P, Muir L, Martinez-Santibanez G, Lumeng CN. Diet-induced obesity promotes myelopoiesis in hematopoietic stem cells. Mol Metab. 2014 Jul 10;3(6):664-75. doi: 10.1016/j.molmet.2014.06.005. eCollection 2014 Sep. PMID: 25161889; PMCID: PMC4142398.
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TRAP-seq defines markers for novel populations of hypothalamic and brainstem LepRb neurons.

Molecular metabolism

Allison MB, Patterson CM, Krashes MJ, Lowell BB, Myers MG, Olson DP.
PMID: 25830093
Mol Metab. 2015 Feb 07;4(4):299-309. doi: 10.1016/j.molmet.2015.01.012. eCollection 2015 Apr.

OBJECTIVE: Leptin acts via its receptor (LepRb) on multiple subpopulations of LepRb neurons in the brain, each of which controls specific aspects of energy balance. Despite the importance of LepRb-containing neurons, the transcriptome and molecular identity of many LepRb...

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Allison MB, Patterson CM, Krashes MJ, et al. TRAP-seq defines markers for novel populations of hypothalamic and brainstem LepRb neurons. Mol Metab. 2015;4(4):299-309doi: 10.1016/j.molmet.2015.01.012.
Allison, M. B., Patterson, C. M., Krashes, M. J., Lowell, B. B., Myers, M. G., & Olson, D. P. (2015). TRAP-seq defines markers for novel populations of hypothalamic and brainstem LepRb neurons. Molecular metabolism, 4(4), 299-309. https://doi.org/10.1016/j.molmet.2015.01.012
Allison, Margaret B, et al. "TRAP-seq defines markers for novel populations of hypothalamic and brainstem LepRb neurons." Molecular metabolism vol. 4,4 (2015): 299-309. doi: https://doi.org/10.1016/j.molmet.2015.01.012
Allison MB, Patterson CM, Krashes MJ, Lowell BB, Myers MG, Olson DP. TRAP-seq defines markers for novel populations of hypothalamic and brainstem LepRb neurons. Mol Metab. 2015 Feb 07;4(4):299-309. doi: 10.1016/j.molmet.2015.01.012. eCollection 2015 Apr. PMID: 25830093; PMCID: PMC4354921.
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Perceptive costs of reproduction drive ageing and physiology in male Drosophila.

Nature ecology & evolution

Harvanek ZM, Lyu Y, Gendron CM, Johnson JC, Kondo S, Promislow DEL, Pletcher SD.
PMID: 28812624
Nat Ecol Evol. 2017 May 15;1(6):152. doi: 10.1038/s41559-017-0152.

Costs of reproduction are thought to result from natural selection optimizing organismal fitness within putative physiological constraints. Phenotypic and population genetic studies of reproductive costs are plentiful across taxa, but an understanding of their mechanistic basis would provide important...

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Harvanek ZM, Lyu Y, Gendron CM, et al. Perceptive costs of reproduction drive ageing and physiology in male Drosophila. Nat Ecol Evol. 2017;1(6):152doi: 10.1038/s41559-017-0152.
Harvanek, Z. M., Lyu, Y., Gendron, C. M., Johnson, J. C., Kondo, S., Promislow, D. E. L., & Pletcher, S. D. (2017). Perceptive costs of reproduction drive ageing and physiology in male Drosophila. Nature ecology & evolution, 1(6), 152. https://doi.org/10.1038/s41559-017-0152
Harvanek, Zachary M, et al. "Perceptive costs of reproduction drive ageing and physiology in male Drosophila." Nature ecology & evolution vol. 1,6 (2017): 152. doi: https://doi.org/10.1038/s41559-017-0152
Harvanek ZM, Lyu Y, Gendron CM, Johnson JC, Kondo S, Promislow DEL, Pletcher SD. Perceptive costs of reproduction drive ageing and physiology in male Drosophila. Nat Ecol Evol. 2017 May 15;1(6):152. doi: 10.1038/s41559-017-0152. PMID: 28812624; PMCID: PMC5657004.
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Concurrent activation of growth factor and nutrient arms of mTORC1 induces oxidative liver injury.

Cell discovery

Cho CS, Kowalsky AH, Namkoong S, Park SR, Wu S, Kim B, James A, Gu B, Semple IA, Tohamy MA, Solanki S, Cho US, Greenson JK, Shah YM, Kim M, Lee JH.
PMID: 31754457
Cell Discov. 2019 Nov 19;5:60. doi: 10.1038/s41421-019-0131-9. eCollection 2019.

mTORC1 is a protein kinase important for metabolism and is regulated by growth factor and nutrient signaling pathways, mediated by the Rheb and Rag GTPases, respectively. Here we provide the first animal model in which both pathways were upregulated...

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Cho CS, Kowalsky AH, Namkoong S, et al. Concurrent activation of growth factor and nutrient arms of mTORC1 induces oxidative liver injury. Cell Discov. 2019;5:60doi: 10.1038/s41421-019-0131-9.
Cho, C. S., Kowalsky, A. H., Namkoong, S., Park, S. R., Wu, S., Kim, B., James, A., Gu, B., Semple, I. A., Tohamy, M. A., Solanki, S., Cho, U. S., Greenson, J. K., Shah, Y. M., Kim, M., & Lee, J. H. (2019). Concurrent activation of growth factor and nutrient arms of mTORC1 induces oxidative liver injury. Cell discovery, 560. https://doi.org/10.1038/s41421-019-0131-9
Cho, Chun-Seok, et al. "Concurrent activation of growth factor and nutrient arms of mTORC1 induces oxidative liver injury." Cell discovery vol. 5 (2019): 60. doi: https://doi.org/10.1038/s41421-019-0131-9
Cho CS, Kowalsky AH, Namkoong S, Park SR, Wu S, Kim B, James A, Gu B, Semple IA, Tohamy MA, Solanki S, Cho US, Greenson JK, Shah YM, Kim M, Lee JH. Concurrent activation of growth factor and nutrient arms of mTORC1 induces oxidative liver injury. Cell Discov. 2019 Nov 19;5:60. doi: 10.1038/s41421-019-0131-9. eCollection 2019. PMID: 31754457; PMCID: PMC6868011.
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Persistent epigenetic reprogramming of sweet taste by diet.

Science advances

Vaziri A, Khabiri M, Genaw BT, May CE, Freddolino PL, Dus M.
PMID: 33177090
Sci Adv. 2020 Nov 11;6(46). doi: 10.1126/sciadv.abc8492. Print 2020 Nov.

Diets rich in sugar, salt, and fat alter taste perception and food preference, contributing to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here, we show that in response to a high sugar...

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Vaziri A, Khabiri M, Genaw BT, et al. Persistent epigenetic reprogramming of sweet taste by diet. Sci Adv. 2020;6(46)doi: 10.1126/sciadv.abc8492.
Vaziri, A., Khabiri, M., Genaw, B. T., May, C. E., Freddolino, P. L., & Dus, M. (2020). Persistent epigenetic reprogramming of sweet taste by diet. Science advances, 6(46), . https://doi.org/10.1126/sciadv.abc8492
Vaziri, Anoumid, et al. "Persistent epigenetic reprogramming of sweet taste by diet." Science advances vol. 6,46 (2020). doi: https://doi.org/10.1126/sciadv.abc8492
Vaziri A, Khabiri M, Genaw BT, May CE, Freddolino PL, Dus M. Persistent epigenetic reprogramming of sweet taste by diet. Sci Adv. 2020 Nov 11;6(46). doi: 10.1126/sciadv.abc8492. Print 2020 Nov. PMID: 33177090; PMCID: PMC7673743.
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Expecting the Unexpected: Lack of In Vivo Network Defects in an .

Epilepsy currents

Hull JM, Isom LL.
PMID: 27857626
Epilepsy Curr. 2016 Nov-Dec;16(6):408-410. doi: 10.5698/1535-7511-16.6.408.

No abstract available.

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Hull JM, Isom LL. Expecting the Unexpected: Lack of In Vivo Network Defects in an . Epilepsy Curr. 2016;16(6):408-410doi: 10.5698/1535-7511-16.6.408.
Hull, J. M., & Isom, L. L. (2016). Expecting the Unexpected: Lack of In Vivo Network Defects in an . Epilepsy currents, 16(6), 408-410. https://doi.org/10.5698/1535-7511-16.6.408
Hull, Jacob M, and Isom, Lori L. "Expecting the Unexpected: Lack of In Vivo Network Defects in an ." Epilepsy currents vol. 16,6 (2016): 408-410. doi: https://doi.org/10.5698/1535-7511-16.6.408
Hull JM, Isom LL. Expecting the Unexpected: Lack of In Vivo Network Defects in an . Epilepsy Curr. 2016 Nov-Dec;16(6):408-410. doi: 10.5698/1535-7511-16.6.408. PMID: 27857626; PMCID: PMC5106108.
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Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity.

Molecular metabolism

Chhabra KH, Adams JM, Jones GL, Yamashita M, Schlapschy M, Skerra A, Rubinstein M, Low MJ.
PMID: 27689000
Mol Metab. 2016 Aug 05;5(10):869-881. doi: 10.1016/j.molmet.2016.07.012. eCollection 2016 Oct.

OBJECTIVE: A major challenge for obesity treatment is the maintenance of reduced body weight. Diet-induced obese mice are resistant to achieving normoweight once the obesogenic conditions are reversed, in part because lowered circulating leptin leads to a reduction in...

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Chhabra KH, Adams JM, Jones GL, et al. Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity. Mol Metab. 2016;5(10):869-881doi: 10.1016/j.molmet.2016.07.012.
Chhabra, K. H., Adams, J. M., Jones, G. L., Yamashita, M., Schlapschy, M., Skerra, A., Rubinstein, M., & Low, M. J. (2016). Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity. Molecular metabolism, 5(10), 869-881. https://doi.org/10.1016/j.molmet.2016.07.012
Chhabra, Kavaljit H, et al. "Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity." Molecular metabolism vol. 5,10 (2016): 869-881. doi: https://doi.org/10.1016/j.molmet.2016.07.012
Chhabra KH, Adams JM, Jones GL, Yamashita M, Schlapschy M, Skerra A, Rubinstein M, Low MJ. Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity. Mol Metab. 2016 Aug 05;5(10):869-881. doi: 10.1016/j.molmet.2016.07.012. eCollection 2016 Oct. PMID: 27689000; PMCID: PMC5034612.
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Brain on food: The neuroepigenetics of nutrition.

Neurochemistry international

Vaziri A, Dus M.
PMID: 34133954
Neurochem Int. 2021 Oct;149:105099. doi: 10.1016/j.neuint.2021.105099. Epub 2021 Jun 13.

Humans have known for millennia that nutrition has a profound influence on health and disease, but it is only recently that we have begun mapping the mechanisms via which the dietary environment impacts brain physiology and behavior. Here we...

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Vaziri A, Dus M. Brain on food: The neuroepigenetics of nutrition. Neurochem Int. 2021;149:105099doi: 10.1016/j.neuint.2021.105099.
Vaziri, A., & Dus, M. (2021). Brain on food: The neuroepigenetics of nutrition. Neurochemistry international, 149105099. https://doi.org/10.1016/j.neuint.2021.105099
Vaziri, Anoumid, and Dus, Monica. "Brain on food: The neuroepigenetics of nutrition." Neurochemistry international vol. 149 (2021): 105099. doi: https://doi.org/10.1016/j.neuint.2021.105099
Vaziri A, Dus M. Brain on food: The neuroepigenetics of nutrition. Neurochem Int. 2021 Oct;149:105099. doi: 10.1016/j.neuint.2021.105099. Epub 2021 Jun 13. PMID: 34133954; PMCID: PMC8387356.
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Loss of neurotensin receptor-1 disrupts the control of the mesolimbic dopamine system by leptin and promotes hedonic feeding and obesity.

Molecular metabolism

Opland D, Sutton A, Woodworth H, Brown J, Bugescu R, Garcia A, Christensen L, Rhodes C, Myers M, Leinninger G.
PMID: 24327958
Mol Metab. 2013 Aug 07;2(4):423-34. doi: 10.1016/j.molmet.2013.07.008. eCollection 2013.

Neurons of the lateral hypothalamic area (LHA) control motivated behaviors such as feeding and ambulatory activity, in part by modulating mesolimbic dopamine (DA) circuits. The hormone, leptin, acts via the long form of the leptin receptor (LepRb) in the...

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Opland D, Sutton A, Woodworth H, et al. Loss of neurotensin receptor-1 disrupts the control of the mesolimbic dopamine system by leptin and promotes hedonic feeding and obesity. Mol Metab. 2013;2(4):423-34doi: 10.1016/j.molmet.2013.07.008.
Opland, D., Sutton, A., Woodworth, H., Brown, J., Bugescu, R., Garcia, A., Christensen, L., Rhodes, C., Myers, M., & Leinninger, G. (2013). Loss of neurotensin receptor-1 disrupts the control of the mesolimbic dopamine system by leptin and promotes hedonic feeding and obesity. Molecular metabolism, 2(4), 423-34. https://doi.org/10.1016/j.molmet.2013.07.008
Opland, Darren, et al. "Loss of neurotensin receptor-1 disrupts the control of the mesolimbic dopamine system by leptin and promotes hedonic feeding and obesity." Molecular metabolism vol. 2,4 (2013): 423-34. doi: https://doi.org/10.1016/j.molmet.2013.07.008
Opland D, Sutton A, Woodworth H, Brown J, Bugescu R, Garcia A, Christensen L, Rhodes C, Myers M, Leinninger G. Loss of neurotensin receptor-1 disrupts the control of the mesolimbic dopamine system by leptin and promotes hedonic feeding and obesity. Mol Metab. 2013 Aug 07;2(4):423-34. doi: 10.1016/j.molmet.2013.07.008. eCollection 2013. PMID: 24327958; PMCID: PMC3857883.
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Showing 1 to 12 of 18 entries