13 research outputs found

    Viscosity bounds in liquids with different structure and bonding types

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    Recently, it was realized that liquid viscosity has a lower bound which is nearly constant for all liquids and is governed by fundamental physical constants. This was supported by experimental data in noble and molecular liquids. Here, we perform large-scale molecular dynamics simulations to ascertain this bound in two other important liquid types: the ionic molten salt system LiF and metallic Pb. We find that these ionic and metallic systems similarly have lower viscosity bounds corresponding to the minimum of kinematic viscosity of ∼10-7m2/s. We show that this agrees with experimental data in other systems with different structures and bonding types, including noble, molecular, metallic, and covalent liquids. This expands the universality of viscosity bounds into the main system types known

    Regulated transcription of the histone H2B genes of Trypanosoma brucei.

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    In Trypanosoma brucei, the genes encoding histone H2B are organized in a cluster of about 10-15 tandemly linked copies per haploid genome. The H2B transcripts are processed by trans-splicing and polyadenylation, and encode a polypeptide of 111 residues with a molecular mass of 12.5 kDa. H2B mRNAs are differentially expressed during the parasite life-cycle and are present at higher levels in dividing procyclic and bloodstream slender forms than in the nondividing bloodstream stumpy forms. Analysis of H2B mRNA levels during the synchronous differentiation from stumpy to procyclics forms revealed that the abundance of these transcripts is regulated through the cell-cycle, reaching maximum levels during S-phase. Addition of hydroxyurea to procyclic forms in culture specifically decreased H2B mRNA levels by about twofold, an effect not linked to its 3' untranslated region. Inhibition of protein synthesis prevented this decrease.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe

    Impaired left ventricular filling in hypertensive left ventricular hypertrophy as a marker of the presence of an arrhythmogenic substrate.

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    OBJECTIVE--To assess the prevalence of ventricular late potentials and ventricular tachycardia in hypertensive subjects with left ventricular hypertrophy and to study their relation to clinical characteristics. SETTING--Teaching and general hospital in Padua. METHODS--107 hypertensive subjects with echocardiographic signs of left ventricular hypertrophy were studied with signal averaged electrocardiography and 24 hour Holter monitoring. Signal averaged electrocardiogram analysis was performed with high pass filters of 25 Hz, 40 Hz, and 80 Hz. Ventricular late potentials were considered to be present if at least two determinants of the signal averaged electrocardiogram were abnormal in one of the three filters. 70 normotensive subjects served as age matched controls. RESULTS--25% (27) of the hypertensive subjects and 6% (four) of the controls showed late potentials on signal averaged electrocardiography (P < 0.0001). The hypertensive subjects with late potentials had a higher prevalence of ventricular tachycardia (33%, 9/27) than those without late potentials (13%, 10/80; P = 0.035). Twenty nine per cent (31/107) of the hypertensive subjects had an inversion of the early to atrial filling velocity (E/A ratio < 1) on Doppler analysis of transmitral flow. Within this group the percentage of subjects with late potentials (55%, 17/31) and ventricular tachycardia (42%, 13/31) was much greater than that within the group of subjects without an inverted E/A ratio (13%, 10/76 (P < 0.0001) and 12%, 9/76 (P = 0.001) respectively). In a multivariate analysis only the E/A ratio was related to the presence or absence of either late potentials (P = 0.0001) or ventricular tachycardia (P = 0.0008). Both late potentials and ventricular tachycardia were unrelated to left ventricular mass, geometry, and systolic performance. CONCLUSIONS--A relation was found between the occurrence of ventricular tachycardia and the presence of late potentials in hypertensive subjects with left ventricular hypertrophy. Impaired left ventricular filling was the main marker for the arrhythmogenic substrate present in this disease
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