Filip Swirski

Last updated
Filip Swirski
NationalityPolish, Canadian, US
CitizenshipUnited States
Alma mater McMaster University, Harvard Medical School
Known forLinking atherosclerosis with blood monocytosis, identifying how sleep interruption accelerates atherosclerosis and neutral drift, demonstrating IL-3 role in protecting against Alzheimer's disease
AwardsOutstanding Investigator Award, NHLBI; Established Investigator Award, American Heart Association
Scientific career
FieldsCardiology, immunology
Institutions Icahn School of Medicine at Mount Sinai, Harvard Medical School, Massachusetts General Hospital
Website Swirski Lab

Filip Swirski is a Polish-Canadian-American scientist and educator serving as the Arthur and Janet C. Ross Professor of Medicine, Cardiology and Professor of Radiology at the Icahn School of Medicine at Mount Sinai and is the Director of the Cardiovascular Research Institute. He is also a member of the Biomedical Engineering and Imaging Institute (BMEII), the Marc and Jennifer Lipschultz Precision Immunology Institute (PrIISM), and The Friedman Brain Institutes (FBI) at Mount Sinai. His research partly focuses on innate and inflammatory mechanisms in cardiovascular disease. He is known for his work in cardioimmunology and notably for linking atherosclerosis with blood monocytosis. [1] [2] [3]

Contents

Education and career

Swirski earned his Bachelor of Arts and Science specializing in biochemistry and a Ph.D. in immunology at McMaster University, Hamilton, Canada. He received an honorary MS from Harvard Medical School in 2020 for accomplishing a full professorship. He was professor at the Center for Systems Biology at Massachusetts General Hospital and at Harvard Medical School. [4] [5]

Research and scientific contributions

Swirski focuses on understanding how leukocytes shape and are shaped by inflammation. His research uses in vivo models of acute and chronic inflammation relevant to cardiovascular, neurodegenerative, infectious, and metabolic diseases. [5] His writings reflect translational and fundamental cardiovascular and neurodegenerative science research, including cell development, mind-marrow communication, and function. [6] [7]

Novel findings

Monocytes and macrophages

  • Swirski described that increased blood monocyte levels, otherwise known as monocytosis, develop in response to hypercholesterolemia [1] and is progressive and proportional to disease severity. [8]
  • Although monocytes develop predominantly in bone marrow, Swirski showed that hypercholesterolemia leads to monocyte production in the spleen [9] in a process called extramedullary hematopoiesis, which further drives atherosclerosis progression.
  • Showed that monocyte-derived macrophages recruited to the atherosclerotic plaque self-renew in the lesion, further accelerating atherosclerosis. [10]
  • Described monocyte recruitment during myocardial infarction [11] [12] and showed a role for a splenic monocyte reservoir as a source of monocytes after myocardial infarction. [13]

Lifestyle and brain-body communication

  • Swirski explores how cardiovascular health is affected by diet, sleep, exercise, and other lifestyle patterns. [14] He showed that sleep limits monocyte production, thereby protecting against atherosclerosis. [15] [16] [17]
  • Showed that sleep fragmentation increases atherogenesis in a mouse model and demonstrated that sleep disruption increases myelopoiesis in the bone marrow, leading to monocytosis and larger atherosclerotic lesions. The results yielded that the marrow contains a pre-neutrophil that regulates monocyte production via hypocretin-dependent CSF-1. Hypocretin, a wake-promoting hormone in the hypothalamus, communicates with bone marrow and regulates leukocyte production. This demonstrates a brain-marrow axis involving a secreted neuropeptide. [17]
  • He demonstrated that sleep interruption increases the rate of hematopoiesis in the bone marrow, which accelerates neutral drift. [18]
  • Showed that IL-3 is a crucial communicator between glial cells (microglia) located throughout the brain and spinal cord, and astrocytes. Using mouse models of Alzheimer’s Disease (AD), data showed that IL-3 protects against AD by programming microglia. [19]
  • Under psychological stress, neurons from different brain regions control the migration of immune cells in the body. [20] Mice under stress were more prone to higher inflammation and death in response to infection with influenza and SARS-CoV-2. [21]
  • Fasting in mice prompts monocytes to re-enter the bone marrow, which increases their lifespan. This process is mediated by the hypothalamic-pituitary-adrenal axis (HPA). Upon re-feeding, distinct monocytes mobilize back to the blood, altering the host's response to infection. The underlying study showed the body can limit energy expenditure when nutrition is scarce. Without it, the body slows down metabolic expenditure, limiting production and preserving—and thus extending—the lifespan of already-made, short-lived monocytes. [22]

Immunometabolic communication

  • Swirski identified an on-demand mechanism by which transient monocyte-derived macrophages dispose of erythrocytes and recycle iron. [23]
  • Identified a population of intraepithelial T cells that are strategically positioned in the gut that modulate systemic dietary metabolism. Without these, mice were metabolically hyperactive, and resisted the development of obesity, hypertension, diabetes, and hypercholesterolemia/atherosclerosis. [24]
  • Showed that cholesterol sensors called Liver X Receptors were important in developing and functioning T cells in the thymus, the lymphoid gland where T cells are produced. [25]

Influence of hematopoietic growth factors

  • Swirski showed the influence of growth factors in disease, where he described a GM-CSF-producing B cell that protects against sepsis and pneumonia. [26] [27]
  • Demonstrated that the growth factor interleukin 3 (IL-3) aggravates sepsis by eliciting a cytokine storm, heightening inflammation leading to death. [28]
  • Identified a critical role for IL-3 in myocarditis [29] and showed that IL-3 regulates microglial function in Alzheimer’s Disease. [19]

Honors and awards

Partial list:

Publications

As of 2024, Swirski is credited with 38,923 citations and has an h-index of 95. [36] His most cited contributions to date are on myocardial infarction, ventricular remodeling, inflammation, stem cell niche, hematopoiesis and hematopoietic stem cells. [37] Between 2018 and 2019, articles reportedly focused mostly on inflammation (43.72%), bone marrow (17.21%) and immune system (17.21%). [38]

Articles

Five most-cited peer-reviewed publications as of 2024 include: [36]

Book chapters

See also

Related Research Articles

<span class="mw-page-title-main">Haematopoiesis</span> Formation of blood cellular components

Haematopoiesis is the formation of blood cellular components. All cellular blood components are derived from haematopoietic stem cells. In a healthy adult human, roughly ten billion to a hundred billion new blood cells are produced per day, in order to maintain steady state levels in the peripheral circulation.

<span class="mw-page-title-main">Spleen</span> Organ recycling old red blood cells and also housing lymphocytes

The spleen is an organ found in almost all vertebrates. Similar in structure to a large lymph node, it acts primarily as a blood filter. The word spleen comes from Ancient Greek σπλήν (splḗn).

<span class="mw-page-title-main">Atherosclerosis</span> Inflammatory disease involving buildup of lesions in the walls of arteries

Atherosclerosis is a pattern of the disease arteriosclerosis, characterized by development of abnormalities called lesions in walls of arteries. This is a chronic inflammatory disease involving many different cell types, and driven by elevated levels of cholesterol in the blood. These lesions may lead to narrowing of the arterial walls due to buildup of atheromatous plaques. At onset there are usually no symptoms, but if they develop, symptoms generally begin around middle age. In severe cases, it can result in coronary artery disease, stroke, peripheral artery disease, or kidney disorders, depending on which body part(s) the affected arteries are located in the body.

<span class="mw-page-title-main">Macrophage</span> Type of white blood cell

Macrophages are a type of white blood cell of the innate immune system that engulf and digest pathogens, such as cancer cells, microbes, cellular debris, and foreign substances, which do not have proteins that are specific to healthy body cells on their surface. This process is called phagocytosis, which acts to defend the host against infection and injury.

Monocytosis is an increase in the number of monocytes circulating in the blood. Monocytes are white blood cells that give rise to macrophages and dendritic cells in the immune system.

<span class="mw-page-title-main">Monocyte</span> Subtype of leukocytes

Monocytes are a type of leukocyte or white blood cell. They are the largest type of leukocyte in blood and can differentiate into macrophages and monocyte-derived dendritic cells. As a part of the vertebrate innate immune system monocytes also influence adaptive immune responses and exert tissue repair functions. There are at least three subclasses of monocytes in human blood based on their phenotypic receptors.

<span class="mw-page-title-main">Endothelial dysfunction</span>

In vascular diseases, endothelial dysfunction is a systemic pathological state of the endothelium. The main cause of endothelial dysfunction is impaired bioavailability of nitric oxide,

The fibrous cap is a layer of fibrous connective tissue, which is thicker and less cellular than the normal intima, found in atherosclerotic plaques. The fibrous cap contains macrophages and smooth muscle cells. The fibrous cap of an atheroma is composed of bundles of muscle cells, macrophages, foam cells, lymphocytes, collagen and elastin.

The cords of Billroth are found in the red pulp of the spleen between the sinusoids, consisting of fibrils and connective tissue cells with a large population of monocytes and macrophages. These cords contain half of the mouse body's monocytes as a reserve so that after tissue injury these monocytes can move in and aid locally sourced monocytes in wound healing.

<span class="mw-page-title-main">Foam cell</span> Fat-laden M2 macrophages seen in atherosclerosis

Foam cells, also called lipid-laden macrophages, are a type of cell that contain cholesterol. These can form a plaque that can lead to atherosclerosis and trigger myocardial infarction and stroke.

<span class="mw-page-title-main">Macrophage colony-stimulating factor</span> Mammalian protein found in humans

The colony stimulating factor 1 (CSF1), also known as macrophage colony-stimulating factor (M-CSF), is a secreted cytokine which causes hematopoietic stem cells to differentiate into macrophages or other related cell types. Eukaryotic cells also produce M-CSF in order to combat intercellular viral infection. It is one of the three experimentally described colony-stimulating factors. M-CSF binds to the colony stimulating factor 1 receptor. It may also be involved in development of the placenta.

<span class="mw-page-title-main">CX3C motif chemokine receptor 1</span> Protein-coding gene in the species Homo sapiens

CX3C motif chemokine receptor 1 (CX3CR1), also known as the fractalkine receptor or G-protein coupled receptor 13 (GPR13), is a transmembrane protein of the G protein-coupled receptor 1 (GPCR1) family and the only known member of the CX3C chemokine receptor subfamily.

<span class="mw-page-title-main">Epithelioid cell</span>

Epithelioid cells are derivatives of activated macrophages resembling epithelial cells.

<span class="mw-page-title-main">Hydroxycarboxylic acid receptor 2</span> Protein-coding gene in the species Homo sapiens

Hydroxycarboxylic acid receptor 2 (HCA2), also known as GPR109A and niacin receptor 1 (NIACR1), is a protein which in humans is encoded (its formation is directed) by the HCAR2 gene and in rodents by the Hcar2 gene. The human HCAR2 gene is located on the long (i.e., "q") arm of chromosome 12 at position 24.31 (notated as 12q24.31). Like the two other hydroxycarboxylic acid receptors, HCA1 and HCA3, HCA2 is a G protein-coupled receptor (GPCR) located on the surface membrane of cells. HCA2 binds and thereby is activated by D-β-hydroxybutyric acid (hereafter termed β-hydroxybutyric acid), butyric acid, and niacin (also known as nicotinic acid). β-Hydroxybutyric and butyric acids are regarded as the endogenous agents that activate HCA2. Under normal conditions, niacin's blood levels are too low to do so: it is given as a drug in high doses in order to reach levels that activate HCA2.

An inflammatory cytokine or proinflammatory cytokine is a type of signaling molecule that is secreted from immune cells like helper T cells (Th) and macrophages, and certain other cell types that promote inflammation. They include interleukin-1 (IL-1), IL-6, IL-12, and IL-18, tumor necrosis factor alpha (TNF-α), interferon gamma (IFNγ), and granulocyte-macrophage colony stimulating factor (GM-CSF) and play an important role in mediating the innate immune response. Inflammatory cytokines are predominantly produced by and involved in the upregulation of inflammatory reactions.

Many human blood cells, such as red blood cells (RBCs), immune cells, and even platelets all originate from the same progenitor cell, the hematopoietic stem cell (HSC). As these cells are short-lived, there needs to be a steady turnover of new blood cells and the maintenance of an HSC pool. This is broadly termed hematopoiesis. This event requires a special environment, termed the hematopoietic stem cell niche, which provides the protection and signals necessary to carry out the differentiation of cells from HSC progenitors. This stem-cell niche relocates from the yolk sac to eventually rest in the bone marrow of mammals. Many pathological states can arise from disturbances in this niche environment, highlighting its importance in maintaining hematopoiesis.

<span class="mw-page-title-main">Mikael Pittet</span> Swiss research scientist

Mikaël Pittet is a Swiss research scientist.

<span class="mw-page-title-main">Gwendalyn J. Randolph</span> American immunologist

Gwendalyn J. Randolph is an American immunologist, the Emil R. Unanue Distinguished Professor in the Department of Immunology and Pathology at Washington University School of Medicine where she is currently co-director of the Immunology Graduate Program. During her postdoctoral work, Randolph characterized monocyte differentiation to dendritic cells and macrophages and made advances in our understanding of dendritic cell trafficking and the fate of monocytes recruited to sites of inflammation. Her lab has contributed to the Immunological Genome Project by characterizing macrophage gene expression. Her work now focuses on the immunological mechanisms driving atherosclerosis and inflammatory bowel disease (IBD) by exploring lymphatic function and lipoprotein trafficking.

Immune system contribution to regeneration of tissues generally involves specific cellular components, transcription of a wide variety of genes, morphogenesis, epithelia renewal and proliferation of damaged cell types. However, current knowledge reveals more and more studies about immune system influence that cannot be omitted. As the immune system exhibits inhibitory or inflammatory functions during regeneration, the therapies are focused on either stopping these processes or control the immune cells setting in a regenerative way, suggesting that interplay between damaged tissue and immune system response must be well-balanced. Recent studies provide evidence that immune components are required not only after body injury but also in homeostasis or senescent cells replacement.

Apoptosis inhibitor of macrophage (AIM) is a protein produced by macrophages that regulates immune responses and inflammation. It plays a crucial role in key intracellular processes like lipid metabolism and apoptosis.

References

  1. 1 2 3 Swirski, Filip K.; Libby, Peter; Aikawa, Elena; Alcaide, Pilar; Luscinskas, F. William; Weissleder, Ralph; Pittet, Mikael J. (2007-01-02). "Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata". The Journal of Clinical Investigation. 117 (1): 195–205. doi:10.1172/JCI29950. ISSN   0021-9738. PMC   1716211 . PMID   17200719.
  2. ↑ Swirski, Filip K.; Nahrendorf, Matthias (2018-09-18). "Cardioimmunology: the immune system in cardiac homeostasis and disease". Nature Reviews Immunology. 18 (12): 733–744. doi:10.1038/s41577-018-0065-8. ISSN   1474-1741. PMID   30228378.
  3. ↑ Swirski, Filip K.; Nahrendorf, Matthias (2013-01-11). "Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure". Science. 339 (6116): 161–166. Bibcode:2013Sci...339..161S. doi:10.1126/science.1230719. ISSN   1095-9203. PMC   3891792 . PMID   23307733.
  4. ↑ "ORCID". orcid.org. Retrieved 2022-08-15.
  5. 1 2 Jansen, Jaclyn M. (2018-05-11). "Filip Swirski: Understanding How Inflammation Both Heals and Hurts the Heart". Circulation Research. 122 (10): 1334–1337. doi:10.1161/CIRCRESAHA.118.313204. ISSN   0009-7330. PMID   29748362.
  6. ↑ "Filip Swirski, PhD, MGH Research Scholar Profile". Massachusetts General Hospital. Retrieved 2022-08-15.
  7. 1 2 3 4 5 6 "Filip Swirski". Cure Alzheimer's Fund. Retrieved 2022-08-15.
  8. ↑ Swirski, Filip K.; Pittet, Mikael J.; Kircher, Moritz F.; Aikawa, Elena; Jaffer, Farouc A.; Libby, Peter; Weissleder, Ralph (2006-07-05). "Monocyte accumulation in mouse atherogenesis is progressive and proportional to extent of disease". Proceedings of the National Academy of Sciences of the United States of America. 103 (27): 10340–10345. Bibcode:2006PNAS..10310340S. doi: 10.1073/pnas.0604260103 . ISSN   0027-8424. PMC   1502459 . PMID   16801531.
  9. ↑ Robbins, Clinton S.; Chudnovskiy, Aleksey; Rauch, Philipp J.; Figueiredo, Jose-Luiz; Iwamoto, Yoshiko; Gorbatov, Rostic; Etzrodt, Martin; Weber, Georg F.; Ueno, Takuya; van Rooijen, Nico; Mulligan-Kehoe, Mary Jo; Libby, Peter; Nahrendorf, Matthias; Pittet, Mikael J.; Weissleder, Ralph (2012-01-17). "Extramedullary hematopoiesis generates Ly-6C(high) monocytes that infiltrate atherosclerotic lesions". Circulation. 125 (2): 364–374. doi:10.1161/CIRCULATIONAHA.111.061986. ISSN   1524-4539. PMC   3263762 . PMID   22144566.
  10. 1 2 Robbins, Clinton S.; Hilgendorf, Ingo; Weber, Georg F.; Theurl, Igor; Iwamoto, Yoshiko; Figueiredo, Jose-Luiz; Gorbatov, Rostic; Sukhova, Galina K.; Gerhardt, Louisa M. S.; Smyth, David; Zavitz, Caleb C. J.; Shikatani, Eric A.; Parsons, Michael; van Rooijen, Nico; Lin, Herbert Y. (2013-09-11). "Local proliferation dominates lesional macrophage accumulation in atherosclerosis". Nature Medicine. 19 (9): 1166–1172. doi:10.1038/nm.3258. ISSN   1546-170X. PMC   3769444 . PMID   23933982.
  11. 1 2 Nahrendorf, Matthias; Swirski, Filip K.; Aikawa, Elena; Stangenberg, Lars; Wurdinger, Thomas; Figueiredo, Jose-Luiz; Libby, Peter; Weissleder, Ralph; Pittet, Mikael J. (2007-11-26). "The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions". The Journal of Experimental Medicine. 204 (12): 3037–3047. doi:10.1084/jem.20070885. ISSN   1540-9538. PMC   2118517 . PMID   18025128.
  12. ↑ Hilgendorf, Ingo; Gerhardt, Louisa M.S.; Tan, Timothy C.; Winter, Carla; Holderried, Tobias A.W.; Chousterman, Benjamin G.; Iwamoto, Yoshiko; Liao, Ronglih; Zirlik, Andreas; Scherer-Crosbie, Marielle; Hedrick, Catherine C.; Libby, Peter; Nahrendorf, Matthias; Weissleder, Ralph; Swirski, Filip K. (2014-05-09). "Ly-6C high Monocytes Depend on Nr4a1 to Balance Both Inflammatory and Reparative Phases in the Infarcted Myocardium". Circulation Research. 114 (10): 1611–1622. doi:10.1161/CIRCRESAHA.114.303204. ISSN   0009-7330. PMC   4017349 . PMID   24625784.
  13. 1 2 Swirski, Filip K.; Nahrendorf, Matthias; Etzrodt, Martin; Wildgruber, Moritz; Cortez-Retamozo, Virna; Panizzi, Peter; Figueiredo, Jose-Luiz; Kohler, Rainer H.; Chudnovskiy, Aleksey; Waterman, Peter; Aikawa, Elena; Mempel, Thorsten R.; Libby, Peter; Weissleder, Ralph; Pittet, Mikael J. (2009-07-31). "Identification of splenic reservoir monocytes and their deployment to inflammatory sites". Science. 325 (5940): 612–616. Bibcode:2009Sci...325..612S. doi:10.1126/science.1175202. ISSN   1095-9203. PMC   2803111 . PMID   19644120.
  14. ↑ Janssen, Henrike; Koekkoek, Laura L.; Swirski, Filip K. (2023-09-26). "Effects of lifestyle factors on leukocytes in cardiovascular health and disease". Nature Reviews. Cardiology. 21 (3): 157–169. doi:10.1038/s41569-023-00931-w. ISSN   1759-5010. PMID   37752350.
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  17. 1 2 McAlpine, Cameron S.; Kiss, Máté G.; Rattik, Sara; He, Shun; Vassalli, Anne; Valet, Colin; Anzai, Atsushi; Chan, Christopher T.; Mindur, John E.; Kahles, Florian; Poller, Wolfram C.; Frodermann, Vanessa; Fenn, Ashley M.; Gregory, Annemijn F.; Halle, Lennard (2019-02-13). "Sleep modulates haematopoiesis and protects against atherosclerosis". Nature. 566 (7744): 383–387. Bibcode:2019Natur.566..383M. doi:10.1038/s41586-019-0948-2. ISSN   1476-4687. PMC   6442744 . PMID   30760925.
  18. ↑ "Sleep exerts lasting effects on hematopoietic stem cell function and diversity". rupress.org. Retrieved 2024-03-18.
  19. 1 2 McAlpine, Cameron S.; Park, Joseph; Griciuc, Ana; Kim, Eunhee; Choi, Se Hoon; Iwamoto, Yoshiko; Kiss, Máté G.; Christie, Kathleen A.; Vinegoni, Claudio; Poller, Wolfram C.; Mindur, John E.; Chan, Christopher T.; He, Shun; Janssen, Henrike; Wong, Lai Ping (2021-07-22). "Astrocytic interleukin-3 programs microglia and limits Alzheimer's disease". Nature. 595 (7869): 701–706. Bibcode:2021Natur.595..701M. doi:10.1038/s41586-021-03734-6. ISSN   1476-4687. PMC   8934148 . PMID   34262178.
  20. ↑ Poller, Wolfram C.; Downey, Jeffrey; Mooslechner, Agnes A.; Khan, Nargis; Li, Long; Chan, Christopher T.; McAlpine, Cameron S.; Xu, Chunliang; Kahles, Florian; He, Shun; Janssen, Henrike; Mindur, John E.; Singh, Sumnima; Kiss, Máté G.; Alonso-Herranz, Laura (2022-05-30). "Brain motor and fear circuits regulate leukocytes during acute stress". Nature. 607 (7919): 578–584. Bibcode:2022Natur.607..578P. doi:10.1038/s41586-022-04890-z. ISSN   1476-4687. PMC   9798885 . PMID   35636458.
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  24. ↑ He, Shun; Kahles, Florian; Rattik, Sara; Nairz, Manfred; McAlpine, Cameron S.; Anzai, Atsushi; Selgrade, Daniel; Fenn, Ashley M.; Chan, Christopher T.; Mindur, John E.; Valet, Colin; Poller, Wolfram C.; Halle, Lennard; Rotllan, Noemi; Iwamoto, Yoshiko (2019). "Gut intraepithelial T cells calibrate metabolism and accelerate cardiovascular disease". Nature. 566 (7742): 115–119. Bibcode:2019Natur.566..115H. doi:10.1038/s41586-018-0849-9. ISSN   1476-4687. PMC   6367023 . PMID   30700910.
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  33. ↑ "Jeffrey M. Hoeg Arteriosclerosis, Thrombosis, and Vascular Biology Award for Basic Science and Clinical Research". professional.heart.org. Retrieved 2024-03-23.
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  35. ↑ "Howard M. Goodman Fellowship Recipients". ecor.mgh.harvard.edu. 2014-03-01. Retrieved 2024-03-23.
  36. 1 2 "Filip K. Swirski". scholar.google.com. Retrieved 2022-08-16.
  37. ↑ "Scopus preview - Swirski, Filip K. - Author details - Scopus". www.scopus.com. Retrieved 2022-08-15.
  38. ↑ "Filip K. Swirski: H-index & Awards - Academic Profile". Research.com. Retrieved 2022-08-15.
  39. ↑ Chousterman, Benjamin G.; Swirski, Filip K.; Weber, Georg F. (2017-07-01). "Cytokine storm and sepsis disease pathogenesis". Seminars in Immunopathology. 39 (5): 517–528. doi:10.1007/s00281-017-0639-8. ISSN   1863-2300. PMID   28555385.
  40. ↑ Swirski, Filip K.; Nahrendorf, Matthias; Libby, Peter (2017-01-12), Gordon, Siamon (ed.), "Mechanisms of Myeloid Cell Modulation of Atherosclerosis", Myeloid Cells in Health and Disease, Washington, DC, USA: ASM Press, pp. 813–824, doi:10.1128/9781555819194.ch47, ISBN   978-1-68367-066-7 , retrieved 2022-08-16
  41. ↑ Pittet, Mikael J.; Nahrendorf, Matthias; Swirski, Filip K. (2014). "The journey from stem cell to macrophage: Macrophage development". Annals of the New York Academy of Sciences. 1319 (1): 1–18. doi:10.1111/nyas.12393. PMC   4074243 . PMID   24673186.
  42. ↑ "Scopus preview - Scopus - Welcome to Scopus". www.scopus.com. Retrieved 2022-08-16.
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