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Biomedical subjects

B Weiss

Publications and source records attributed to B Weiss.

At least 253 records · Page 14Linked to original sources
PubMed1985

Effect of age on the rate of recovery of beta-adrenergic receptors in rat brain following desmethylimipramine-induced subsensitivity.

Brain tissues from aged rats have an impaired ability to increase beta-adrenergic receptors in response to reduced noradrenergic input, but can down-regulate these receptors in response to repeated administration of desmethylimipramine (DMI). In this study we compared the ability of brain tissues from young (3-month) and aged (20- to 26-month) rats to restore their density of beta-adrenergic receptors following desmethylimipramine (DMI)-induced receptor subsensitivity. Either DMI or saline was administered i.p. twice daily for 7 days to groups of young and aged rats. At various times after drug administration [3H]dihydroalprenolol (DHA) binding was determined in homogenates of pineal gland and cerebral cortex. Four hours after the last dose of DMI there was a decrease in DHA binding in both brain areas of young and aged rats. In young rats DHA binding in these tissues returned to control levels by 2 days after DMI administration. In contrast, in aged rats it took 8 and 16 days for DHA binding to recover in cerebrum and pineal, respectively. The concentration and half-life for the disappearance of DMI from serum and cerebrum were significantly greater in aged rats than in young rats, but the differences do not entirely explain the delayed recovery of beta-receptors in the aged rats. The results suggest that beta-adrenergic receptors of brain tissues from aged rats cannot recover from beta-receptor subsensitivity as readily as those from young rats. If this recovery process requires the synthesis of new receptors, then this synthetic mechanism may be impaired with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1985

[Acute myocardial infarct in a metropolitan area].

In a retrospective study the course of acute myocardial infarction was investigated in 1840 patients treated in 1980 in eleven Hamburg hospitals (90% of hospitals admitting emergencies). 71% of patients were over 60 years of age, infarction frequency reached its peak in the eighth decade. Compared to prior investigations the percentage of women was higher both as a whole and in patients over 70 years of age (ratio men to women = 1.8 : 1). In comparison with the overall population of Hamburg, infarction rate was not increased in certain social classes. Frequency of "silent" infarctions was 4 to 5 times higher in patients of 70 years of age than in younger ones. Left ventricular failure and conduction disturbances increased with age, while extrasystoles occurred at all ages without difference. Hospital mortality of acute infarction was 29% for men and 37% for women. Striking results are the higher mortality of younger women and the considerable increase of mortality in patients over 70 years of age, probably due to change of age structure, the large number of acute reinfarctions (29%), and the short admission time. 40% of patients of all age-groups were admitted within 3 hours after onset of infarction.

Adult↗
PubMed1985

Performance and exposure indices of rats exposed to low concentrations of lead.

To further characterize the lower end of the function relating lead exposure and biological exposure indices to behavior, male weanling rats were exposed chronically to drinking solutions containing 25 ppm sodium acetate (controls) or 25 ppm lead acetate. Behavioral training began when the animals reached 50 days of age, and performance on a fixed-interval 1-min schedule of food reinforcement was then assessed over 90 experimental sessions (136 days). This exposure produced overall response rate increases over the first 40 sessions that were similar to those observed previously with higher concentrations of lead. Response rates of the two groups tended to merge subsequently. The increased overall response rates in the treated group derived primarily from an increased frequency of shorter interresponse times (IRTs) and increased running rates (calculated without the postreinforcement interval). Blood lead (PbB) and zinc protoporphyrin (ZPP) values were determined following sessions 30, 60, and 90. PbB values of the lead-exposed group averaged 15 to 20 micrograms/dl throughout the study; ZPP did not differ. The mean brain lead value of the treated group was 0.07 micrograms Pb/g. Blood-brain ratios (1.38 to 4.06) were substantially greater than those previously observed at higher exposures. These data extend to even lower exposures, and lower blood lead concentrations, the effective concentration for behavioral effects, and further emphasize the importance of the sensitivity of the endpoint in assessing behavioral toxicity.

Animals↗
PubMed1985

Alterations in behavior produced by inhaled ozone or ammonia.

Ozone, a lower-airway irritant, produces fatigue, lethargy, and increased respiratory rates in several species, including man. Ammonia, an upper-airway irritant, produces burning of the eyes, nose, and throat, and a decrease in respiratory rate. The effects of exposure to these two prototypical irritants were examined to see if behavioral changes during and after exposure occurred at concentrations comparable to those that produce symptoms in humans. Long-Evans rats and Swiss mice, individually housed in running wheels, were exposed either to ozone (0.08, 0.12, 0.25, or 0.5 ppm) or to ammonia (100 or 300 ppm) for 6 hr. Each animal's behavior was compared with its own control performance. Running in both species decreased in a concentration-related manner during exposure to either irritant. The decrease in running activity produced by high concentrations of ozone persisted for several hours after exposure. Concentrations of ammonia that eliminated running during exposure led to an increase in activity following exposure. At comparable concentrations of both compounds, activity in rats decreased more than in mice.

Ammonia↗
PubMed1985

Endonuclease III (nth) mutants of Escherichia coli.

Two strains that overproduce endonuclease III were found in a colony bank containing hybrid ColE1-Escherichia coli plasmids. The enzyme was identified in crude extracts by the degradation of partially depyrimidinated DNA in the presence of EDTA, by its sedimentation velocity, and by its associated thymine glycol-DNA glycosylase activity. An insertion mutation was produced by cloning the kanamycin-resistance gene of Tn5 into the plasmid copy of the nth gene. The mutation was then transferred to the chromosome in the following steps: (i) selection for chromosomal integration of the plasmid at 42 degrees C in a temperature-sensitive polA strain, (ii) curing via temperature shifts, and (iii) phage P1-mediated transduction of a new host. The insertion mutant, as well as a separately isolated deletion mutant, had no measurable glycosylase activity for DNA containing thymine glycol. Although such residues are common lesions in oxidized or irradiated DNA, the mutants were not unusually sensitive to H2O2 or gamma-rays. The insertion mutation had a mutator effect (4- to 22-fold enhancement) on one tested allele.

Chromatography, High Pressure Liquid↗
PubMed1985

Inhibition of calmodulin-stimulated phosphodiesterase activity by vasoactive intestinal peptide.

The effects of certain peptides of the glucagon family on calmodulin activity were determined from their capacity to inhibit a calmodulin-dependent form of phosphodiesterase. Vasoactive intestinal peptide and secretin were potent inhibitors of calmodulin activity, having IC50 values of 0.5 microM and 2 microM, respectively. By contrast, glucagon failed to inhibit calmodulin activity even at concentrations of 100 microM. None of these compounds significantly inhibited the basal activity of phosphodiesterase at concentrations up to 100 microM. These findings support the suggestion that important structural features of peptides for anticalmodulin activity include a net positive charge and a hydrophobic surface.

Animals↗
PubMed1985

Regional distribution of calmodulin activity in rat brain.

Calmodulin activity in 68 discrete areas of rat brain, obtained by micropunch technique, was assessed by its capacity to activate a calmodulin-sensitive form of phosphodiesterase. In general, the activity of calmodulin was higher in the telencephalon, limbic system, and hypothalamus than in the mesencephalon, pons, cerebellum, and medulla. However, there were substantial differences in calmodulin activity in discrete nuclei of each region. The regional distribution of calmodulin activity in rat brain does not appear to correlate with that of any of the known putative neurotransmitters or peptides.

Animals↗
PubMed1985

Genetic mapping of nth, a gene affecting endonuclease III (thymine glycol-DNA glycosylase) in Escherichia coli K-12.

The nth gene of Escherichia coli affects the production of endonuclease III, a glycosylase-endonuclease that attacks DNA damaged by oxidizing agents or by ionizing radiation. An nth insertion mutant and a deletion mutant were studied. nth is located between add and tyrS on the linkage map of E. coli K-12 and was 97% linked to tyrS in a transduction with phage P1.

Chromosome Deletion↗
PubMed1985

dfp Gene of Escherichia coli K-12, a locus affecting DNA synthesis, codes for a flavoprotein.

The cloned dfp gene complements dna-707 (now designated dfp-707), a temperature-sensitive conditionally lethal mutation that results in a slow cessation of DNA synthesis while protein synthesis is maintained. In vitro and in vivo experiments failed to demonstrate a specific defect in the initiation of DNA replication, and turn-off of DNA synthesis at high temperature was slower than that of a typical initiation (dnaA) mutant. The gene was localized, and its product was identified through the construction and analysis of deletion and insertion mutants of dfp-containing plasmids. dfp is located between the rpmB and dut genes at 81 min on the linkage map of Escherichia coli K-12. It is transcribed clockwise, independently of dut. The ability of a plasmid to complement a chromosomal dfp-707 mutation was correlated with its ability to produce a 45-kilodalton polypeptide. The purified protein contained 1 mol of flavin mononucleotide per mol of polypeptide.

Bacterial Proteins↗
PubMed1984

Interaction of alpha adrenergic antagonists with calmodulin.

Several alpha-adrenergic antagonists inhibited the activation of calmodulin-stimulated phosphodiesterase at concentrations that had little or no effect on basal phosphodiesterase activity. The most potent of these compounds were phenoxybenzamine and dibenamine (IC50 values of about 1 microM); the amino acid ergot alkaloids ergocryptine, ergocristine, ergotamine and their dihydrogenated derivatives were less potent calmodulin-inhibitors (IC50 values of 35-80 microM). The amino ergot alkaloids ergonovine and methysergide were essentially devoid of inhibitory activity. A variety of other alpha 1-antagonists (phentolamine, tolazoline and prazosin), an alpha 2-antagonist (yohimbine), alpha-agonists (norepinephrine, phenylephrine and clonidine), beta-adrenergic antagonists (propranolol and practolol) and the beta-adrenergic agonist methoxyphenamine displayed little or no anti-calmodulin activity (IC50 values greater than 300 microM). Similarly, the alkylating agents chlorambucil and mechlorethamine also failed to inhibit calmodulin activity. Phenoxybenzamine and dibenamine inhibited calmodulin activity irreversibly, whereas the inhibition caused by other alpha adrenergic blocking agents was reversible. Phenoxybenzamine inhibited calmodulin activity by binding directly to it. This binding was calcium-dependent and irreversible. The irreversible binding and inhibition of calmodulin activity by phenoxybenzamine (or dibenamine) may serve as a useful tool for studying the sites at which drugs bind to calmodulin and may also be useful for studying the distribution and turnover of calmodulin.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

Impaired recovery of alpha 1- and alpha 2-adrenergic receptors in brain tissue of aged rats.

The influence of age on the rate of recovery of alpha 1- and alpha 2-adrenergic receptors was determined in rat brain following their irreversible inhibition by phenoxybenzamine (PBZ). Fischer 344 rats (3- or 24-months old) were administered two doses of vehicle or PBZ at 12-hour intervals. At various times after the last dose of PBZ, alpha-adrenergic receptors were quantified in washed membranes of cerebral cortex and hypothalamus, using [3H]prazosin and [3H]rauwolscine to label alpha 1- and alpha 2-adrenergic receptors, respectively. Recovery of prazosin binding sites in cortex and hypothalamus and of rauwolscine binding sites in cortex was significantly delayed in aged versus young rats. Administration of [3H]PBZ to young and aged rats revealed no apparent differences in the concentration or rate of disappearance of PBZ or its metabolites that could account for these age-related changes. These data suggest that the synthesis of both alpha 1- and alpha 2-adrenergic receptors is impaired in brain tissue from aged rats.

Aging↗
PubMed1984

Interaction of various peptides with calmodulin.

In summary, we have demonstrated the existence of several endogenous substances capable of inhibiting the action of calmodulin and have identified certain structural features of a peptide that confer calmodulin inhibitory activity. These include a net positive charge, a region of hydrophobic amino acids, and the ability to form a hydrophobic alpha-helix. We believe that these properties can be used to predict the calmodulin inhibitory potency of other peptides and can also provide an insight into the structural characteristics present in calmodulin-sensitive enzymes.

3',5'-Cyclic-AMP Phosphodiesterases↗