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Biomedical subjects

S Sommer

Publications and source records attributed to S Sommer.

At least 19 recordsLinked to original sources
PubMed1992

Preventive care in general practice.

Preventive care is an integral component of general practice teaching in all Australian medical schools. While curriculum time and teaching methods vary, the overriding emphasis remains on integrating both epidemiological and behavioural science approaches into the primary care setting. Preventive aspects are stressed during attachments with general practitioners. Use of appropriate theoretical frameworks and models allows the role of the general practitioner in disease prevention to be formalized. Undergraduate teaching is further reinforced by programs within the Family Medicine Programme at a vocational training level, and the Royal Australian College of General Practitioners at a continuing medical education level.

Australia↗
PubMed1991

Use of neural network analysis to classify electroencephalographic patterns against depth of midazolam sedation in intensive care unit patients.

The electroencephalographic (EEG) analog signal is complex and cannot easily be described by univariate variables. Clear visual changes in the EEG power spectrum can be present with little or no change in univariate variable values. A method that could produce a single value based on the total data available in the EEG power spectrum would be very useful in monitoring EEG changes. Neural network analysis is a technique that can take multiple inputs and produce a single output value using complicated processing patterns that require training to establish. We examined the usefulness of a series of neural network models to classify 63 EEG patterns against sedation level in 26 mechanically ventilated patients requiring midazolam for long-term sedation. During a stable period of sedation, a 4- to 60-minute period of EEG data was obtained concurrently with a sedation level from 1 (follows commands) to 7 (no or gag response to suctioning of the endotracheal tube). The EEG power spectrum was divided into equal frequency bands, and the log absolute powers in each of these bands were used as inputs for a series of neural network models. The output target was the sedation level associated with each set of EEG data. Networks were trained on a subset of EEG power/sedation score data pairs, and the ability to classify the remaining data pairs was tested. Using a t-test comparison with a random set of sedation levels, we found that trained neural network models classified EEG patterns against sedation level successfully (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Gestational age in relation to marine n-3 fatty acids in maternal erythrocytes: a study of women in the Faroe Islands and Denmark.

Gestation is longer in Faroese than Danish women, possibly because of the high intake of marine long-chain n-3 fatty acids that down regulates formation of prostaglandins from arachidonic acid. Polyunsaturated fatty acids were quantified in erythrocytes obtained within 2 days of delivery from randomly selected groups of 62 Faroese and 37 Danish women with an assessable gestational age. Average ratio of long-chain n-3 fatty acids to arachidonic acid [(3/6) ratio] was 0.73 (SD = 0.11) in Faroese women and 0.61 (SD = 0.12) in Danish women (p less than 0.0001), corresponding to the higher intake of marine n-3 fatty acids in the Faroes. A 20% increase in the (3/6) ratio was associated with an increase in pregnancy duration of 5.7 days in Danish women (95% confidence interval, 1.4 to 10.1 days; p = 0.02) and 0.7 days in Faroese women (95% confidence interval, -2.0 to 3.3; p = 0.6). The hypothesized exposure-effect relationship may be weaker or absent at the higher level of exposure seen in the Faroese group.

Arachidonic Acid↗
PubMed1991

Substitution of UmuD' for UmuD does not affect SOS mutagenesis.

In order to study the role of UmuDC proteins in SOS mutagenesis, we have constructed new Escherichia coli K-12 strains to avoid i) over-production of Umu proteins, ii) the formation of unwanted mixed plasmid and chromosomal Umu proteins upon complementation. We inserted a mini-kan transposon into the umuD gene carried on a plasmid. The insertion at codon 24 ends protein translation and has a polar effect on the expression of the downstream umuC gene. We transferred umuD24 mutation to the E coli chromosome. In parallel, we subcloned umuD+ umuC+ or umuD' umuC+ genes into pSC101, a low copy number plasmid. In a host with the chromosomal umuD24 mutation, plasmids umuD+ umuC+ or umuD' umuC+ produced elevated resistance to UV light and increased SOS mutagenesis related to a gene dosage of about 3. UV mutagenesis was as high in umuD' umuC+ hosts devoid of UmuD+ protein as in umuD+ umuC+ hosts. UmuD' protein, the maturated form of UmuD, can substitute for UmuD in SOS mutagenesis.

Bacterial Proteins↗
PubMed1991

A RecA protein mutant deficient in its interaction with the UmuDC complex.

recA1730 is a dominant point mutation preventing SOS mutagenesis. We demonstrate here that: i) RecA1730 fails to produce mutagenesis even though UmuD' is formed, ii) recA1730, when complemented by recA+, can cleave LexA protein and it displays a UmuDC- phenotype in spite of adequate concentrations of matured UmuD' and UmuC proteins, iii) the Mut- phenotype caused by RecA1730 is partially alleviated by MucAB proteins, functional analogs of UmuDC. To explain the mutant phenotype, we postulate that recA1730 impairs a RecA function required for the positioning of the UmuD'C complex within the replisome at the site of lesions.

Bacterial Proteins↗
PubMed1991

Introduction of a UV-damaged replicon into a recipient cell is not a sufficient condition to produce an SOS-inducing signal.

Three models have been proposed for the nature of the SOS-inducing signal in E. coli. One model postulates that degradation products of damaged DNA generate an SOS-inducing signal; another model surmises that the very lesions produced by UV damage constitute the SOS-inducing signal in vivo; a third model proposes that DNA damage is processed upon DNA replication to form single-stranded DNA (the SOS signal) that activates RecA protein. We tested the models by measuring SOS induction produced by introducing into recipient cells the UV-damaged DNA of 2 constructed phagemids. We used phagemids since they transferred DNA to the recipients with 100% efficiency. The origin of replication of the phagemids was either oriC from the E. coli chromosome, or oriF from F plasmid. Replication of the oriC phagemid was dependent on methylation. A UV-damaged oriC phagemid failed to induce SOS functions in a recipient cell whereas an oriF phagemid did induce them. Our results disprove the first and the second model proposed for the nature of the SOS-inducing signal. The failure of a UV-damaged oriC replicon to induce SOS can be explained by the third model if one assumes that replication of a UV-damaged oriC plasmid does not generate single-stranded DNA as does the E. coli chromosome after UV damage.

Bacteriophage lambda↗
PubMed1989

[Postoperative analgesia with morphine versus morphine and paracetamol. A double-blind clinically controlled study with a placebo].

The effect of paracetamol on the postoperative employment of morphine was investigated in a double-blind clinically controlled investigation with a placebo. The operations concerned were elective gynaecological laparotomies and hip replacements. During the first 60 hours postoperatively, the employment of morphine was reduced significantly in the patients who received paracetamol. Reductions of 16, 22 and 26% were concerned. The differences between the various types of operation were not significant. Patients for joint replacements who had been treated preoperatively with non-steroid anti-inflammatory preparations did not have any significantly greater consumption of morphine postoperatively but the reduction in consumption of morphine in the paracetamol group was significantly greater with a saving of 43%. Patients who had received treatment with morphine preparations preoperatively had significantly greater consumption of morphine postoperatively but the additive analgesic effect of paracetamol remained unchanged at approximately 25%.

Acetaminophen↗
PubMed1989

An intronic region within the human factor VIII gene is duplicated within Xq28 and is homologous to the polymorphic locus DXS115 (767).

The genomic sequences recognized by the anonymous probe 767 (DXS115) are localized to two sites within Xq28. One site lies within intron 22 of the factor VIII gene (FBC). Physical mapping suggests that the second site lies within 1.2 megabases of the F8C gene. The RFLPs detected by 767 are located within the second site. Genetic data suggest that F8C and DXS115 are tightly linked (theta max = .04; Zmax = 8.30). Recombination events in meioses informative for DXS52 (St14), DXS115, and F8C suggest that DXS115 and F8C lie distal to DXS52.

Chromosome Deletion↗
PubMed1989

Personal adjustments and regimen compliance 1 year after myocardial infarction.

The relationship of attitudes and perceived beliefs of others to regimen compliance and personal psychologic and social adjustments of patients with myocardial infarction was investigated 1 year after the infarction. Eighty-one patients (39 in the experimental group, 42 in the control group) who participated in a prior study on the effect of a nursing intervention on regimen compliance, completed scales that assessed attitudes toward regimen prescriptions (diet, medications, activity, smoking, and stress response), perceived beliefs of others concerning compliance, personal adjustments, and regimen compliance. At 1 year, no differences were found between experimental and control groups for regimen compliance or personal adjustments. There was a significant decrease in mean scores for all variables from the time the patient was in the hospital to 30 days afterward, but no change at 1 year from the 30- or 60-day visit. At 1 year, attitudes were predictive of compliance for all regimen prescriptions. Perceived beliefs of others were predictive of diet, activity, and medication prescriptions.

Adaptation, Psychological↗
PubMed1988

Identification of psiB genes of plasmids F and R6-5. Molecular basis for psiB enhanced expression in plasmid R6-5.

PsiB protein of plasmid R6-5 inhibits the induction of the SOS pathway. The F sex factor also carries a psiB gene homologous to that of R6-5. Yet, it fails to inhibit SOS induction. In order to solve this difference, we characterized the psiB genes of R6-5 and F. We found that (i) the sequences of the two psiB genes share extensive homology the predicted amino acid sequences of the two proteins differing by 5 residues, (ii) the expression of R6-5 psiB is 4 times higher than F psiB gene, (iii) in plasmid R6-5, a Tn10 transposon upstream from the psiB gene enhances psiB expression. Hence, the F sex factor may be unable to prevent SOS induction for two non-exclusive reasons: (i) F PsiB protein, being slightly different from R6-5, may be less active, (ii) the level of synthesis of F PsiB protein may be insufficient to prevent SOS induction.

Amino Acid Sequence↗
PubMed1988

PsiB polypeptide prevents activation of RecA protein in Escherichia coli.

We further characterize a novel plasmid function preventing SOS induction called Psi (Plasmid SOS Inhibition). We show that Psi function is expressed by psiB, a gene located at coordinate 54.9 of plasmid R6-5 and near oriT, the origin of conjugal transfer. Deletions and amber mutations of the psiB gene permitted us to demonstrate that PsiB polypeptide (apparent molecular weight, 12 kDa) is responsible for Psi function. PsiB protein prevents recA730-promoted mutagenesis and intra-chromosomal recombination but not recombination following conjugation. Overproduction of PsiB protein sensitizes the host cell to UV irradiation. We propose that PsiB polypeptide has an anti-SOS action by inhibiting activation of RecA protein, thus preventing the occurrence of LexA-controlled functions.

Bacterial Proteins↗