Search

While the two types of intransitive verbs, i.e. unergative and unaccusative, are hypothesised to be syntactically represented, many have proposed a semantic account where abstract properties related to agentivity and telicity, often conceptualised as binary properties, determine the classification. Here we explore the extent to which graded, embodied features rooted in neurobiological systems contribute to the distinction, representing verb meanings as continuous human ratings over various experiential dimensions. Unlike prior studies that classified verbs based on categorical intuition, we assessed the degree of unaccusativity by acceptability of the prenominal past participle construction, one of the unaccusativity diagnostics. Five models were constructed to explain these data: categorical syntactic/semantic, feature-based event-semantic, experiential, and distributional models. The experiential model best explained the diagnostic test data, suggesting that the unaccusative/unergative distinction may be an emergent phenomenon related to differences in underlying experiential content. The experiential model's advantages, including interpretability and scalability, are also discussed. [ABSTRACT FROM AUTHOR]

Herein, we have directly investigated a 2 delta L as the diffusion length in a‐IGZO TFT using a scanning capacitance microscopy (SCM) technique at the cross section of TFTs instead of indirect normal transmission line method (TLM). Moreover, we revealed that the difference of 2 delta L leads the variation of total parastic capacitance in devices, which play a key role in the properites of EL currents in case of display devices. [ABSTRACT FROM AUTHOR]

In recent years, with the approval of preventative vaccines for pandemics, lipid nanoparticles have become a prominent RNA delivery vehicle. The lack of long-lasting effects of non-viral vectors is an advantage for infectious disease vaccines. With the introduction of microfluidic processes that facilitate the encapsulation of nucleic acid cargo, lipid nanoparticles are being studied as delivery vehicles for various RNA-based biopharmaceuticals. In particular, using microfluidic chip-based fabrication processes, nucleic acids such as RNA and proteins can be effectively incorporated into lipid nanoparticles and utilized as delivery vehicles for various biopharmaceuticals. Due to the successful development of mRNA therapies, lipid nanoparticles have emerged as a promising approach for the delivery of biopharmaceuticals. Biopharmaceuticals of various types (DNA, mRNA, short RNA, proteins) possess expression mechanisms that are suitable for manufacturing personalized cancer vaccines, while also requiring formulation with lipid nanoparticles. In this review, we describe the basic design of lipid nanoparticles, the types of biopharmaceuticals used as carriers, and the microfluidic processes involved. We then present research cases focusing on lipid-nanoparticle-based immune modulation and discuss the current status of commercially available lipid nanoparticles, as well as future prospects for the development of lipid nanoparticles for immune regulation purposes. [ABSTRACT FROM AUTHOR]

A gene homologous to rpoS was cloned from a fatal human pathogen, Vibrio vulnificus. The functional role of rpoS in V. vulnificus was accessed by using an rpoS knockout mutant strain. This mutant was impaired in terms of the ability to survive under oxidative stress, nutrient starvation, UV irradiation, or acidic conditions. The increased susceptibility of the V. vulnificus mutant in the exponential phase to [H.sub.2][O.sub.2] was attributed to the reduced activity of hydroperoxidase I (HPI). Although [[sigma].sup.s] synthesis was induced and HPI activity reached the maximal level in the stationary phase, the mutant in the stationary phase showed the same susceptibility to [H.sub.2][O.sub.2] as the wild-type strain in the stationary phase. In addition, HPII activity, which is known to be controlled by [[sigma].sup.s] in Escherichia coli, was not detectable in V. vulnificus strains under the conditions tested. The mutant in the exponential phase complemented with multiple copies of either the rpoS or katG gene of V. vulnificus recovered both resistance to [H.sub.2] [O.sub.2] and HPI activity compared with the control strain. Expression of the katG gene encoding HPI in V. vulnificus was monitored by using a katG::luxAB transcriptional fusion. The expression of this gene was significantly reduced by deletion of [[sigma].sup.s] in both the early exponential and late stationary phases. Thus, [[sigma].sup.s] is necessary for increased synthesis and activity of HPI, and [[sigma].sup.s] is required for exponentially growing V. vulnificus to develop the ability to survive in the presence of [H.sub.2][O.sub.2].

Abstract Background Helicobacter pylori causes acute and chronic gastric inflammation induced by proinflammatory cytokines and chemokines secreted by cells of the gastric mucosa, including gastric epithelial cells. Previous studies have demonstrated that the bacterial arginase, RocF, is involved in inhibiting T cell proliferation and CD3ζ expression, suggesting that arginase could be involved in a more general dampening of the immune response, perhaps by down-regulation of certain pro-inflammatory mediators. Results Global transcriptome analysis was performed on AGS gastric epithelial cells infected for 16 hours with a wild type Helicobacter pylori strain 26695, an arginase mutant (rocF-) or a rocF+ complemented strain. H. pylori infection triggered altered host gene expression in genes involved in cell movement, death/growth/proliferation, and cellular function and maintenance. While the wild type strain stimulates host inflammatory pathways, the rocF- mutant induced significantly more expression of IL-8. The results of the microarray were verified using real-time PCR, and the differential levels of protein expression were confirmed by ELISA and Bioplex analysis. MIP-1B was also significantly secreted by AGS cells after H. pylori rocF- mutant infection, as determined by Bioplex. Even though not explored in this manuscript, the impact that the results presented here may have on the development of gastritis, warrant further research to understand the underlying mechanisms of the relationship between H. pylori RocF and IL-8 induction. Conclusions We conclude that H. pylori arginase modulates multiple host signaling and metabolic pathways of infected gastric epithelial cells. Arginase may play a critical role in anti-inflammatory host responses that could contribute to the ability of H. pylori to establish chronic infections.

In semitransparent perovskite solar cells with n–i–p configuration, thermal evaporation is the common method to deposit the sputter buffer material, such as molybdenum oxide and tungsten oxide. Buffer layers are especially necessary when using organic hole transporting layers, as they are more susceptible to get damaged when sputtering the top transparent conducting oxide. However, there is a limited selection of possible materials and limited control of the materials properties by thermal evaporation, which leads to inefficient protection against sputtering and poor air stability. While there have been well‐established buffer layers by atomic layer deposition, including tin oxide, for p–i–n structured semitransparent perovskite solar cells, this is not the case for n–i–p structured devices. Here, copper oxide is demonstrated by pulsed‐chemical vapor deposition incorporated into perovskite solar cells for the sputter buffer layer, which result in stable encapsulated semitransparent devices maintaining over 95% of the maximum efficiency under AM 1.5 G at maximum power point tracking for 150 h without any temperature control. [ABSTRACT FROM AUTHOR]

Vaccination is an effective measure to control the diffusion of infectious disease such as COVID-19. This paper analyzes the basic reproduction number in South Korea which enables us to identify a necessary level of vaccine stockpile to achieve herd immunity. An susceptible-infected-susceptible model is adopted that allows a stochastic diffusion. The result shows that the basic reproduction number of South Korea is approximately 2 which is substantially lower than those of the other regions. The herd immunity calculated from economic-epidemiological model suggests that at least 62% of the susceptible population be vaccinated when COVID-19 vaccine becomes available. [ABSTRACT FROM AUTHOR]

For semitransparent devices with n‐i‐p structures, a metal oxide buffer material is commonly used to protect the organic hole transporting layer from damage due to sputtering of the transparent conducting oxide. Here, a surface treatment approach is addressed for tungsten oxide‐based transparent electrodes through slight modification of the tungsten oxide surface with niobium oxide. Incorporation of this transparent electrode technique to the protective buffer layer significantly recovers the fill factor from 70.4% to 80.3%, approaching fill factor values of conventional opaque devices, which results in power conversion efficiencies over 18% for the semitransparent perovskite solar cells. Application of this approach to a four‐terminal tandem configuration with a silicon bottom cell is demonstrated. [ABSTRACT FROM AUTHOR]

Buffer Layers: Copper Oxide Buffer Layers by Pulsed-Chemical Vapor Deposition for Semitransparent Perovskite Solar Cells (Adv. Keywords: buffer layers; copper oxide; perovskite photovoltaics; pulsed-chemical vapor deposition; semitransparent solar cells EN buffer layers copper oxide perovskite photovoltaics pulsed-chemical vapor deposition semitransparent solar cells 1 1 1 01/15/21 20210108 NES 210108 In article number 2001482, Helen Hejin Park, Jangwon Seo, and co-workers introduce copper oxide by pulsed-chemical vapor deposition as a buffer layer, which protects the organic hole transport layer from sputtering damage during sputtering of the transparent conducting oxide. Buffer layers, copper oxide, perovskite photovoltaics, pulsed-chemical vapor deposition, semitransparent solar cells. [Extracted from the article]

A gene homologous to rpoS was cloned from a fatal human pathogen, Vibrio vulnificus. The functional role of rpoS in V. vulnificus was accessed by using an rpoS knockout mutant strain. This mutant was impaired in terms of the ability to survive under oxidative stress, nutrient starvation, UV irradiation, or acidic conditions. The increased susceptibility of the V. vulnificus mutant in the exponential phase to H2O2 was attributed to the reduced activity of hydroperoxidase I (HPI). Although σS synthesis was induced and HPI activity reached the maximal level in the stationary phase, the mutant in the stationary phase showed the same susceptibility to H2O2 as the wild-type strain in the stationary phase. In addition, HPII activity, which is known to be controlled by ers in Escherichia coli, was not detectable in V. vulnificus strains under the conditions tested. The mutant in the exponential phase complemented with multiple copies of either the rpoS or katG gene of V. vulnificus recovered both resistance to H2O2 and HPI activity compared with the control strain. Expression of the katG gene encoding HPI in V. vulnificus was monitored by using a katG::luxAB transcriptional fusion. The expression of this gene was significantly reduced by deletion of ers in both the early exponential and late stationary phases. Thus, σS is necessary for increased synthesis and activity of HPI, and σS is required for exponentially growing V. vulnificus to develop the ability to survive in the presence of H2O2. [ABSTRACT FROM AUTHOR]

The Gram-negative opportunistic pathogen, Pseudomonas aeruginosa , has multiple multidrug efflux pumps. MexT, a LysR-type transcriptional regulator, functions as a transcriptional activator of the MexEF-OprN efflux system. MexT consists of an N-terminal DNA-binding domain and a C-terminal regulatory domain (RD). Little is known regarding MexT ligands and its mechanism of activation. We elucidated the crystal structure of the MexT RD at 2.0 Å resolution. The structure comprised two protomer chains in a dimeric arrangement. MexT possessed an arginine-rich region and a hydrophobic patch lined by a variable loop, both of which are putative ligand-binding sites. The three-dimensional structure of MexT provided clues to the interacting ligand structure. A DNase I footprinting assay of full-length MexT identified two MexT-binding sequence in the mexEF oprN promoter. Our findings enhance the understanding of the regulation of MexT-dependent activation of efflux pumps.

The binding of MS2 bacteriophage coat protein (MCP) to MS2 binding site (MBS) RNA stem-loop sequences has been widely used to label mRNA for live-cell imaging at single-molecule resolution. However, concerns have been raised recently from studies with budding yeast showing aberrant mRNA metabolism following the MS2-GFP labeling. To investigate the degradation pattern of MS2-GFP-labeled mRNA in mammalian cells and tissues, we used Northern blot analysis of β-actin mRNA extracted from the Actb-MBS knock-in and MBS×MCP hybrid mouse models. In the immortalized mouse embryonic cell lines and various organ tissues derived from the mouse models, we found no noticeable accumulation of decay products of β-actin mRNA compared with the wild-type mice. Our results suggest that accumulation of MBS RNA decay fragments does not always happen depending on the mRNA species and the model organisms used.

We show here that NdgR, a known transcriptional activator of isopropylmalate dehydratase in actinomycetes, may have other targets in the cell. An in-frame deletion mutant of ndgR showed unexpectedly poor growth in defined minimal medium even in the presence of leucine. To our surprise, it was supplementation of cysteine and methionine that corrected the growth. Based on this, we propose that NdgR induces cysteine-methionine biosynthesis. Direct involvement of NdgR in the very last steps of methionine synthesis with methionine synthase (metH) and 5,10-methylenetetrahydrofolate reductase (metF) was examined. From a pulldown assay, it was seen that NdgR was enriched from crude cell lysates with a strong affinity to metH and metF upstream sequences. Direct physical interaction of NdgR with these targets was further examined with a gel mobility shift assay. ndgR, leuC, metH, and metF were inducible in M145 cells upon nutrient downshift from rich to minimal medium but were not induced in the ndgR knockout mutant. Taking these observations together, NdgR-dependent metH-metF expression would account for the abnormal growth phenotype of the ndgR mutant although there may be additional NdgR-dependent genes in the Cys-Met metabolic pathways. As the first transcriptional factor reported for regulating Cys-Met metabolism in Streptomyces, NdgR links two disparate amino acid families, branched-chain amino acids (BCAAs) and sulfur amino acids, at the transcriptional level. Considering that Cys-Met metabolism is connected to mycothiol and one-carbon metabolism, NdgR may have broad physiological impacts.

Aim: To investigate the role of host and bacterial arginases in the colonization of mice by Helicobacter pylori (H. pylori)., Methods: H. pylori produces a very powerful urease that hydrolyzes urea to carbon dioxide and ammonium, which neutralizes acid. Urease is absolutely essential to H. pylori pathogenesis; therefore, the urea substrate must be in ample supply for urease to work efficiently. The urea substrate is most likely provided by arginase activity, which hydrolyzes L-arginine to L-ornithine and urea. Previous work has demonstrated that H. pylori arginase is surprisingly not required for colonization of wild-type mice. Hence, another in vivo source of the critical urea substrate must exist. We hypothesized that the urea source was provided by host arginase II, since this enzyme is expressed in the stomach, and H. pylori has previously been shown to induce the expression of murine gastric arginase II. To test this hypothesis, wild-type and arginase (rocF) mutant H. pylori strain SS1 were inoculated into arginase II knockout mice., Results: Surprisingly, both the wild-type and rocF mutant bacteria still colonized arginase II knockout mice. Moreover, feeding arginase II knockout mice the host arginase inhibitor S-(2-boronoethyl)-L-cysteine (BEC), while inhibiting > 50% of the host arginase I activity in several tissues, did not block the ability of the rocF mutant H. pylori to colonize. In contrast, BEC poorly inhibited H. pylori arginase activity., Conclusion: The in vivo source for the essential urea utilized by H. pylori urease is neither bacterial arginase nor host arginase II; instead, either residual host arginase I or agmatinase is probably responsible.

The eye colour mutant sepia (se1) is defective in PDA {6-acetyl-2-amino-3,7,8,9-tetrahydro-4H-pyrimido[4,5-b]-[1,4]diazepin-4-one or pyrimidodiazepine} synthase involved in the conversion of 6-PTP (2-amino-4-oxo-6-pyruvoyl-5,6,7,8-tetrahydropteridine; also known as 6-pyruvoyltetrahydropterin) into PDA, a key intermediate in drosopterin biosynthesis. However, the identity of the gene encoding this enzyme, as well as its molecular properties, have not yet been established. Here, we identify and characterize the gene encoding PDA synthase and show that it is the structural gene for sepia. Based on previously reported information [Wiederrecht, Paton and Brown (1984) J. Biol. Chem. 259, 2195-2200; Wiederrecht and Brown (1984) J. Biol. Chem. 259, 14121-14127; Andres (1945) Drosoph. Inf. Serv. 19, 45; Ingham, Pinchin, Howard and Ish-Horowicz (1985) Genetics 111, 463-486; Howard, Ingham and Rushlow (1988) Genes Dev. 2, 1037-1046], we isolated five candidate genes predicted to encode GSTs (glutathione S-transferases) from the presumed sepia locus (region 66D5 on chromosome 3L). All cloned and expressed candidates exhibited relatively high thiol transferase and dehydroascorbate reductase activities and low activity towards 1-chloro-2,4-dinitrobenzene, characteristic of Omega class GSTs, whereas only CG6781 catalysed the synthesis of PDA in vitro. The molecular mass of recombinant CG6781 was estimated to be 28 kDa by SDS/PAGE and 56 kDa by gel filtration, indicating that it is a homodimer under native conditions. Sequencing of the genomic region spanning CG6781 revealed that the se1 allele has a frameshift mutation from 'AAGAA' to 'GTG' at nt 190-194, and that this generates a premature stop codon. Expression of the CG6781 open reading frame in an se1 background rescued the eye colour defect as well as PDA synthase activity and drosopterins content. The extent of rescue was dependent on the dosage of transgenic CG6781. In conclusion, we have discovered a new catalytic activity for an Omega class GST and that CG6781 is the structural gene for sepia which encodes PDA synthase.