Planar penta-transition metal phosphide and arsenide as narrow-bandgap semiconductors from first principle calculations

Searching for materials with single atom-thin as well as planar structure, like graphene and borophene, is one of the most attractive themes in two dimensional materials. Herein, using density functional theory calculations, we have proposed a series of single layer planar penta-transition metal phosphide and arsenide, i.e. TM$\mathrm{_2}$X$\mathrm{_4}$ (TM= Ni, Pd and Pt; X=P, As). According to the calculated phonon dispersion relation and elastic constants, as well as ab initio molecular dynamics simulation results, monolayers of planar penta-TM$\mathrm{_2}$X$\mathrm{_4}$ are dynamically, mechanically, and thermally stable. In addition, the band structures calculated with the screened HSE06 hybrid functional including spin-orbit coupling show that these monolayers are direct-gap semiconductors with sizeable band gaps ranging from 0.14 eV to 0.69 eV. Besides, the optical properties in these monolayers are further investigated, where strong in-plane optical absorption with wide spectral range has been revealed. Our results indicate that planar penta-TM$\mathrm{_2}$X$\mathrm{_4}$ monolayers are interesting narrow gap semiconductors with excellent optical properties, and may find potential applications in photoelectronics.Comment: 6 figures, with Supporting Informatio

The role of China in the global spread of the current cholera pandemic

Epidemics and pandemics of cholera, a severe diarrheal disease, have occurred since the early 19th century and waves of epidemic disease continue today. Cholera epidemics are caused by individual, genetically monomorphic lineages of Vibrio cholerae: the ongoing seventh pandemic, which has spread globally since 1961, is associated with lineage L2 of biotype El Tor. Previous genomic studies of the epidemiology of the seventh pandemic identified three successive sub-lineages within L2, designated waves 1 to 3, which spread globally from the Bay of Bengal on multiple occasions. However, these studies did not include samples from China, which also experienced multiple epidemics of cholera in recent decades. We sequenced the genomes of 71 strains isolated in China between 1961 and 2010, as well as eight from other sources, and compared them with 181 published genomes. The results indicated that outbreaks in China between 1960 and 1990 were associated with wave 1 whereas later outbreaks were associated with wave 2. However, the previously defined waves overlapped temporally, and are an inadequate representation of the shape of the global genealogy. We therefore suggest replacing them by a series of tightly delineated clades. Between 1960 and 1990 multiple such clades were imported into China, underwent further microevolution there and then spread to other countries. China was thus both a sink and source during the pandemic spread of V. cholerae, and needs to be included in reconstructions of the global patterns of spread of cholera

Arginine deiminase pathway is far more important than urease for acid resistance and intracellular survival in Laribacter hongkongensis: a possible result of arc gene cassette duplication

BACKGROUND: Laribacter hongkongensis is a Gram-negative, urease-positive bacillus associated with invasive bacteremic infections in liver cirrhosis patients and fish-borne community-acquired gastroenteritis and traveler's diarrhea. Its mechanisms of adaptation to various environmental niches and host defense evasion are largely unknown. During the process of analyzing the L. hongkongensis genome, a complete urease cassette and two adjacent arc gene cassettes were found. We hypothesize that the urease cassette and/or the arc gene cassettes are important for L. hongkongensis to survive in acidic environment and macrophages. In this study, we tested this hypothesis by constructing single, double and triple non-polar deletion mutants of the urease and two arc gene cassettes of L. hongkongensis using the conjugation-mediated gene deletion system and examining their effects in acidic environment in vitro, in macrophages and in a mouse model. RESULTS: HLHK9ureA, HLHK9ureC, HLHK9ureD and HLHK9ureE all exhibited no urease activity. HLHK9arcA1 and HLHK9arcA2 both exhibited arginine deiminase (ADI) activities, but HLHK9arcA1/arcA2 double deletion mutant exhibited no ADI activity. At pH 2 and 3, survival of HLHK9arcA1/arcA2 and HLHK9ureA/arcA1/arcA2 were markedly decreased (p < 0.001) but that of HLHK9ureA was slightly decreased (p < 0.05), compared to wild type L. hongkongensis HLHK9. Survival of HLHK9ureA/arcA1/arcA2 and HLHK9arcA1/arcA2 in macrophages were also markedly decreased (p < 0.001 and p < 0.01 respectively) but that of HLHK9ureA was slightly decreased (p < 0.05), compared to HLHK9, although expression of arcA1, arcA2 and ureA genes were all upregulated. Using a mouse model, HLHK9ureA exhibited similar survival compared to HLHK9 after passing through the murine stomach, but survival of HLHK9arcA1/arcA2 and HLHK9ureA/arcA1/arcA2 were markedly reduced (p < 0.01). CONCLUSIONS: In contrast to other important gastrointestinal tract pathogens, ADI pathway is far more important than urease for acid resistance and intracellular survival in L. hongkongensis. The gene duplication of the arc gene cassettes could be a result of their functional importance in L. hongkongensis.published_or_final_versio

Co-existence of multiple distinct lineages in Vibrio parahaemolyticus serotype O4:K12

Vibrio parahaemolyticus is an important cause of foodborne gastroenteritis globally. Thermostable direct haemolysin (TDH) and the TDH-related haemolysin are the two key virulence factors in V. parahaemolyticus. Vibrio pathogenicity islands harbour the genes encoding these two haemolysins. The serotyping of V. parahaemolyticus is based on the combination of O and K antigens. Frequent recombination has been observed in V. parahaemolyticus , including in the genomic regions encoding the O and K antigens. V. parahaemolyticus serotype O4:K12 has caused gastroenteritis outbreaks in the USA and Spain. Recently, outbreaks caused by this serotype of V. parahaemolyticus have been reported in China. However, the relationships among this serotype of V. parahaemolyticus strains isolated in different regions have not been addressed. Here, we investigated the genome variation of the V. parahaemolyticus serotype O4:K12 using the whole-genome sequences of 29 isolates. We determined five distinct lineages in this strain collection. We observed frequent recombination among different lineages. In contrast, little recombination was observed within each individual lineage. We showed that the lineage of this serotype of V. parahaemolyticus isolated in America was different from those isolated in Asia and identified genes that exclusively existed in the strains isolated in America. Pan-genome analysis showed that strain-specific and cluster-specific genes were mostly located in the genomic islands. Pan-genome analysis also showed that the vast majority of the accessory genes in the O4:K12 serotype of V. parahaemolyticus were acquired from within the genus Vibrio . Hence, we have shown that multiple distinct lineages exist in V. parahaemolyticus serotype O4:K12 and have provided more evidence about the gene segregation found in V. parahaemolyticus isolated in different continents

Virulence regulator AphB enhances toxR transcription in Vibrio cholerae

<p>Abstract</p> <p>Background</p> <p><it>Vibrio cholerae </it>is the causative agent of cholera. Extensive studies reveal that complicated regulatory cascades regulate expression of virulence genes, the products of which are required for <it>V. cholerae </it>to colonize and cause disease. In this study, we investigated the expression of the key virulence regulator ToxR under different conditions.</p> <p>Results</p> <p>We found that compared to that of wild type grown to stationary phase, the <it>toxR </it>expression was lower in an <it>aphB </it>mutant strain. AphB has been previously shown to be a key virulence regulator that is required to activate the expression of <it>tcpP</it>. When expressed constitutively, AphB is able to activate the <it>toxR </it>promoter. Furthermore, gel shift analysis indicates that AphB binds <it>toxR </it>promoter region directly. We also characterize the effect of AphB on the levels of the outer membrane porins OmpT and OmpU, which are known to be regulated by ToxR.</p> <p>Conclusions</p> <p>Our data indicate that <it>V. cholerae </it>possesses an additional regulatory loop that use AphB to activate the expression of two virulence regulators, ToxR and TcpP, which together control the expression of the master virulence regulator ToxT.</p

Spatiotemporal evolution of air cargo networks and its impact on economic development - An analysis of China's domestic market before and during the COVID-19 pandemic

China's domestic air cargo network plays a crucial role in economic development by enabling the efficient and reliable transportation of goods, ensuring regional competitiveness, and supporting sustained economic growth. This study aimed to examine and analyse the spatiotemporal evolution of China's domestic air cargo network and structural configuration and its relationship with local economic development before and during the COVID-19 pandemic, thereby enhancing a better understanding of the mechanisms linking air cargo networks/operations and economic development. By applying the complex network theory and the seemingly unrelated regression framework, this study revealed a significant expansion of China's domestic air cargo network, even amidst the COVID-19 pandemic. The results showed the substantial growth of smaller airports in the western region that were involved in air cargo operations and the enhanced connectivity of major hub airports in coastal cities in the east. Moreover, this study established a causal relationship between the development of the air cargo network and economic growth. These findings have significant implications for various stakeholders, including policymakers at both the central and local levels, as well as airports and airlines, strengthening the development of air cargo networks

Characters of homogentisate oxygenase gene mutation and high clonality of the natural pigment-producing Vibrio cholerae strains

<p>Abstract</p> <p>Background</p> <p>Some microorganisms can produce pigments such as melanin, which has been associated with virulence in the host and with a survival advantage in the environment. In <it>Vibrio cholerae</it>, studies have shown that pigment-producing mutants are more virulent than the parental strain in terms of increased UV resistance, production of major virulence factors, and colonization. To date, almost all of the pigmented <it>V. cholerae </it>strains investigated have been induced by chemicals, culture stress, or transposon mutagenesis. However, during our cholera surveillance, some nontoxigenic serogroup O139 strains and one toxigenic O1 strain, which can produce pigment steadily under the commonly used experimental growth conditions, were obtained in different years and from different areas. The genes VC1344 to VC1347, which correspond to the El Tor strain N16961 genome and which comprise an operon in the tyrosine catabolic pathway, have been confirmed to be associated with a pigmented phenotype. In the present study, we investigated the mechanism of pigment production in these strains.</p> <p>Results</p> <p>Sequencing of the VC1344, VC1345, VC1346, and VC1347 genes in these pigmented strains suggested that a deletion mutation in the homogentisate oxygenase gene (VC1345) may be associated with the pigmented phenotype, and gene complementation confirmed the role of this gene in pigment production. An identical 15-bp deletion was found in the VC1345 gene of all six O139 pigment-producing strains examined, and a 10-bp deletion was found in the VC1345 gene of the O1 strain. Strict sequence conservation in the VC1344 gene but higher variance in the other three genes of this operon were observed, indicating the different stress response functions of these genes in environmental adaption and selection. On the basis of pulsed-field gel electrophoresis typing, the pigment-producing O139 strains showed high clonality, even though they were isolated in different years and from different regions. Additionally all these O139 strains belong to the rb4 ribotype, which contains the O139 strains isolated from diarrheal patients, although these strains are cholera toxin negative.</p> <p>Conclusion</p> <p>Dysfunction of homogentisate oxygenase (VC1345) causes homogentisate accumulation and pigment formation in naturally pigmented strains of <it>V. cholerae</it>. The high clonality of these strains may correlate to an environmental survival advantage in the <it>V. cholerae </it>community due to their pigment production, and may imply a potential protective function of melanin in environmental survival of such strains.</p