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Biomedical subjects

P May

Publications and source records attributed to P May.

At least 73 records · Page 4Linked to original sources
PubMed1995

In vitro activity of RP 59500 (quinupristin/dalfopristin) against antibiotic-resistant strains of Streptococcus pneumoniae and enterococci.

The activity of RP 59500 (quinupristin/dalfopristin) was evaluated in vitro against antibiotic-resistant strains of Streptococcus pneumoniae (N = 15) and Enterococcus spp. (N = 43). By broth dilution MIC tests RP 59500 was highly active against penicillin-resistant S. pneumoniae and vancomycin-resistant Enterococcus faecium, but showed poor activity against E. faecalis. In time-kill studies the drug was rapidly bactericidal against S. pneumoniae but failed to kill most enterococci, even in the presence of gentamicin or human serum.

Drug Resistance, Microbial↗
PubMed1995

A study of the clinical outcome of patients with profound mental retardation gradually withdrawn from chronic neuroleptic medication.

In a naturalistic study of 23 severely and profoundly mentally retarded adult male patients undergoing slow "diagnostic" neuroleptic taper, it was determined that at least 60% could eventually be managed without psychoactive medication. However, many of these demonstrated a remarkably long, but nonetheless transient, period of worsening. This suggests that behavioral deterioration during drug reduction trials does not always indicate a need for chronic neuroleptic maintenance since these behaviors may return to baseline without pharmacological intervention. On the other hand, 40% demonstrated persistent (> 2 years) behavioral worsening. Those individuals who demonstrated persistent deterioration had been generally well controlled on neuroleptics, were somewhat older, and were receiving a higher baseline dose. Most of these persistently worsened subjects currently require some type of psychoactive medication (although only two have been returned to neuroleptics).

Adult↗
PubMed1995

[P53 and cancers].

The p53 gene, located on chromosome 17p 13.1 and coding for a nuclear 393 amino-acids phosphoprotein acts to constrain or antagonize cell growth, and as such, is a tumor suppressor gene. In fact, inactivation of p53 tumor suppressor gene is a common event in the development of all or most types of human cancers. About half of cell cancer cases analysed thus far involve missense mutation of one p53 allele combined with the deletion of the second allele, and many of the remaining cases involve a functional inactivation of p53 protein through non mutational mechanisms. The importance of p53 as an inherited cancer susceptibility gene has been demonstrated in Li-Fraumeni syndrome. In some circumstances, it has been shown that in response to DNA damage, the p53 level in the cell increases considerably and induces a cell growth arrest late in G1 phase. This cycle arrest allows the altered DNA to be repaired before entry of the cell into S phase. This function of p53 helps to insure the genomic stability of the cell. Mutations in p53 eliminate this response and result in enhanced frequency of genomic rearrangements. In other circumstances wild type p53 may act by triggering cell death by apoptosis. The p53 protein exerts its physiological functions through various biochemical activities. These include its ability to be a site-specific transcriptional transactivator as well as a repressor of transcription. The oncoproteins derived from several oncogenic DNA viruses including SV40 large T antigen, the adenovirus E1B protein, and papillomavirus E6 protein, as well as specific cellular gene products e.g. mdm2 form complexes with the p53 protein, causing its inactivation.(ABSTRACT TRUNCATED AT 250 WORDS)

Genes, Tumor Suppressor↗
PubMed1994

The auditory transient 40-Hz response is insensitive to changes in stimulus features.

Ten subjects were presented with tone pips occasionally interspersed with deviant tone pips of a higher frequency. The transient 40-Hz response was insensitive to change in qualitative stimulus features. In contrast, stimulus changes elicited a later and slower event-related potential, the mismatch negativity (MMN). As a response to changes in stimulus features implies the existence of a memory system, and because changes in qualitative stimulus aspects do not activate the generator mechanisms underlying the 40-Hz response, the 40-Hz response can be dissociated from memory mechanisms. Furthermore, the analysis of phase-locked (synchronous) and non-phase-locked (asynchronous) responses revealed that the 40-Hz response might be caused by the synchronization of already active oscillators.

Acoustic Stimulation↗
PubMed1994

Attentive novelty detection in humans is governed by pre-attentive sensory memory.

Being able to detect unusual, possibly dangerous events in the environment is a fundamental ability that helps ensure the survival of biological organisms. Novelty detection requires a memory system that models (builds neural representations of) events in the environment, so that changes are detected because they violate the predictions of the model. The earliest physiologically measurable brain response to novel auditory stimuli is the mismatch negativity, MMN, a component of the event-related potential. It is elicited when a predictable series of unvarying stimuli is unexpectedly followed by a deviating stimulus. As the occurrence of MMN is not usually affected by the direction of attention, MMN reflects the operation of automatic sensory (echoic) memory, the earliest memory system that builds traces of the acoustic environment against which new stimuli can be compared. The dependence of attentive novelty detection on earlier, pre-attentive processes, however, has remained elusive. Previous, related studies seem to suggest a relationship between MMN and attentive processes, although no conclusive evidence has so far been shown. Here we address novelty detection in humans both on a physiological and behavioural level, and show how attentive novelty detection is governed by a pre-attentive sensory memory mechanism.

Acoustic Stimulation↗
PubMed1994

Long-term stimulation attenuates the transient 40-Hz response.

The effect of long-term stimulation on the transient 40-Hz response was studied in 5-h long experimental sessions. Ten human subjects were presented with series of 1000 Hz tone pips occasionally replaced by 1200 Hz tone pips. The transient 40-Hz response was compared with two event-related potential (ERP) components, the N1 and the mismatch negativity (MMN) during the different phases of the long-lasting sessions. The 40-Hz and N1 onset responses attenuated while the MMN did not. Thus, the 40-Hz response might indicate vigilance.

Acoustic Stimulation↗
PubMed1994

Enhanced cytotoxicity of amyloid beta-peptide by a complement dependent mechanism.

Amyloid beta-peptide (A beta) has been shown to activate the classical complement pathway in vitro. Here, we demonstrate that this interaction is fully capable of killing cells and damaging cellular processes in mixed hippocampal cultures from embryonic day 18 rat fetuses. Lactic acid dehydrogenase (LDH) release and morphologic changes were used to evaluate toxicity.

Amyloid beta-Protein Precursor↗
PubMed1994

Concomitant p53 gene mutation and increased radiosensitivity in rat lung embryo epithelial cells during neoplastic development.

A rat lung cell population had been treated with benzo(a)pyrene, and a set of different epithelial cell lines was derived from it. These cell lines carried either a wild-type or mutant p53 gene and represented grading states of neoplastic development. We demonstrate here that the cells lacking both wild-type p53 alleles display a significant decrease in survival after gamma-irradiation with doses of 2 to 12 Gy, compared with their counterparts carrying wild-type p53 alleles. This is the first reported model in which cells bearing a mutation of the p53 gene display enhanced sensitivity to ionizing radiation.

Animals↗
PubMed1994

Directional selection associated with clonal expansion of p53 mutant cells during neoplastic development of carcinogen-treated rat embryo lung epithelial cells.

In this study, rat embryo lung organ cultures were exposed to benzo[a]pyrene (B[a]P). After carcinogen-treatment the cells were dissociated and an epithelial cell line (BP) was developed from the primary cell culture derived from the carcinogen-treated explants. Investigations were performed on the sequential changes occurring in the course of neoplastic progression of BP cells and in the tumor cells that arose in vivo from implanted BP cells. During the neoplastic progression a mutation was shown to occur in p53 gene at codon 130 (AAG > AGG; Lys > Arg) in a single cell which expanded and gave rise to a predominant subpopulation. This mutational event was already detected at passage 14 but was probably not a direct consequence of a specific alteration caused by the carcinogen in the target cell. This mutation was retained through the subsequent progressional steps first as a heterozygous mutation, then converted to a homozygous state. From passage 18 on, it was possible in BP cell cultures to detect foci of larger morphologically distinct cells emerging on a background of cells maintaining the original morphology. These foci were shown to derive from a single cell carrying the p53 mutation in a homozygous state. During the neoplastic progression the mutant p53 allele frequency steadily increased and this mutant allele eventually came to predominate completely in the late stages of the neoplastic progression, including in the transplantation-induced tumors. The pattern of a directional selection for mutant p53 gene towards fixation is probably applicable to a wide range of human malignancies and may reflect the particular importance of this gene for tumorigenesis.

Animals↗
PubMed1993

p53-mediated cell death: relationship to cell cycle control.

M1 clone S6 myeloid leukemic cells do not express detectable p53 protein. When stably transfected with a temperature-sensitive mutant of p53, these cells undergo rapid cell death upon induction of wild-type (wt) p53 activity at the permissive temperature. This process has features of apoptosis. In a number of other cell systems, wt p53 activation has been shown to induce a growth arrest. Yet, wt 53 fails to induce a measurable growth arrest in M1 cells, and cell cycle progression proceeds while viability is being lost. There exists, however, a relationship between the cell cycle and p53-mediated death, and cells in G1 appear to be preferentially susceptible to the death-inducing activity of wt p53. In addition, p53-mediated M1 cell death can be inhibited by interleukin-6. The effect of the cytokine is specific to p53-mediated death, since apoptosis elicited by serum deprivation is refractory to interleukin-6. Our data imply that p53-mediated cell death is not dependent on the induction of a growth arrest but rather may result from mutually incompatible growth-regulatory signals.

Animals↗
PubMed1992

Hospital-acquired infection with vancomycin-resistant Enterococcus faecium transmitted by electronic thermometers.

OBJECTIVES: To describe an epidemic of vancomycin-resistant Enterococcus faecium causing bacteremia and bacteriuria, to identify the source of infection, to delineate risk factors associated with acquisition of the organism, and to determine antibiotic sensitivities for the organism. DESIGN: Investigation of an epidemic, including a case-control study. SETTING: Medical-surgical intensive care unit and ward in a university medical center. PATIENTS: Nine patients infected or colonized with vancomycin-resistant Enterococcus faecium and 20 noninfected controls. MEASUREMENTS: Clinical data, environmental surveillance cultures, and in-vitro microbiologic studies. RESULTS: Colonization or infection by vancomycin-resistant E. faecium was associated with an increased duration of treatment with ceftazidime, 13.2 compared with 4.6 days, and a greater number of nonisolated days of hospitalization in the intensive care unit, 19.9 compared with 6.4 days for infected and noninfected patients, respectively (P less than 0.05). Environmental surveillance cultures recovered the organism repeatedly from the rectal probe handles of three electronic thermometers used exclusively on nonisolated patients in the intensive care unit. Restriction endonuclease analysis of plasmid DNA showed that all clinical and environmental isolates were identical. Infection control measures, including isolation of colonized or infected patients and removal of the rectal thermometer probes suspected to be responsible for transmission, resulted in termination of the outbreak. In-vitro, time-kill studies showed that the combination of ciprofloxacin, rifampin, and gentamicin resulted in bactericidal activity against the organism. CONCLUSIONS: This nosocomial outbreak of infection due to a highly vancomycin-resistant strain of Enterococcus is the first epidemic in which an electronic thermometer has been implicated as the vehicle of transmission for an infectious agent.

Adolescent↗
PubMed1992

Rainbow trout p53: cDNA cloning and biochemical characterization.

We have cloned and sequenced the p53-encoding cDNA of rainbow trout (Salmo gairdneri). The encoded product contains the characteristics found in all p53 proteins: (i) the five highly conserved domains, (ii) an acidic N terminus, (iii) a hydrophilic C terminus, and (iv) a penultimate serine residue. Furthermore, we demonstrate that the rainbow trout p53 is able to specifically interact with the SV40 large T antigen.

Amino Acid Sequence↗
PubMed1992

Bactericidal activity of ramoplanin against antibiotic-resistant enterococci.

Ramoplanin, a new lipoglycodepsipeptide antibiotic, was uniformly active against 65 strains of enterococci, including strains highly resistant to vancomycin, penicillin G, and gentamicin. MBCs were usually within a fourfold dilution of the MICs. In time-kill studies, ramoplanin alone demonstrated dose-dependent bactericidal activity against enterococcal strains that resisted killing by vancomycin or penicillin in combination with gentamicin.

Anti-Bacterial Agents↗
PubMed1992

p53 mutations in Raji cells: characterization and localization relative to other Burkitt's lymphomas.

The nuclear phosphoprotein p53 is an important regulator of cell proliferation in normal cells. Interestingly, the gene encoding p53 has usually undergone mutations in a wide range of tumor types. Recent studies of the p53 gene in Burkitt's lymphomas have demonstrated that mutations are extremely common, and in fact it is rare that both alleles of the p53 gene in these tumors are not inactivated by mutation or deletion. We present here genetic data regarding the status of the p53 gene in the Burkitt lymphoma cell line, Raji. As is typical for this type of tumor, both alleles have undergone point mutations. Further, statistical analysis of available data from a large number of Burkitt's lymphomas indicates an apparent tumor-specific distribution of p53 mutations. The possibility that specific mutations of the p53 gene may be important for different tumor types is discussed.

Alleles↗