Search PubMed⌕ Search

Biomedical subjects

J A Kark

Publications and source records attributed to J A Kark.

26 records · Page 2Linked to original sources
PubMed1982

Erythrocytosis in patients on long-term hemodialysis.

Erythrocytosis was seen in two men during maintenance hemodialysis therapy for end-stage renal disease secondary to apparent chronic glomerulonephritis. Nonrenal causes of erythrocytosis such as polycythemia vera, chronic hypoxemia, high-oxygen affinity hemoglobin, and hepatoma were excluded by appropriate clinical studies. A computed tomographic scan of the abdomen showed numerous renal cysts in each patient consistent with acquired cystic disease of end-stage kidneys. Peripheral serum erythropoietin levels were elevated as measured by sensitive radioimmunoassay. The findings suggest that the erythrocytosis is caused by an erythropoietic mechanism related to the diseased kidneys. A review of the literature failed to show previous reports of this clinical association.

Erythropoietin↗
PubMed1982

Modification of intracellular hemoglobin with pyridoxal and pyridoxal 5'-phosphate.

The aldehyde forms of vitamin B6, pyridoxal and pyridoxal 5'-phosphate (PLP) have aroused interest as antisickling agents because of their ability to modify hemoglobin (Hb) and their low toxicity. To study their rate of formation and stability inside red cells, pyridoxal-Hb and PLP-Hb were measured in lysates from treated normal and sickle erythrocytes using isocratic high pressure liquid chromatography on Bio-Rex 70. The validity of this assay was confirmed by isoelectric focussing, fluorescence scans of reduced globin, and treatment of cells with pyridoxal 14C. Optimal conditions were described for treatment of whole blood with pyridoxal and washed erythrocytes with PLP. Although there was competition between 2,3-DPG and PLP, but not pyridoxal, for binding to Hb, depletion of 2,3-DPG prior to treatment was unnecessary. No special requirements were noted for the anticoagulants or buffers used. Sickle erythrocytes formed PLP-Hb more rapidly than normal erythrocytes, but pyridoxal-Hb appeared at the same rate in both types of erythrocytes. During incubation of treated erythrocytes in untreated plasma, the stability of pyridoxal-Hb varied inversely with the hematocrit, but PLP-Hb was stable at all hematocrits tested. The absence of hemolysis during a 4 day incubation of treated normal red cells implies that treatment with pyridoxal or PLP did not severely impair red cell metabolism.

Anemia, Sickle Cell↗
PubMed1980

Optic atrophy in experimental vitamin B12 deficiency in monkeys.

The clinical findings and pathological changes of the visual pathway of vitamin B12 deficient monkeys have been described. The cellular morphology and counts of the peripheral blood and bone marrow remained normal during the study (nine deficient, three controls: one still alive in each group). Visual impairment was noted in all seven of the deficient animals that were evaluated by clinical observations. Ophthalmoscopic examination disclosed optic atrophy in six of the seven deficient monkeys. Degeneration of the visual pathway was demonstrated by pathological examination in eight of the deficient group of nine (one is still alive). Loss of ganglion cells was noted in the maculae of two of three deficient animals with completed studies. In the three control animals there were neither visual disturbances nor ophthalmoscopic changes and in two animals autopsies disclosed no lesions in the visual pathways. The third animal is still alive and well.

Animals↗
PubMed1978

Low erythrocyte pyridoxal-kinase activity in Blacks: Its possible relation to falciparum malaria.

The red-cell glucose-6-phosphate dehydrogenase (G.-6-P.D.) activity and red-cell pyridoxal-kinase (P.L.K.) activity of 27 Nigerian children with severe Plasmodium falciparum parasitaemia were compared with those of 26 healthy Nigerian children and 6 White adults. The mean P.L.K. activity of the malaria patients was similar to that of the Whites but significantly higher than that of the Nigerian controls. Correction for reduced mean red-cell age in patients was made by comparing the P.L.K.: G.-6-P.D. ratio for those subjects with stable G.-6-P.D. phenotypes. The mean P.L.K.:G.-6-P.D. ratio was the same for malaria patients and adult White but significantly higher than that for the Nigerian controls. These results suggest that the relatively high frequency of low red-cell P.L.K. activity among Blacks may have been selected for by falciparum malaria.

Adult↗
PubMed1978

An ultrastructural study of subacute combined degeneration of the spinal cord in vitamin B12-deficient rhesus monkeys.

Prolonged deprivation of vitamin B12 in rhesus monkeys produced changes in the central nervous system that were indistinguishable topographically and histologically from those of human subacute combined degeneration. Ultrastructural studies of early lesions of the spinal cord disclosed a degeneration of myelin characterized by separation of myelin lamellae and formation of intramyelinic vacuoles, leading eventually to complete destruction of myelin sheaths. At a later stage, there was degeneration and loss of axons, and marked gliosis. The theories of pathogenesis of subacute combined degeneration are reviewed in the light of these observations.

Animals↗
PubMed1978

Inhibition of erythrocyte sickling in vitro by pyridoxal.

To test the antisickling activity of pyridoxal, we compared the oxygen affinity and the percent sickling at low PO2 of untreated erythrocytes with values for cells from the same blood sample incubated with pyridoxal, glyceraldehyde, or pyridoxine. Pyridoxal increased oxygen affinity much more than glyceraldehyde. 20 mM pyridoxal and glyceraldehyde had equivalent antisickling activity. At PO2 levels above 20 mm Hg, both agents reduced sickling to less than 2%. In samples examined by electron microscopy, pyridoxal reduced the percent sickled cells and the percent cells that contain hemoglobin S fibers by the same amount (from 74 to 3%). Pyridoxine had no effect on oxygen affinity or sockling. Pyridoxal reacts with intracellular hemoglobin to increase oxygen affinity, which inhibits hemoglobin S polymerization and sickling.

Anemia, Sickle Cell↗
PubMed1976

Neuropathology of experimental vitamin B12 deficiency in monkeys.

We have produced severe vitamin B12 deficiency in rhesus monkeys by feeding them a defined experimental diet under controlled conditions. Five years after institution of the deficient diet, the morphology and counts of peripheral blood and bone marrow are normal. Gross visual impairment appeared in five of the monkeys between 33 and 45 months after the institution of the vitamin B12 deficient diet. Subsequently, in three of the visually impaired animals, a gradually progressive spastic paralysis of their hind limbs developed. Autopsies of six deficient animals showed degeneration of the peripheral visual pathway in all and of white matter in the spinal cord in four. Degeneration of several cranial nerve roots was found in four monkeys and a mild diffuse degeneration of cerebral white matter in four. The lesions in all affected parts of the central nervous system were bilaterally symmetrical and were indistinguishable from those due to B12 deficiency in the human. No abnormalities were found in one B12 supplemented control animal.

Animals↗