Mark T. Gladwin

Last updated
Mark T. Gladwin
Mark Gladwin (cropped).jpg
Alma mater University of Miami
Scientific career
FieldsHeart and vascular medicine
Institutions National Institutes of Health
University of Pittsburgh
University of Maryland, Baltimore
Website University of Maryland School of Medicine Office of the Dean

Mark T. Gladwin is an American physician-scientist and academic administrator serving as the dean of the University of Maryland School of Medicine since 2022. He is also the John Z. and Akiko K. Bowers Distinguished Professor and vice president for medical affairs of the University of Maryland, Baltimore. [1] [2]

Contents

Education and career


Gladwin earned a B.S. and M.D. (1991) from the University of Miami. [3] He completed an internal medicine internship and residency in 1994 and served as chief resident in 1995 at the Oregon Health & Science University. [3] He was a critical care fellow at the National Institutes of Health Clinical Center in 1996. [3] In 1998, he completed a fellowship in pulmonary critical care at the University of Washington. [3] He returned to the NIH Clinical Center as a senior research fellow in critical care medicine until 2000, also serving as the Chief of the Pulmonary and Vascular Medicine Branch of the National Heart, Lung, and Blood Institute. [4] [3]

Gladwin joined the University of Pittsburgh School of Medicine in 2008 as a professor and the inaugural director of the University’s Vascular Medicine Institute. [5] In 2015, he was appointed chair of the department of medicine. By the time Gladwin left the university in 2022, the department employed more than 1,000 faculty and had combined clinical and research revenues of almost $600 million. [6] [7]

On August 1, 2022, Gladwin was appointed dean of the University of Maryland School of Medicine, [3] succeeding longtime dean E. Albert Reece. [5] He oversees 46 academic departments with a total annual operating budget of $1.3 billion and more than 7,000 faculty, trainees, students and staff. [8]

Gladwin is co-author of two medical textbooks in the "Made Ridiculously Simple" series from publisher Medmaster Inc. He wrote Clinical Microbiology Made Ridiculously Simple with physicians William Trattler and C. Scott Mahan, and Critical Care and Hospitalist Medicine Made Ridiculously Simple with physician Michael Donahoe. [9] [10]

Research

Gladwin is a vascular, heart, and lung physician-scientist who has specialized in the study of reactive nitrogen molecules, like nitric oxide and nitrite, and how they regulate blood flow via reactions with hemoglobin. Researchers in the late 1970s [11] discovered that nitric oxide (NO) regulated blood flow by triggering vasodilation, the widening of blood vessels. However, scientists considered metabolites of NO, such as nitrite (NO2), to be inert. [12] But in 2003, Gladwin and a team of researchers published a paper in Nature Medicine demonstrating that nitrite could also trigger vasodilation, through conversion to NO, under low oxygen conditions in the body such as during a heart attack or stroke. [13] Subsequent studies by other researchers suggest nitrite administered before or immediately following a heart attack could help preserve heart tissue. [14]

Gladwin has also conducted research on hemoglobin-related proteins, such as neuroglobin, and their possible application as antidotes to carbon monoxide poisoning. [15] [16] [17] He currently serves as Chair of the Board of Directors of Globin Solutions, Inc., a pre-clinical stage biopharmaceutical company researching rapidly acting antidotes for carbon monoxide poisoning, including a modified form of neuroglobin. [18] [19]  In December 2023, Gladwin and his team of researchers published a study in Nature Communications on the discovery of the first-ever link between hemoglobin-like protein and normal cardiac development. [20]

Gladwin's work on blood flow and hemoglobin also led to discoveries related to sickle cell disease. In 2004, Gladwin and his colleagues found that 10% of sickle cell patients also exhibited pulmonary hypertension, high blood pressure in the blood vessels that supply the lung, and determined that hypertension was a major cause of death among sickle cell patients. They described this new human disease syndrome, called hemolysis-associated pulmonary hypertension, in the New England Journal of Medicine. [21]

In June 2020, Gladwin initiated a 22-site Phase II clinical trial in France, Brazil, and the U.S. that is exploring whether blood transfusions that use the patient's own blood can improve outcomes and extend survival in patients with sickle cell disease. [22] [23]

Personal life

Dr. Gladwin was born in Palo Alto, California, and was raised in various locations in the U.S. as well as in remote locations in Ghana, Guatemala, and Mexico. His parents, Hugh Gladwin, Ph.D., a professor of anthropology at Florida International University, and Christina Gladwin, Ph.D., a professor of food and resource economics at the University of Florida, studied in these locations.

He is married to Dr. Tammy Shields, an epidemiologist and scientific investigator who has published research on cancer epidemiology and prevention. They have three children. Dr. Gladwin is an avid soccer and fitness enthusiast, currently playing competitive soccer in an over-40 outdoor premier league.

Related Research Articles

<span class="mw-page-title-main">Hemoglobin</span> Metalloprotein that binds with oxygen

Hemoglobin is a protein containing iron that facilitates the transport of oxygen in red blood cells. Almost all vertebrates contain hemoglobin, with the exception of the fish family Channichthyidae. Hemoglobin in the blood carries oxygen from the respiratory organs to the other tissues of the body, where it releases the oxygen to enable aerobic respiration which powers the animal's metabolism. A healthy human has 12 to 20 grams of hemoglobin in every 100 mL of blood. Hemoglobin is a metalloprotein, a chromoprotein, and globulin.

<span class="mw-page-title-main">Hemolysis</span> Rupturing of red blood cells and release of their contents

Hemolysis or haemolysis, also known by several other names, is the rupturing (lysis) of red blood cells (erythrocytes) and the release of their contents (cytoplasm) into surrounding fluid. Hemolysis may occur in vivo or in vitro.

<span class="mw-page-title-main">Hemoglobinopathy</span> Any of various genetic disorders of blood

Hemoglobinopathy is the medical term for a group of inherited blood disorders involving the hemoglobin, the protein of red blood cells. They are single-gene disorders and, in most cases, they are inherited as autosomal co-dominant traits.

<span class="mw-page-title-main">Myoglobin</span> Iron and oxygen-binding protein

Myoglobin is an iron- and oxygen-binding protein found in the cardiac and skeletal muscle tissue of vertebrates in general and in almost all mammals. Myoglobin is distantly related to hemoglobin. Compared to hemoglobin, myoglobin has a higher affinity for oxygen and does not have cooperative binding with oxygen like hemoglobin does. Myoglobin consists of non-polar amino acids at the core of the globulin, where the heme group is non-covalently bounded with the surrounding polypeptide of myoglobin. In humans, myoglobin is found in the bloodstream only after muscle injury.

<span class="mw-page-title-main">Thalassemia</span> Family of inherited blood disorders

Thalassemias are inherited blood disorders that result in abnormal hemoglobin. Symptoms depend on the type of thalassemia and can vary from none to severe. Often there is mild to severe anemia as thalassemia can affect the production of red blood cells and also affect how long the red blood cells live. Symptoms of anemia include feeling tired and having pale skin. Other symptoms of thalassemia include bone problems, an enlarged spleen, yellowish skin, pulmonary hypertension, and dark urine. Slow growth may occur in children. Symptoms and presentations of thalassemia can change over time. Older terms included Cooley's anemia and Mediterranean anemia for beta-thalassemia. These have been superseded by the terms Transfusion-Dependent Thalassemia (TDT) and non-Transfusion-Dependent Thalassemia (NTDT). Patients with TDT require regular transfusions, typically every two to five weeks. TDTs include Beta-thalassemia major, nondeletional HbH disease, survived Hb Bart's disease, and severe HbE/beta-thalassemia.

<span class="mw-page-title-main">Paroxysmal nocturnal hemoglobinuria</span> Medical condition

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired, life-threatening disease of the blood characterized by destruction of red blood cells by the complement system, a part of the body's innate immune system. This destructive process occurs due to deficiency of the red blood cell surface protein DAF, which normally inhibits such immune reactions. Since the complement cascade attacks the red blood cells within the blood vessels of the circulatory system, the red blood cell destruction (hemolysis) is considered an intravascular hemolytic anemia. There is ongoing research into other key features of the disease, such as the high incidence of venous blood clot formation. Research suggests that PNH thrombosis is caused by both the absence of GPI-anchored complement regulatory proteins on PNH platelets and the excessive consumption of nitric oxide (NO).

<span class="mw-page-title-main">Polycythemia</span> Laboratory diagnosis of high hemoglobin content in blood

Polycythemia is a laboratory finding in which the hematocrit and/or hemoglobin concentration are increased in the blood. Polycythemia is sometimes called erythrocytosis, and there is significant overlap in the two findings, but the terms are not the same: polycythemia describes any increase in hematocrit and/or hemoglobin, while erythrocytosis describes an increase specifically in the number of red blood cells in the blood.

<span class="mw-page-title-main">Hemolytic anemia</span> Reduced oxygen-carrying ability of the blood due to breakdown of red blood cells

Hemolytic anemia or haemolytic anaemia is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels or elsewhere in the human body (extravascular). This most commonly occurs within the spleen, but also can occur in the reticuloendothelial system or mechanically. Hemolytic anemia accounts for 5% of all existing anemias. It has numerous possible consequences, ranging from general symptoms to life-threatening systemic effects. The general classification of hemolytic anemia is either intrinsic or extrinsic. Treatment depends on the type and cause of the hemolytic anemia.

<span class="mw-page-title-main">Pulmonary hypertension</span> Increased blood pressure in lung arteries

Pulmonary hypertension is a condition of increased blood pressure in the arteries of the lungs. Symptoms include shortness of breath, fainting, tiredness, chest pain, swelling of the legs, and a fast heartbeat. The condition may make it difficult to exercise. Onset is typically gradual. According to the definition at the 6th World Symposium of Pulmonary Hypertension in 2018, a patient is deemed to have pulmonary hypertension if the pulmonary mean arterial pressure is greater than 20mmHg at rest, revised down from a purely arbitrary 25mmHg, and pulmonary vascular resistance (PVR) greater than 3 Wood units.

<span class="mw-page-title-main">Hydroxycarbamide</span> Medication

Hydroxycarbamide, also known as hydroxyurea, is a medication used in sickle-cell disease, essential thrombocythemia, chronic myelogenous leukemia, polycythemia vera, and cervical cancer. In sickle-cell disease it increases fetal hemoglobin and decreases the number of attacks. It is taken by mouth.

Hemoglobin A2 (HbA2) is a normal variant of hemoglobin A that consists of two alpha and two delta chains (α2δ2) and is found at low levels in normal human blood. Hemoglobin A2 may be increased in beta thalassemia or in people who are heterozygous for the beta thalassemia gene.

Gasotransmitters is a class of neurotransmitters. The molecules are distinguished from other bioactive endogenous gaseous signaling molecules based on a need to meet distinct characterization criteria. Currently, only nitric oxide, carbon monoxide, and hydrogen sulfide are accepted as gasotransmitters. According to in vitro models, gasotransmitters, like other gaseous signaling molecules, may bind to gasoreceptors and trigger signaling in the cells.

<span class="mw-page-title-main">Beta thalassemia</span> Blood disorder

Beta thalassemias are a group of inherited blood disorders. They are forms of thalassemia caused by reduced or absent synthesis of the beta chains of hemoglobin that result in variable outcomes ranging from severe anemia to clinically asymptomatic individuals. Global annual incidence is estimated at one in 100,000. Beta thalassemias occur due to malfunctions in the hemoglobin subunit beta or HBB. The severity of the disease depends on the nature of the mutation.

<span class="mw-page-title-main">Hemoglobin subunit alpha</span> Human hemoglobin protein

Hemoglobin subunit alpha, Hemoglobin, alpha 1, is a hemoglobin protein that in humans is encoded by the HBA1 gene.

Biological functions of nitric oxide are roles that nitric oxide plays within biology.

<span class="mw-page-title-main">Sickle cell nephropathy</span> Medical condition

Sickle cell nephropathy is a type of kidney disease associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla, coupled with the slow blood flow in the vasa recta, favors sickling of red blood cells, with resultant local infarction. Functional tubule defects in patients with sickle cell disease are likely the result of partial ischemic injury to the renal tubules.

<span class="mw-page-title-main">Riociguat</span> Chemical compound

Riociguat, sold under the brand name Adempas, is a medication by Bayer that is a stimulator of soluble guanylate cyclase (sGC). It is used to treat two forms of pulmonary hypertension (PH): chronic thromboembolic pulmonary hypertension (CTEPH) and pulmonary arterial hypertension (PAH). Riociguat constitutes the first drug of the class of sGC stimulators. The drug has a half-life of 12 hours and will decrease dyspnea associated with pulmonary arterial hypertension.

Medical gas therapy is a treatment involving the administration of various gases. It has been used in medicine since the use of oxygen therapy. Most of these gases are drugs, including oxygen. Many other gases, collectively known as factitious airs, were explored for medicinal value in the late eighteenth century. In addition to oxygen, medical gases include nitric oxide (NO), and helium-O2 mixtures (Heliox). Careful considerations and close monitoring needed when medical gases are in use. For the purpose of this article only gas mixtures are described.

Gaseous signaling molecules are gaseous molecules that are either synthesized internally (endogenously) in the organism, tissue or cell or are received by the organism, tissue or cell from outside and that are used to transmit chemical signals which induce certain physiological or biochemical changes in the organism, tissue or cell. The term is applied to, for example, oxygen, carbon dioxide, sulfur dioxide, nitrous oxide, hydrogen cyanide, ammonia, methane, hydrogen, ethylene, etc.

<span class="mw-page-title-main">Jonathan Stamler</span> English-American physician and biochemist

Jonathan Solomon Stamler is an English-born American physician and scientist. He is known for his discovery of protein S-nitrosylation, the addition of a nitric oxide (NO) group to cysteine residues in proteins, as a ubiquitous cellular signal to regulate enzymatic activity and other key protein functions in bacteria, plants and animals, and particularly in transporting NO on cysteines in hemoglobin as the third gas in the respiratory cycle.

References

  1. ↑ Baltimore, University of Maryland. "Mark T. Gladwin, MD". University of Maryland, Baltimore. Retrieved 2024-01-12.
  2. ↑ Staff, Daily Record (2022-04-20). "Next dean, VP of medical affairs for UM School of Medicine selected". Maryland Daily Record. Retrieved 2024-01-12.
  3. 1 2 3 4 5 6 "Gladwin, Mark | University of Maryland School of Medicine". www.medschool.umaryland.edu. Retrieved 2023-12-26.
  4. ↑ "Vascular Medicine Branch, Division of Intramural Research, NHLBI, NIH". dir.nhlbi.nih.gov. Retrieved 2024-01-12.
  5. 1 2 Cohn, Meredith (2022-04-20). "University of Maryland School of Medicine names Pittsburgh medical professor as new dean". Baltimore Sun. Retrieved 2023-12-26.
  6. ↑ "Gladwin Named Department of Medicine Chair at Pitt School of Medicine". UPMC | Life Changing Medicine. Retrieved 2024-02-15.
  7. ↑ "Noted physician-scientist, Anne Marie Lennon, MBBCh, PhD, named Chair of Medicine". Department of Medicine. 2023-11-20. Retrieved 2024-08-14.
  8. ↑ Staff, Daily Record (2022-10-18). "FEATURED MOVER | Dr. Mark Gladwin, UMD School of Medicine". Maryland Daily Record. Retrieved 2024-02-15.
  9. ↑ "Clinical Microbiology Made Ridiculously Simple". MedMaster. Retrieved 2024-03-15.
  10. ↑ "Critical Care and Hospitalist Medicine Made Ridiculously Simple". MedMaster. Retrieved 2024-03-15.
  11. ↑ Ignarro, Louis J. (2000), Kadowitz, Philip J.; McNamara, Dennis B. (eds.), "Nitric Oxide in the Regulation of Blood Flow: A Historical Overview", Nitric Oxide and the Regulation of the Peripheral Circulation, Nitric Oxide in Biology and Medicine, Boston, MA: Birkhäuser, pp. 1–12, doi:10.1007/978-1-4612-1326-0_1, ISBN   978-1-4612-1326-0 , retrieved 2024-01-12
  12. ↑ Wink, David A. (December 2003). "Ion implicated in blood pact". Nature Medicine. 9 (12): 1460–1461. doi:10.1038/nm1203-1460. ISSN   1546-170X. PMID   14647519. S2CID   29815156.
  13. ↑ Cosby, Kenyatta; Partovi, Kristine S.; Crawford, Jack H.; Patel, Rakesh P.; Reiter, Christopher D.; Martyr, Sabrina; Yang, Benjamin K.; Waclawiw, Myron A.; Zalos, Gloria; Xu, Xiuli; Huang, Kris T.; Shields, Howard; Kim-Shapiro, Daniel B.; Schechter, Alan N.; Cannon, Richard O. (December 2003). "Nitrite reduction to nitric oxide by deoxyhemoglobin vasodilates the human circulation". Nature Medicine. 9 (12): 1498–1505. doi:10.1038/nm954. ISSN   1546-170X. PMID   14595407. S2CID   6370323.
  14. ↑ Griffiths, Kayleigh; Lee, Jordan J.; Frenneaux, Michael P.; Feelisch, Martin; Madhani, Melanie (2021-07-01). "Nitrite and myocardial ischaemia reperfusion injury. Where are we now?". Pharmacology & Therapeutics. 223: 107819. doi:10.1016/j.pharmthera.2021.107819. ISSN   0163-7258. PMID   33600852. S2CID   231963701.
  15. ↑ Azarov, Ivan; Wang, Ling; Rose, Jason J.; Xu, Qinzi; Huang, Xueyin N.; Belanger, Andrea; Wang, Ying; Guo, Lanping; Liu, Chen; Ucer, Kamil B.; McTiernan, Charles F.; O’Donnell, Christopher P.; Shiva, Sruti; Tejero, Jesús; Kim-Shapiro, Daniel B. (2016-12-07). "Five-coordinate H64Q neuroglobin as a ligand-trap antidote for carbon monoxide poisoning". Science Translational Medicine. 8 (368): 368ra173. doi:10.1126/scitranslmed.aah6571. ISSN   1946-6234. PMC   5206801 . PMID   27928027.
  16. ↑ Rose, Jason J.; Bocian, Kaitlin A.; Xu, Qinzi; Wang, Ling; DeMartino, Anthony W.; Chen, Xiukai; Corey, Catherine G.; Guimarães, Danielle A.; Azarov, Ivan; Huang, Xueyin N.; Tong, Qin; Guo, Lanping; Nouraie, Mehdi; McTiernan, Charles F.; O'Donnell, Christopher P. (2020-05-08). "A neuroglobin-based high-affinity ligand trap reverses carbon monoxide-induced mitochondrial poisoning". The Journal of Biological Chemistry. 295 (19): 6357–6371. doi: 10.1074/jbc.RA119.010593 . ISSN   1083-351X. PMC   7212636 . PMID   32205448.
  17. ↑ Rose, Jason J.; Wang, Ling; Xu, Qinzi; McTiernan, Charles F.; Shiva, Sruti; Tejero, Jesus; Gladwin, Mark T. (2017-03-01). "Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy". American Journal of Respiratory and Critical Care Medicine. 195 (5): 596–606. doi:10.1164/rccm.201606-1275CI. ISSN   1535-4970. PMC   5363978 . PMID   27753502.
  18. ↑ "Our Team | Globin Solutions, Inc" . Retrieved 2024-01-12.
  19. ↑ "Technology | Globin Solutions, Inc" . Retrieved 2024-01-12.
  20. ↑ Rochon, Elizabeth R.; Xue, Jianmin; Mohammed, Manush Sayd; Smith, Caroline; Hay-Schmidt, Anders; DeMartino, Anthony W.; Clark, Adam; Xu, Qinzi; Lo, Cecilia W.; Tsang, Michael; Tejero, Jesus; Gladwin, Mark T.; Corti, Paola (14 December 2023). "Cytoglobin regulates NO-dependent cilia motility and organ laterality during development". Nature Communications. 14 (8333): 8333. Bibcode:2023NatCo..14.8333R. doi:10.1038/s41467-023-43544-0. PMC   10721929 . PMID   38097556.
  21. ↑ Gladwin, Mark T.; Sachdev, Vandana; Jison, Maria L.; Shizukuda, Yukitaka; Plehn, Jonathan F.; Minter, Karin; Brown, Bernice; Coles, Wynona A.; Nichols, James S.; Ernst, Inez; Hunter, Lori A.; Blackwelder, William C.; Schechter, Alan N.; Rodgers, Griffin P.; Castro, Oswaldo (2004-02-26). "Pulmonary Hypertension as a Risk Factor for Death in Patients with Sickle Cell Disease". New England Journal of Medicine. 350 (9): 886–895. doi:10.1056/NEJMoa035477. ISSN   0028-4793. PMID   14985486.
  22. ↑ Gladwin, Mark (4 December 2023). "Sickle Cell Disease and CardiovAscular Risk - Red Cell Exchange Trial (SCD-CARRE) (SCD-CARRE)". ClinicalTrials.gov. Retrieved 3 January 2024.
  23. ↑ Cohn, Sarah True,Meredith (2024-01-12). "Maryland doctors are loosening sickle cell's painful grip on patients worldwide". The Baltimore Banner. Retrieved 2024-01-12.{{cite web}}: CS1 maint: multiple names: authors list (link)
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