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Biomedical subjects

G Herrera

Publications and source records attributed to G Herrera.

At least 55 records · Page 3Linked to original sources
PubMed1991

Diagnosis of cysticercosis in endemic regions. The Cysticercosis Working Group in Peru.

Taenia solium cysticercosis is a frequent cause of neurological disease in developing countries. Specific diagnosis of cysticercosis is difficult. We obtained serum and/or CSF samples from 204 consecutive patients admitted to a neurological ward in Lima, Peru, and looked for antibodies specific for T solium with the enzyme-linked immunoelectrotransfer blot (EITB) assay. 21 (12%) of 173 serum samples from these patients were EITB-positive. In contrast, only 2 (1.5%) of 135 patients attending a public endoscopy clinic and 1 (1%) of 88 patients attending a private endoscopy clinic were seropositive. 1 (1%) of 98 pregnant women living in a Lima shanty town was EITB-positive. 15 (58%) of 26 neurology patients diagnosed clinically as having cysticercosis were seronegative. Routine screening by EITB of all patients with neurological symptoms from areas of endemic cysticercosis would avoid misdiagnosis of this common and treatable disease.

Adolescent↗
PubMed1991

Influence of recA mutations on gyrA dependent quinolone resistance.

We examined, in Escherichia coli, the influence of recA mutant alleles on the level of quinolone resistance promoted by mutations in the gyrA gene. We found that the recA142 mutation, abolishing all the activities of RecA protein, greatly reduced the level of resistance to the quinolone ciprofloxacin, whereas the recA430 allele affecting the SOS inducing ability of RecA, reduced ciprofloxacin resistance to a lesser extent. The recA142 mutation did not cause enhancement of ciprofloxacin induced DNA breakage in gyrA mutants, indicating that the stabilization of DNA-gyrase complexes by the quinolone is not influenced by a RecA mutant protein. We suggest that RecA protein plays a role in the repair of quinolone damage, principally through a recombinational mechanism and, to a lesser degree, through the induction of the SOS response.

DNA Repair↗
PubMed1991

Effects of ciprofloxacin on plasmid DNA supercoiling of Escherichia coli topoisomerase I and gyrase mutants.

Changes in plasmid DNA supercoiling were measured following treatment of Escherichia coli cells, carrying topoisomerase mutations, with the quinolone ciprofloxacin. In quinolone-susceptible cells (top+ gyr+) as well as in topA mutants and in gyrB mutants, plasmid DNA was relaxed after the addition of ciprofloxacin. In cells partially resistant to quinolones, low ciprofloxacin levels led to an increase in negative superhelicity of plasmid DNA, whereas at higher ciprofloxacin concentrations, DNA became relaxed. Cells exhibiting partial resistance to quinolones carried either a gyrA mutation alone or a combination of gyrA and gyrB mutations. Moreover, they showed a reduction in gyrase activity, indicated by the supercoiling of a reporter plasmid. Therefore, we conclude that a low level of quinolone action and a DNA with a lower-than-normal level of superhelicity are the two essential conditions for obtaining a ciprofloxacin-promoted increase in plasmid DNA supercoiling. In contrast, deficiency in topoisomerase I is not required for this effect.

Ciprofloxacin↗
PubMed1991

[Non tumor intracranial expansive processes: clinico-topographical correlation].

Presentation of clinical-tomographic correlation in 111 cases of non tumoral intracranial expansive processes seen between 1984-1988 in the Hospital Cayetano Heredia (Lima, Peru). Emphasis is given fundamentally to: (1) the importance of establishing the organicity of partial and late epilepsy; (2) the high incidence rate of inflammatory infectious processes with CNS compromise in underdeveloping countries; (3) the necessity of making public the importance of two parasitic diseases in the differential diagnosis of non tumoral intracranial expansive processes: free living amebiasis, and toxoplasmosis (especially in association with AIDS).

Adolescent↗
PubMed1990

Expression of the recA gene is reduced in Escherichia coli topoisomerase I mutants.

We studied the influence of DNA topological changes on Escherichia coli recA gene expression. This was monitored by measuring beta-galactosidase activity in cells containing a recA-lacZ fusion. To modulate DNA supercoiling we used mutations in the genes encoding for topoisomerase I and DNA gyrase. After either UV irradiation or treatment with the gyrase inhibitor ciprofloxacin, induction of the recA gene was reduced in topA10 mutants, this reduction being alleviated when gyrA or gyrB mutations causing DNA relaxation were present. A reduced induction of recA was also observed after incubation of cells carrying the recA441 mutation at 42 degrees C in the presence of adenine. Using bacteria deficient in the LexA repressor, we have demonstrated that the topA10 mutation reduces the constitutive expression of the recA gene. We suggest that the increase in negative supercoiling resulting from topoisomerase I deficiency interferes with transcription from the recA promoter. The reduction in the expression of the recA gene in topA10 bacteria could determine their increased UV sensitivity as well as their partial defectiveness in SOS mutability.

Ciprofloxacin↗
PubMed1990

[Partial epilepsy in children].

It is reported the analysis of a retrospective and prospective study on a series of 101 patients suffering from partial epilepsy who have been examined at the Neuropediatric Clinics of Hospital General Base Cayetano Heredia during the period that lasted from January 1984 to July 1988. The observation time varied from 6 months to 4 years. The patients age varied from 6 months to 3 years old. There were found 19% of idiopathic epilepsy with 7.7% from benign epilepsies in childhood. The symptomatic epilepsies corresponded to sequels of problems short after birth, followed by tuberculosis granulomata and sequels of infections in the central nervous system.

Adolescent↗
PubMed1989

New Escherichia coli gyrA and gyrB mutations which have a graded effect on DNA supercoiling.

We isolated new gyrA and gyrB mutations in Escherichia coli which have a graded effect on DNA supercoiling. The mutants, selected respectively for resistance to nalidixic acid and coumermycin, were sorted by means of a rapid in vivo assay of DNA gyrase activity (Aleixandre and Blanco 1987). Cells carrying a gyrB (Cour) mutation usually showed a decrease in DNA supercoiling, which would indicate a reduction in gyrase activity. In contrast, most of the gyrA (Nalr) mutations had no significant effect on DNA supercoiling. Moreover, they conferred a high level of resistance to nalidixic acid and other quinolones, thus being similar to the gyrA (Nalr) mutants currently used. We also detected rare gyrA mutants showing a reduction in DNA gyrase activity. These mutants were, in addition, resistant to only low concentrations of quinolones, which allowed us to use the phenotype of partial quinolone resistance as an indicator to score gyrA mutations affecting DNA supercoiling. When gyrB mutations were introduced into the gyrA mutants, these became more sensitive to quinolones and a decrease in supercoiling was observed. Moreover, the topA10 mutation sensitized gyrA (Nalr) cells to quinolones. We conclude therefore that the GyrA-dependent quinolone resistance is diminished as a consequence of the reduction either in topoisomerase I or gyrase activities.

Aminocoumarins↗
PubMed1988

UV-light-induced mutability in Salmonella strains containing the umuDC or the mucAB operon: evidence for a umuC function.

Multicopy plasmids carrying either the umuDC operon of Escherichia coli or its analog mucAB operon, were introduced into Ames Salmonella strains in order to analyze the influence of UmuDC and MucAB proteins on repair and mutability after UV irradiation. It was found that in uvr+ bacteria, plasmid pICV80:mucAB increased the frequency of UV-induced His+ revertants whereas pSE117:umuDC caused a smaller increase in UV mutagenesis. In delta uvrB bacteria, the protective role of pSE117 against UV killing was weak, and there was a great reduction in the mutant yield. In contrast, in these cells, pICV80 led to a large increase in both cell survival and mutation frequency. These results suggest that in Salmonella, as in E. coli, MucAB proteins mediate UV mutagenesis more efficiently than UmuDC proteins do. Plasmid pICV84:umuD+ C- significantly increased UV mutagenesis of TA2659: delta uvrB cells whereas in them, pICV77:mucA+ B- had no effect on mutability indicating the presence in Salmonella TA2659 of a gene functionally homologous to umuC.

Bacterial Proteins↗
PubMed1987

Mutagenic DNA repair in Escherichia coli. XIII. Proofreading exonuclease of DNA polymerase III holoenzyme is not operational during UV mutagenesis.

We have introduced a mutD5 mutation (which results in defective 3'-5'-exonuclease activity of the epsilon proofreading subunit of DNA polymerase III holoenzyme) into excision-defective Escherichia coli strains with varying SOS responses to UV light. MutD5 increased the spontaneous mutation frequency in all strains tested, including recA430, umuC122::Tn5, and umuC36 derivatives. It had no effect on UV mutability or immutability in any strain or on misincorporation revealed by delayed photoreversal in UV-irradiated umuC36, umuC122::Tn5, or recA430 bacteria. It is concluded that the epsilon proofreading subunit of DNA polymerase III holoenzyme is excluded, inhibited, or inoperative during misincorporation and mutagenesis after UV.

Arginine↗
PubMed1986

Different efficiency of UmuDC and MucAB proteins in UV light induced mutagenesis in Escherichia coli.

Two multicopy plasmids carrying either the umuDC or the mucAB operon were used to compare the efficiency of UmuDC and MucAB proteins in UV mutagenesis of Escherichia coli K12. It was found that in recA+ uvr+ bacteria, plasmid pIC80, mucAB+ mediated UV mutagenesis more efficiently than did plasmid pSE117, umuDC+. A similar result was obtained in lexA41 (Def) cells, excluding the possibility that this was due to a differential regulation by LexA of the umuDC and mucAB operons. We conclude that some structural characteristic of the UmuDC and MucAB proteins determines their different efficiency in UV mutagenesis. This characteristic could be also responsible for the observation that in the recA430 mutant, pIC80 but no pSE117 can mediate UV mutagenesis. In the recA142 mutant, pIC80 also promoted UV mutagenesis more efficiently than pSE117. In this mutant, the recombination proficiency, the protease activity toward LexA and the mutation frequency were increased by the presence of adenine in the medium. In recA+ uvrB5 bacteria, plasmid pSE117, umuDC caused both an increase in UV sensitivity as well as a reduction in the mutation frequency. These negative effects resulting from the overproduction of UmuDC proteins were higher in recA142 uvrB5 than in recA+ uvrB5 cells. In contrast, overproduction of MucAB protein in excision-deficient bacteria containing pIC80 led to a large increase in the mutation frequency. We suggest that the functional differences between UmuDC and MucAB proteins might be due to their different dependence on the direct role of RecA protease in UV mutagenesis.

Bacterial Proteins↗
PubMed1986

New role for photoreversible pyrimidine dimers in induction of prototrophic mutations in excision-deficient Escherichia coli by UV light.

UV mutagenesis to His+ in certain recA441 lexA51 bacteria was not photoreversible, indicating that pyrimidine dimers are not target lesions. Photoreversibility was observed in recA+ lexA51 bacteria, showing that pyrimidine dimers are needed to activate the recA+ protein (unlike the recA441 protein) to perform a function in UV mutagenesis distinct from cleavage of the lexA repressor.

DNA Repair↗
PubMed1984

Dysgerminoma with syncytiotrophoblastic giant cells presenting as a hydatidiform mole.

There have been a total of 11 cases of pure dysgerminoma with syncytiotrophoblastic giant cells (SGC) previously reported in the literature as of June 1981. All were Stage IA, all were treated with unilateral salpingo-oophorectomy, and the preoperative serum human chorionic beta-gonadotropin (beta-hCG) titers ranged from 2000 to 3160 mlU/ml. A recent case at William Beaumont Army Medical Center involved a 20-year-old Hispanic female who presented with a 20 weeks' size pelvic-abdominal mass which was sonographically consistent with a hydatidiform mole. An initial preoperative serum beta subunit hCG was 193,000 mlU/ml. At the time of surgery a Stage IC dysgerminoma of the right ovary was discovered and right salpingo-oophorectomy performed. In reviewing all 11 previously reported cases, not only is this case the first Stage IC reported, but it also is the first to present as a hydatidiform mole, has the highest ever reported preoperative beta-hCG, and provides the first ultrastructural study of this tumor type. The unusual clinical presentation and management of this case are discussed and a brief review of the clinical and pathological features of this unusual tumor is given.

Adult↗
PubMedDate not supplied

Influence of the processing of MucA protein on the reversion of the frameshift hisD3052 and the base substitution hisG46 mutations by chemical mutagens in Salmonella typhimurium.

The correlation between the proficiency at promoting mutagenesis of MucA/B proteins and MucA processing has been considered to be very high (Hauser et al., 1992) on the basis of the results of UV mutagenicity (Shiba et al., 1990). Here we show that this correlation is only partial. We have assayed the mutagenicity of benzo[a]pyrene (B[a]P) and aflatoxin B1 (AFB1) in Salmonella typhimurium tester strains containing plasmids which encode MucA proteins with an altered cleavage site. Reversion of the frameshift hisD3052 mutation by B[a]P or AFB1 was observed in the presence of non-cleavable MucA protein although at a lower level than that found in cells containing wild-type MucA protein. Reversion of the base substitution hisG46 mutation by AFB1 requires a significant processing of MucA, while lower levels of this processing would be enough for the hisG46 reversion by B[a]P. These results suggest that the specificity of mutations induced by mutagens forming DNA adducts is influenced by the activity of MucA protein. They also show the relevance of mutagenicity assays in the mechanistic studies of mutagenesis.

Aflatoxin B1↗