Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Species
Language
Sex
Age
Showing 13 to 24 of 122 entries
Sorted by: Best Match Show Resources per page
Varicella zoster virus-infected cerebrovascular cells produce a proinflammatory environment.

Neurology(R) neuroimmunology & neuroinflammation

Jones D, Neff CP, Palmer BE, Stenmark K, Nagel MA.
PMID: 29159203
Neurol Neuroimmunol Neuroinflamm. 2017 Jul 13;4(5):e382. doi: 10.1212/NXI.0000000000000382. eCollection 2017 Sep.

OBJECTIVE: To test whether varicella zoster virus (VZV) infection of human brain vascular cells and of lung fibroblasts directly increases proinflammatory cytokine levels, consistent with VZV as a causative agent in intracerebral VZV vasculopathy and giant-cell arteritis (GCA).METHODS: Conditioned...

Cite
Jones D, Neff CP, Palmer BE, et al. Varicella zoster virus-infected cerebrovascular cells produce a proinflammatory environment. Neurol Neuroimmunol Neuroinflamm. 2017;4(5):e382doi: 10.1212/NXI.0000000000000382.
Jones, D., Neff, C. P., Palmer, B. E., Stenmark, K., & Nagel, M. A. (2017). Varicella zoster virus-infected cerebrovascular cells produce a proinflammatory environment. Neurology(R) neuroimmunology & neuroinflammation, 4(5), e382. https://doi.org/10.1212/NXI.0000000000000382
Jones, Dallas, et al. "Varicella zoster virus-infected cerebrovascular cells produce a proinflammatory environment." Neurology(R) neuroimmunology & neuroinflammation vol. 4,5 (2017): e382. doi: https://doi.org/10.1212/NXI.0000000000000382
Jones D, Neff CP, Palmer BE, Stenmark K, Nagel MA. Varicella zoster virus-infected cerebrovascular cells produce a proinflammatory environment. Neurol Neuroimmunol Neuroinflamm. 2017 Jul 13;4(5):e382. doi: 10.1212/NXI.0000000000000382. eCollection 2017 Sep. PMID: 29159203; PMCID: PMC5682918.
Copy Download .nbib Format: NLM
Identification of Infants at Risk for Chronic Lung Disease at Birth. Potential for a Personalized Approach to Disease Prevention.

American journal of respiratory and critical care medicine

D'Alessandro A, Nozik-Grayck E, Stenmark KR.
PMID: 28613077
Am J Respir Crit Care Med. 2017 Oct 15;196(8):951-952. doi: 10.1164/rccm.201706-1065ED.

No abstract available.

Cite
D'Alessandro A, Nozik-Grayck E, Stenmark KR. Identification of Infants at Risk for Chronic Lung Disease at Birth. Potential for a Personalized Approach to Disease Prevention. Am J Respir Crit Care Med. 2017;196(8):951-952doi: 10.1164/rccm.201706-1065ED.
D'Alessandro, A., Nozik-Grayck, E., & Stenmark, K. R. (2017). Identification of Infants at Risk for Chronic Lung Disease at Birth. Potential for a Personalized Approach to Disease Prevention. American journal of respiratory and critical care medicine, 196(8), 951-952. https://doi.org/10.1164/rccm.201706-1065ED
D'Alessandro, Angelo, et al. "Identification of Infants at Risk for Chronic Lung Disease at Birth. Potential for a Personalized Approach to Disease Prevention." American journal of respiratory and critical care medicine vol. 196,8 (2017): 951-952. doi: https://doi.org/10.1164/rccm.201706-1065ED
D'Alessandro A, Nozik-Grayck E, Stenmark KR. Identification of Infants at Risk for Chronic Lung Disease at Birth. Potential for a Personalized Approach to Disease Prevention. Am J Respir Crit Care Med. 2017 Oct 15;196(8):951-952. doi: 10.1164/rccm.201706-1065ED. PMID: 28613077; PMCID: PMC5649991.
Copy Download .nbib Format: NLM
Hemodynamically Unloading the Distal Pulmonary Circulation in Pulmonary Hypertension: A Modeling Study.

Journal of biomechanical engineering

Walter R, Hunter K, Stenmark K, Kheyfets VO.
PMID: 34251418
J Biomech Eng. 2022 Feb 01;144(2). doi: 10.1115/1.4051719.

Pulmonary hypertension (PH) is a progressive disease that is characterized by a gradual increase in both resistive and reactive pulmonary arterial (PA) impedance. Previous studies in a rodent model of PH have shown that reducing the hemodynamic load in...

Cite
Walter R, Hunter K, Stenmark K, et al. Hemodynamically Unloading the Distal Pulmonary Circulation in Pulmonary Hypertension: A Modeling Study. J Biomech Eng. 2022;144(2)doi: 10.1115/1.4051719.
Walter, R., Hunter, K., Stenmark, K., & Kheyfets, V. O. (2022). Hemodynamically Unloading the Distal Pulmonary Circulation in Pulmonary Hypertension: A Modeling Study. Journal of biomechanical engineering, 144(2), . https://doi.org/10.1115/1.4051719
Walter, Rachelle, et al. "Hemodynamically Unloading the Distal Pulmonary Circulation in Pulmonary Hypertension: A Modeling Study." Journal of biomechanical engineering vol. 144,2 (2022). doi: https://doi.org/10.1115/1.4051719
Walter R, Hunter K, Stenmark K, Kheyfets VO. Hemodynamically Unloading the Distal Pulmonary Circulation in Pulmonary Hypertension: A Modeling Study. J Biomech Eng. 2022 Feb 01;144(2). doi: 10.1115/1.4051719. PMID: 34251418; PMCID: PMC8547017.
Copy Download .nbib Format: NLM
Potential long-term effects of SARS-CoV-2 infection on the pulmonary vasculature: a global perspective.

Nature reviews. Cardiology

Halawa S, Pullamsetti SS, Bangham CRM, Stenmark KR, Dorfmüller P, Frid MG, Butrous G, Morrell NW, de Jesus Perez VA, Stuart DI, O'Gallagher K, Shah AM, Aguib Y, Yacoub MH.
PMID: 34873286
Nat Rev Cardiol. 2021 Dec 06; doi: 10.1038/s41569-021-00640-2. Epub 2021 Dec 06.

The lungs are the primary target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, with severe hypoxia being the cause of death in the most critical cases. Coronavirus disease 2019 (COVID-19) is extremely heterogeneous in terms of severity,...

Cite
Halawa S, Pullamsetti SS, Bangham CRM, et al. Potential long-term effects of SARS-CoV-2 infection on the pulmonary vasculature: a global perspective. Nat Rev Cardiol. 2021;doi: 10.1038/s41569-021-00640-2.
Halawa, S., Pullamsetti, S. S., Bangham, C. R. M., Stenmark, K. R., Dorfmüller, P., Frid, M. G., Butrous, G., Morrell, N. W., de Jesus Perez, V. A., Stuart, D. I., O'Gallagher, K., Shah, A. M., Aguib, Y., & Yacoub, M. H. (2021). Potential long-term effects of SARS-CoV-2 infection on the pulmonary vasculature: a global perspective. Nature reviews. Cardiology, . https://doi.org/10.1038/s41569-021-00640-2
Halawa, Sarah, et al. "Potential long-term effects of SARS-CoV-2 infection on the pulmonary vasculature: a global perspective." Nature reviews. Cardiology vol. (2021). doi: https://doi.org/10.1038/s41569-021-00640-2
Halawa S, Pullamsetti SS, Bangham CRM, Stenmark KR, Dorfmüller P, Frid MG, Butrous G, Morrell NW, de Jesus Perez VA, Stuart DI, O'Gallagher K, Shah AM, Aguib Y, Yacoub MH. Potential long-term effects of SARS-CoV-2 infection on the pulmonary vasculature: a global perspective. Nat Rev Cardiol. 2021 Dec 06; doi: 10.1038/s41569-021-00640-2. Epub 2021 Dec 06. PMID: 34873286; PMCID: PMC8647069.
Copy Download .nbib Format: NLM
Association between time-related changes in routine blood morphological parameters and renal function after transcatheter aortic valve implantation - a preliminary study.

Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery

Stelmark K, Zaher EA, Olasińska-Wiśniewska A, Adesina M, Dragone A, Isaac M, Misterski M, Grygier M, Puślecki M, Lesiak M, Jemielity M, Perek B.
PMID: 34703472
Kardiochir Torakochirurgia Pol. 2021 Sep;18(3):152-158. doi: 10.5114/kitp.2021.109368. Epub 2021 Oct 05.

INTRODUCTION: Transcatheter aortic valve implantation (TAVI) although minimally invasive is still accompanied by changes in blood morphological parameters, some of them linked to unfavorable outcomes.AIM: To find any association between changes in blood morphology reflecting an inflammatory response and...

Cite
Stelmark K, Zaher EA, Olasińska-Wiśniewska A, et al. Association between time-related changes in routine blood morphological parameters and renal function after transcatheter aortic valve implantation - a preliminary study. Kardiochir Torakochirurgia Pol. 2021;18(3):152-158doi: 10.5114/kitp.2021.109368.
Stelmark, K., Zaher, E. A., Olasińska-Wiśniewska, A., Adesina, M., Dragone, A., Isaac, M., Misterski, M., Grygier, M., Puślecki, M., Lesiak, M., Jemielity, M., & Perek, B. (2021). Association between time-related changes in routine blood morphological parameters and renal function after transcatheter aortic valve implantation - a preliminary study. Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery, 18(3), 152-158. https://doi.org/10.5114/kitp.2021.109368
Stelmark, Konrad, et al. "Association between time-related changes in routine blood morphological parameters and renal function after transcatheter aortic valve implantation - a preliminary study." Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery vol. 18,3 (2021): 152-158. doi: https://doi.org/10.5114/kitp.2021.109368
Stelmark K, Zaher EA, Olasińska-Wiśniewska A, Adesina M, Dragone A, Isaac M, Misterski M, Grygier M, Puślecki M, Lesiak M, Jemielity M, Perek B. Association between time-related changes in routine blood morphological parameters and renal function after transcatheter aortic valve implantation - a preliminary study. Kardiochir Torakochirurgia Pol. 2021 Sep;18(3):152-158. doi: 10.5114/kitp.2021.109368. Epub 2021 Oct 05. PMID: 34703472; PMCID: PMC8525280.
Copy Download .nbib Format: NLM
Book review on hypoxic respiratory failure in the newborn - from origins to clinical management.

Pulmonary circulation

Stenmark K.
PMID: 34925763
Pulm Circ. 2021 Dec 14;11(4):20458940211060161. doi: 10.1177/20458940211060161. eCollection 2021.

No abstract available.

Cite
Stenmark K. Book review on hypoxic respiratory failure in the newborn - from origins to clinical management. Pulm Circ. 2021;11(4):20458940211060161doi: 10.1177/20458940211060161.
Stenmark, K. (2021). Book review on hypoxic respiratory failure in the newborn - from origins to clinical management. Pulmonary circulation, 11(4), 20458940211060161. https://doi.org/10.1177/20458940211060161
Stenmark, Kurt. "Book review on hypoxic respiratory failure in the newborn - from origins to clinical management." Pulmonary circulation vol. 11,4 (2021): 20458940211060161. doi: https://doi.org/10.1177/20458940211060161
Stenmark K. Book review on hypoxic respiratory failure in the newborn - from origins to clinical management. Pulm Circ. 2021 Dec 14;11(4):20458940211060161. doi: 10.1177/20458940211060161. eCollection 2021. PMID: 34925763; PMCID: PMC8679030.
Copy Download .nbib Format: NLM
Publisher Correction: Stable isotope metabolomics of pulmonary artery smooth muscle and endothelial cells in pulmonary hypertension and with TGF-beta treatment.

Scientific reports

Hernandez-Saavedra D, Sanders L, Freeman S, Reisz JA, Lee MH, Mickael C, Kumar R, Kassa B, Gu S, D' Alessandro A, Stenmark KR, Tuder RM, Graham BB.
PMID: 32132567
Sci Rep. 2020 Mar 04;10(1):4349. doi: 10.1038/s41598-020-60500-w.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cite
Hernandez-Saavedra D, Sanders L, Freeman S, et al. Publisher Correction: Stable isotope metabolomics of pulmonary artery smooth muscle and endothelial cells in pulmonary hypertension and with TGF-beta treatment. Sci Rep. 2020;10(1):4349doi: 10.1038/s41598-020-60500-w.
Hernandez-Saavedra, D., Sanders, L., Freeman, S., Reisz, J. A., Lee, M. H., Mickael, C., Kumar, R., Kassa, B., Gu, S., D' Alessandro, A., Stenmark, K. R., Tuder, R. M., & Graham, B. B. (2020). Publisher Correction: Stable isotope metabolomics of pulmonary artery smooth muscle and endothelial cells in pulmonary hypertension and with TGF-beta treatment. Scientific reports, 10(1), 4349. https://doi.org/10.1038/s41598-020-60500-w
Hernandez-Saavedra, Daniel, et al. "Publisher Correction: Stable isotope metabolomics of pulmonary artery smooth muscle and endothelial cells in pulmonary hypertension and with TGF-beta treatment." Scientific reports vol. 10,1 (2020): 4349. doi: https://doi.org/10.1038/s41598-020-60500-w
Hernandez-Saavedra D, Sanders L, Freeman S, Reisz JA, Lee MH, Mickael C, Kumar R, Kassa B, Gu S, D' Alessandro A, Stenmark KR, Tuder RM, Graham BB. Publisher Correction: Stable isotope metabolomics of pulmonary artery smooth muscle and endothelial cells in pulmonary hypertension and with TGF-beta treatment. Sci Rep. 2020 Mar 04;10(1):4349. doi: 10.1038/s41598-020-60500-w. PMID: 32132567; PMCID: PMC7055208.
Copy Download .nbib Format: NLM
Author Correction: STEEP mediates STING ER exit and activation of signaling.

Nature immunology

Zhang BC, Nandakumar R, Reinert LS, Huang J, Laustsen A, Gao ZL, Sun CL, Jensen SB, Troldborg A, Assil S, Berthelsen MF, Scavenius C, Zhang Y, Windross SJ, Olagnier D, Prabakaran T, Bodda C, Narita R, Cai Y, Zhang CG, Stenmark H, Doucet CM, Noda T, Guo Z, Goldbach-Mansky R, Hartmann R, Chen ZJ, Enghild JJ, Bak RO, Thomsen MK, Paludan SR.
PMID: 32929276
Nat Immunol. 2020 Nov;21(11):1468-1469. doi: 10.1038/s41590-020-0803-5.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cite
Zhang BC, Nandakumar R, Reinert LS, et al. Author Correction: STEEP mediates STING ER exit and activation of signaling. Nat Immunol. 2020;21(11):1468-1469doi: 10.1038/s41590-020-0803-5.
Zhang, B. C., Nandakumar, R., Reinert, L. S., Huang, J., Laustsen, A., Gao, Z. L., Sun, C. L., Jensen, S. B., Troldborg, A., Assil, S., Berthelsen, M. F., Scavenius, C., Zhang, Y., Windross, S. J., Olagnier, D., Prabakaran, T., Bodda, C., Narita, R., Cai, Y., Zhang, C. G., Stenmark, H., Doucet, C. M., Noda, T., Guo, Z., Goldbach-Mansky, R., Hartmann, R., Chen, Z. J., Enghild, J. J., Bak, R. O., Thomsen, M. K., & Paludan, S. R. (2020). Author Correction: STEEP mediates STING ER exit and activation of signaling. Nature immunology, 21(11), 1468-1469. https://doi.org/10.1038/s41590-020-0803-5
Zhang, Bao-Cun, et al. "Author Correction: STEEP mediates STING ER exit and activation of signaling." Nature immunology vol. 21,11 (2020): 1468-1469. doi: https://doi.org/10.1038/s41590-020-0803-5
Zhang BC, Nandakumar R, Reinert LS, Huang J, Laustsen A, Gao ZL, Sun CL, Jensen SB, Troldborg A, Assil S, Berthelsen MF, Scavenius C, Zhang Y, Windross SJ, Olagnier D, Prabakaran T, Bodda C, Narita R, Cai Y, Zhang CG, Stenmark H, Doucet CM, Noda T, Guo Z, Goldbach-Mansky R, Hartmann R, Chen ZJ, Enghild JJ, Bak RO, Thomsen MK, Paludan SR. Author Correction: STEEP mediates STING ER exit and activation of signaling. Nat Immunol. 2020 Nov;21(11):1468-1469. doi: 10.1038/s41590-020-0803-5. PMID: 32929276.
Copy Download .nbib Format: NLM
Brief Report: Case Comparison of Therapy With the Histone Deacetylase Inhibitor Vorinostat in a Neonatal Calf Model of Pulmonary Hypertension.

Frontiers in physiology

Applegate TJ, Krafsur GM, Boon JA, Zhang H, Li M, Holt TN, Ambler SK, Abrams BA, Gustafson DL, Bartels K, Garry FB, Stenmark KR, Brown RD.
PMID: 34552503
Front Physiol. 2021 Sep 06;12:712583. doi: 10.3389/fphys.2021.712583. eCollection 2021.

Pulmonary hypertension (PH) is an incurable condition in humans; driven by pulmonary vascular remodeling partially mediated by epigenetic mechanisms; and leading to right ventricular hypertrophy, failure, and death. We hypothesized that targeting chromatin-modifying histone deacetylases may provide benefit. In...

Cite
Applegate TJ, Krafsur GM, Boon JA, et al. Brief Report: Case Comparison of Therapy With the Histone Deacetylase Inhibitor Vorinostat in a Neonatal Calf Model of Pulmonary Hypertension. Front Physiol. 2021;12:712583doi: 10.3389/fphys.2021.712583.
Applegate, T. J., Krafsur, G. M., Boon, J. A., Zhang, H., Li, M., Holt, T. N., Ambler, S. K., Abrams, B. A., Gustafson, D. L., Bartels, K., Garry, F. B., Stenmark, K. R., & Brown, R. D. (2021). Brief Report: Case Comparison of Therapy With the Histone Deacetylase Inhibitor Vorinostat in a Neonatal Calf Model of Pulmonary Hypertension. Frontiers in physiology, 12712583. https://doi.org/10.3389/fphys.2021.712583
Applegate, Tanya J, et al. "Brief Report: Case Comparison of Therapy With the Histone Deacetylase Inhibitor Vorinostat in a Neonatal Calf Model of Pulmonary Hypertension." Frontiers in physiology vol. 12 (2021): 712583. doi: https://doi.org/10.3389/fphys.2021.712583
Applegate TJ, Krafsur GM, Boon JA, Zhang H, Li M, Holt TN, Ambler SK, Abrams BA, Gustafson DL, Bartels K, Garry FB, Stenmark KR, Brown RD. Brief Report: Case Comparison of Therapy With the Histone Deacetylase Inhibitor Vorinostat in a Neonatal Calf Model of Pulmonary Hypertension. Front Physiol. 2021 Sep 06;12:712583. doi: 10.3389/fphys.2021.712583. eCollection 2021. PMID: 34552503; PMCID: PMC8450341.
Copy Download .nbib Format: NLM
Structure and functions of stable intercellular bridges formed by incomplete cytokinesis during development.

Communicative & integrative biology

Haglund K, Nezis IP, Stenmark H.
PMID: 21509167
Commun Integr Biol. 2011 Jan;4(1):1-9. doi: 10.4161/cib.4.1.13550.

Cytokinesis, the final step of cell division, normally proceeds to completion in living organisms, so that daughter cells physically separate by abscission. In certain tissues and developmental stages, on the other hand, the cytokinesis process is incomplete, giving rise...

Cite
Haglund K, Nezis IP, Stenmark H. Structure and functions of stable intercellular bridges formed by incomplete cytokinesis during development. Commun Integr Biol. 2011;4(1):1-9doi: 10.4161/cib.4.1.13550.
Haglund, K., Nezis, I. P., & Stenmark, H. (2011). Structure and functions of stable intercellular bridges formed by incomplete cytokinesis during development. Communicative & integrative biology, 4(1), 1-9. https://doi.org/10.4161/cib.4.1.13550
Haglund, Kaisa, et al. "Structure and functions of stable intercellular bridges formed by incomplete cytokinesis during development." Communicative & integrative biology vol. 4,1 (2011): 1-9. doi: https://doi.org/10.4161/cib.4.1.13550
Haglund K, Nezis IP, Stenmark H. Structure and functions of stable intercellular bridges formed by incomplete cytokinesis during development. Commun Integr Biol. 2011 Jan;4(1):1-9. doi: 10.4161/cib.4.1.13550. PMID: 21509167; PMCID: PMC3073259.
Copy Download .nbib Format: NLM
Complement-containing small extracellular vesicles from adventitial fibroblasts induce proinflammatory and metabolic reprogramming in macrophages.

JCI insight

Kumar S, Frid MG, Zhang H, Li M, Riddle S, Brown RD, Yadav SC, Roy MK, Dzieciatkowska ME, D'Alessandro A, Hansen KC, Stenmark KR.
PMID: 34499621
JCI Insight. 2021 Nov 08;6(21). doi: 10.1172/jci.insight.148382.

Pulmonary hypertension (PH) is a severe cardiopulmonary disease characterized by complement-dependent, fibroblast-induced perivascular accumulation and proinflammatory activation of macrophages. We hypothesized that, in PH, nanoscale-sized small extracellular vesicles (sEVs), released by perivascular/adventitial fibroblasts, are critical mediators of complement-dependent proinflammatory...

Cite
Kumar S, Frid MG, Zhang H, et al. Complement-containing small extracellular vesicles from adventitial fibroblasts induce proinflammatory and metabolic reprogramming in macrophages. JCI Insight. 2021;6(21)doi: 10.1172/jci.insight.148382.
Kumar, S., Frid, M. G., Zhang, H., Li, M., Riddle, S., Brown, R. D., Yadav, S. C., Roy, M. K., Dzieciatkowska, M. E., D'Alessandro, A., Hansen, K. C., & Stenmark, K. R. (2021). Complement-containing small extracellular vesicles from adventitial fibroblasts induce proinflammatory and metabolic reprogramming in macrophages. JCI insight, 6(21), . https://doi.org/10.1172/jci.insight.148382
Kumar, Sushil, et al. "Complement-containing small extracellular vesicles from adventitial fibroblasts induce proinflammatory and metabolic reprogramming in macrophages." JCI insight vol. 6,21 (2021). doi: https://doi.org/10.1172/jci.insight.148382
Kumar S, Frid MG, Zhang H, Li M, Riddle S, Brown RD, Yadav SC, Roy MK, Dzieciatkowska ME, D'Alessandro A, Hansen KC, Stenmark KR. Complement-containing small extracellular vesicles from adventitial fibroblasts induce proinflammatory and metabolic reprogramming in macrophages. JCI Insight. 2021 Nov 08;6(21). doi: 10.1172/jci.insight.148382. PMID: 34499621; PMCID: PMC8663554.
Copy Download .nbib Format: NLM
Activation of the unfolded protein response is associated with pulmonary hypertension.

Pulmonary circulation

Yeager ME, Reddy MB, Nguyen CM, Colvin KL, Ivy DD, Stenmark KR.
PMID: 22837864
Pulm Circ. 2012 Apr-Jun;2(2):229-40. doi: 10.4103/2045-8932.97613.

Pulmonary hypertension remains an important cause of morbidity and mortality. Although there is currently no cure, descriptions of defective intracellular trafficking and protein misfolding in vascular cell models of pulmonary hypertension have been recently reported. We tested the hypothesis...

Cite
Yeager ME, Reddy MB, Nguyen CM, et al. Activation of the unfolded protein response is associated with pulmonary hypertension. Pulm Circ. 2012;2(2):229-40doi: 10.4103/2045-8932.97613.
Yeager, M. E., Reddy, M. B., Nguyen, C. M., Colvin, K. L., Ivy, D. D., & Stenmark, K. R. (2012). Activation of the unfolded protein response is associated with pulmonary hypertension. Pulmonary circulation, 2(2), 229-40. https://doi.org/10.4103/2045-8932.97613
Yeager, Michael E, et al. "Activation of the unfolded protein response is associated with pulmonary hypertension." Pulmonary circulation vol. 2,2 (2012): 229-40. doi: https://doi.org/10.4103/2045-8932.97613
Yeager ME, Reddy MB, Nguyen CM, Colvin KL, Ivy DD, Stenmark KR. Activation of the unfolded protein response is associated with pulmonary hypertension. Pulm Circ. 2012 Apr-Jun;2(2):229-40. doi: 10.4103/2045-8932.97613. PMID: 22837864; PMCID: PMC3401877.
Copy Download .nbib Format: NLM
Showing 13 to 24 of 122 entries