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Biomedical subjects

B K Lee

Publications and source records attributed to B K Lee.

144 records · Page 8Linked to original sources

Micromonospora-produced gentamicin components.

After the chromatographic separation of [methyl-(14)C]gentamicin major (C) components from a large-scale radioactive fermentation (Lee et al., 1974), [methyl-(14)C]gentamicin minor (polar) components (A, B, B(1), X(2), and G-418) were isolated from subsequent chromatography of the remaining antibiotic mixture. When l-[methyl-(14)C]methionine was added at the onset of biosynthesis of the gentamicin components, incorporation of label into the minor components preceded incorporation into the major components. Degradation occurred when [methyl-(14)C]gentamicin major components (C(1), C(2) and C(1)a) were added respectively to the gentamicin-producing culture medium and shaken.

Biodegradation, Environmental↗

Micromonospora-produced sisomicin components.

A sisomicin fermentation carried out in the presence of (methyl-14C)-L-methionine resulted in a crude mixture, composed of methyl-14C-labeled sisomicin as a major component; and two 4''-C-desmethylsisomicin (66-40B and 66-40D) isomer-like components, an unidentified component and a gentamicin A-like antibiotic as minor components. When (methyl-14C)-L-methionine was added in an early stage of the fermentation (24 hours), incorporation of methyl-14C-label into polar components (e.g., gentamicin A-like antibiotic) preceded that into sisomicin. Chromatographic evidence for the bioconversion of (methyl-14C)-gentamicin A to a radioactive sisomicin-like product (possibly (3''-N-methyl-14C)-sisomicin) was seen, when a Micromonospora blocked mutant was incubated in the presence of the former antibiotic.

Anti-Bacterial Agents↗

Mouse mammary tumor virus polypeptide precursors in intracytoplasmic A particles.

Intracytoplasmic A particles were analyzed by immunodiffusion and sodium dodecyl sulfate--polyacrylamide gel electrophoresis (SDS--PAGE) before and after enzymatic cleavage with trypsin. A common antigen in A particles was detected by antisera prepared against purified intracytoplasmic A particles, purified mouse mammary tumor virus (MMTV), and a purified MMTV core polypeptide (p28). Despite this correlation, no SDS--polyacrylamide band migrating at p28 was observed in purified intracytoplasmic A particles. However, after incubation with trypsin, A particles subjected to SDS--PAGE produced only two polypeptide bands. They were observed at p28 and p15-10. Ouchterlony analysis of the trypsin-cleaved A particles revealed no alteration in the antigenicity of the particles. These results suggested that some structural components of intracytoplasmic A particles are polypeptide precursors of MMTV core proteins.

Animals↗

Inheritance of T-associated sex reversal in mice.

We previously identified a primary sex-determining locus, Tas, on mouse Chr 17 that causes ovarian tissue development in C57BL/6J Thp/+ and TOrl/+ individuals if the AKR/JY chromosome is present. We hypothesized that Tas is located within the region of Chr 17 deleted by Thp and TOrl and that C57BL/6J carries a diagnostic Tas allele, based on the observation that ovarian tissue develops in XY mice when Thp is on a C57BL/6J inbred strain background, whereas normal testicular development occurs when Thp is on a C3H/HeSnJ inbred strain background. To test this hypothesis, we mated (C57BL/6J x C3H/HeSnJ)F1 females to C57BL/6J Thp/+ hermaphrodites. As expected, half of the XY Thp/+ offspring developed ovarian and testicular tissue while half developed exclusively testicular tissue. Unexpectedly, the inheritance of selected Chr 17 molecular loci was independent of gonadal development, as half of the male and hermaphroditic offspring inherited C3H/HeSnJ-derived Chr 17 loci and half inherited C57BL/6J-derived Chr 17 loci. We conclude that for ovarian tissue to develop in an XY Thp/+ or XY TOrl/+ individual (1) Tas must be present in a hemizygous state, which is accomplished by heterozygosity for the Thp or TOrl deletions; (2) the AKR/J-derived Y chromosome must be present; and (3) an additional locus involved in primary sex determination must be present in a homozygous C57BL/6J state. This newly identified gene may be one of the previously defined loci, tda-1 or tda-2.

Animals↗

Associations of subtypes of hemoglobin with delta-aminolevulinic acid dehydratase genotype and dimercaptosuccinic acid-chelatable lead levels.

Hemoglobin in erythrocytes may be an important intravascular site of lead binding. We examined associations of hemoglobin subtypes A1 and A2 with delta-aminolevulinic acid dehydratase (ALAD) genotype, a protein that is another important site of erythrocyte lead binding. After oral administration of dimercaptosuccinic acid (DMSA-chelatable lead), we also examined 4-h lead excretion, which provides an estimate of bioavailable lead stores. We randomly selected 57 South Korean current lead battery manufacturing workers from two plants (N = 290 employees) and from two ALAD genotype strata (ALAD1-1 and ALAD1-2). These workers voluntarily administered 5 mg/kg oral DMSA. We frequency-matched subjects with ALAD1-1 (n = 38) to subjects with ALAD1-2 (n = 19) with respect to duration of employment in the lead industry. Blood lead levels ranged from 11 to 53 microg/dl (mean +/- standard deviation, 25.4 +/- 10.2 microg/dl). After administration of oral DMSA, workers excreted a mean lead level of 85.4 (standard deviation, 45.0 microg; range, 16.5-184.1 microg). Hemoglobin A1 and A2 ranged from 3.7% to 9.9% and 1.6% to 5.9%, respectively (mean +/- standard deviation, 6.2 +/- 1.0% and 2.7 +/- 0.8%, respectively). Subjects with ALAD1-1 had elevated mean hemoglobin A1 levels (adjusted p = .05). In addition, higher hemoglobin A1 levels were associated with higher DMSA-chelatable lead levels (adjusted p = .03). This, as well as the results of prior research, suggest that both ALAD and hemoglobin A1 may be important lead-binding sites that influence urinary lead excretion after administration of DMSA.

Administration, Oral↗

Reduced lymphocyte proliferation and interleukin-2 production in anxiety disorders.

OBJECTIVE: The purpose of this study was to examine the effect of anxiety on cell-mediated immunity. METHOD: The subjects consisted of 31 patients with anxiety disorders and 31 normal controls, who were gender-matched. Cell-mediated immune function was measured by the lymphocyte proliferative response to phytohemagglutinin (PHA), Interleukin-2 (IL-2) production, and natural killer cell activity (NKA). The extent of anxiety was assessed by the Hamilton rating scale for anxiety and the anxiety subscale of symptom checklist-90 revised (SCL-90-R). RESULTS: The patients with anxiety disorders were significantly lower than the normal controls in lymphocyte proliferative response to PHA and IL-2 production. However, there was no significant difference in NKA between the two groups. Also, no significant correlation was found between the duration of illness or the degree of anxiety and each immune measure in patients with anxiety disorders. CONCLUSIONS: The results suggest a reduced cell-mediated immune function in patients with anxiety disorders, compared with normal controls. These findings also imply that a variety of immune measures should be assessed at the same time in this kind of psychoneuroimmunology research. This would help elucidate the relationship between anxiety and immune function, which has been unclear in most previous research using a single immune measure.

Adult↗