The association between expressive suppression and anxiety in Chinese left-behind children in middle school: serial mediation roles of psychological resilience and self-esteem.

BACKGROUND: Left-behind children (LBC) have become a special population to be concerned due to the negative consequences of parental absence during their physical and psychological development in China. Expressive suppression (ES) is a response-focused emotion regulation and may be frequently used by LBC to suppress their emotions resulting in different forms of internalizing problems. The objective of the present study was to investigate the role of ES as an emotion regulation strategy on anxiety in Chinese left-behind children in middle school (LBC-MS) by considering the mediating role(s) of psychological resilience and self-esteem. METHODS: 820 middle school students aged between 12 and 17 years from a middle school in Xiangtan, Hunan Province, participated in the study. Screen for Child Anxiety Related Emotional Disorders (SCARED), Emotion Regulation Questionnaire (ERQ), Resilience Scale for Chinese Adolescents (RSCA), and Rosenberg Self-Esteem Scale (SES) were administered. Variables measured using the above scales in left-behind children in middle school (LBC-MS) and non-left-behind children in middle school (non-LBC-MS) were compared, and descriptive statistics were used to present the overall characteristics. Then the PROCESS macro of SPSS was used to conduct regression-based statistical mediation for the data of 211 left-behind children. RESULTS: This study revealed that LBC-MS had higher anxiety and ES scores and lower psychological resilience and self-esteem scores than non-LBC-MS (Ps < 0.01). ES was found positively associated with anxiety in LBC-MS and negatively associated with psychological resilience and self-esteem (Ps < 0.05 - 0.01). Specifically, both psychological resilience and self-esteem significantly mediated the association between ES and anxiety, accounting for 7.50% and 10.68%, respectively, of the total associations. Moreover, psychological resilience and self-esteem had a chain mediating effect between ES and anxiety in LBC-MS. CONCLUSION: The findings indicated that LBC-MS in China may frequently engage in the use of ES which correlated with higher level of anxiety. Psychological interventions should be dedicated to this underserved group. Intervention approaches that improve emotion regulation strategies (i.e., decrease the use of ES) and increase psychological resilience and self-esteem may help to alleviate anxiety in LBC-MS.

Overexpression of blaGES-1 due to a strong promoter in the class 1 integron contributes to decreased ceftazidime-avibactam susceptibility in carbapenem-resistant Pseudomonas aeruginosa ST235.

Sequence type 235 (ST235) Pseudomonas aeruginosa, harboring so-called international, high-risk, or widespread clones, is associated with relatively high morbidity and mortality, partly due to multiantibiotic and high-level antibiotic resistance. Treatment of infections caused by such strains with ceftazidime-avibactam (CZA) is often successful. However, CZA resistance in carbapenem-resistant P. aeruginosa (CRPA) strains has been consistently reported with the increasing use of this drug. Likewise, we identified thirty-seven CZA-resistant ST235 P. aeruginosa strains from among 872 CRPA isolates. A total of 10.8% of the ST235 CRPA strains were resistant to CZA. Site-directed mutagenesis, cloning, expression, and whole-genome sequencing analysis revealed that overexpression of blaGES-1, which was carried in a class 1 integron of the complex transposon Tn6584, occurred due to a strong promoter, contributing to CZA resistance. Moreover, such overexpression of blaGES-1 combined with an efflux pump resulted in high-level resistance to CZA, considerably reducing the therapeutic options available for treating infections caused by ST235 CRPA. Considering the widespread presence of ST235 P. aeruginosa strains, clinicians should be aware of the risk of CZA resistance development in high-risk ST235 P. aeruginosa. Surveillance initiatives for preventing further dissemination of high-risk ST235 CRPA isolates with CZA resistance are essential.

Pseudomonas aeruginosa High-Risk Sequence Type 463 Co-Producing KPC-2 and AFM-1 Carbapenemases, China, 2020-2022.

We report the clonal spread and evolution of high-risk Pseudomonas aeruginosa sequence type 463 co-producing KPC-2 and AFM-1 carbapenemases isolated from hospital patients in China during 2020-2022. Those strains pose a substantial public health threat and surveillance and stricter infection-control measures are essential to prevent further infections.

PCK1 activates oncogenic autophagy via down-regulation Serine phosphorylation of UBAP2L and antagonizes colorectal cancer growth.

Phosphoenolpyruvate carboxykinase 1 (PCK1) is the rate-limiting enzyme in gluconeogenesis. PCK1 is considered an anti-oncogene in several human cancers. In this study, we aimed to determine the functions of PCK1 in colorectal cancer (CRC). PCK1 expression in CRC tissues was tested by western blot and immunohistochemistry analyses and associations of PCK1 level with clinicopathological characteristics and disease survival evaluated. Further, we studied the effect of PCK1 on CRC cell proliferation and the underlying mechanisms. Our results show that PCK1 is expressed at significantly lower levels in CRC than in control tissues. High PCK1 expression was correlated with smaller tumor diameter and less bowel wall invasion (T stage). Overexpression and knockdown experiments demonstrated that PCK1 inhibits CRC cell growth both in vitro and in vivo. Mechanistically, PCK1 antagonizes CRC growth via inactivating UBAP2L phosphorylation at serine 454 and enhancing autophagy. Overall, our findings reveal a novel molecular mechanism involving PCK1 and autophagy, and highlight PCK1 as a promising candidate therapeutic target in CRC.

Improving spatial resolution and diagnostic confidence with thinner slice and deep learning image reconstruction in contrast-enhanced abdominal CT.

OBJECTIVE: To evaluate image quality and diagnostic confidence improvement using a thin slice and a deep learning image reconstruction (DLIR) in contrast-enhanced abdominal CT. METHODS: Forty patients with hepatic lesions in enhanced abdominal CT were retrospectively analyzed. Images in the portal phase were reconstructed at 5 mm and 1.25 mm slice thickness using the 50% adaptive statistical iterative reconstruction (ASIR-V) (ASIR-V50%) and at 1.25 mm using DLIR at medium (DLIR-M) and high (DLIR-H) settings. CT number and standard deviation of the hepatic parenchyma, spleen, portal vein, and subcutaneous fat were measured, and contrast-to-noise ratio (CNR) was calculated. Edge-rise-slope (ERS) was measured on the portal vein to reflect spatial resolution and the CT number skewness on liver parenchyma was calculated to reflect image texture. Two radiologists blindly assessed the overall image quality including subjective noise, image contrast, visibility of small structures using a 5-point scale, and object sharpness and lesion contour using a 4-point scale. RESULTS: For the 1.25-mm images, DLIR significantly reduced image noise, improved CNR and overall subjective image quality compared to ASIR-V50%. Compared to the 5-mm ASIR-V50% images, DLIR images had significantly higher scores in the visibility and contour for small structures and lesions; as well as significantly higher ERS and lower CT number skewness. At a quarter of the signal strength, the 1.25-mm DLIR-H images had a similar subjective noise score as the 5-mm ASIR-V50% images. CONCLUSION: DLIR significantly reduces image noise and maintains a more natural image texture; image spatial resolution and diagnostic confidence can be improved using thin slice images and DLIR in abdominal CT. KEY POINTS: • DLIR further reduces image noise compared with ASIR-V while maintaining favorable image texture. • In abdominal CT, thinner slice images improve image spatial resolution and small object visualization but suffer from higher image noise. • Thinner slice images combined with DLIR in abdominal CT significantly suppress image noise for detecting low-density lesions while significantly improving image spatial resolution and overall image quality.

Two Arabidopsis MYB-SHAQKYF transcription repressors regulate leaf wax biosynthesis via transcriptional suppression on DEWAX.

Plant cuticular wax accumulation limits nonstomatal transpiration and is regulated by external environmental stresses. DEWAX (DECREASE WAX BIOSYNTHESIS) plays a vital role in diurnal wax biosynthesis. However, how DEWAX expression is controlled and the molecular mechanism of wax biosynthesis regulated by the diurnal cycle remains largely unknown. Here, we identified two Arabidopsis MYB-SHAQKYF transcription factors, MYS1 and MYS2, as new regulators in wax biosynthesis and drought tolerance. Mutations of both MYS1 and MYS2 caused significantly reduced leaf wax, whereas overexpression of MYS1 or MYS2 increased leaf wax biosynthesis and enhanced drought tolerance. Our results demonstrated that MYS1 and MYS2 act as transcription repressors and directly suppress DEWAX expression via ethylene response factor-associated amphiphilic repression motifs. Genetic interaction analysis with DEWAX, SPL9 (SQUAMOSA PROMOTER BINDING PROTEIN-LIKE 9), and CER1 (ECERIFERUM 1) in wax biosynthesis and under drought stresses demonstrated that MYS1 and MYS2 act upstream of the DEWAX-SPL9 module, thus regulating CER1 expression. Expression analysis suggested that the diurnal expression pattern of DEWAX is partly regulated by MYS1 and MYS2. Our findings demonstrate the roles of two unidentified transcription repressors, MYS1 and MYS2, in wax biosynthesis and provide insights into the mechanism of diurnal cycle-regulated wax biosynthesis.

Differentiating total from subtotal arterial occlusion in lower extremities by using reverse attenuation gradient sign in CT angiography.

OBJECTIVES: To investigate the use of reverse attenuation gradient sign (RAGS) in CT angiography (CTA) to differentiate total from subtotal occlusion in lower extremities which poses different challenges for the procedure and carries different prognoses. METHODS: Eighty patients with 91 lesions in the lower extremities were divided into total occlusion (TO) group and subtotal occlusion (SO) group confirmed by digital subtraction angiography. The CT numbers of vascular lumen at the end of lesion (proximal, P) and at the first entrance (distal, D) of the lateral branch were measured and their difference (CT(PD) = CT(P) - CT(D)) of each lesion was calculated. The CT number gradient (G(DP) = 2 * CT(PD)/[CT(P) + CT(D)]) was calculated by dividing the CT number difference by the average CT number of the two points. The existence of RAGS where the CT number at the distal point is higher than that at the proximal point (CT(PD) and G(PD) < 0) was determined and the diagnostic efficacy of using RAGS in CTA for differentiating total from subtotal occlusive lesions in lower extremities was calculated. RESULTS: The SO group had higher CT numbers than the TO group (p < 0.001). More importantly, the SO group had positive CT number gradient (G(PD) > 0), while the gradient was negative (G(PD) < 0) in the TO group. The specificity and sensitivity of using RAGS (G(PD) < 0) in images for diagnosing TO of lower extremity were 97.6% and 92.0%, respectively, and 87.8% and 88.0% using the standard CTA images. CONCLUSION: The use of RAGS in CTA images has high diagnostic accuracy to differentiate TO from SO in lower extremities. KEY POINTS: • Total occlusions often exhibit higher CT number at distal point than at proximal point to the occlusion. • The reverse attenuation gradient sign (RAGS) may be determined using the CT number measurements between the proximal and distal points after occlusion. • RAGS can be used to improve the diagnostic efficiency in CTA to differentiate between total and subtotal occlusions of lower extremity arteries.

A fatal case of Exophiala dermatitidis meningoencephalitis in an immunocompetent host: A case report and literature review.

BACKGROUND: Central nervous system (CNS) infection due to Exophiala dermatitidis is rare and fatal, and primarily reported in immunocompromised patients or those with caspase recruitment domain-containing protein 9 deficiency. Herein, we describe a case of an otherwise healthy person (without underlying disease or gene deficiency) diagnosed with Exophiala dermatitidis meningoencephalitis. The patient achieved clinical remission under high-dose antifungal therapy in the first 14 months but died after 2 years of the therapy. CASE PRESENTATION: A 15-year-old student with headache and fever was admitted to our department. Lumbar puncture showed increased cerebrospinal fluid (CSF) pressure, moderately high CSF protein levels and cell counts, and a remarkable decrease in CSF glucose and chloride. Magnetic resonance imaging of the brain revealed multiple lesions and cerebral pia mater enhancement. CSF culture confirmed E. dermatitidis infection. We administered 4-week antifungal therapy of amphotericin B, but his CSF culture remained positive. After receiving the 12-week standard dose of voriconazole (200 mg q12h), the patient's CSF culture became negative, but his condition deteriorated with intracranial lesion enlargement. We administered a high-dose voriconazole therapy (600-800 mg per day) for 12 months, which led to clinical remission. The voriconazole dose was reduced due to adverse effects including hepatic dysfunction and hypokalemia, and the disease progressed with high intracranial pressure and epileptic seizures. CONCLUSIONS: CNS infection caused by E. dermatitidis is fatal and the most serious form of fungal infection. Initially, high-dose and long-term antifungal therapy could be effective. Gene defect and related antifungal immunodeficiency may be the most important pathogenic and lethal factor.

Tandem amplification of the vanM gene cluster drives vancomycin resistance in vancomycin-variable enterococci.

BACKGROUND: Vancomycin-variable enterococci (VVE) are a potential risk factor for vancomycin resistance gene dissemination and clinical treatment failure. vanM has emerged as a new prevalent resistance determinant among clinical enterococci in China. A total of 54 vancomycin-susceptible enterococci (VSE) isolates carrying incomplete vanM gene clusters were isolated in our previous study. OBJECTIVES: To determine the potential of vanM-carrying VSE to develop vancomycin resistance and investigate the mechanism of alteration of the resistance phenotype. METHODS: Fifty-four vanM-positive VSE strains were induced in vitro by culturing in increasing concentrations of vancomycin. Genetic changes between three parent VVE strains and their resistant variants were analysed using Illumina and long-read sequencing technologies, quantitative PCR and Southern blot hybridization. Changes in expression level were determined by quantitative RT-PCR. RESULTS: Twenty-five of the 54 VSE strains carrying vanM became resistant upon vancomycin exposure. A significant increase in vanM copy number was observed ranging from 5.28 to 127.64 copies per cell in induced resistant VVE strains. The vanM transposon was identified as tandem repeats with IS1216E between them, and occurred in either the plasmid or the chromosome of resistant VVE cells. In addition, an increase in vanM expression was observed after resistance conversion in VVE. CONCLUSIONS: This study identified tandem amplification of the vanM gene cluster as a new mechanism for vancomycin resistance in VVE strains, offering a competitive advantage for VVE under antibiotic pressure.

Histopathological diagnosis of persistent pruritic eruptions associated with adult-onset Still's disease.

AIMS: Persistent pruritic eruptions (PPEs), presenting with dyskeratotic keratinocytes histologically, are characteristic skin rash in patients with adult-onset Still's disease (AOSD). The lesions may be histologically similar to other entities that present with dyskeratosis. In the present study, we compared the histopathological features between PPEs and other entities presenting with dyskeratosis. METHODS AND RESULTS: To investigate whether histopathological findings can be used to discriminate among PPEs and other entities presenting with dyskeratotic keratinocytes, cutaneous histopathological changes of PPEs associated with AOSD (n = 26) were compared with those of systemic lupus erythematosus (SLE) (n = 16), dermatomyositis (n = 19), and drug eruption (n = 16). Dyskeratosis was observed in the upper one-third of the epidermal layer in all 26 PPEs. The rate of dyskeratosis for PPEs was higher than that for SLE (18.8%) and dermatomyositis (15.8%). In drug eruptions, the dyskeratotic cells were distributed in all levels of the epidermis. Variable densities of neutrophils were found in the dermis in all PPEs. CONCLUSIONS: Although this was a retrospective study conducted at a single centre, presentation of dyskeratotic keratinocytes in the upper one-third of the epidermal layer is a distinctive histopathological reactive pattern of PPEs. This pattern may be a useful histopathological marker for early diagnosis of AOSD.

PCAF-mediated acetylation of Lin28B increases let-7 biogenesis in lung adenocarcinoma H1299 cells.

BACKGROUND: Lin28B and its paralog Lin28A are small RNA binding proteins that have similar inhibitory effects, although they target separate steps in the maturation of let-7 miRNAs in mammalian cells. Because Lin28B participates in the promotion and development of tumors mostly by blocking the let-7 tumor suppressor family members, we sought to explore the associated mechanisms to gain insights into how Lin28B might be decreased in human cancer cells to increase let-7 levels and reverse malignancy. RESULTS: We demonstrated that the histone acetyltransferase PCAF, via its cold shock domain, directly interacts with and subsequently acetylates Lin28B in lung adenocarcinoma-derived H1299 cells. RT-qPCR assays showed that both let-7a-1 and let-7g were increased in PCAF-transfected H1299 cells. Lin28B is acetylated by ectopic PCAF and translocates from the nucleus to the cytoplasm in H1299 cells. CONCLUSIONS: The effects of acetylated Lin28B on let-7a-1 and let-7g are similar to that of stable knockdown of Lin28B in H1299 cells. The new role of PCAF in mediating Lin28B acetylation and the specific release of its target microRNAs in H1299 cells may shed light on the potential application of let-7 in the clinical treatment of lung cancer patients.

Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells.

Wnt1-inducible signaling pathway protein-1 is a cysteine-rich protein that belongs to the CCN family, which has been implicated in mediating the occurrence and progression through distinct molecular mechanisms in several tumor types. However, the association of Wnt1-inducible signaling pathway protein-1 with gastric cancer and the related molecular mechanisms remain to be elucidated. Therefore, this study aimed to clarify the biological role of Wnt1-inducible signaling pathway protein-1 in the proliferation, migration, and invasion in gastric cancer cells and further investigated the associated molecular mechanism on these biological functions. We first detected the expression level of Wnt1-inducible signaling pathway protein-1 in gastric cancer, and the reverse transcription polymerase chain reaction have shown that Wnt1-inducible signaling pathway protein-1 expression levels were upregulated in gastric cancer tissues. The expression of Wnt1-inducible signaling pathway protein-1 in gastric cancer cell lines was also detected by quantitative real-time polymerase chain reaction and Western blotting. Furthermore, two gastric cancer cell lines with high expression of Wnt1-inducible signaling pathway protein-1 were selected to explore the biological function of Wnt1-inducible signaling pathway protein-1 in gastric cancer. Function assays indicated that knockdown of Wnt1-inducible signaling pathway protein-1 suppressed cell proliferation, migration, and invasion in BGC-823 and AGS gastric cancer cells. Further investigation of mechanisms suggested that cyclinD1 was identified as one of Wnt1-inducible signaling pathway protein-1 related genes to accelerate proliferation in gastric cancer cells. In addition, one pathway of Wnt1-inducible signaling pathway protein-1 induced migration and invasion was mainly through the enhancement of epithelial-to-mesenchymal transition progression. Taken together, our findings presented the first evidence that Wnt1-inducible signaling pathway protein-1 was upregulated in gastric cancer and acted as an oncogene by promoting proliferation, migration, and invasion in gastric cancer cells.

Whole-Genome Analysis of an Extensive Drug-Resistant Acinetobacter Baumannii ST195 Isolate from a Recipient After DCD Renal Transplantation in China.

BACKGROUND/AIMS: Infection with Acinetobacter baumannii was emerging as one of the leading causes of mortality after donation after cardiac death transpalantion. METHODS: We reported a case of a recipient who underwent DCD renal transplantation and later got infected by A.baumannii. Etests were done to verify the susceptibility test results in clinic. Whole-genome analysis was applied to investigate the resistant mechanism at gene level. RESULTS: The pathogen was isolated from his draining liquid the day after the surgery, and susceptibility test reavealed that it was sensitive to tigecycline. However, the isolate obtained from the draining liquid became tigecycline-resistant after fifteen-day administration of tigecycline. The Susceptibility tests showed that the pathogen recovered from tigecycline resistance and became intermediated to tigecycline. Whole-Genome analysis revealed the genetic level change leading to tigecycline resistance and we identified the location of mutation by comparing the whole genome sequence of the isolates. Three loci were figured out which may contribute to drug resistance, including genes encoding HTH domain protein, MFS transporter and AdeS. CONCLUSION: Understanding the genetic characteristics associated with drug resistance mechanism and antimicrobial profiles of pathogen is important in controlling infection outbreak and preventing serious complications and gives a new insight into the development of antimicrobial agents.

MAGI1 inhibits migration and invasion via blocking MAPK/ERK signaling pathway in gastric cancer.

OBJECTIVE: To explore the association of membrane-associated guanylate kinase inverted 1 (MAGI1) with gastric cancer (GC) and the related molecular mechanisms. METHODS: The reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were utilized to measure the MAGI1 expression level in GC tissues. Quantitative real-time PCR and Western blotting were used to ensure the MAGI1 expression in GC cell lines. Small hairpin RNA (shRNA) was applied for knockdown of endogenous MAGI1 in GC cells. MTT assay and colony formation assay, scratch wounding migration assay and transwell chamber migration assay, as well as transwell chamber invasion assay were employed respectively to investigate the GC cell proliferation, migration and invasion in MAGI1-knockdown and control GC cells. The potential molecular mechanism mediated by MAGI1 was studied using Western blotting and RT- PCR. RESULTS: RT-PCR and IHC verified MAGI1 was frequently expressed in matched adjacent noncancerous mucosa compared with GC tissues and the expression of MAGI1 was related to clinical pathological parameters. Functional assays indicated that MAGI1 knockdown significantly promoted GC cell migration and invasion. Further mechanism investigation demonstrated that one pathway of MAGI1 inhibiting migration and invasion was mainly by altering the expression of matrix metalloproteinases (MMPs) and epithelial-mesenchymal transition (EMT)-related molecules via inhibiting MAPK/ERK signaling pathway. CONCLUSIONS: MAGI1 was associated with GC clinical pathological parameters and acted as a tumor suppressor via inhibiting of MAPK/ERK signaling pathway in GC.

Reversible acetylation of Lin28 mediated by PCAF and SIRT1.

Lin28 is a small RNA-binding protein that plays an important role in regulating developmental timing, stem cell reprogramming, and oncogenesis. However, the significance of the effect of post-translational modifications on Lin28 activity is not fully understood. In this study, we demonstrated that PCAF directly interacted with and acetylated Lin28. We also showed that the acetylation of Lin28 can be specifically reversed by the deacetylase SIRT1. These findings suggest that the PCAF/SIRT1 balance plays an important role in regulating Lin28 activity. Furthermore, we found that the cold shock domain of Lin28 is the major target of PCAF-mediated acetylation, which leads to a severe reduction in the Lin28 protein levels and an increase in the level of mature let-7a. This study provides the first demonstration that post-translational modification regulates Lin28 activity during let-7a biogenesis and sheds light on the regulation of Lin28 in ES cells and carcinogenesis.

Clinical and microbiological characteristics of Klebsiella pneumoniae liver abscess in East China.

BACKGROUND: Klebsiella pneumoniae has been the dominant pathogen for liver abscesses in several Asian countries. Although the prevalence of K. pneumoniae liver abscess (KLA) in mainland China is increasing recently, the clinical and microbiological characteristics of KLA in China have not been elucidated. METHODS: Clinical and microbiology characteristics of 45 consecutive patients with KLA from a tertiary teaching hospital in China between June 2008 and June 2012 were retrospectively evaluated. RESULTS: Vast majority of the strains were susceptible to main antimicrobial agents. Most of K. pneumoniae strains from pyogenic liver abscess patients belonged to K1/K2 serotype (68.9% for K1 serotype and 20% for K2 serotype). All K. pneumoniae strains were rmpA positive, and 68.9% of these strains were magA positive. Overall, 57.8% (26/45) of K. pneumoniae strains belonged to ST23. Twenty-five of 26 ST23 K. pneumoniae isolates (96.2%) from KLA patients were magA-positive and K1 serotype. Only 28.9% (13/45) of KLA isolates exhibited hypermucoviscous phenotype, which is clinically used as the characteristic of hypervirulent K. pneumoniae (hvKP). Liver abscess sizes in patients infected with hvKP were tend to be larger than those in patients infected with cKP. There was no significant association between the microbiological and clinical characteristics including serotypes, magA and rmpA genotypes, and STs with the metastatic infection and prognosis of KLA. CONCLUSIONS: Neither the serotypes, magA and rmpA genotypes, nor the STs of K. pneumoniae were associated with the metastatic infection and prognosis of KLA. However, further studies with larger sample are needed in the future.

Evolutionary adaptation of KPC-2-producing Pseudomonas aeruginosa high-risk sequence type 463 in a lung transplant patient.

OBJECTIVES: KPC-2-producing Pseudomonas aeruginosa high-risk sequence type (ST) 463 is increasingly prevalent in China and poses severe threats to public health. In this study, we aimed to investigate within-host adaptive evolution of this clone during therapy. METHODS: Using nine serial respiratory isolates from a post-lung transplantation patient undergoing multiple antibiotic treatments, we conducted genomic, transcriptomic and phenotypic analyses to uncover the adaptive mechanisms of a KPC-2-producing ST463 P. aeruginosa strain. RESULTS: The early-course isolates exhibited low-level resistance to ceftazidime/avibactam (CZA), facilitated by the blaKPC-2 gene's presence on both chromosome and plasmid, and its overexpression. Comparative genomic analysis revealed that chromosomal integration of blaKPC-2 resulted from intracellular replicative transposition of the plasmid-derived IS26-blaKPC-2-IS26 composite transposon. As the infection progressed, selective pressures, predominantly from antibiotic interventions and host immune response, led to significant genomic and phenotypic changes. The late-course isolates developed a Δ242-GT-243 deletion in plasmid-encoded blaKPC-2 (blaKPC-14) after sustained CZA exposure, conferring high-level CZA resistance. Increased expression of pili and extracellular polysaccharides boosted biofilm formation. A D143N mutation in the global regulator vfr rendered the strain aflagellate by abrogating the ability of fleQ to positively regulate flagellar gene expression. The enhancement of antibiotic resistance and immune evasion collaboratively facilitated the prolonged survival of ST463 P. aeruginosa within the host. CONCLUSIONS: Our findings highlight the remarkable capacity of ST463 P. aeruginosa in adapting to the dynamic host pressures, supporting its persistence and dissemination in healthcare.

Tix+ in-situ intercalation and interlayer modification via titanium foil/vanadium ion solution interface of VO2.375 as sulfur-wrapped matrix enabling long-life lithium sulfur battery.

Lithium sulfur battery (LSB) has great potential as a promising next-generation energy storage system owing to ultra-high theoretical specific capacity and energy density. However, the polysulfide shuttle effect and slow redox kinetics are recognized the most stumbling blocks on the way of commercializing LSB. On this account, for the first time, we use Tix+ in-situ intercalation strategy via titanium foil/vanadium ion (V5+) solution interface to modify the layer of vanadium oxide for long cycle LSB. The inserted Tix+ strengthens interlayer interaction and enhances lithium-ion mobility rate. Meanwhile, based on density functional theory (DFT) calculation, the mixed valence of V5+/V4+ in the vanadium oxide structure reduces the stress and strain of lithium-ion intercalation through the interlayer support of titanium ions (Tix+). Also, Tix+ refines the structural stability of the sulfur wrapped composite matrix so as to facilitate the LiPSs transformation, and improve the electrochemical performances. Consequently, the Ti-VO2.375/S cathode delivers a lower capacity decay of 0.037 % per cycle over 1500 cycles with a stable coulombic efficiency around 100 %.