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At least 955 records · Page 53Linked to original sources
PubMed1982

The discharge of primary and secondary granules during immune phagocytosis by normal and chronic granulocytic leukaemia polymorphonuclear neutrophils.

The two types of granule in polymorphonuclear neutrophils may have distinct functions. The primary granule enzymes are responsible for killing and digesting ingested micro-organisms while the secondary granule constituents may have regulatory functions outside the cell. This hypothesis is supported by finding that during immune phagocytosis of a yeast, nearly all of the neutrophil's secondary granule vitamin B12-binding protein is lost from the cell and 80% can be accounted for in the medium. Much less of the primary granule enzymes, beta-glucuronidase and acid phosphatase, are lost from the cells and very little can be detected in the medium. Lysozyme is a constituent of both types of granule and its behaviour is intermediate. There is no difference in the release of these granule constituents from chronic granulocytic leukaemia neutrophils compared with normal neutrophils.

Acid Phosphatase↗
PubMed1980

Studies on the effect of folic acid supplement on folate and vitamin B12 status in children.

The effect of folic acid supplement (15 mg folic acid per day) for 5 weeks was studied on a group of 5 children aged 8-12 years who were admitted to hospital. The result was compared to a control group of 5 children who were given a placebo. After supplementation, both serum and red cell folate levels in the experimental group significantly increased, i.e., 15 fold (82.0 ng/ml) and 4 fold (880 ng/ml), respectively. Serum UFBP decreased considerably while TFBP showed no significant alteration which resulted in the elevation of the % saturation to its maximum value. These findings indicated that the supplementary folic acid not only increased both serum and red cell folate levels and saturated nearly all serum UFBP but also elevated the % saturation markedly. There were no definite changes of serum vitamin B12, UBBC, TBBC and TC levels of the experimental group from those of the control group. There were slightly but not significantly increased blood haemoglobin and haematocrit levels in both groups of children. This indicated that folic acid supplement had no definite effect on vitamin B12 and haematological findings in this study.

Carrier Proteins↗
PubMed1982

A new case of deficiency of the R binder for cobalamin, with observations on minor cobalamin-binding proteins in serum and saliva.

A patient presented at the age of 77 yr with a low serum cobalamin level. Subsequent study showed that he had persistently very low R binder (TC I) cobalamin-binding capacity in serum (less than 5 ng/liter versus 213 +/- 171 ng/liter in normal controls), and that almost all of his endogenous serum cobalamin was carried by TC II instead of TC I. His saliva also demonstrated virtually undetectable R binder (binding capacity of 31-38 ng/liter versus 41,690 +/- 23,820 ng/liter for control subjects). Unlike previous cases of R binder deficiency, he seemed to maintain normal serum cobalamin levels while receiving monthly cyanocobalamin injections. This and his normal serum unsaturated binding capacity were due to elevated TC II levels. TC II carried 72%-98% of his endogenous cobalamin, the rest being attached to minor binders. As incidental findings, the patient had a serum component of molecular weight of approximately 70,000 that carried 7%-8% of his endogenous cobalamin and also had small quantities of TC II demonstrable in his saliva. Both these heretofore unappreciated minor peaks were identifiable because of the lack of R binder. The patient's clinical presentation supports the conclusion that R binder deficiency is a benign disorder. Whether his mild hypersegmentation of neutrophils and neuropathy were related to the R binder deficiency or, more likely, arose from coexisting folate deficiency and alcohol abuse, the overall picture contrasts dramatically with the severe clinical sequelae of TC II deficiency.

Aged↗
PubMed1982

Cobalamin contents of the brains in some clinical and pathologic states.

To study the cobalamin content of the brains in various clinico-pathologic states in the elderly, the patho-histology and cobalamin content were examined in autopsy brains with special attention to the temporal and frontal lobes. Consequently, a decrease of cobalamin contents and its binding protein (binder) was found in brains with dementia, severe neuronal loss, myelin degeneration, brain atrophy, ventricular dilatation, and vascular lesions in comparison with those in the controls.

Aged↗
PubMed1980

Commercially-supplied binders for plasma cobalamin (vitamin B12), analysis--"purified" intrinsic factor, "cobinamide"-blocked R-protein binder, and non-purified intrinsic factor-R-protein binder--compared to microbiological assay.

Recent evidence (Kolhouse et al., N. Engl. J. Med. 299: 785-792, 1978) demonstrates that commercial cobalamin (Vitamin B12) radioassay kits contain nonspecific R-protein binding agents that can give falsely normal results in patients who are actually cobalamin deficient. We tested three kits: with "purified" intrinsic factor as the binder, with intrinsic factor and the nonspecific R-protein sites blocked with "cobinamide," and non-purified intrinsic factor-R-protein binder. Results with use of the first two compared well with those by a microbiological assay (Lactobacillus leichmannii) and are in harmony with clinical impressions.

Biological Assay↗
PubMed1981

Enterohepatic circulation of cobalamin in the nonhuman primate.

Biliary excretion of cobalamin was studied in baboons after intravenous injection of 57Co-radiolabeled cyanocobalamin. Radioactivity appeared in bile after 20 min, and up to 4.4% of the dose was recovered in 6 h. It was estimated that 4 microgram cobalamin traverses the baboon biliary tract each day. These studies in the nonhuman primate confirm that there is considerable biliary excretion of cobalamin and that enterohepatic circulation of the vitamin is important for maintenance of normal cobalamin balance.

Animals↗
PubMed1981

Cobalamin binding and uptake in vitro in the human central nervous system.

Little information exists about the CNS transport of cobalamin. Therefore we undertook to characterize the cobalamin-binding proteins of CSF and to examine uptake of the vitamin by homogenates of CNS tissue. CSF from 24 patients had a mean unsaturated cobalamin-binding capacity of 335 +/- 282 pg/ml. The vast majority of this was TC II (302 +/- 276 pg/ml). The remainder consisted of R binder and a binder eluting with the void volume on Sephadex G-200 gel chromatography. CSF TC II was identical to serum TC II immunologically, functionally, in molecular size, and in electrophoretic mobility, but the levels of the two did not correlate. CSF TC II levels may correlate best with CSF protein levels and tended to be higher in abnormal fluids. Unlike serum TC II, CSF TC II tended to adhere to glass surfaces; uncorrected, this may be a source of artifact in studying various fluids. CSF contains little cobalamin, but most of the endogenous cobalamin was carried by TC II instead of by R binder. Thus CSF appears to have a much higher total TC II: R binder ratio than does plasma. TC II enhanced 57CoB12 uptake by neonatal and adult human brain homogenate and by mouse brain homogenate. The primary phase of TC II-57CoB12 uptake in vitro by human brain cortex homogenate occurred mostly within 30 min and was maximal at 22 degrees C. Uptake was specific, but apo-and holo-TC II appeared to have equal affinity for the receptors. Spinal cord homogenate took up less TC II-57CoB12 per wet weight of tissue than did brain homogenate. R binders did not enhance cobalamin uptake; in fact, they inhibited it. We conclude that uptake of cobalamin by CNS tissue is dependent on TC II and that TC II may be even more prominent in cobalamin transport in the CSF than it is in plasma.

Animals↗
PubMed1978

Vitamin B12 and vitamin B12 binding proteins in iron deficiency anaemia.

Vitamin B12 and vitamin B12 binding proteins were determined in 20 patients with iron deficiency anaemia who showed low haemoglobin, haematocrit, serum iron levels and hypochromic microcytic red blood cells. The serum vitamin B12 levels in these patients were significantly lower than that of the normal subjects. Nine of 20 patients had serum vitamin B12 less than 350 pg/ml. There was a significant increase in serum UBBC and TBBC levels in patient group and 9 of 20 patients had higher UBBC values than those of the normal subjects. The absolute values of TCI and TCII increased significantly while TCIII was within the normal limit even though the percentage of UBBC were not different from that of the normal subjects.

Anemia, Hypochromic↗