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At least 1,063 records · Page 59Linked to original sources
PubMed1978

Stuttering: high-level mistranslation in animal and bacterial cells.

In both bacterial and mammalian cells, extreme starvation for certain amino acids resulted in translational errors that could be easily detected by two-dimensional polyacrylamide gel electrophoresis. On two-dimensional gels, the faulty proteins were shown as a trail of spots with molecular weights similar to those of the authentic proteins but separated in the isoelectric focusing dimension, a phenomenon we call "stuttering." The direction of charge shift depended on the amino acid substituted and could be predicted from misreading of pyrimidines for purines at the third position of the codon. It is expected that this phenomenon will provide a rapid means of measuring the fidelity of the translational machinery from cell type to cell type.

Amino Acids↗
PubMed1986

Temporal disruptions in the "accurate" speech of articulatory defective speakers and stutterers.

Durational measures of vocalic steady states and transitions were made on phonetically accurate and fluently produced vowel-plosive, consonant-vowel bisyllables embedded in a carrier phrase. in the first experiment, these measures were taken from the speech of ten articulatory defective adult speakers and ten matched normal speakers. The second experiment analyzed durational measures in the speech of ten adult stutterers and ten matched nonstutterers. Using wideband spectrography, durational measurements were used to infer timing of articulatory movements during the subsegments of the VCV sequences. The results of both experiments suggest that the two groups of speech disordered subjects were able to produce transitional shifts appropriate to the phonetic environment but appeared to delay the initiation of coarticulatory movements. Aberrant speech timing may imply an involvement in the planning or integration of articulatory/coarticulatory movements rather than difficulty with movement execution per se.

Journal Article↗
PubMed1991

SP6 RNA polymerase stutters when initiating from an AAA... sequence.

The 16S ribosomal RNA gene of Escherichia coli was placed under the transcriptional control of consensus and modified T7 promoters and a modified SP6 promoter. Both T7 and SP6 polymerases faithfully transcribed the coding sequence (beginning at the +1 position) of each construct, although SP6 polymerase was five-fold more effective than T7 polymerase in initiating with the AAAUUG... sequence. An appreciable fraction of the SP6 transcript molecules contained additional adenosines in the -1, -2, -3, -4, and -5 positions. The transcripts containing additional residues constituted approximately 40-50% of the total SP6 transcription products. Neither the nature nor extent of the additional residues was affected by replacing the pppA 5'-end by pA. Since the identity of the inserted residues does not correspond to the sequence of the template, these additional nucleosides must result from 'stuttering' of the SP6 enzyme at the -1 to +3 positions during initiation of transcription.

Bacteriophages↗
PubMed2005

Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2.

Emerging evidence suggests that restoration of blood flow in a stuttering manner may limit lethal myocardial ischemia-reperfusion injury. However, the mechanisms contributing to this phenomenon, termed postconditioning (post-C), remain poorly defined. Our aim was to test the hypothesis that activation of classic "survival kinases," phosphatidylinositol 3-kinase (PI3-kinase) and/or extracellular signal-regulated kinase (ERK)1/2, may play a role in post-C-induced cardioprotection. In protocol 1, isolated buffer-perfused rabbit hearts underwent 30 min of sustained coronary artery occlusion and were randomized to receive abrupt reperfusion (controls) or four cycles of 30 s of reperfusion and 30 s of reocclusion before full restoration of flow (post-C). Protocol 2 was identical except control and postconditioned hearts received the PI3-kinase inhibitor LY-294002 (protocol 2A) or the ERK1/2 antagonist PD-98059 (protocol 2B) throughout the first 25 min of reperfusion, whereas in protocol 3, myocardial samples were obtained during the early minutes of reflow from additional control, postconditioned, and nonischemic sham hearts for the assessment, by standard immunoblotting, of phospho-Akt (downstream target of PI3-kinase) and phospho-ERK. Protocols 1 and 2 corroborated that infarct size (delineated by tetrazolium staining and expressed as a percent of risk region) was reduced in postconditioned hearts vs. control hearts and also revealed that post-C-induced cardioprotection was maintained despite LY-294002 treatment but was abrogated by PD-98059. These pharmacological data were supported by protocol 3, which showed increased immunoreactivity of phospho-ERK but not phospho-Akt with post-C. Thus our results implicate the involvement of ERK1/2 rather than PI3-kinase/Akt in the reduction of infarct size achieved with post-C.

Animals↗
PubMed1983

A response to "On token reinforcement and stuttering therapy: Another view on findings reported by Howie and Woods (1982)".

Ingham's (1983) critique of our research is based on the unwarranted assumption that it claimed to be a replication of Ingham and Andrews' (1973a) study. Our report did not claim to be a replication. Procedural differences between treatments do not preclude the possibility of drawing general conclusions that may apply to related treatments, or suggesting possible confounding variables that might be operating in another study. We have nevertheless dealt with each of Ingham's methodological objections. In general, we believe that we struck an acceptable compromise between the needs of clients and theoretical and research demands. We stand by our original conclusions, and note with satisfaction that Ingham concurs with our emphasis on systematic structure rather than the presence or absence of rewards as the crucial component of this type of stuttering treatment.

Journal Article↗
PubMedDate not supplied

Penile fracture in a patient with stuttering priapism.

Penile fracture commonly results from trauma of sexual intercourse or masturbation. It is common in the Middle East and America, but rare in Nigeria and sub-Sahara Africa. We present a case of penile fracture, an uncommon urologic emergency, complicating priapism, another urologic emergency; precipitated in an unusual circumstance. This report illustrates a 30-year-old undergraduate who has suffered stuttering priapism for about a week and developed penile fracture while forcefully packing the erect organ. He presented early in the hospital and had emergency surgical repair. Prognosis was good. A review of literature is also presented. Immediate surgical repair offers good prognosis in the management of this emergency.

Adult↗
PubMed2003

Activity-dependent depression of excitability and calcium transients in the neurohypophysis suggests a model of "stuttering conduction".

Using millisecond time-resolved optical recordings of transmembrane voltage and intraterminal calcium, we have determined how activity-dependent changes in the population action potential are related to a concurrent modulation of calcium transients in the neurohypophysis. We find that repetitive stimulation dramatically alters the amplitude of the population action potential and significantly increases its temporal dispersion. The population action potentials and the calcium transients exhibit well correlated frequency-dependent amplitude depression, with broadening of the action potential playing only a limited role. High-speed camera recordings indicate that the magnitude of the spike modulation is uniform throughout the neurohypophysis, thereby excluding propagation failure as the underlying mechanism. In contrast, temporal dispersion and latency of the population spike do increase with distance from the stimulation site. This increase is enhanced during repeated stimulation and by raising the stimulation frequency. Changes in Ca influx directly affect the decline in population spike amplitude, consistent with electrophysiological measurements of the local loss of excitability in nerve terminals and varicosities, mediated by a Ca-activated K conductance. Our observations suggest a model of "stuttering conduction": repeated action potential stimulation causes excitability failures limited to nerve terminals and varicosities, which account for the rapid decline in the population spike amplitude. These failures, however, do not block action potential propagation but generate the cumulative increases in spike latency.

Action Potentials↗