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In this study, peptides designed using fragments of an antifreeze protein (AFP) from the freeze-tolerant insect Tenebrio molitor, TmAFP, were evaluated as inhibitors of clathrate hydrate formation. It was found that these peptides exhibit inhibitory effects by both direct and indirect mechanisms. The direct mechanism involves the displacement of methane molecules by hydrophobic methyl groups from threonine residues, preventing their diffusion to the hydrate surface. The indirect mechanism is characterized by the formation of cylindrical gas bubbles, the morphology of which reduces the pressure difference at the bubble interface, thereby slowing methane transport. The transfer of methane to the hydrate interface is primarily dominated by gas bubbles in the presence of antifreeze peptides. Spherical bubbles facilitate methane migration and potentially accelerate hydrate formation; conversely, the promotion of a cylindrical bubble morphology by two of the designed systems was found to mitigate this effect, leading to slower methane transport and reduced hydrate growth. These findings provide valuable guidance for the design of effective peptide-based inhibitors of natural-gas hydrate formation with potential applications in the energy and environmental sectors. [ABSTRACT FROM AUTHOR]

A new gate driver with metal oxide thin‐film transistors (MO‐TFTs) has been presented for micro‐light‐emitting diode (Micro‐LED) display. The proposed gate driver employing linearly decreasing sweep signal generated module could realize the line‐by‐line pulse width modulation (PWM) driving method, which is valuable for application in high‐resolution Micro‐LED display compared with the conventional driving method employing global sweep signal. A simple Micro‐LED pixel circuit including an inverter module driven by the analog PWM method is employed to demonstrate the feasibility of the proposed gate driver. A 10 × 10 green Micro‐LED display array has been fabricated with MO‐TFTs backplane technology. It is shown that a 10‐μs width pulse and linearly scanning sweep signal can be successfully output. Consequently, the pixel circuit array can be driven properly under analog line‐by‐line PWM driving method. [ABSTRACT FROM AUTHOR]

The flexible control in burning rate and stable combustion of solid propellants over a broad range of pressures essentially determine the performance of solid rocket motors. The nanoscale metals and their oxides are usually utilized as the traditional burn rate modifiers in adjusting the combustion behaviors of solid propellants, but the energy characteristics of propellants are greatly compromised owing to the inert nature of additives used. In this paper, a series of metal complexes of triaminoguanidine-glyoxal polymer (TAGP-Ms) with high nitrogen content were synthesized and employed as energetic burn rate inhibitors in tunning the combustion properties of composite modified double-based (CMDB) propellants. The influences of prepared TAGP-Ms on the thermal decomposition and combustion of CMDB propellants were comprehensively investigated based on thermal analysis technique and combustion characterization methods. It was found that the peak temperatures of the second exotherm displayed for the propellants containing TAGP-Ms inhibitors were significantly increased by more than 30°C (except for TAGP-Cu), indicating the TAGP-Ms is capable of suppressing the thermal decomposition of CMDB propellants. More importantly, the heat releases of CMDB propellants were substantially enhanced by 16%~34% determined by DSC analysis. In comparison to the blank reference, the energetic TAGP-Ms inhibitors could promote the heat of combustion for the involved CMDB propellants by 5%~9%. The burning rates of CMDB propellants were notably reduced over a wide range of pressures by adding TAGP-Ms, whereas the calculated pressure exponents at pressures ranging from 10 to ~ 22 MPa appear to be relatively high due to the accelerated HMX decomposition. The measured combustion wave temperatures suggest that the CMDB propellants with TAGP-Ms undergo a three-stage combustion process with the highest temperatures in the range of 2160 ~ 2230°C. [ABSTRACT FROM AUTHOR]

Two new species of Polyporales, Cerrena caulinicystidiata and Polyporus minutissimus, are illustrated and described on the basis of morphological studies and phylogenetic analyses from southern China and Vietnam. C. caulinicystidiata is characterized by annual, resupinate, sometimes effused-reflexed basidiocarps, greyish orange to brownish orange pore surface, irregular pores (3–8 per mm), a trimitic hyphal system, pyriform to ventricose cystidia, and subglobose basidiospores 3.2–4.5 × 2.8–3.5 µm in size. P. minutissimus is characterized by annual, solitary, fan-shaped with a depressed center or infundibuliform basidiocarps, obvious black stipe, cream to buff yellow pileal surface with glabrous, occasionally zonate and radially aligned stripes, angular pores (6–9 per mm), a dimitic hyphal system, and cylindrical basidiospores, 5–9.2 × 2.2–4 μm. Detailed descriptions and illustrations of the two new species are provided. The differences between the two new species and their morphologically similar and phylogenetically related species are discussed. [ABSTRACT FROM AUTHOR]

Roxithromycin is an oral macrolide antibiotic agent that has been repeatedly reported to provoke excessive prolongation of the Q-T interval and torsades de pointes in clinical settings. To investigate the mechanisms underlying the arrhythmogenic side effects of roxithromycin, we studied the molecular mechanisms of roxithromycin on human etfier-a-go-go-related gene (hERG)[K.sup.+] channels expressed in human embryonic kidney (HEK293) cells. Roxithromycin was found to inhibit wild-type (WT) hERG currents in a concentration-dependent manner with a half-maximum block concentration ([IC.sub.50]) of 55.8 ± 9.1 µmol/L. S6 residue hERG mutants (Y652A and F656C) showed reduced levels of hERG current blockage attributable to roxithromycin. Roxithromycin also inhibited the trafficking of hERG protein to the cell membrane, as confirmed by Western blot analysis and confocal microscopy. These findings indicate that roxithromycin may cause acquired long-QT syndrome via direct inhibition of hERG current and by disruption of hERG protein trafficking. Mutations in drug- binding sites (Y652A or F656C) of the hERG channel were found to attenuate hERG current blockage by roxithromycin, but did not significantly alter the disruption of trafficking. Key words: roxithromycin, Q-T interval, hERG channel, HEK293 cells, long-QT syndrome, hERG protein trafficking, hERG mutants. La roxithromycine est antibiotique de la classe des macrolides qui, selon de nombreux rapports, provoque une prolongation excessive de l'intervalle Q-T et des torsades de pointe en contexte clinique. Afin d'examiner les mecanismes sous-jacents aux effets secondaires arythmogenes de la roxithromycine, nous avons etudie les mecanismes moleculaires de la roxithromycine sur le gene codant le canal potassique hERG (ether-a-go-go- related gene) exprime chez les cellules de rein embyronnaire HEK293. La roxithromycine inhibait les courants du hERG sauvage en fonction de la concentration, avec une [IC.sub.50] de 55,8 ± 9,1 µmol/L. L'inhibition du courant par la roxithromycine etait reduite chez les mutants du segment S6 du hERG (Y652A et F656C). La roxithromycine inhibait aussi le trafic de hERG a la membrane cellulaire, comme l'ont confirme le buvardage Western et la microscopie confocale. Ces donnees indiquent que la roxithromycine peut provoquer un syndrome du QT long au moyen de l'inhibition directe du courant du hERG et par la perturbation du trafic de hERG. Des mutations des sites de liaison du medicament (Y652A ou F656C) du canal hERG attenuent le blocage du courant de hERG par la roxithromycine mais n'affectent pas la perturbation du trafic. [Traduit par la Redaction] Mots-cles: roxithromycine, intervalle Q-T, canal hERG, cellules HEK293, syndrome du QT long, trafic de hERG, mutants du hERG., Introduction Acquired long-QT syndrome (LQTS) is associated with many clinically available drugs and developmental compounds (Mitcheson et al. 2000). Most drugs that can cause acquired LQTS do so through direct [...]