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Biomedical subjects

B J Meyer

Publications and source records attributed to B J Meyer.

At least 19 recordsLinked to original sources
PubMed1992

[Epidemiology and pathophysiology of heart failure].

The role of coronary artery disease in the epidemiology of congestive heart failure is important. In the pathophysiologic process of congestive heart failure, a number of adaptive mechanisms (hypertrophy, dilatation, neurohumoral stimulation) compensate for the decreased cardiac output by the failing heart. A new understanding of the pathophysiology of heart failure has lead to the identification of important cellular alterations. In the final stage of overcompensation these adaptive mechanisms are deleterious. Associated ventricular arrhythmias indicate a high incidence of sudden cardiac death. Recent considerations of clinical relevance are taken into account in tailoring treatment for patients with congestive heart failure.

Autonomic Nervous System↗
PubMed1992

[Anti-angina effect of amiodarone in therapy-resistant angina pectoris].

In a double-blind randomized trial 63 patients on the waiting list for coronary artery bypass grafting, with stable angina NYHA III and a positive stress test on triple (nitrates, beta- and calcium entry blockers) combination therapy, were studied for an additional antianginal effect of amiodarone over a period of 2 months. In the treatment group an increase in exercise duration and a decrease of the double product and of ST-depression were noted. Thus, amiodarone is an effective antianginal agent in patients with limiting angina pectoris on conventional triple therapy.

Adrenergic beta-Antagonists↗
PubMed1992

Alterations in human enamel surface morphology following vital bleaching.

Extracted intact human teeth (n = 4) were treated for 30 days by three protocols: Home 1 (Proxigel, n = 4) for 8 hours daily, Home 2 (White & Bright, n = 4) for 24 hours with 3 minutes of stannous fluoride gel, or an Office protocol (n = 4) using 30% hydrogen peroxide (Superoxol) warmed by a high-intensity light while the controls remained untreated. "Home" bleaching agents contain approximately 10% carbamide peroxide. After treatment, the coronal surfaces were examined with a scanning electron microscope (SEM) at 2000 power magnification, and the surface topography was measured by a profilometer. The SEM photomicrographs of the controls and office-treated groups were similar to previously reported descriptions, while the home bleached surfaces appeared similar to each other. Profilometric analysis was used to examine surface roughness and surface waviness. Mean surface roughness in microns was: control, 1.9; Home 1, 0.6; Home 2, 0.9; and Office, 0.6. Surface waviness was ranked control > office > Home 1 = Home 2. Enamel surface alterations were evident after the three bleaching methods. The differences between the office and home-treated surfaces were unrelated to the pH of the bleaching agents.

Carbamide Peroxide↗
PubMed1992

Characterization of cat messenger RNA decay suggests that turnover occurs by endonucleolytic cleavage in a 3' to 5' direction.

Turnover of the chloramphenicol acetyltransferase (cat) messenger RNA in Escherichia coli was investigated by analysis of cellular mRNA decay intermediates and the transcript sequence. Analysis of the sequence has revealed the presence of a repetitive extragenic palindromic (REP) element at the 3' end of the transcript as well as several 5'-UUAU-3' sequences, two elements which have roles in modulating turnover of other E. coli mRNAs. For cat mRNA, however, removal of the REP sequence has no effect on the half-life of the transcript, indicating that the REP sequence does not stabilize the upstream region of this message. Results from mapping of the mRNA decay products by several techniques suggest that the message is instead subject to endonucleolytic attack at five sites 5' of the REP element. The sequence UUAU is present at three of these five sites. It also appears that the cat mRNA is sequentially cleaved in a 3' to 5' direction during turnover of this mRNA in vivo. A model for cat mRNA turnover is discussed.

Base Sequence↗
PubMed1992

[Malignant ventricular arrhythmia in congenital aneurysms of the left ventricle in adulthood].

Congenital aneurysms of the left ventricle (ALV) are rare cardiac lesions. Beyond that an association with malignant ventricular arrhythmias (MVA, symptomatic ventricular tachycardia--VT or ventricular fibrillation--VF) is reported only in sporadic cases. Since 1988 we had the opportunity to study 5 patients (pts) with MVA (4 sustained VT, 1 VF; 1 female, 4 males; mean age 38 years) without cardiovascular risk factors, history of myocardial infarction, trauma or inflammatory disease. Left ventricular contrast angiography and echocardiography disclosed ALV's. At programmed electrical stimulation clinically documented MVA (4 VT, 1 resuscitated VF) were reproducible in all 5 cases, the respective VT was located in the area of the ALV in 4 cases. In 2 pts aneurysmectomy combined with subendocardial resection and cryotherapy (1 apical, 1 posterobasal ALV) was performed. In both pts histopathology confirmed a congenital disorder, without evidence of inflammatory lesions. In 2 pts MVA was controlled with antiarrhythmic therapy. The pt with VF and an ALV adjacent to the anulus of the aortic valve received an implantable cardioverter defibrillator. In congenital aneurysms of the left ventricle complicated by malignant ventricular arrhythmias surgical intervention offers a potential cure in selected cases.

Adolescent↗
PubMed1991

[Clinical experience with a second-generation cardioverter-defibrillator].

Implantable cardioverter defibrillators (ICD's) are effective for reducing mortality in refractory malignant ventricular arrhythmias (MVA). Second generation ICD's (Telectronics Guardian 4202/4203) were implanted in 7 patients (all male, mean age 58.1 years) with ventricular fibrillation (VF) in 2, ventricular tachycardia (VT) in 1, and both VF and VT in 4. Underlying heart disease was coronary artery disease in 4 patients, and valvular heart disease, dilated cardiomyopathy and no obvious cause (documented primary VF, reproducible at electrophysiologic study) in 1 patient each. Mean ejection fraction was 40 +/- 14%. Mean defibrillation threshold of the two epicardial patches at implantation by means of median sternotomy was 18 +/- 9 joule, and patch impedance 35 +/- 7 ohms. Post defibrillation bradypacing via epicardial electrode was programmed in 5 patients (70%). Mean follow-up was 10.1 months (1-25 months). Successful defibrillation of 28 spontaneous VT/VF episodes was noted in 2 patients, while the other 5 have had no further episodes of MVA so far. One device was explanted following tissue necrosis at the battery site after a MVA-recurrence-free interval of 15 months. The reconfirmation algorithm prevented false shock delivery in 2 patients.

Cardiac Pacing, Artificial↗
PubMed1991

Early aspects of Caenorhabditis elegans sex determination and dosage compensation are regulated by a zinc-finger protein.

The sdc-1 gene acts at an early step in the regulatory hierarchy that controls the choice of sexual fate in Caenorhabditis elegans. It functions at a point before the control of sex determination and X-chromosome dosage compensation diverge. Here we report that sdc-1 encodes a protein of 1,203 amino acids containing seven zinc fingers. This protein motif in combination with other genetic and molecular information suggests that sdc-1 is likely to function as an embryonic transcription factor regulating downstream genes involved specifically in the sex determination and dosage compensation pathways, or regulating other genes involved in the coordinate control of both processes. These results enhance our general understanding of sex determination strategies, which are already known to involve transcriptional regulation and alternative RNA splicing in Drosophila melanogaster, DNA rearrangements in Saccharomyces cerevisiae, and transcriptional regulation in mammals.

Amino Acid Sequence↗
PubMed1991

A novel transcriptional response by the cat gene during slow growth of Escherichia coli.

A novel response to growth rate was found with expression of the chloramphenicol acetyltransferase (cat) gene in Escherichia coli. The amount of cat mRNA relative to total RNA increased about 11-fold as growth rates decreased 5- to 6-fold, without an increase in translation. The accumulation of cat mRNA was in contrast to decreased cellular concentrations of total RNA, trxA, ompA, or 23S rRNA as the growth rate decreased and was not due to changes in gene dosage or mRNA stability. Stability of the cat mRNA does not appear to be regulated by growth rate. No significant change in either chemical or functional stability was observed within a five- to sixfold range of growth rates when chemostat-grown cells were used. However, cat mRNA stability was affected by growth medium composition. The half-life of cat mRNA decreased about threefold, with an approximate fourfold increase in generation time due to changes in growth medium. Transcriptional studies have indicated that accumulation of cat mRNA at slow growth rates is the result of a specific transcriptional response to changes in cellular generation times. We propose that increases in the cellular concentration of a specific message at slow growth rates may reflect an additional type of survival response in E. coli.

Cell Division↗
PubMed1990

The role of sdc-1 in the sex determination and dosage compensation decisions in Caenorhabditis elegans.

Our previous work demonstrated that mutations in the X-linked gene sdc-1 disrupt both sex determination and dosage compensation in Caenorhabditis elegans XX animals, suggesting that sdc-1 acts at a step that is shared by the sex determination and dosage compensation pathways prior to their divergence. In this report, we extend our understanding of early events in C. elegans sex determination and dosage compensation and the role played by sdc-1 in these processes. First, our analysis of 14 new sdc-1 alleles suggests that the phenotypes resulting from the lack of sdc-1 function are (1) an incompletely penetrant sexual transformation of XX animals toward the male fate, and (2) increased levels of X-linked gene transcripts in XX animals, correlated with XX-specific morphological defects but not significant XX-specific lethality. Further, all alleles exhibit strong maternal rescue for all phenotypes assayed. Second, temperature-shift experiments suggest that sdc-1 acts during the first half of embryogenesis in determining somatic sexual phenotype, long before sexual differentiation actually takes place, and consistent with our previous proposal that sdc-1 acts at an early step in the regulatory hierarchy controlling the choice of sexual fate. Other temperature-shift experiments suggest that sdc-1 may be involved in establishing but not maintaining the XX mode of dosage compensation. Third, a genetic mosaic analysis of sdc-1 produced an unusual result: the genotypic mosaics failed to display the sdc-1 sexual transformation phenotypes. This result suggests several possible interpretations: (1) sdc-1 is expressed immediately, in the one- or two-celled embryo; (2) sdc-1 acts non-cell-autonomously, such that expression of the gene in either the AB or P1 lineage can supply sdc-1(+) function to cells of the other lineage; (3) the X/A ratio is assessed immediately, in the one- or two-celled embryo; or (4) the X/A signal directs the choice of sexual fate in a non-cell-autonomous fashion. Finally, examination of the classes of sexual phenotypes produced in sdc-1 mutant strains suggests that different cells in the organism may not choose their sexual fates independently.

Alleles↗
PubMed1990

Plasma melatonin in patients with breast cancer.

Daytime plasma melatonin values were measured by radioimmune assay in 86 patients with breast cancer; 280 assays were done and compared with the clinical status of the patients. Patients in the advanced disease group had significantly higher levels than those in the adjuvant treatment group, and patients with progressive disease had significantly higher values than those in remission or with stable disease. No significant differences were found between different dominant metastatic disease sites. Multiple-regression tests showed a significant inverse correlation between survival and melatonin values.

Biomarkers, Tumor↗
PubMed1990

[Optimization of the powder application in the Cerec method with environment-friendly propellant systems].

This study compared the thickness of powder layers sprayed on Cerec inlay cavity preparations before taking the "optical impression". 6 different powder propellant methods were evaluated. 60 MOD inlay cavities were prepared in vitro in extracted human molars and mounted in phantom-head jaws. 10 clinicians powdered 1 cavity each for each of the 6 methods. The powdered teeth were embedded in acrylic and the preparations sectioned parallel to the cavity floor, mesio-distally and bucco-lingually. The powder layer thickness on the proximo-lateral walls (PLW), cavity floors (CF) and occlusal margins (OM) were measured using a light microscope. The means and SD are: [Table; see text] This study showed that propane-butane propellants were as effective as the fluoridated hydrocarbons. A wet system (5) was good despite the transient surface cooling (-43 degrees C) effect. However, the air-flow system (6) produced acceptable powder layers as well, avoiding any chemical contamination of the room air.

Aerosol Propellants↗
PubMed1989

Effects of experimental hypothyroidism on the distribution of lipids and lipoproteins in the plasma of rats.

Male Sprague-Dawley rats were treated for up to 4 weeks with propylthiouracil in a study designed to determine the effects of experimental hypothyroidism on plasma lipoproteins. The distribution of lipid constituents across the plasma lipoprotein spectrum was assessed by size exclusion chromatography and the lipoprotein particle size was assessed by gradient gel electrophoresis. A reduction in the concentration of thyroid hormones was accompanied by changes to plasma lipoproteins within 1 week of commencing treatment with propylthiouracil. These changes progressed for a further week, after which the pattern remained relatively stable for up to 4 weeks of treatment. In the animals treated with propylthiouracil, there was a marked reduction in the concentration of all constituents of very-low-density lipoproteins (VLDL). There was a coincident increase in concentration of all constituents of low-density lipoproteins (LDL), with an increase in LDL triacylglycerol being particularly obvious. There was also a marked and sustained increase in the concentration of cholesterol in high-density lipoproteins (HDL), but in this case, there were no sustained increases in the concentrations of other HDL constituents. There was, however, an appearance of new populations of very large HDL particles comparable to the HDLc which accumulate in the plasma of cholesterol-fed animals.

Animals↗
PubMed1989

Induction of osteogenesis.

Bone induction studies on baboons using standard millipore tissue chambers showed that lyophilised bone, bone marrow and thrombocytes (growth factors) are necessary for optimal osteogenesis. The decalcification of bone tissue before transplantation leads to the impairment of new bone growth.

Animals↗
PubMed1989

Genes that implement the hermaphrodite mode of dosage compensation in Caenorhabditis elegans.

We report a genetic characterization of several essential components of the dosage compensation process in Caenorhabditis elegans. Mutations in the genes dpy-26, dpy-27, dpy-28, and the newly identified gene dpy-29 disrupt dosage compensation, resulting in elevated X-linked gene expression in XX animals and an incompletely penetrant maternal-effect XX-specific lethality. These dpy mutations appear to cause XX animals to express each set of X-linked genes at a level appropriate for XO animals. XO dpy animals are essentially wild type. Both the viability and the level of X-linked gene expression in XX animals carrying mutations in two or more dpy genes are the same as in animals carrying only a single mutation, consistent with the view that these genes act together in a single process (dosage compensation). To define a potential time of action for the gene dpd-28 we performed reciprocal temperature-shift experiments with a heat sensitive allele. The temperature-sensitive period for lethality begins 5 hr after fertilization at the 300-cell stage and extends to about 9 hr, a point well beyond the end of cell proliferation. This temperature-sensitive period suggests that dosage compensation is functioning in XX animals by mid-embryogenesis, when many zygotically transcribed genes are active. While mutations in the dpy genes have no effect on the sexual phenotype of otherwise wild-type XX or XO animals, they do have a slight feminizing effect on animals whose sex-determination process is already genetically perturbed. The opposite directions of the feminizing effects on sex determination and the masculinizing effects on dosage compensation caused by the dpy mutations are inconsistent with the wild-type dpy genes acting to coordinately control both processes. Instead, the feminizing effects are most likely an indirect consequence of disruptions in dosage compensation caused by the dpy mutations. Based on the cumulative evidence, the likely mechanism of dosage compensation in C. elegans involves reducing X-linked gene expression in XX animals to equal that in XO animals via the action of the dpy genes.

Animals↗
PubMed1989

The Caenorhabditis elegans gene sdc-2 controls sex determination and dosage compensation in XX animals.

We have identified a new X-linked gene, sdc-2, that controls the hermaphrodite (XX) modes of both sex determination and X chromosome dosage compensation in Caenorhabditis elegans. Mutations in sdc-2 cause phenotypes that appear to result from a shift of both the sex determination and dosage compensation processes in XX animals to the XO modes of expression. Twenty-eight independent sdc-2 mutations have no apparent effect in XO animals, but cause two distinct phenotypes in XX animals: masculinization, reflecting a defect in sex determination, and lethality or dumpiness, reflecting a disruption in dosage compensation. The dosage compensation defect can be demonstrated directly by showing that sdc-2 mutations cause elevated levels of several X-linked transcripts in XX but not XO animals. While the masculinization is blocked by mutations in sex determining genes required for male development (her-1 and fem-3), the lethality, dumpiness and overexpression of X-linked genes are not, indicating that the effect of sdc-2 mutations on sex determination and dosage compensation are ultimately implemented by two independent pathways. We propose a model in which sdc-2 is involved in the coordinate control of both sex determination and dosage compensation in XX animals and acts in the regulatory hierarchy at a step prior to the divergence of the two pathways.

Animals↗