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Biomedical subjects

S Kim

Publications and source records attributed to S Kim.

At least 1,441 records · Page 80Linked to original sources
PubMed1980

Characterization of the viral ribonucleic acids and structural polypeptides of Anopheles A, Bunyamwera, Group C, California, Capim, Guama, Patois, and Simbu bunyaviruses.

Analyses of the viral ribonucleic acids and structural polypeptides of 17-22 of the 119 accepted or proposed members of the Bunyavirus genus of arboviruses (family Bunyaviridae), have shown that from the standpoint of their structural components these viruses are highly comparable to each other. The average molecular weights for the three viral RNA species (L, large, M, medium, S, small) of 17 bunyaviruses were 2.93 X 10(6) (L, range 2.7-3.1 X 10(6)), 2.0 X 10(6) (M, range 1.8-2.3 X 10(6)), and 0.435 X 10(6) (Sm range 0.28-0.50 X 10(6)). The average molecular weights of the three major virion polypeptides (glycoproteins G1 and G2, and nucleocapsid protein, N) of 22 bunyaviruses were 115 X 10(3) (G1, range 108-120 X 10(3)), 37 X 10(3) (G2, range 20-41 X 10(3)) and 22 X 10(3) (N, range 19-25 X 10(3)). These results indicate that the structural components of bunyaviruses are different from those reported for Phlebotomus fever, Uukuniemi, and Crimean-Congo hemorrhagic fever, and other members of the Bunyaviridae family that are not currently assigned to a genus.

Animals↗
PubMed1980

Segmental demyelinating disease: reliability of nerve conduction measurements.

Serial nerve conduction studies were done in 5 patients with Guillain-Barre syndrome, 4 of whom were recovering and 1 who did not recover. In a total of 20 paired studies, the nerve conduction velocity deteriorated in spite of improvement in distal and proximal latencies in 5 cases, and nerve conduction velocity improved in spite of deterioration of latencies in 1 case. This seeming contradiction is explained by the following hypothesis: when the conduction velocity is not homogeneous along the course of the nerve because of a segmental demyelination which takes place in a spotty pattern, both longitudinally and transversely, the fastest fiber from the proximal stimulation point may not necessarily be the fastest from the distal stimulation point. If the fastest fibers from the 2 stimulating points are not the same fibers, the conduction time between these 2 points as calculated by measuring the onset of motor response may be artificially prolonged. This will give a falsely slow conduction velocity. Using this hypothesis in segmental demyelinating disease, latency alone is a better parameter of nerve conductivity than nerve conduction velocity, and serial latencies may correlate better with the clinical course than do serial conduction velocities.

Adult↗
PubMed1979

Idiotype in myeloma terminating in erythroleukemia.

A patient with multiple myeloma, IgG kappa type, developed erythroleukemia with cytogenetic abnormalities three years after diagnosis. The latter disease progressed terminally to acute granulocytic leukemia. Anti-idiotype antibody reagents were prepared by injecting rabbits with the purified monoclonal IgG kappa obtained from the patient's serum and subsequent absorption of the antisera with normal IgG coupled to Sepharose 4B. These reagents reacted specifically with autologous myeloma cells but failed to react with all tested allogeneic cells: these included myeloma cells, reactive lymphocytes and plasma cells, and established lymphoid cell lines. Common idiotypic determinants were found in lymphoid and plasmacytic cells of the patient's marrow, spleen, lymph node, and gastrointestinal tract at autopsy that were not present in the leukemic population. The findings indicate that myeloma and granulocytic leukemia cells have separate clonal origins.

Antibodies, Anti-Idiotypic↗
PubMed1979

Enzymatic methyl esterification of specific glutamyl residue in corticotropin.

Ovine corticotropin (alpha s-ACTH) was enzymatically methylated with purified calf brain protein methylase II (protein O-methyltransferase; S-adenosyl-L-methionine: protein-carboxyl O-methyltransferase, EC 2.1.1.24) and S-adenosyl-L-[methyl-14C]methionine. After incubation for 60 min at 37 degrees C, 30 mol % of the hormone was methylated on the basis of the [14C]methyl incorporation. In order to assess the location of methylation, the modified peptide was digested with pepsin. Analytical results derived from studies on the peptic digest led to the suggestion that the alpha s-ACTH-(6--28) peptide fragment was esterified. Because there is only one available methylation site at Glu-28, these results indicate that Glu-28 of alpha s-ACTH was specifically methyl esterified to yield [Glu(OMe)28]-alpha s-ACTH.

Adrenocorticotropic Hormone↗
PubMed1979

Enzymatic methyl esterification of pituitary polypeptides.

Methyl esterification of pituitary polypeptides by protein methylase II (S-adenosylmethionine:protein-carboxyl O-methyltransferase, EC. 2.1.1.24) has been investigated. Ovine lutropin and adrenocorticotropin (alpha1-39-ACTH) were found to be good methyl acceptor substrates, followed by beta-lipotropin. While the alpha-subunit of lutropin had nearly equal the methyl accepting activity of lutropin, the beta-subunit was devoid of accepting activity. The maximum amount of esterification occurred between 15 and 30 min at 37 degrees C) depending on the methyl acceptor molecule. The rate of the methyl esterification of adrenocorticotropin fragments was also studied. While alpha7-38-ACTH had less than half of alpha1-37-ACTH methyl accepting capacity, alpha1-17-ACTH did not serve as methyl acceptor. However, when a mixture of the two fragments was preincubated, the resulting mixture had full alpha1-39-ACTH activity.

Adrenocorticotropic Hormone↗
PubMed1979

Methyl acceptors for protein methylase II from human-erythrocyte membrane.

Membrane proteins from human erythrocytes were methylated with purified protein methylase II (S-adenosylmethionine:protein-carboxyl O-methyltransferase, EC.2.1.1.24). The methylated proteins were analyzed by dodecyl sulfate/polyacrylamide gel electrophoresis. Monomeric and dimeric glycophorin A (NaIO4/Schiff-2 and NaIO4/Schiff-1 positive bands) and 'band 4.5' were identified as two major classes of methyl-acceptor polypeptides for protein methylase II. In rabbit erythrocyte membrane where glycophorin A is absent, 'band 4.5' was the only major methyl-acceptor protein component. Extracted and purified glycophorin A from human erythrocytes was also found to be an excellent substrate for protein methylase II with a Km of 35.7 microM. The role of erythrocyte membrane protein methylation is discussed with regard to membrane function.

Animals↗
PubMed1979

[Morphological changes of platelets in disturbed cerebral microcirculation--a clinical study using a scanning electron microscope (author's transl)].

Many factors are known that contribute to the pathogenesis of the cerebral microcirculatory disturbances, but, there are few reports investigating the roles of the intravascular components directly. The present study was undertaken to evaluate morphological changes of platelets in patients with cerebral damage, in relation to neurological signs, especially consciousness levels. Morphological changes of platelets were observed in 72 patients with intracranial organic lesions. These lesions included subarachnoid hemorrhages, hypertensive cerebral hemorrhages, cerebral infarctions, brain tumors, chronic subdural hematomas, and acute epidural hematomas. Two blood samples were taken, one from the internal jugular vein (the blood after cerebral perfusion), the other from the cubital vein (systemic blood). After fixative procedures with 1% glutaraldehyde, the differences in the three-dimensional structures of platelets were compared, using a scanning electron microscope. In general, remarkably activated forms of platelets were found in the blood after cerebral perfusion in cases with severely impaired consciousness in the acute stage. But, in cases without severe neurological deficits, such changes of platelet forms were rarely seen. A close relationship was suggested between the degree of neurological damage (especially consciousness levels) and that of platelet activation in the acute stage. In the chronic stage, these changes of platelets in the cerebral blood disappeared. Changes of platelet forms were not found in the systemic blood from the cubital vein, even in the acute stage. It is clinically suggested that morphological changes of platelets play an important role in the pathogenesis of the disturbed cerebral microcirculation. Obstruction of cerebral microvasculature may be caused, mechanically by the activated platelets themselves, and/or chemically by vasoconstrictive substances released from these platelets. Therefore, in the treatment of these intracranial organic lesions, it is concluded that the possible roles of activated platelets should be taken into consideration.

Adolescent↗
PubMed1978

Selective methyl esterification of erythrocyte membrane proteins by protein methylase II.

Methyl esterification of erythrocyte membrane proteins have been demonstrated by incubating the isolated membrane with purified protein methylase II (S-adenosyl-methionine:protein-carboxyl O-methyltransferase, EC 2.1.1.24) and S-adenosyl-L-[methyl-14C]methionine. Methyl esterification of membrane-bound proteins occurred selectively to proteins corresponding to bands 3 (mol wt 97 000), 4 (mol wt 75 000), and 4.5 (mol wt 48 000) [designated according to Steck, T. L. (1974), J. Cell Biol. 62, 1] as identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Mild alkali treated depleted vesicles which lacked bands 1, 2, 5, and 6 had a higher methyl accepting capacity; 500 pmol of methyl groups/mg of depleted vesicle proteins vs. 200 pmol of methyl groups/mg of intact membrane proteins. Alkali-extractable membrane components were not methylated.

Animals↗
PubMed1978

Improvement of in vitro mitogen proliferative responses in non-Hodgkin's lymphoma patients exposed to fractionated total body irradiation.

Patients with non-Hodgkin's lymphomas who failed to respond to chemotherapy were treated with low dose fractionated total body irradiation (TBI). Prior to during and after scheduled therapy, their clinical status was evaluated and peripheral blood studies were performed to enumerate EAC and E rosetting cells and to measure proliferative responses to mitogens. Peripheral blood abnormalities were present prior to TBI using these in vitro assays. Patients who obtained clinical remissions following therapy had restoration of mitogen progressive disease had no change in their ability to proliferate in response to mitogens. Normalization of EAC and E rosetting profiles often occurred regardless of clinical response. These data indicate that low dose fractionated TBI produces clinical and in vitro detectable immunological changes. Furthermore, they show that improvement in mitogen responsiveness correlates best with good clinical responses.

Erythrocytes↗