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Biomedical subjects

B Bednarczyk

Publications and source records attributed to B Bednarczyk.

11 recordsLinked to original sources
PubMed1991

Importance of the lay press in the transmission of medical knowledge to the scientific community.

BACKGROUND: Efficient, undistorted communication of the results of medical research is important to physicians, the scientific community, and the public. Information that first appears in the scientific literature is frequently retransmitted in the popular press. Does popular coverage of medical research in turn amplify the effects of that research on the scientific community? METHODS: To test the hypothesis that researchers are more likely to cite papers that have been publicized in the popular press, we compared the number of references in the Science Citation Index to articles in the New England Journal of Medicine that were covered by The New York Times with the number of references to similar articles that were not covered by the Times. We also performed the comparison during a three-month period when the Times was on strike but continued to prepare an "edition of record" that was not distributed; doing so enabled us to address the possibility that coverage in the Times was simply a marker of the most important articles, which would therefore be cited more frequently, even without coverage in the popular press. RESULTS: Articles in the Journal that were covered by the Times received a disproportionate number of scientific citations in each of the 10 years after the Journal articles appeared. The effect was strongest in the first year after publication, when Journal articles publicized by the Times received 72.8 percent more scientific citations than control articles. This effect was not present for articles published during the strike; articles covered by the Times during this period were no more likely to be cited than those not covered. CONCLUSIONS: Coverage of medical research in the popular press amplifies the transmission of medical information from the scientific literature to the research community.

Bibliographies as Topic↗
PubMed1988

Improved receptor assay for measuring digoxin activity.

We describe a receptor assay of digoxin activity involving Na+/K+-ATPase (EC 3.6.1.37) derived from human heart tissue. The procedure requires 500 microL of serum or plasma and incorporates one purification step, with Sep-Pak C18 cartridges (Waters). The method appears to be considerably more specific for digoxin and its cardio-active metabolites than are conventional immunoassays. Cardio-inactive metabolites and several digoxin-like factors cross react only slightly. The between-day coefficient of variation for the procedure ranged from 8.10% to 1.37% for digoxin concentrations between 0.5 and 5.0 nmol/L.

Animals↗
PubMed1982

Different effects of 3-chlorophenylpiperazine on locomotor activity and acquisition of conditioned avoidance response in different strains of mice.

Mice of C57BL/6 (C57), Balb/c (BALB), and CD-1 (CD) strains were injected with 3-chlorophenylpiperazine (CPP), 1-10 mg/kg ip, and their exploratory and basal locomotor activities and acquisition of conditioned avoidance response in a shuttle-box were tested. In C57 mice CPP did not affect either locomotor activity or shuttle-box performance. In BALB mice CPP inhibited both basal and exploratory activities (the latter only in higher doses) and facilitated the acquisition of conditioned avoidance response. In CD mice CPP did not affect exploration, but inhibited basal locomotor activity and facilitated the shuttle-box performance. It is concluded that there exist large interstrain differences in responsiveness of mice to CPP, and that the drug may facilitate acquisition of conditioned avoidance response through a strain-specific, serotonin-independent mechanism.

Animals↗
PubMed1979

Central dopamine receptors regulate blood eosinophilia in the rat.

Dopaminergic agents, dopa and apomorphine, affected biphasically the blood eosinophil count in the rat: low doses of the drug elevated, while high doses lowered it. The response to a high dose of dopa was retained in rats pretreated with an inhibitor of dopamine-beta-hydroxylase, U 10, 157, but prevented by a centrally acting dopa decarboxylase inhibitor, NSD 1015. This indicates that the eosinopenia observed after large doses of dopa is due to the action of dopamine formed from the precursor. As intracerebroventricular injections of Ldopa also produce eosinopenia, the central site of dopamine action is indicated. The eosinopenic response to apomorphine was antagonized by a dopamine receptor blocking agent, haloperidol. This indicates that some central dopamine receptors are involved in the regulation of the eosinophil count in circulating blood. The hypophysis seems to play a crucial role in the phenomenon observed, as no eosinopenia was produced by dopa in hypophysectomized rats.

Animals↗
PubMed1978

Inhibition of "wet shakes" during morphine abstinence by an antagonist of opiate analgesia.

An antagonist of morphine analgesia, N-cyclopropylmethylnorazidomorphine (CAM) inhibited the"wet shakes" appearing during spontaneous or nalorphine-precipitated morphine abstinence. CAM inhibited the pinna reflex more strongly than did morphine and selectively antagonized quipazine-induced head twitches; its inhibition of head twitches induced by 5-hydroxytryptophan or LSD seemed unspecific. The results suggest that the opiate receptors involved in the inhibition of some symptoms of morphine abstinence and of the pinna reflex differ from those involved in opiate analgesia.

5-Hydroxytryptophan↗
PubMedDate not supplied

Stimulatory and inhibitory action of clonidine on the locomotor activity in the rat.

Clonidine depresses "motivated" but stimulates "basal" locomotor activity of normal rats. It does not affect the "dopaminergic", but inhibits "noradrenergic" locomotor stimulation produced by intraventricularly administered L-dopa methyl ester to nialamide-pretreated rats, although it does not affect the brain norepinephrine accumulation observed after administration of the dopa derivative. The importance of experimental protocol and the possible mechanism of "antiadrenergic" action of clonidine are discussed.

Animals↗