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16 Facts About Clement Finch

1.

Clement Alfred Finch was an American physician specializing in hematology whose research on iron metabolism in the bloodstream at the University of Washington led to significant advancements in accurately diagnosing and treating anemia during a time period in which little was known about this aspect of the body.

2.

Clement Finch graduated in 1941 from the University of Rochester Medical School and a year later was married to the first of three wives.

3.

Clement Finch experienced a 60-year tenure at the University of Washington, and has published many scholarly articles pertaining to iron in the bloodstream and is the author of three books entitled: Iron Metabolism, Red Cell Manual and Fulfilling the Dream: A History of the University of Washington School of Medicine 1946 to 1988.

4.

Clement Finch was elected as a Fellow of the National Academy of Sciences in 1974, and elected as a Fellow of the American Academy of Arts and Sciences in 1976.

5.

Clement Finch's studies are importantly recognized as significant in helping the World Health Organization make dietary recommendations for developing countries to aid in preventing anemia and poor development.

6.

Clement Finch was born in Broadalbin, New York, on July 4,1915, into a line of physicians which included both his father and grandfather.

7.

Clement Finch graduated from Union College in 1936 and enrolled at the University of Rochester Medical School in the late 1930s, from which he worked with Nobel Prize-winner George Whipple and published his first paper on hemoglobin regeneration in dogs in the Journal of Experimental Medicine as a second-year student.

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8.

In 1948 after not being able to join the military due to pneumonia, Clement Finch started his career at the University of Washington, which he preferred for the landscape and surrounding environment which offered him access to his favorite hobbies such as mountain climbing.

9.

Clement Finch's research on how iron metabolizes in the blood helped with blood disorders characterized by either an excess or inadequate supply of iron in the blood stream, such as anemia and hemochromatosis, and focused his work on further understanding erythropoiesis, a process by which red blood cells are produced.

10.

Clement Finch was able to discover how iron is incorporated in hemoglobin, and was able to aid doctors in expanding their abilities from simply detecting iron-deficiency anemia to detecting different types of anemia in an increasingly accurate manner.

11.

Clement Finch has published Scientific Journal articles specifically pertaining to Erythropoiesis and anemia such as Erythropoiesisin Pernicious Anemia, Treatment of Iron Deficiency Anemia in the Adult, The Diagnosing of Iron deficiency Anemia, Pathophysiologic Aspects of Sickle Cell Anemia, and Erythroid Marrow Function in Anemic Patients.

12.

Clement Finch researched and published studies on transferrin in the blood such as intact transferrin receptors in human plasma, human deferric transferrin's interaction with reticulocytes, the uptake and release of iron in human transferrin, rat transferrin and gene expression, the iron binding sites of human transferrin, its saturation, and clinical implications.

13.

Clement Finch additionally showed that hemochromatosis which causes the body to absorb too much iron from food consumption could be treated through periodic bleeding.

14.

Clement Finch described how the body tries to maintain adequate stores after significant iron stores are depleted during menstruation and recommended that most women take supplements to prevent them from suffering signs of iron deficiency such as fatigue.

15.

Clement Finch showed how to extend the life of blood stored to transfuse injured soldiers, work inspired by his desire to help serve his country after being unable to serve in the military.

16.

Research in the early 1960s by Clement Finch showed that most women were not getting enough iron in their diet and suggested that supplements be taken by women to avoid problems such as fatigue caused by iron deficiency.