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Biomedical subjects

K Richardson

Publications and source records attributed to K Richardson.

At least 55 records · Page 3Linked to original sources
PubMed1992

Sister chromatid exchanges in peripheral lymphocytes in newborns treated with phototherapy and vitamin E.

A study was undertaken to determine whether blue fluorescent light might affect the sister chromatid exchange (SCE) frequency of peripheral lymphocytes in icteric newborns undergoing continuous phototherapy treatment (72 h). Also, the potential preventive effect of vitamin E on SCE frequency was studied in a subgroup of 11 preterm and 9 fullterm newborns after daily administration of vitamin E (46.44 mumol/kg/d, im). The results revealed that only the preterm icteric newborns showed an increase in mean SCE frequency of peripheral lymphocytes after phototherapy (9%, p = 0.02), but in no case did the highest SCEs/cell ratio exceed the normal values. No correlation was found between the average SCE rate and birth weight, gestational age or bilirubin levels. Also, no difference in SCEs was observed between newborns treated or untreated with vitamin E.

Evaluation Studies as Topic↗
PubMed1991

Analysis of the potential promoter sequences of African cassava mosaic virus by transient expression of the beta-glucuronidase gene.

DNA fragments from promoter regions of the geminivirus, African cassava mosaic virus, were cloned into pG1, a vector based on pUC18, producing transcriptional fusions with the beta-glucuronidase (GUS) gene and nopaline synthase termination sequence. The activity of each promoter construct was assessed by analysing the transient expression of GUS in Nicotiana clevelandii protoplasts. The results demonstrated that constructs containing the common region of DNA A showed much stronger promoter activity in the complementary sense than in the viral sense. These results were supported by the analysis of promoter activity in transgenic N. benthamiana plants. In comparison, in protoplasts a region upstream of the AC2 open reading frame was shown to have moderate promoter activity. Unlike DNA A, the complementary sense DNA B promoter constructs had weak activity; the viral sense DNA B promoter constructs appeared to be regulated by host factors. The implications of these results for the regulation of early and late genes are discussed.

Base Sequence↗
PubMed1991

Mutagenesis of the AC3 open reading frame of African cassava mosaic virus DNA A reduces DNA B replication and ameliorates disease symptoms.

Small insertions were made independently at each of four unique restriction sites on African cassava mosaic virus (ACMV) DNA A to disrupt the three overlapping complementary-sense open reading frames (ORFs) herein designated AC1, AC2 and AC3. The DNA A mutants were assayed for their infectivity by agroinoculation of monomeric constructs to Nicotiana benthamiana plants containing chromosomal insertions of ACMV DNA B. Disruption of the AC3 ORF alone resulted in a delay and amelioration of disease symptoms which correlated with reduced replication of DNA B. Normal replication of DNA A still carrying the AC3 ORF mutation was found in extracts from these plants. No ACMV DNA or symptoms were observed in corresponding inoculations with either the simultaneous disruption of the overlapping AC2 and AC3 ORFs or disruption of the AC1 ORF. Complementation by the inoculation of different mutant pairs produced a delay in disease symptoms followed by repair of mutated sites. A DNA A construct with the virus-sense AV1 (coat protein) ORF deleted was infectious producing typical ACMV disease symptoms. A similar construct with a larger deletion encompassing the complementary-sense AC3 ORF produced symptomless infections. The DNA recovered from plants revealed DNA A of normal size where the position of the deleted ORF was replaced with cloning vector DNA. Significantly reduced DNA B replication was observed for the AC3 deletion construct.

Blotting, Southern↗
PubMed1991

Urinary IL-6: a marker for mesangial proliferative glomerulonephritis?

A prospective study of plasma and urinary interleukin-6 (IL-6) levels was performed in 54 patients undergoing renal biopsy to determine whether detectable urinary IL-6 was a reliable marker for mesangial proliferation. Interleukin-6 was found in both the urine and plasma of seven patients, the urine alone of 15 patients, and the plasma alone of two patients. Interleukin-6 was not detected in the urine or the plasma of the remaining 30 patients, the urine of 10 healthy controls or the urine of 10 patients with rheumatoid arthritis with raised plasma IL-6. Interleukin-6 was found in the urine of only one out of an additional seven patients with lupus nephritis. Urinary IL-6 was associated with a variety of renal abnormalities and was not restricted to those with mesangial hypercellularity. Furthermore, many patients with mesangial hypercellularity did not have detectable urinary IL-6. There was no correlation between urinary IL-6 and plasma IL-6, urinary albumin excretion or urinary creatinine. These results suggest that IL-6 detected in the urine is a marker of renal IL-6 production, but not specifically of mesangial hypercellularity. The patients with IL-6 in the urine had a mean serum creatinine significantly higher than those without IL-6. It is not possible to distinguish at present whether IL-6 contributes to renal dysfunction or whether it reflects renal damage.

Adolescent↗
PubMed1991

Autoradiographic localization of angiotensin-converting enzyme and angiotensin II binding sites in early atheroma-like lesions in rabbit arteries.

1. Early atheroma-like lesions in rabbits are associated with increased sensitivity to serotonin. The localization and distribution of angiotensin-converting enzyme (ACE) and angiotensin II (AII) binding sites has been studied in these developing lesions by quantitative in vitro autoradiography. 2. In sham-operated control vessels, ACE was localized predominantly to intimal and adventitial sites, whereas in lesioned arteries the level of ACE detected in these regions was significantly reduced. 3. In control vessels AII receptor binding was distributed largely in the outer media, whereas in lesioned vessels AII receptor binding was dispersed throughout the media with the highest levels of binding in the outer media. 4. There was a significant amount of binding associated with ACE and with AII receptors in the extra-adventitial inflammatory tissue of lesioned arteries. 5. Apparent loss of ACE from intimal and adventitial sites may be a consequence of tissue remodelling and cellular proliferation, while the appearance of ACE in abnormal sites could play a role in AII production by the vessel wall. The role of ACE and AII in the developing atheroma-like lesions needs to be investigated further.

Angiotensin II↗
PubMed1991

Roles of motility and flagellar structure in pathogenicity of Vibrio cholerae: analysis of motility mutants in three animal models.

Wild-type Vibrio cholerae of both El Tor and classical biotypes (strains N16961 and 395, respectively) and nonmotile mutant derivatives with and without flagellar structures were characterized in three different animal models: (i) the rabbit ileal loop, (ii) the removable intestinal tie adult rabbit diarrhea (RITARD) model, and (iii) the suckling mouse model. Both the wild-type strains and nonmotile mutants were toxinogenic in the rabbit ileal loop and the suckling mouse models. However, all of the nonmotile mutants produced significantly less fluid accumulation than did the wild-type parental strains. The two nonmotile mutants of strain N16961 did not adhere to rabbit ileal mucosa, but both nonmotile mutants derived from strain 395 exhibited adherence. In the RITARD model, the motile El Tor strains were more virulent than both the flagellate and aflagellate nonmotile mutants (all infected rabbits died within 18 h), while the nonmotile mutants, when fatalities occurred, required 78 to 105 h to produce a fatal outcome. Likewise, the motile classical parent 395 produced a fatal outcome within ca. 25 h, while nonmotile mutants required 69 to 96 h. The nonmotile flagellate strain KR31 was not significantly more virulent than the nonmotile aflagellate strain KR26. Of the two classical nonmotile mutants, KR1, which produces a coreless sheathlike structure, was clearly more virulent (5 of 10 rabbits died within 96 h), while KR3 (nonmotile, aflagellate) did not produce fatalities in any of the 10 rabbits tested. Similarly, no significant difference in diarrheagenicity or colonizing ability was detected between the two nonmotile mutants derived from the El Tor strain, but the classical nonmotile mutant with the coreless sheath caused significantly greater diarrhea and colonized for a longer time than did the isogenic nonmotile aflagellate strain, KR3. No significant differences between the nonmotile mutants were detected in competition studies done with suckling mice. Analysis of the wild-type and mutant strains in these three animal models clearly demonstrated a role for motility in V. cholerae pathogenicity, while analysis of only the nonmotile mutants derived from the classical parent suggested a role for flagellar structures.

Animals↗
PubMed1990

The discovery and profile of fluconazole.

Fluconazole is a bis-triazolyl, difluorophenyl propyl alcohol derivative being developed for treatment of life-threatening and superficial fungal infections. The presence of a triazole and a difluorophenyl produces potent antifungal activity but replacement of the usual imidazole group by triazole leads to improved selectivity. Fluconazole is much less lipophilic than other azole antifungals and this leads to excellent penetration throughout the body, low protein-binding and water-solubility. Fluconazole is stable to metabolism resulting in excellent oral absorption and a long half-life. These properties have resulted in excellent efficacy and safety in a wide range of clinical situations.

Biological Availability↗
PubMed1990

Transposon-induced non-motile mutants of Vibrio cholerae.

Non-motile mutants of Vibrio cholerae were isolated after transposon insertion mutagenesis with either Tn5 on a plasmid or Tn10ptac mini-kan in bacteriophage lambda. The physical location and number of transposon insertions was determined. Eighteen Tn5 insertion mutants and 11 Tn10ptac mini-kan insertion mutants had single unique insertion sites. The 18 Tn5 insertions were contained within six different EcoRI fragments and the 11 Tn10ptac mini-kan insertions were contained within eight different fragments of V. cholerae chromosomal DNA. These data suggest that multiple genes are involved in motility. Immunoblot analysis of non-motile mutants with antibody to wild-type flagellar core protein indicated that two of the non-motile mutants made flagellar core protein. Three additional mutants reacted weakly with the antibodies. However, these mutants with immunopositive reactions did not produce any structures which resembled flagella by transmission electron microscopy. In addition, none of the other non-motile mutants produced wild-type flagella. However, five mutants which did not react in the immunoblot produced a structure which resembled a flagellar sheath without the internal flagellar core. In addition to having no filamentous core, the sheaths often extended from the sides of the bacteria, rather than from the poles where the flagellum is normally located. The data suggest that sheath formation is independent of flagellar filament formation, but that proper positioning of the sheath may require the flagellar filament.

DNA Transposable Elements↗
PubMed1990

High-frequency spontaneous mutation of classical Vibrio cholerae to a nonmotile phenotype.

The species Vibrio cholerae contains within it two biotypes, classical and El Tor, both of which are motile. Phenotypic expression of motility was unaffected by type of growth medium, salt concentration, pH, or temperature of incubation. However, seven strains of classical V. cholerae produced spontaneous nonmotile mutants at an unusually high frequency (ca. 10(-4)), while no mutants were detected for all three El Tor strains examined. No revertants of these nonmotile mutants were detected. Four independent mutants of classical strain 395 were isolated to characterize this phenomenon. By transmission electron microscopy, one of the nonmotile mutants was found to be flagellated, while the other three were found to be aflagellate. Chromosomal DNA from the mutants and parental wild-type strain 395 was examined by Southern blot analysis with, as probes, V. cholerae mutagenic prophages VcA-1 and VcA-2 and six cloned motility gene regions isolated from transposon insertion motility mutants of strains 395 and N16961 (El Tor, Inaba). The parental wild-type strain and all of the mutants exhibited the same pattern of bands when probed with VcA-1 and VcA-2 DNAs. Four of the cloned motility gene regions hybridized to the same fragments of DNA in both the wild-type and mutant isolates. However, two other probes detected a new fragment for a single aflagellate mutant. The observations that spontaneous nonmotile mutants occurred at a high frequency and that these mutants did not revert at a detectable frequency suggested that a genetic event is involved. The phenomenon appears to be limited to classical V. cholerae and may explain why classical V. cholerae is only sporadically associated with disease in the current pandemic.

Animals↗
PubMed1990

Amy remembered.

Explore the source record for details and available documents.

Chicago↗
PubMed1989

Human immune response to Vibrio cholerae O1 whole cells and isolated outer membrane antigens.

The serum immunoglobulin G (IgG) and mucosal secretory IgA (SIgA) response of human volunteers challenged with Vibrio cholerae O1 was analyzed for reactivity to V. cholerae O1 antigens by the immunoblot technique. Components of both in vitro- and in vivo (rabbit ligated ileal loop)-grown V. cholerae O1 were separated by sodium dodecyl sulfate-urea-polyacrylamide gel electrophoresis. Postchallenge serum IgG reacted uniquely with 15 antigens and with greater intensity than did prechallenge serum with at least 16 antigens. Serum IgG and SIgA reacted with antigens present in preparations from the homologous challenge strain of V. cholerae as well as antigens from strains of heterologous biotype or serotype. These heterologous antigens may represent antigens responsible for protection to rechallenge with a heterologous strain of V. cholerae. All the antigens detected by postchallenge jejunal fluid SIgA had an apparent molecular size of less than 25 kilodaltons. Serum IgG and jejunal fluid SIgA also reacted with antigens unique to in vivo-grown cells and several antigens in outer membrane preparations, suggesting that studies of protective immunity and V. cholerae O1 pathogenesis should include examination of both in vitro- and in vivo-grown V. cholerae O1 cellular antigens.

Animals↗