A Gram-stain-negative, aerobic, and rod-shaped bacterium, designated H14T, was isolated from a tidal flat in Zhoushan, Zhejiang Province, China. Colonies of strain H14T were yellow, round, smooth and convex after cultivating on marine agar at 37 ℃ for 72 h. Cells were catalase-positive and oxidase-negative. Growth occurred at 16–40 ℃ (optimum, 37 ℃), pH 5.0–8.5 (optimum, pH 6.5) and with 0.5–10.0

IntroductionHeart failure (HF) and chronic kidney disease (CKD) frequently coexist and share chronic low-grade inflammation, oxidative stress, and thrombotic activation. Natriuretic peptides remain the cornerstone of HF prognostication, but their interpretation is confounded by reduced renal clearance, leading to false elevations and attenuated prognostic specificity in CKD. The systemic immune-inflammation index (SII), derived from routine blood counts, integrates neutrophil-driven inflammation, lymphocyte-mediated immunity, and platelet-associated thrombosis, and may provide a renal-function–independent adjunct to natriuretic peptides among patients with non-dialysis CKD. We aimed to evaluate whether SII provides incremental prognostic information to BNP and NT-proBNP in HF, with particular attention to the non-dialysis cardiorenal spectrum.MethodsWe conducted a two-cohort study. The derivation cohort included 1,284 adults hospitalized for chronic HF at Guangdong Medical University Affiliated Hospital (2018–2023). The external validation cohort comprised adults with a first HF hospitalization from MIMIC-IV v3.1 (2008–2022). After excluding patients without SII data and those with incomplete covariates, 11,767 patients were included in the primary analysis. The systemic immune-inflammation index (SII), a composite inflammatory marker derived from routine complete blood count, was calculated as platelet count (×109/L) × neutrophil count (×109/L) / lymphocyte count (×109/L). Patients were stratified by CKD-EPI estimated glomerular filtration rate (eGFR) into >=60, 30–59, and <30 mL/min/1.73 m2. Cox proportional hazards regression, C-index comparisons, net reclassification improvement (NRI), integrated discrimination improvement (IDI), and SII × CKD-stage interaction tests were performed.ResultsSII predicted mortality in the derivation cohort (HR 1.012, 95% CI 1.007–1.017, P = 7.5 × 10⁻⁶) and added modest incremental value to NT-proBNP.ConclusionSII is an inexpensive, universally available prognostic marker in HF patients with non-dialysis CKD. It does not replace NT-proBNP, but provides a statistically significant yet clinically modest incremental signal in CKD—across the non-dialysis CKD spectrum. SII may serve as a practical adjunct, not a substitute, for risk stratification across the non-dialysis cardiorenal spectrum.

Acute myeloid leukemia remains a highly aggressive hematological malignancy with poor clinical outcomes. Long non-coding RNAs are increasingly recognized as regulators of leukemia biology, but the role of PHKA2-AS1 in AML remains unclear. MCOLN1-related lysosome–mitochondria stress and zinc homeostasis have been implicated in cancer cell fate; however, whether AML-associated lncRNAs are transcriptionally associated with this axis has not been fully explored. We integrated public transcriptomic analyses with in vitro and in vivo assays to evaluate the clinical relevance and biological effects of PHKA2-AS1 in AML. PHKA2-AS1 expression, subcellular localization, and functional effects were examined using qRT-PCR, FISH, nuclear/cytoplasmic fractionation, proliferation, cell-cycle, apoptosis, and xenograft assays. Correlations between PHKA2-AS1 and MCOLN1 or mitochondrial stress-related genes were assessed as exploratory co-expression analyses. PHKA2-AS1 was upregulated in AML in public transcriptomic analyses and in local bone marrow samples, and it was predominantly localized in the nucleus. PHKA2-AS1 overexpression promoted MV4-11 cell proliferation, facilitated G1/S cell-cycle transition, and showed a trend toward increased xenograft tumor growth, whereas its effect on apoptosis was limited. In the TCGA-LAML cohort, higher PHKA2-AS1 expression was associated with poorer overall survival and showed weak-to-moderate correlations with MCOLN1 and several mitochondrial stress-related genes, including BID, CASP9, and PINK1. An internally assessed exploratory PHKA2-AS1-related lncRNA prognostic signature showed apparent within-cohort prognostic performance in TCGA-LAML; however, no external or additional resampling-based validation was performed. Computational immune analyses suggested differences in immune-related transcriptional signatures between groups stratified by PHKA2-AS1 expression or risk score. PHKA2-AS1 is upregulated in AML, associated with shorter overall survival in the TCGA-LAML cohort, and promotes leukemic proliferation in the models examined. Its co-expression with MCOLN1 and mitochondrial stress-related genes suggests a potential lysosome–mitochondria stress-related transcriptional context, providing a rationale for future mechanistic studies.

A yellow, Gram-stain-negative, facultatively anaerobic and rod-shaped strain, designated as HB62T, was isolated from seawater in the tidal region of Danzhou, Hainan Island, People's Republic of China. Growth of strain HB62T occurs at 16-40 °C, 0.5-10.0% (w/v) and pH 6.0-9.5 with the optima of 37 °C, 1.5-2.0% (w/v) and pH 6.5-7.0. Strain HB62T could grow anaerobically by using nitrate and sulphate as electron acceptors. The 16S rRNA gene sequence identity analysis showed that strain HB62T shared the highest sequence identity of 98.0% with Salinimicrobium soli CAU 1287T and those of ≤97.9% and ≤94.6% with the rest of Salinimicrobium type strains and other genera type strains, respectively. Phylogenetic trees based on 16S rRNA genes and single-copy orthologous clusters revealed that strain HB62T was stably clustered into the genus Salinimicrobium. Average nucleotide identity and digital DNA-DNA hybridization values of strain HB62T and Salinimicrobium type strains were 72.1-78.2% and 17.8-21.2%, respectively, which were lower than the species delineation thresholds. The sole respiratory quinone was identified as menaquinone-6. Major fatty acids (>10%) are iso-C15:0, iso-C16:0 and summed feature 9 (iso-C17:1  ω9c and/or C16:0 10-methyl). Polar lipids included phosphatidylethanolamine, two unidentified glycolipids, three unidentified lipids and two unidentified aminolipids. Based on the genetic, chemotaxonomic and phenotypic results, strain HB62T is concluded to represent a novel Salinimicrobium species, for which the name Salinimicrobium aquimaris sp. nov. is proposed. The type strain is HB62T (=KCTC 102226T=MCCC 1K08856T).

BACKGROUND:Dioxin has emerged as a major and modifiable determinant of tumor burden worldwide. Building on this premise, we investigated whether dioxin-interacting genes (DIGs) are connected to diffuse large B-cell lymphoma (DLBCL) and sought genes that might function as molecular bridges between exposure and clinical outcome. METHODS:DIGs were gathered (based on the Comparative Toxicogenomics Database) for differential expression analysis and combined univariable Cox regression with Least Absolute Shrinkage and Selection Operator (LASSO) to screen for DIGs robustly associated with overall survival in DLBCL. A multigene risk equation was trained in the GSE10846 cohort and evaluated in an external GSE181063 cohort. In parallel, we compared biological pathways, tumor immune contexture, and drug sensitivity between risk strata, and profiled signature genes at single‑cell resolution. Finally, independent clinical sample queue and in vitro experiments confirmed the potential therapeutic value of DIGs in DLBCL. RESULTS:3 DIGs (CCT5, INHBA and PTPRF) were identified as genes associated with the prognosis of DLBCL. A prognostic risk model for DLBCL patients was constructed based on 3 DIGs. The independent dataset confirms the diagnostic value of the prognostic model. High‑risk and low‑risk groups displayed distinct immune infiltration patterns, and the three genes correlated with multiple immune lineages. An independent clinical sample cohort confirmed the differential expression of CCT5 in DLBCL. Cell experiments have confirmed CCT5 can affect DLBCL cells' function significantly. CONCLUSION:Our analysis delineates a plausible link between DIGs and DLBCL outcome, nominating CCT5 as environmentally relevant biomarkers with prognostic and potential therapeutic implications.

OBJECTIVES:To analyze the global burden, drivers, and disparities of oral diseases among adults aged 70 years and older from 1990 to 2021 and project trends to 2040. METHODS:Using Global Burden of Disease Study 2021 data, we analyzed incidence, prevalence, and disability-adjusted life-years (DALYs). Decomposition, inequality, and Bayesian age-period-cohort modeling assessed trends, drivers, and future burden. RESULTS:From 1990 to 2021, global incidence, prevalence, and DALYs of oral diseases in adults aged 70 years and older increased substantially (prevalence: 133.26 to 313.37 million), although age-standardized rates all declined slightly. Decomposition analysis showed population growth accounted for 107.01% to 111.36% of the increase, exceeding 100% due to an offsetting reduction from favorable epidemiological changes. Critically, the disease burden exhibited clear stratification: trends diverged by disease type, and significant disparities persisted across gender and geographic regions. By 2040, the age-standardized incidence rate is projected to reach 18,024 per 100,000 population, and the age-standardized DALY rate is expected to increase. CONCLUSION:The global burden of elderly oral diseases is growing in absolute terms, driven by population growth. Given the stratified patterns identified by disease type, gender, and region, targeted and context-specific public health strategies are urgently needed to improve elderly oral health worldwide.

OBJECTIVES:Acute respiratory infections (ARIs) are driven by multiple co-circulating pathogens. We investigated pathogen co-detection patterns and interactions at multiple levels to identify factors shaping their dynamics. STUDY DESIGN:Population-based surveillance study. METHODS:From November 2023 to December 2024, a multi-center surveillance of ARIs was conducted in 26 sentinel hospitals across Zhejiang Province, China. 14 respiratory pathogens were tested using PCR-based capillary electrophoresis. Population-level pathogen associations were assessed by Spearman's rank correlation and Granger causality tests. Pathogen interactions at the host level were analyzed using proportional distribution model and multivariable logistic regression. RESULTS:Of 39,115 enrolled ARIs cases, 38,606 were tested for 14 respiratory pathogens. The overall pathogen positivity was 54.84% (21,173/38,606), with co-detections observed in 12.47% (4815/38,606) of ARIs cases. Streptococcus pneumoniae was the most prevalent pathogen and the primary driver of co-detections. A directed predictive network was identified, with RSV, HRV, and HPIV as key hubs. Viral-bacterial synergy was common in children, while adults and the elderly showed significant viral interference, most notably between IFV-A and IFV-B (OR = 0.06). Strong influenza interference was observed in the cold season (IFV-A-IFV-B, OR = 0.10), whereas the warm season was dominated by broader pathogen synergy, alongside notable negative associations such as IFV-A-SARS-CoV-2 (OR = 0.17). CONCLUSIONS:This study reveals that age- and season-dependent pathogen interactions may shape the dynamic patterns of multiple respiratory pathogens, thereby highlighting the importance of considering such interactions in public health strategies.

Avian influenza H7 viruses pose a significant zoonotic and pandemic threat, yet their evolutionary dynamics, spatial transmission patterns, and host-specific roles remain underexplored. This study integrates phylodynamic and phylogeographic analyses to map global H7 dissemination, quantify host-specific contributions, and identify key ecological and anthropogenic drivers. Epidemiological data show key epidemic waves in Asia during 2013-2014 and 2016-2017, and in Africa in 2023. The Eurasian and American lineages of H7 viruses exhibit transmission with a median velocity of ~661 km/year and ~354 km/year, though spread varies significantly by virus subtype. Anseriformes (~587 km/year) and wild birds (~654 km/year) spread the Eurasian lineage of H7 viruses more rapidly and over greater distances than Galliformes and domestic birds. Geographic distance is negatively associated with the spread of the H7 virus, while temperature and poultry density show positive association. In this work, we identify Asia as an important H7 virus evolutionary epicenter. Anseriformes drives transcontinental spread, whereas Galliformes facilitates local amplification. The dynamics of the H7 virus are shaped by ecological and socioeconomic factors. A One Health approach emphasizing targeted surveillance and global cooperation is essential to mitigate cross-species transmission and future pandemic threats.

BACKGROUND:Atrial fibrosis drives atrial structural remodeling and plays a crucial role in the initiation and maintenance of atrial fibrillation (AF). This study aimed to investigate the underlying mechanism of circ_0004090 in atrial fibrosis. METHOD:AngiotensinⅡ (Ang Ⅱ) was used to treat mouse cardiac fibroblasts (MCFs) and C57/B6J mice to establish in vitro and in vivo models of atrial fibrosis. mRNA and protein expression levels were detected using quantitative real-time reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting, respectively. CCK-8 assay, EdU proliferation assay, and cell scratch wound healing assay were performed to assess MCFs proliferation and migration. Dual-luciferase reporter assay was employed to validate the interaction between circ_0004090 and miR-590-5p/TGF-β1. Pathological staining was conducted to analyze histopathological changes in mouse atrial tissues. RESULT:Expression of circ_0004090 was elevated in the serum of AF patients and in Ang Ⅱ-treated MCFs. Silencing circ_0004090 inhibited the proliferation and migration of Ang Ⅱ-treated fibroblasts and reduced the expression of fibrosis-related genes. Circ_0004090 acted as a molecular sponge to inhibit miR-590-5p expression. Overexpression of miR-590-5p abolished the promoting effects of elevated circ_0004090 on the proliferation, migration, and fibrosis of MCFs. Transforming growth factor-β1 (TGF-β1) was identified as a downstream target of miR-590-5p; circ_0004090 sponged miR-590-5p to regulate TGF-β1 expression. Importantly, experiments in mice confirmed that knockdown of circ_0004090 inhibited atrial fibrosis. CONCLUSION:The circ_0004090 downregulates miR-590-5p expression via its molecular sponge function. Reduced miR-590-5p levels lead to derepression of TGF-β1and subsequent activation of the related signaling pathway, thereby promoting Ang Ⅱ-induced atrial fibrosis.

Ubiquitination and liquid-liquid phase separation has been reported to be closely related to the development and occurrence of tumors, but its role in multiple myeloma (MM) remains unexplored. For the first time, based on ubiquitination and liquid-liquid phase separation prognosis related genes (ULLPSRGs), consistent clustering analysis and prognostic difference analysis were conducted, and a prognostic model was constructed through multivariate Cox regression. The model was validated on an independent dataset. Simultaneously conduct immune infiltration analysis, enrichment analysis and drug sensitivity evaluation. Then, the potential therapeutic targets of MM were confirmed through cell experiments. We have identified for the first time four ULLPSRGs associated with MM prognosis. Consensus cluster analysis based on four ULLPSRGs revealed that the two identified clusters had prognostic differences. A prognostic model was constructed based on ULLPSRGs and validated in an independent dataset. The signature is an independent risk factor for MM patients and significantly correlates with clinical factors, the signature was associated with the tumor microenvironment. Cell experiments have confirmed that inhibiting the expression of UBA1 can inhibit the cycle progression of MM cells and promote apoptosis. Our signature can provide clinicians with prognostic predictions and help guide the treatment of patients with MM.

Microbe-mineral interactions play a crucial role in microbial energy conservation and mineral mobilization within deep-sea hydrothermal vents, yet the specific microorganisms involved remain largely underexplored. In this study, sulfide minerals and iron-rich sediment samples from a hydrothermal field on the Indian Ocean Ridge were obtained and subjected to long-term enrichment experiments to simulate microbe-mineral interaction. Sulfur-oxidizing communities were established with 36 isolated sulfur-oxidizing bacteria (SOB). Among them, Methylophaga sp. F7, Sulfitobacter sp. L-8 and Roseovarius sp. B-10 exhibited thiosulfate oxidation capabilities. Scanning electron microscopy-energy dispersive X-ray spectroscopy (SEM-EDS) showed diverse nanoscale signatures of microbial weathering after 30 and 90 days incubation, including metal oxide particles, secondary mineral precipitates, and irregular dissolution pits. Overall, this research connects microbial sulfur-oxidizing metabolisms with morphological transformation of polymetallic sulfide minerals, highlighting the important role of SOB in mineral weathering, metal mobilization, and resource sharing on hydrothermal environments.

Background:Metabolic multimorbidity is prevalent in high-risk populations for diabetes and is linked to cardiovascular disease (CVD) and gut microbiota composition. The relationship between metabolic clusters (MCs), microbial age (MA), and metabolic markers remains poorly understood. Objective:This study aimed to investigate the characteristics of MCs and MA in high-risk diabetic populations, focusing on their associations with gut microbiota, metabolic dysregulation, and CVD risk. Methods:Using data from the NIH Integrative Human Microbiome Project, we performed metabolomic and microbiomic analyses. K-means clustering identified MCs, and redundancy analysis examined the relationship between metabolic variables and microbiota. A random forest (RF) model predicted MA and CVD risk, while the linear discriminant analysis effect size identified microbial species associated with MCs and MA. Co-occurrence network analysis explored microbial interactions. Results:We included 103 high-risk individuals (56/103, 54.4% female, mean age 50.6, SD 54.6 years). In total, 3 MCs were identified: MC1 (high glucose or blood urea nitrogen), MC2 (relatively healthy), and MC3 (lipid dysregulation). Age explained 3% of gut microbiota variation (R2=0.03; P=.006). The RF model predicting microbial age showed a strong correlation with chronological age in training data (ρ=0.97, root mean square error=3.33; P<.001) and moderate correlation in test data (ρ=0.35; P<.001). High microbial age was associated with elevated lipid markers (low-density lipoprotein and triglycerides; P<.001) and higher cardiovascular risk. The RF model for CVD risk prediction achieved excellent discrimination (area under the curve=0.95 for the low-risk and 0.95 for the high-risk groups). Conclusions:This study highlights the relationship between MCs, MA, and gut microbiota, providing insights for early intervention and personalized treatment strategies for diabetes and related metabolic disorders.

Although the global burden of pertussis has declined steadily over recent decades, the COVID-19 pandemic coincided with a marked disruption of its established epidemic trajectory. We assessed pandemic-associated changes using spatiotemporal trend analysis, health inequality assessment, multivariable regression, and Mendelian randomization. Globally, the age-standardized disability-adjusted life years (DALYs) rate decreased from 378.01 per 100,000 in 1990 to 70.92 in 2021, accelerating steeply after 2019. Despite reductions, burden remained concentrated in low-sociodemographic index (SDI) countries, with widening relative inequalities. Macro-scale multivariable regression stratified by SDI revealed no robust independent association between COVID-19 and pertussis incidence after adjusting for population density. Consistently, Mendelian randomization analyses found no evidence of a causal effect of genetic liability to COVID-19 on pertussis risk. These findings suggest the pandemic-era decline is driven by disruptions to transmission and health services rather than biological cross-protection. We interpret this transient suppression as contributing to an emerging immunity gap - an accumulation of susceptible individuals following reduced natural exposure and interruptions to routine immunization. As social contact patterns normalize, this immunity gap increases the risk of rebound transmission. Strengthening life-course vaccination, including catch-up programmes and prioritization of low-SDI settings, is essential to mitigate post-pandemic resurgence.

Heart failure (HF) is a leading cause of hospitalization and death worldwide, yet most prognostic models target long-term outcomes and are not optimized for acute-phase risk stratification. This study developed and externally validated an 8-variable Cox model for predicting 28-day and 1-year all-cause mortality in hospitalized HF patients, following the TRIPOD statement. Using the MIMIC-IV v3.1 database (n = 12,269) for development and temporal validation and a Chinese cohort (n = 1284; 1,278 with complete data) for geographic external validation, LASSO-penalized Cox regression was used for variable selection. The 28-day model achieved C-index values of 0.738, 0.736, and 0.830 in the development, temporal validation, and Guangdong cohorts, respectively, and showed better discrimination than the 1-year model (ΔC-index = 0.058 in the development set). The systemic immune-inflammation index (SII) showed a stronger association with 28-day mortality (HR 1.40, 95% CI 1.32–1.48) than with 1-year mortality (HR 1.18, 95% CI 1.14–1.23; bootstrap interaction P = 0.001). A web-based risk calculator was externally validated after slope + intercept recalibration. The 8-variable model and calculator provide practical tools for early HF risk stratification.

BackgroundThe global burden of injury is a key indicator for assessing public health and medical needs. During the COVID-19 pandemic, this burden was impacted. This study aims to explore how the pandemic influenced the injury burden globally and regionally, and provide recommendations to relieve this burden.MethodsThe burden of injury-related data is derived from the Global Burden of Disease (GBD) 2021 Study. Autoregressive integrated moving average (ARIMA) and ARIMA-Long short-Term Memory (LSTM) models were adopted for counterfactual inference to predict the scenario without the pandemic.ResultsDuring the COVID-19 pandemic, the observed global age-standardized incidence rate (ASIR) of injury exceeded the predicted value by 107.31 per 100,000, and the observed age-standardized prevalence rate (ASPR) was higher than the predicted value by 102.81 per 100,000. Self-harm and interpersonal violence saw the largest deviations above predicted values in Europe and parts of Asia. Specifically, Armenia's ASIR was 7,829.33 per 100,000 higher than predicted, and its ASDR exceeded projections by 5,186.32 per 100,000. Besides, traffic injuries exceeded predicted levels most significantly in Southeast Asia, with Indonesia's ASIR 25.48 per 100,000 higher than projected. And the observed ASIR of unintentional injuries in China was 379.61 per 100,000 higher than the predicted value.ConclusionDuring the COVID-19 pandemic, the global burden of injuries surpassed the predicted levels for a scenario without the pandemic in 2020-2021, especially in Europe and Asia. In addressing an epidemic, prevention and emergency measures for high-burden injury types and key populations should be strengthened based on local socio-cultural contexts.

Human adenovirus (HAdV) is an important cause of respiratory infections, yet community-level burden estimates remain limited. We aimed to estimate post-pandemic HAdV burden in China. Using nationwide respiratory pathogen surveillance data and a multiplier model, we estimated the incidence of HAdV infections, symptomatic illnesses (SI), and medically attended illnesses (MAI) in China from 2023 to 2024. Age-, species-, and province-specific analyses were conducted. Uncertainty was assessed using Monte Carlo simulations. We estimated 44.21 million HAdV infections (95% UI, 26.68-77.08 million) over the 19-month study period, corresponding to an average monthly incidence of 1.58 per 1000 persons (95% UI, 1.01-2.61), equivalent to an annualized incidence of 18.96 per 1000 persons (95% UI, 12.12-31.32). The estimated average monthly incidences of SI and MAI were 0.41 (95% UI, 0.30-0.57) and 0.30 (95% UI, 0.21-0.40) per 1000 persons, corresponding to annualized incidences of 4.92 (95% UI, 3.60-6.84) and 3.60 (95% UI, 2.52-4.80) per 1000 persons, respectively. Children aged 0-4 years had the highest average monthly incidence (16.66 [95% UI, 10.26-28.54] per 1000 persons). HAdV species B showed higher incidence than species C among children aged 5-14 years. The highest incidence rates occurred in several south-central and southwestern provinces, including Hunan, Guangxi, Hubei, Guangdong, and Yunnan. HAdV imposed a substantial and under-recognized respiratory disease burden in China during the post-pandemic period. Children experienced the highest burden, and marked species-specific and geographic heterogeneity were observed. These findings provide community-based evidence to inform adenovirus surveillance and respiratory disease control strategies in China.

Rotavirus (RV) is a leading cause of infectious gastroenteritis and associated deaths worldwide, imposing a substantial disease burden in China. This study aimed to describe the epidemiological characteristics, clinical manifestations and dominant genotypes of rotavirus infection in Zhejiang Province and evaluated risk factors for severe RV-associated diarrhea. A prospective study was conducted on patients with acute gastroenteritis (AGE) from multicenter hospitals in Zhejiang Province between 2023 and 2024. Relevant information was collected through epidemiological questionnaires and electronic medical records. Fecal samples were collected to detect pathogens and G/P serotypes. A total of 4,810 RV-infected patients were enrolled, including 75.95

Two Gram-stain-negative, aerobic, oxidase-negative, non-motile, ellipsoid to short rod-shaped bacteria (~1.2-2.0 µm in length and 0.7-0.8 µm in width) were isolated from soil near a wastewater treatment plant in Hangzhou, Zhejiang Province, China, designated TB0136T and TB0139T. Both strains are able to grow chemolithoautotrophically using hydrogen as an electron donor and perform nitrogen fixation in the absence of ammonium or any organic nitrogen source. Strains TB0136T and TB0139T were observed to grow at temperatures of 15-45 °C (both optimal at 33 °C; TB0139T additionally showed trace growth at 50 °C), at pH of 6.0-10.0 (TB0136T optimal at 7.5-8.0, TB0139T optimal at 8.0-8.5) and in the presence of 0-6.0% (w/v) NaCl (optimal at 1.0%). Chemotaxonomic analyses indicated that the main respiratory quinone in both strains is ubiquinone-10. The DNA G+C contents of strains TB0136T and TB0139T were 63.3 and 61.5 mol%, respectively. Phylogenetic analysis based on the 16S rRNA gene sequence and the whole genome indicated that strains TB0136T and TB0139T formed a unique lineage in the evolutionary branches of the family Xanthobacteraceae. According to the characteristics of polyphasic taxonomy, strains TB0136T and TB0139T are proposed to represent two novel species of a new genus, for which the name Haloleucobacter gen. nov. is proposed. The proposed species names are Haloleucobacter ellipsoideus and Haloleucobacter albus. The type strains are TB0136T (=MCCC 1K09187T=JCM 37006T) and TB0139T (= MCCC1K09185T=JCM 37007T), respectively.

A N,N-dimethylformamide-degrading bacterium, strain HB0163ᵀ, was isolated from activated sludge of a wastewater treatment plant in Hangzhou, Zhejiang Province, China. Cells are Gram-stain-negative, aerobic, oxidase-positive, non-motile rods (0.4–0.6 × 1.0–1.5 μm). Growth occurred at 20–45 °C (optimum 35 °C), pH 5.0–9.5 (optimum 7.5–8.0), and with 0–6.0