Search

Presents a computer simulation of photoconductivity decay in AgBr microcrystals. Factor which controls the decay rate; Role of free-electron/trapped-hole recombination in the photoconductivity decay; Factor attributed to the size dependence.

Sensitometric and spectroscopic techniques are used to study the effect of 4-hydroxy-6-methyl-1,3,3a,7-tetraazaindene (TAI) during the sulphur sensitization of AgBr octahedra. TAI increased the speed of an oversensitized emulsion, causing it to have a speed comparable with the optimally sulphur-sensitized emulsion at high irradiance. TAI decreased the absorption by sulphide centres at 1.5 mmole concentration but not at 1 mmole. The long wavelength sensitivity (> 500 nm) increased at 1 mmole TAI concentration, but decreased at 1.5 mmole TAI concentration, whereas the activation energy for this response was reduced at both TAI levels. These results are interpreted using a model which assumes that TAI interacts with multiple-sulphide centres to lower their ground-state energy level, but not their electron-trapping energy level. This interaction reduces the degree of tree-hole/trapped-electron recombination that occurs at these centres. The enhancement of this recombination channel by high levels of sensitizer is what causes the oversensitization effect. [ABSTRACT FROM AUTHOR]

The increasing prevalence of antibiotic-resistant bacterial infections, particularly methicillin-resistant Staphylococcus aureus (MRSA), presents a significant public health concern. Timely detection of MRSA is crucial to enable prompt medical intervention, limit its spread, and reduce antimicrobial resistance. Here, we introduce a miniaturized nano-sieve device featuring a pneumatically-regulated chamber for highly efficient MRSA purification from human plasma samples. By using packed magnetic beads as a filter and leveraging the deformability of the nano-sieve channel, we achieved an on-chip concentration factor of ∼15-fold for MRSA. We integrated this device with recombinase polymerase amplification (RPA) and clustered regularly interspaced short palindromic repeats (CRISPR)-Cas detection system, resulting in an on-chip limit of detection (LOD) of approximately 100 CFU mL -1 . This developed approach provides a rapid, precise, and centrifuge-free solution suitable for point-of-care diagnostics, with the potential to significantly improve patient outcomes in resource-limited medical conditions.

Traditionally, cellulose nanofiber (CNF) production has primarily relied on virgin cellulose sources. Yet, the shift to using paper mill sludge (PMS) as a source for CNF underscores the significance of reusing and recycling industrial byproducts. PMS contains significant amounts of cellulose that can be extracted as a raw material. The purpose of present study is to provide a sustainable approach to PMS utilization as a paper coating additive in the cellulose nanofibrils (CNF PMS ) form via simply scalable wire-wound rod coating method. The effect of CNF PMS additive amounts at two coating layers on microstructure and surface properties of coatings such as porosity, air permeability surface roughness and optical properties such as brightness, gloss and CIE L*a*b* is studied, which they can also provide insight for the eventual print performance. Results indicated that the obtained CNF PMS in paper coating shows 52% decrease in porosity, presenting significant improvement in the coating microstructure. The marginal increase in permeability coefficient and surface roughness, 54% and 10%, respectively, suggests improving color reproduction and preventing color density losses. Optical analysis showed slight decrease in brightness and gloss, as was expected. Notably, the lightness was improved, which also indicates increasing color gamut volume in printing applications. As a result, the current work offers a sustainable approach to manage PMS for use in paper coatings as a high-value-added material., (© 2023. The Author(s).)

Genetic defects in the repair of DNA single-strand breaks (SSBs) can result in neurological disease triggered by toxic activity of the single-strand-break sensor protein PARP1. However, the mechanism(s) by which this toxic PARP1 activity triggers cellular dysfunction are unclear. Here we show that human cells lacking XRCC1 fail to rapidly recover transcription following DNA base damage, a phenotype also observed in patient-derived fibroblasts with XRCC1 mutations and Xrcc1 -/- mouse neurons. This defect is caused by excessive/aberrant PARP1 activity during DNA base excision repair, resulting from the loss of PARP1 regulation by XRCC1. We show that aberrant PARP1 activity suppresses transcriptional recovery during base excision repair by promoting excessive recruitment and activity of the ubiquitin protease USP3, which as a result reduces the level of monoubiquitinated histones important for normal transcriptional regulation. Importantly, inhibition and/or deletion of PARP1 or USP3 restores transcriptional recovery in XRCC1 -/- cells, highlighting PARP1 and USP3 as possible therapeutic targets in neurological disease., (© 2021. The Author(s).)

Mammalian DNA base excision repair (BER) is accelerated by poly(ADP-ribose) polymerases (PARPs) and the scaffold protein XRCC1. PARPs are sensors that detect single-strand break intermediates, but the critical role of XRCC1 during BER is unknown. Here, we show that protein complexes containing DNA polymerase β and DNA ligase III that are assembled by XRCC1 prevent excessive engagement and activity of PARP1 during BER. As a result, PARP1 becomes "trapped" on BER intermediates in XRCC1-deficient cells in a manner similar to that induced by PARP inhibitors, including in patient fibroblasts from XRCC1-mutated disease. This excessive PARP1 engagement and trapping renders BER intermediates inaccessible to enzymes such as DNA polymerase β and impedes their repair. Consequently, PARP1 deletion rescues BER and resistance to base damage in XRCC1 -/- cells. These data reveal excessive PARP1 engagement during BER as a threat to genome integrity and identify XRCC1 as an "anti-trapper" that prevents toxic PARP1 activity., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Here, we report on a polymer blend consisting of a soft thermoplastic polyurethane (TPU) elastomer and a low melting temperature thermoplastic healing agent (polycaprolactone, PCL). In this study, polymer blends containing up to 60 wt % PCL were prepared and the resulting mechanical, thermal, shape memory, and self-healing properties were studied. These immiscible polymers exhibit two well-separated transitions attributable to the melting of PCL and TPU hard segments. This viscoelastic behavior engendered shape memory capability at moderate processing temperatures (∼90 °C) and melt processability at elevated temperatures (>160 °C). The reversible plasticity shape memory (RPSM) effect was also characterized: when subjected to 125% strain at room temperature and subsequently heated to 90 °C, the samples nearly fully recovered to their original length. Moreover, upon heating to above PCL's melting temperature, the flow of PCL into an undeformed crack was shown to fill the crack void, thus promoting self-repair. Through the action of mild heating (90 °C/30 min), fracture surfaces are brought into intimate contact through the action of the RPSM effect and subsequently healed through the redistribution of molten PCL. The shape memory-assisted self-healing efficiency was evaluated by comparing the tensile force restoration after healing of a highly deformed, notched sample to its behavior prior to notching. It was observed that blends containing up to 30 wt % PCL showed nearly complete restoration of properties. In contrast, pure TPU showed only about 5% healing efficiency because of the absence of the PCL healing agent. Blends containing 50 and 60 wt % PCL likewise did not exhibit appreciable restoration of properties, and this was attributed to their propensity to neck during crack opening and poor mechanical properties at elevated temperatures. Blends may serve as a self-healing replacement for pure TPU in existing applications (e.g., automotive and sporting goods) or as a self-healing shape memory polymer in advanced products in soft robotic, biomedical, and microelectronic applications.

Hereditary mutations in polynucleotide kinase-phosphatase (PNKP) result in a spectrum of neurological pathologies ranging from neurodevelopmental dysfunction in microcephaly with early onset seizures (MCSZ) to neurodegeneration in ataxia oculomotor apraxia-4 (AOA4) and Charcot-Marie-Tooth disease (CMT2B2). Consistent with this, PNKP is implicated in the repair of both DNA single-strand breaks (SSBs) and DNA double-strand breaks (DSBs); lesions that can trigger neurodegeneration and neurodevelopmental dysfunction, respectively. Surprisingly, however, we did not detect a significant defect in DSB repair (DSBR) in primary fibroblasts from PNKP patients spanning the spectrum of PNKP-mutated pathologies. In contrast, the rate of SSB repair (SSBR) is markedly reduced. Moreover, we show that the restoration of SSBR in patient fibroblasts collectively requires both the DNA kinase and DNA phosphatase activities of PNKP, and the fork-head associated (FHA) domain that interacts with the SSBR protein, XRCC1. Notably, however, the two enzymatic activities of PNKP appear to affect different aspects of disease pathology, with reduced DNA phosphatase activity correlating with neurodevelopmental dysfunction and reduced DNA kinase activity correlating with neurodegeneration. In summary, these data implicate reduced rates of SSBR, not DSBR, as the source of both neurodevelopmental and neurodegenerative pathology in PNKP-mutated disease, and the extent and nature of this reduction as the primary determinant of disease severity., (© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.)

Neurodegeneration is a common hallmark of individuals with hereditary defects in DNA single-strand break repair; a process regulated by poly(ADP-ribose) metabolism. Recently, mutations in the ARH3 (ADPRHL2) hydrolase that removes ADP-ribose from proteins have been associated with neurodegenerative disease. Here, we show that ARH3-mutated patient cells accumulate mono(ADP-ribose) scars on core histones that are a molecular memory of recently repaired DNA single-strand breaks. We demonstrate that the ADP-ribose chromatin scars result in reduced endogenous levels of important chromatin modifications such as H3K9 acetylation, and that ARH3 patient cells exhibit measurable levels of deregulated transcription. Moreover, we show that the mono(ADP-ribose) scars are lost from the chromatin of ARH3-defective cells in the prolonged presence of PARP inhibition, and concomitantly that chromatin acetylation is restored to normal. Collectively, these data indicate that ARH3 can act as an eraser of ADP-ribose chromatin scars at sites of PARP activity during DNA single-strand break repair.

XRCC1 accelerates repair of DNA single-strand breaks by acting as a scaffold protein for the recruitment of Polβ, LigIIIα, and end-processing factors, such as PNKP and APTX. XRCC1 itself is recruited to DNA damage through interaction of its central BRCT domain with poly(ADP-ribose) chains generated by PARP1 or PARP2. XRCC1 is believed to interact directly with DNA at sites of damage, but the molecular basis for this interaction within XRCC1 remains unclear. We now show that the central BRCT domain simultaneously mediates interaction of XRCC1 with poly(ADP-ribose) and DNA, through separate and non-overlapping binding sites on opposite faces of the domain. Mutation of residues within the DNA binding site, which includes the site of a common disease-associated human polymorphism, affects DNA binding of this XRCC1 domain in vitro and impairs XRCC1 recruitment and retention at DNA damage and repair of single-strand breaks in vivo., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)