Auger Recombination and Carrier–Lattice Thermalization in Semiconductor Quantum Dots under Intense Excitation

A thorough understanding of the photocarrier relaxation dynamics in semiconductor quantum dots (QDs) is essential to optimize their device performance. However, resolving hot carrier kinetics under high excitation conditions with multiple excitons per dot is challenging because it convolutes several ultrafast processes, including Auger recombination, carrier–phonon scattering, and phonon thermalization. Here, we report a systematic study of the lattice dynamics induced by intense photoexcitation in PbSe QDs. By probing the dynamics from the lattice perspective using ultrafast electron diffraction together with modeling the correlated processes collectively, we can differentiate their roles in photocarrier relaxation. The results reveal that the observed lattice heating time scale is longer than that of carrier intraband relaxation obtained previously using transient optical spectroscopy. Moreover, we find that Auger recombination efficiently annihilates excitons and speeds up lattice heating. This work can be readily extended to other semiconductor QDs systems with varying dot sizes

Additional file 1 of Effects of iron on the growth, biofilm formation and virulence of Klebsiella pneumoniae causing liver abscess

Additional file 1: Table S1. Primers used for PCR amplification of virulence gene

Additional file 2 of Effects of iron on the growth, biofilm formation and virulence of Klebsiella pneumoniae causing liver abscess

Additional file 2: Table S2. Primers used for qRT-PCR of siderophore gene

Additional file 2 of Effects of iron on the growth, biofilm formation and virulence of Klebsiella pneumoniae causing liver abscess

Additional file 2: Table S2. Primers used for qRT-PCR of siderophore gene

Restoring Colistin Sensitivity and Combating Biofilm Formation: Synergistic Effects of Colistin and Usnic Acid against Colistin-Resistant <i>Enterobacteriaceae</i>

Colistin (COL), the last line of defense in clinical medicine, is an important therapeutic option against multidrug-resistant Gram-negative bacteria. In this context, the emergence of colistin-resistant (COL-R) bacteria mediated by broad-spectrum efflux pumps, mobile genetic elements, and biofilm formation poses a significant public health concern. In response to this challenge, a novel approach of combining COL with usnic acid (UA) has been proposed in this study. UA is a secondary metabolite derived from lichens and is well-known for its anti-inflammatory properties. This study aimed to investigate the synergistic effects of UA and COL against COL-R Enterobacteriaceae both in vitro and in vivo. The exceptional synergistic antibacterial activity exhibited by the combination of COL and UA was demonstrated by performing a comprehensive set of assays, including the checkerboard assay, time-dependent killing assay, and Live/Dead bacterial cell viability assay. Furthermore, crystal violet staining and scanning electron microscopy assays revealed the inhibitory effect of this combination on the biofilm formation. Mechanistically, the combination of UA and COL exacerbated cell membrane rupture, induced DNA damage, and generated a significant amount of reactive oxygen species, which ultimately resulted in bacterial cell death. In addition, erythrocyte hemolysis and cell viability tests confirmed the biocompatibility of the combination. The evaluation of the COL/UA combination in vivo using Galleria mellonella larvae and a mouse infection model showed a significant improvement in the survival rate of the infected larvae as well as a reduction in the bacterial load in the mouse thigh muscle. These findings, for the first time, provide strong evidence for the potential application of COL/UA as an effective alternative therapeutic option to combat infections caused by COL-R Enterobacteriaceae strains

Complete genome sequence of the emerging pathogen <i>Cysteiniphilum</i> spp. and comparative genomic analysis with genus <i>Francisella</i>: Insights into its genetic diversity and potential virulence traits

Cysteiniphilum is a newly discovered genus in 2017 and is phylogenetically closely related to highly pathogenic Francisella tularensis. Recently, it has become an emerging pathogen in humans. However, the complete genome sequence of genus Cysteiniphilum is lacking, and the genomic characteristics of genetic diversity, evolutionary dynamics, and pathogenicity have not been characterized. In this study, the complete genome of the first reported clinical isolate QT6929 of genus Cysteiniphilum was sequenced, and comparative genomics analyses to Francisella genus were conducted to unveil the genomic landscape and diversity of the genus Cysteiniphilum. Our results showed that the complete genome of QT6929 consists of one 2.61 Mb chromosome and a 76,819 bp plasmid. The calculated average nucleotide identity and DNA–DNA hybridization values revealed that two clinical isolates QT6929 and JM-1 should be reclassified as two novel species in genus Cysteiniphilum. Pan-genome analysis revealed genomic diversity within the genus Cysteiniphilum and an open pan-genome state. Genomic plasticity analysis exhibited abundant mobile genetic elements including genome islands, insertion sequences, prophages, and plasmids on Cysteiniphilum genomes, which facilitated the broad exchange of genetic material between Cysteiniphilum and other genera like Francisella and Legionella. Several potential virulence genes associated with lipopolysaccharide/lipooligosaccharide, capsule, and haem biosynthesis specific to clinical isolates were predicted and might contribute to their pathogenicity in humans. Incomplete Francisella pathogenicity island was identified in most Cysteiniphilum genomes. Overall, our study provides an updated phylogenomic relationship of members of the genus Cysteiniphilum and comprehensive genomic insights into this rare emerging pathogen.</p

Additional file 1 of Effects of iron on the growth, biofilm formation and virulence of Klebsiella pneumoniae causing liver abscess

Additional file 1: Table S1. Primers used for PCR amplification of virulence gene

Azomycin Orchestrate Colistin-Resistant Enterobacter cloacae Complex’s Colistin Resistance Reversal In Vitro and In Vivo

The Enterobacter cloacae complex (ECC) is a group of nosocomial pathogens that pose a challenge in clinical treatment due to its intrinsic resistance and the ability to rapidly acquire resistance. Colistin was reconsidered as a last-resort antibiotic for combating multidrug-resistant ECC. However, the persistent emergence of colistin-resistant (COL-R) pathogens impedes its clinical efficacy, and novel treatment options are urgently needed. We propose that azomycin, in combination with colistin, restores the susceptibility of COL-R ECC to colistin in vivo and in vitro. Results from the checkerboard susceptibility, time-killing, and live/dead bacterial cell viability tests showed strong synergistic antibacterial activity in vitro. Animal infection models suggested that azomycin–colistin enhanced the survival rate of infected Galleria mellonella and reduced the bacterial load in the thighs of infected mice, highlighting its superior in vivo synergistic antibacterial activity. Crystal violet staining and scanning electron microscopy unveiled the in vitro synergistic antibiofilm effects of azomycin–colistin. The safety of azomycin and azomycin–colistin at experimental concentrations was confirmed through cytotoxicity tests and an erythrocyte hemolysis test. Azomycin–colistin stimulated the production of reactive oxygen species in COL-R ECC and inhibited the PhoPQ two-component system to combat bacterial growth. Thus, azomycin is feasible as a colistin adjuvant against COL-R ECC infection

Table_1_Comparison of Carbapenem-Resistant Klebsiella pneumoniae Strains Causing Intestinal Colonization and Extraintestinal Infections: Clinical, Virulence, and Molecular Epidemiological Characteristics.docx

Carbapenem-resistant Klebsiella pneumonia (CRKP) infections has become a concerning threat. However, knowledge regarding the characteristics of intestinal CRKP isolates is limited. This study aimed to investigate and compare the clinical, virulence and molecular epidemiological characteristics of intestinal colonization and extraintestinal infections CRKP strains. The clinical characteristics were investigated retrospectively. Polymerase chain reaction was used to investigate the capsular serotype, virulence genes and carbapenemase genes. Capsular polysaccharide quantification assay, serum resistance assay, biofilm formation assay, and infection model of Galleria mellonella larvae were performed to compare the virulence and pathogenicity. Besides, multilocus-sequence-typing (MLST) and pulsed-field-gel-electrophoresis (PFGE) were conducted to explore the homology of intestinal CRKP isolates. A total of 54 intestinal CRKP isolates were included. The main capsular serotypes were K14, K64, and K19. C-reactive protein and the proportion of ICU isolation of the infection group were significantly higher than that of the colonization group (P 0.05), but the lethality of the infection group to Galleria mellonella was significantly higher than that of the colonization group (P < 0.05). The MLST categorized the 54 isolates into 13 different sequence types. PFGE revealed that homology among the 54 CRKP strains was <80%. This study suggested that the CRKP strains in the infection group had higher virulence than those in the colonization group. The development of CRKP isolates colonizing in the intestine should be addressed in future clinical surveillance.</p

Additional file 1: of Evolution of resistance mechanisms and biological characteristics of rifampicin-resistant Staphylococcus aureus strains selected in vitro

Table S1. The details of bacterial growth curves for all strains derived in this study, the optical density of the bacterial culture at 595 nm was measured after 0 to 24 h of incubation. Experiments were performed in duplicate, and the averages were used for estimating growth parameters. (DOCX 41 kb