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Showing 1 to 11 of 11 entries
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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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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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Vascular Network Formation by Human Microvascular Endothelial Cells in Modular Fibrin Microtissues.

ACS biomaterials science & engineering

Tiruvannamalai Annamalai R, Rioja AY, Putnam AJ, Stegemann JP.
PMID: 29503863
ACS Biomater Sci Eng. 2016 Nov 14;2(11):1914-1925. doi: 10.1021/acsbiomaterials.6b00274. Epub 2016 Sep 27.

Microvascular endothelial cells (MVEC) are a preferred cell source for autologous revascularization strategies, since they can be harvested and propagated from small tissue biopsies. Biomaterials-based strategies for therapeutic delivery of cells are aimed at tailoring the cellular microenvironment to...

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Tiruvannamalai Annamalai R, Rioja AY, Putnam AJ, et al. Vascular Network Formation by Human Microvascular Endothelial Cells in Modular Fibrin Microtissues. ACS Biomater Sci Eng. 2016;2(11):1914-1925doi: 10.1021/acsbiomaterials.6b00274.
Tiruvannamalai Annamalai, R., Rioja, A. Y., Putnam, A. J., & Stegemann, J. P. (2016). Vascular Network Formation by Human Microvascular Endothelial Cells in Modular Fibrin Microtissues. ACS biomaterials science & engineering, 2(11), 1914-1925. https://doi.org/10.1021/acsbiomaterials.6b00274
Tiruvannamalai Annamalai, Ramkumar, et al. "Vascular Network Formation by Human Microvascular Endothelial Cells in Modular Fibrin Microtissues." ACS biomaterials science & engineering vol. 2,11 (2016): 1914-1925. doi: https://doi.org/10.1021/acsbiomaterials.6b00274
Tiruvannamalai Annamalai R, Rioja AY, Putnam AJ, Stegemann JP. Vascular Network Formation by Human Microvascular Endothelial Cells in Modular Fibrin Microtissues. ACS Biomater Sci Eng. 2016 Nov 14;2(11):1914-1925. doi: 10.1021/acsbiomaterials.6b00274. Epub 2016 Sep 27. PMID: 29503863; PMCID: PMC5830175.
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Electrophilic and Drug-Induced Stimulation of NOTCH3 N-terminal Fragment Oligomerization in Cerebrovascular Pathology.

Translational stroke research

Young KZ, Cartee NMP, Lee SJ, Keep SG, Ivanova MI, Wang MM.
PMID: 33939102
Transl Stroke Res. 2021 Dec;12(6):1081-1092. doi: 10.1007/s12975-021-00908-2. Epub 2021 May 03.

Small vessel disease is a prevalent age-related condition linked to increased risk of dementia and stroke. We investigate the most commonly inherited form, CADASIL, caused by cysteine-involving mutations in NOTCH3. Recent studies highlight accumulation of NOTCH3 N-terminal fragmentation product...

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Young KZ, Cartee NMP, Lee SJ, et al. Electrophilic and Drug-Induced Stimulation of NOTCH3 N-terminal Fragment Oligomerization in Cerebrovascular Pathology. Transl Stroke Res. 2021;12(6):1081-1092doi: 10.1007/s12975-021-00908-2.
Young, K. Z., Cartee, N. M. P., Lee, S. J., Keep, S. G., Ivanova, M. I., & Wang, M. M. (2021). Electrophilic and Drug-Induced Stimulation of NOTCH3 N-terminal Fragment Oligomerization in Cerebrovascular Pathology. Translational stroke research, 12(6), 1081-1092. https://doi.org/10.1007/s12975-021-00908-2
Young, K Z, et al. "Electrophilic and Drug-Induced Stimulation of NOTCH3 N-terminal Fragment Oligomerization in Cerebrovascular Pathology." Translational stroke research vol. 12,6 (2021): 1081-1092. doi: https://doi.org/10.1007/s12975-021-00908-2
Young KZ, Cartee NMP, Lee SJ, Keep SG, Ivanova MI, Wang MM. Electrophilic and Drug-Induced Stimulation of NOTCH3 N-terminal Fragment Oligomerization in Cerebrovascular Pathology. Transl Stroke Res. 2021 Dec;12(6):1081-1092. doi: 10.1007/s12975-021-00908-2. Epub 2021 May 03. PMID: 33939102; PMCID: PMC8557116.
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High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity.

Obesity (Silver Spring, Md.)

Frieler RA, Vigil TM, Song J, Leung C, Lumeng CN, Mortensen RM.
PMID: 34549547
Obesity (Silver Spring). 2021 Nov;29(11):1868-1881. doi: 10.1002/oby.23264. Epub 2021 Sep 21.

OBJECTIVE: Excess dietary fat and sodium (NaCl) are both associated with obesity and metabolic dysfunction. In mice, high NaCl has been shown to block high-fat (HF) diet-induced weight gain. Here, the impact of an HF/NaCl diet on metabolic function...

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Frieler RA, Vigil TM, Song J, et al. High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity. Obesity (Silver Spring). 2021;29(11):1868-1881doi: 10.1002/oby.23264.
Frieler, R. A., Vigil, T. M., Song, J., Leung, C., Lumeng, C. N., & Mortensen, R. M. (2021). High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity. Obesity (Silver Spring, Md.), 29(11), 1868-1881. https://doi.org/10.1002/oby.23264
Frieler, Ryan A, et al. "High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity." Obesity (Silver Spring, Md.) vol. 29,11 (2021): 1868-1881. doi: https://doi.org/10.1002/oby.23264
Frieler RA, Vigil TM, Song J, Leung C, Lumeng CN, Mortensen RM. High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity. Obesity (Silver Spring). 2021 Nov;29(11):1868-1881. doi: 10.1002/oby.23264. Epub 2021 Sep 21. PMID: 34549547; PMCID: PMC8571049.
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HDL in Endocrine Carcinomas: Biomarker, Drug Carrier, and Potential Therapeutic.

Frontiers in endocrinology

Morin EE, Li XA, Schwendeman A.
PMID: 30555417
Front Endocrinol (Lausanne). 2018 Nov 30;9:715. doi: 10.3389/fendo.2018.00715. eCollection 2018.

High-density lipoprotein (HDL) have long been studied for their protective role against cardiovascular diseases, however recently relationship between HDL and cancer came into focus. Several epidemiological studies have shown an inverse correlation between HDL-cholesterol (HDL-C) and cancer risk, and...

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Morin EE, Li XA, Schwendeman A. HDL in Endocrine Carcinomas: Biomarker, Drug Carrier, and Potential Therapeutic. Front Endocrinol (Lausanne). 2018;9:715doi: 10.3389/fendo.2018.00715.
Morin, E. E., Li, X. A., & Schwendeman, A. (2018). HDL in Endocrine Carcinomas: Biomarker, Drug Carrier, and Potential Therapeutic. Frontiers in endocrinology, 9715. https://doi.org/10.3389/fendo.2018.00715
Morin, Emily E, et al. "HDL in Endocrine Carcinomas: Biomarker, Drug Carrier, and Potential Therapeutic." Frontiers in endocrinology vol. 9 (2018): 715. doi: https://doi.org/10.3389/fendo.2018.00715
Morin EE, Li XA, Schwendeman A. HDL in Endocrine Carcinomas: Biomarker, Drug Carrier, and Potential Therapeutic. Front Endocrinol (Lausanne). 2018 Nov 30;9:715. doi: 10.3389/fendo.2018.00715. eCollection 2018. PMID: 30555417; PMCID: PMC6283888.
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High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity.

Obesity (Silver Spring, Md.)

Frieler RA, Vigil TM, Song J, Leung C, Lumeng CN, Mortensen RM.
PMID: 34549547
Obesity (Silver Spring). 2021 Nov;29(11):1868-1881. doi: 10.1002/oby.23264. Epub 2021 Sep 21.

OBJECTIVE: Excess dietary fat and sodium (NaCl) are both associated with obesity and metabolic dysfunction. In mice, high NaCl has been shown to block high-fat (HF) diet-induced weight gain. Here, the impact of an HF/NaCl diet on metabolic function...

Cite
Frieler RA, Vigil TM, Song J, et al. High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity. Obesity (Silver Spring). 2021;29(11):1868-1881doi: 10.1002/oby.23264.
Frieler, R. A., Vigil, T. M., Song, J., Leung, C., Lumeng, C. N., & Mortensen, R. M. (2021). High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity. Obesity (Silver Spring, Md.), 29(11), 1868-1881. https://doi.org/10.1002/oby.23264
Frieler, Ryan A, et al. "High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity." Obesity (Silver Spring, Md.) vol. 29,11 (2021): 1868-1881. doi: https://doi.org/10.1002/oby.23264
Frieler RA, Vigil TM, Song J, Leung C, Lumeng CN, Mortensen RM. High-fat and high-sodium diet induces metabolic dysfunction in the absence of obesity. Obesity (Silver Spring). 2021 Nov;29(11):1868-1881. doi: 10.1002/oby.23264. Epub 2021 Sep 21. PMID: 34549547; PMCID: PMC8571049.
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Deep mutational scanning of the plasminogen activator inhibitor-1 functional landscape.

Scientific reports

Huttinger ZM, Haynes LM, Yee A, Kretz CA, Holding ML, Siemieniak DR, Lawrence DA, Ginsburg D.
PMID: 34552126
Sci Rep. 2021 Sep 22;11(1):18827. doi: 10.1038/s41598-021-97871-7.

The serine protease inhibitor (SERPIN) plasminogen activator inhibitor-1 (PAI-1) is a key regulator of the fibrinolytic system, inhibiting the serine proteases tissue- and urokinase-type plasminogen activator (tPA and uPA, respectively). Missense variants render PAI-1 non-functional through misfolding, leading to...

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Huttinger ZM, Haynes LM, Yee A, et al. Deep mutational scanning of the plasminogen activator inhibitor-1 functional landscape. Sci Rep. 2021;11(1):18827doi: 10.1038/s41598-021-97871-7.
Huttinger, Z. M., Haynes, L. M., Yee, A., Kretz, C. A., Holding, M. L., Siemieniak, D. R., Lawrence, D. A., & Ginsburg, D. (2021). Deep mutational scanning of the plasminogen activator inhibitor-1 functional landscape. Scientific reports, 11(1), 18827. https://doi.org/10.1038/s41598-021-97871-7
Huttinger, Zachary M, et al. "Deep mutational scanning of the plasminogen activator inhibitor-1 functional landscape." Scientific reports vol. 11,1 (2021): 18827. doi: https://doi.org/10.1038/s41598-021-97871-7
Huttinger ZM, Haynes LM, Yee A, Kretz CA, Holding ML, Siemieniak DR, Lawrence DA, Ginsburg D. Deep mutational scanning of the plasminogen activator inhibitor-1 functional landscape. Sci Rep. 2021 Sep 22;11(1):18827. doi: 10.1038/s41598-021-97871-7. PMID: 34552126; PMCID: PMC8458277.
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Inkjet-printed micro-calibration standards for ultraquantitative Raman spectral cytometry.

The Analyst

LaLone V, Fawaz MV, Morales-Mercado J, Mourão MA, Snyder CS, Kim SY, Lieberman AP, Tuteja A, Mehta G, Standiford TJ, Raghavendran K, Shedden K, Schwendeman A, Stringer KA, Rosania GR.
PMID: 31116195
Analyst. 2019 Jun 21;144(12):3790-3799. doi: 10.1039/c9an00500e. Epub 2019 May 22.

Herein we report the development of a cytometric analysis platform for measuring the contents of individual cells in absolute (picogram) scales; this study represents the first report of Raman-based quantitation of the absolute mass - or the total amount...

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LaLone V, Fawaz MV, Morales-Mercado J, et al. Inkjet-printed micro-calibration standards for ultraquantitative Raman spectral cytometry. Analyst. 2019;144(12):3790-3799doi: 10.1039/c9an00500e.
LaLone, V., Fawaz, M. V., Morales-Mercado, J., Mourão, M. A., Snyder, C. S., Kim, S. Y., Lieberman, A. P., Tuteja, A., Mehta, G., Standiford, T. J., Raghavendran, K., Shedden, K., Schwendeman, A., Stringer, K. A., & Rosania, G. R. (2019). Inkjet-printed micro-calibration standards for ultraquantitative Raman spectral cytometry. The Analyst, 144(12), 3790-3799. https://doi.org/10.1039/c9an00500e
LaLone, Vernon, et al. "Inkjet-printed micro-calibration standards for ultraquantitative Raman spectral cytometry." The Analyst vol. 144,12 (2019): 3790-3799. doi: https://doi.org/10.1039/c9an00500e
LaLone V, Fawaz MV, Morales-Mercado J, Mourão MA, Snyder CS, Kim SY, Lieberman AP, Tuteja A, Mehta G, Standiford TJ, Raghavendran K, Shedden K, Schwendeman A, Stringer KA, Rosania GR. Inkjet-printed micro-calibration standards for ultraquantitative Raman spectral cytometry. Analyst. 2019 Jun 21;144(12):3790-3799. doi: 10.1039/c9an00500e. Epub 2019 May 22. PMID: 31116195; PMCID: PMC6711383.
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Impaired Myocardial Energetics Causes Mechanical Dysfunction in Decompensated Failing Hearts.

Function (Oxford, England)

Lopez R, Marzban B, Gao X, Lauinger E, Van den Bergh F, Whitesall SE, Converso-Baran K, Burant CF, Michele DE, Beard DA.
PMID: 33074265
Function (Oxf). 2020;1(2):zqaa018. doi: 10.1093/function/zqaa018. Epub 2020 Sep 22.

Cardiac mechanical function is supported by ATP hydrolysis, which provides the chemical-free energy to drive the molecular processes underlying cardiac pumping. Physiological rates of myocardial ATP consumption require the heart to resynthesize its entire ATP pool several times per...

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Lopez R, Marzban B, Gao X, et al. Impaired Myocardial Energetics Causes Mechanical Dysfunction in Decompensated Failing Hearts. Function (Oxf). 2020;1(2):zqaa018doi: 10.1093/function/zqaa018.
Lopez, R., Marzban, B., Gao, X., Lauinger, E., Van den Bergh, F., Whitesall, S. E., Converso-Baran, K., Burant, C. F., Michele, D. E., & Beard, D. A. (2020). Impaired Myocardial Energetics Causes Mechanical Dysfunction in Decompensated Failing Hearts. Function (Oxford, England), 1(2), zqaa018. https://doi.org/10.1093/function/zqaa018
Lopez, Rachel, et al. "Impaired Myocardial Energetics Causes Mechanical Dysfunction in Decompensated Failing Hearts." Function (Oxford, England) vol. 1,2 (2020): zqaa018. doi: https://doi.org/10.1093/function/zqaa018
Lopez R, Marzban B, Gao X, Lauinger E, Van den Bergh F, Whitesall SE, Converso-Baran K, Burant CF, Michele DE, Beard DA. Impaired Myocardial Energetics Causes Mechanical Dysfunction in Decompensated Failing Hearts. Function (Oxf). 2020;1(2):zqaa018. doi: 10.1093/function/zqaa018. Epub 2020 Sep 22. PMID: 33074265; PMCID: PMC7552914.
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Obesity results in adipose tissue T cell exhaustion.

JCI insight

Porsche CE, Delproposto JB, Geletka L, O'Rourke R, Lumeng CN.
PMID: 33724954
JCI Insight. 2021 Apr 22;6(8). doi: 10.1172/jci.insight.139793.

Despite studies implicating adipose tissue T cells (ATT) in the initiation and persistence of adipose tissue inflammation, fundamental gaps in knowledge regarding ATT function impedes progress toward understanding how obesity influences adaptive immunity. We hypothesized that ATT activation and...

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Porsche CE, Delproposto JB, Geletka L, et al. Obesity results in adipose tissue T cell exhaustion. JCI Insight. 2021;6(8)doi: 10.1172/jci.insight.139793.
Porsche, C. E., Delproposto, J. B., Geletka, L., O'Rourke, R., & Lumeng, C. N. (2021). Obesity results in adipose tissue T cell exhaustion. JCI insight, 6(8), . https://doi.org/10.1172/jci.insight.139793
Porsche, Cara E, et al. "Obesity results in adipose tissue T cell exhaustion." JCI insight vol. 6,8 (2021). doi: https://doi.org/10.1172/jci.insight.139793
Porsche CE, Delproposto JB, Geletka L, O'Rourke R, Lumeng CN. Obesity results in adipose tissue T cell exhaustion. JCI Insight. 2021 Apr 22;6(8). doi: 10.1172/jci.insight.139793. PMID: 33724954; PMCID: PMC8119198.
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