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The American Journal of Medicine | 1964

A clinical and family study of hereditary proconvertin (factor VII) deficiency

Charles A. Hall; Samuel I. Rapaport; Sara B. Ames; Jean A. DeGroot; Edward S. Allen; Marc A. Ralston

Abstract Severe, hereditary proconvertin (factor VII) deficiency was discovered in a propositus and two of his siblings. An extensive family study (histories and quantitative proconvertin assays) confirmed that the disorder is transmitted by an autosomal intermediate gene which produces severe deficiency in the homozygote and partial deficiency in the heterozygote. The study brought out the unreliability of assessing the mode of transmission of a hereditary bleeding disorder by history alone. The clinical course of the three homozygotes with severe deficiencies was unusual in that bleeding attributable to impaired hemostasis was minimal, if, indeed, present at all. The death of the propositus from pulmonary embolism was most remarkable and clearly establishes that isolated proconvertin deficiency fails to protect against venous thrombotic disease. The implications of this for the etiology of venous thrombosis and for coumarin anticoagulant therapy are discussed.


Journal of Clinical Investigation | 1979

Megaloblastic anemia as a result of an abnormal transcobalamin II (Cardeza).

Farid I. Haurani; Charles A. Hall; Ronald Rubin

A 34-year-old Black woman had severe megaloblastic anemia in childhood. Initially, and over the years, she responded well to massive doses of parenteral cobalamin (Cbl) or oral folic acid. Metabolic reactions involving Cbl and folate enzymes were normal during both relapse and remission except for the absence of thymidylate synthetase in relapse. Amino acid analyses of urine and plasma showed no significant abnormalities. Neither cystathionine, homocystine, formiminoglutamic acid, nor methylmalonic acid was detected in the urine. The serum Cbl level was repeatedly elevated even when the patient was receiving only folic acid therapy. The elevation of the vitamin in the serum was found to be a result of markedly increased levels of transcobalamin II (TC II), as identified by several physicochemical techniques. The patients TC II-Cbl shared immunologic properties with normal TC II but did not facilitate or impede the uptake of Cbl or Cbl bound to normal TC II, respectively, by human cells.


Journal of Clinical Investigation | 1972

Transport function of transcobalamin II

Mary E. Rappazzo; Charles A. Hall

The uptake of free and bound (57)CoB(12), principally to transcobalamin II (TC II), was studied in isolated, perfused liver and kidney of the dog. (1) There was good uptake of canine TC II-B(12) by both organs. (2) In the liver TC II enhanced uptake over that of free B-12. (3) Renal uptake of free B-12 was greater than that of TC II-B(12). Free B-12 was neither lost in the urine nor returned to the circulation. (4) On a per gram tissue basis, renal uptake of TC II-B(12) was greater than hepatic. (5) There was renal release or production of TC II (6) Some TC II but more of a larger molecular size binder came from the liver. (7) Passing free B-12 through the kidney enhanced its uptake by the liver. (8) Passing free B-12 through the liver depressed its uptake by the kidney. (9) It is postulated that the distribution of B-12 can be modified by (a) different responses of tissue to TC II-B(12), (b) synthesis of TC II by an organ, and (c) the effects of B-12 passing through one organ to another.


British Journal of Haematology | 1992

The neurologic aspects of transcobalamin II deficiency

Charles A. Hall

Summary. Thirty‐four symptomatic cases of inherited transcobalamin II (TCII) deficiency were analysed in order to determine the frequency and nature of neurologic manifestations. In no instance was there definite evidence of a neurologic disorder at the time of presentation as a young infant. One child of 21/2 years transiently lost deep tendon reflexes at a time of suboptimal treatment. A syndrome of mental retardation and other neurologic manifestations was observed in three cases, all with the following in common: (1) an extended duration of illness of 2–17 years; (2) inadequate or no treatment with Cbl; (3) treatment with folic or folinic acid. TCII deficiency rarely if ever presents with neurologic manifestations. However, neurologic disorders can be produced subsequently by improper treatment.


British Journal of Haematology | 1969

TRANSPORT OF VITAMIN B12 IN MAN

Charles A. Hall

The plasma transport of vitamin B,, is an important phase of the metabolism of this vital substance. Much has yet to be learnt, but enough is known to permit an outline of current concepts of the transport system. Some of the characteristics of the two participating transport proteins, transcobalamin I and I1 (TC I and 11) are presented in Table I. Two other vitamin-B,, binders (Table I) exist and all four are glycoproteins. A further detailed account of these proteins will be published elsewhere (Hall and Finkler, 1969a).


The American Journal of Clinical Nutrition | 1964

Long-Term Excretion of Co57-Vitamin B12 and Turnover Within the Plasma

Charles A. Hall; Jane G. Hegeman

C LARIFICATION of two aspects of the frequently studied problem of vitamin B12 metabolism in man-excretion and plasma turnover-is needed. Vitamin B12 can be found in urine,’ but recent work2 suggests that bile and feces may be a more important route of excretion. Although microbiologic assay of vitamin B,2 in urine is possible, it can be destroyed or produced in the gut, and assay of vitamin B12 in the feces is meaningless. Moreover, such measurements determine only that the vitamin is sufficiently intact to promote growth of the organism used in the assay, and possibly much of the excreted vitamin B,2 enters the urine or gut in an inactive form. Tracer studies circumvent some of these problems, but in the past neither specific activity of the radioactive vitamin B,2 nor the technic for measurement have been adequate for long-term studies. Consequently, the route and magnitude of vitamin B,2 excretion have remained unknown. Initially, loss of injected vitamin B,2 from the circulation is very rapid even when the vitamin is bound to plasma protein prior to injection.3 A rapid but changing rate of loss persists for one or two months after the vitamin is either ingested or injected.4 However, since the total body turnover of vitamin Bi2 is slow,”6 the question arose as to when this early, rapid plasma loss changed to a rate equivalent to total body turnover. The solution of this problem, too, has been beset by technical difficulties.


Biochimica et Biophysica Acta | 1985

Synthesis of transcobalamin II by cultured human hepatocytes

Charles A. Hall; Pamela D. Green-Colligan; James A. Begley

Cultured HepG2 cells, derived from a human hepatoma synthesized and released unsaturated, immunoreactive transcobalamin II. Synthesis was confirmed by the blocking with inhibitors of protein synthesis and by incorporation of tritiated leucine into transcobalamin II.


Biochemical and Biophysical Research Communications | 1981

Hydrophobic interactions of the apo and holo forms of human cobalamin binding proteins.

James A. Begley; Susan M. Heckman; Charles A. Hall

Abstract The interactions of transcobalamin II (TC II), intrinsic factor (IF) and R-type binding protein of cobalamin (Cb1, vitamin B12) with the hydrophobic chromatography matrix Phenyl-Sepharose CL-4B were investigated. IF-Cb1 and R-Cb1 complexes were not adsorbed on Phenyl-Sepharose at room temperature or at 4°C with buffer containing 50 mM sodium phosphate, pH 7.4 containing 150 mM sodium chloride. The TC II-Cb1 complex adsorbed and could be eluted with buffer containing 50% v v glycerol. IF without Cb1 adsorbed and was eluted with 50% glycerol at room temperature and 4°C. At room temperature, R binder without Cb1 eluted with buffer, but later than the R-Cb1 complex. At 4°C, R binder completely adsorbed to the matrix. TC II-without Cb1 bound to the matrix at 4°C and room temperature and could not be eluted with glycerol. These results suggest that Cb1 binding proteins can be separated and identified based on their hydrophobic properties. In addition, upon binding Cb1, TC II, IF and R-type binders undergo a conformational change such that the protein-Cb1 complex shows reduced hydrophobicity.


Nutrition Research | 1990

The relationship between erythrocyte age and cell content of micronutrients and levels of related enzymes

Richard C. Chu; James A. Begley; Charles A. Hall

Abstract The effects of erythrocyte aging on the contents of certain micronutrients and related enzyme levels were investigated in cells from 11 healthy adult subjects. Young and old red cells were separated by density centrifugation. Erythrocyte zinc, copper, vitamin E, superoxide dismutase and carbonic anhydrase isoenzyme B and C levels, and hemolysis by peroxide were not altered by aging of the red cells. Cobalamin and folate levels declined progressively as erythrocytes aged.


American Journal of Hematology | 1990

Function of vitamin B12 in the central nervous system as revealed by congenital defects

Charles A. Hall

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Alexander E. Finkler

United States Department of Veterans Affairs

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Pamela D. Green-Colligan

United States Department of Veterans Affairs

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Richard C. Chu

United States Department of Veterans Affairs

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Jane G. Hegeman

United States Department of Veterans Affairs

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