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Abstract We perform a theoretical study on the spectrum of the low-lying hidden-bottom ( $$q\bar{q}b\bar{b}$$ q q ¯ b b ¯ with $$q=$$ q = u, d and s) and double-bottom ( $$q\bar{q}bb$$ q q ¯ b b ) tetraquark states within a nonrelativistic quark model, in which the instanton-induced interaction is taken as the residual spin-dependent hyperfine interaction between quarks. All the model parameters are fixed by fitting the spectrum of the ground hadron states. The numerical results indicate that masses of several $$X_{q\bar{q}}$$ X q q ¯ , $$Z_{b}$$ Z b , and $$Z_{bs}$$ Z bs tetraquark states are below and near thresholds of corresponding meson-meson channels, thus these states may form components of exotic meson states with reasonable probabilities. Especially, in present model, masses of several obtained states with quantum number $$I^G(J^P)=1^+(1^{+})$$ I G ( J P ) = 1 + ( 1 + ) are close to $$Z_b^\pm (10610)$$ Z b ± ( 10610 ) , so one may expect these states to be non-negligible components of the experimentally observed $$Z_{b}$$ Z b states. Concerning to the double-bottom tetraquark states, the present results are in general consistent with other previous works. Two possible stable $$T_{bb}$$ T bb states with quark content $$bb\bar{n}\bar{n}$$ b b n ¯ n ¯ ( $$n=u$$ n = u or d quark) lying at energies 10558 MeV and 10650 MeV are found, and one possible stable $$bb\bar{n}\bar{s}$$ b b n ¯ s ¯ state is found, whose energy is $$\sim 10687$$ ∼ 10687 MeV.

Abstract Water is necessary for the alkali aggregate reaction to occur and this study investigates the impact of waterproofing on alkali-aggregate reaction (AAR) in concrete by separating water from alkali reactive aggregates through surface, aggregate, and matrix treatments. Accelerated mortar bar tests (AMBT) are conducted to analyze the expansion caused by alkali aggregates. Furthermore, the suppressive mechanism of waterproofing on AAR is explored using scanning electron microscopy (SEM), while the influence of waterproof concrete aggregate and matrix on pore characteristics and hydration products is assessed using nuclear magnetic resonance (NMR) and X-ray diffraction (XRD). The results demonstrate that surface waterproofing with silane and polyvinyl alcohol (PVA) effectively suppress AAR. Moreover, PVA-coated aggregates significantly enhance the compactness of the interfacial transition zone (ITZ) in concrete. Based on these findings, an improved model considering waterproofness is proposed to quantify the degree of alkali aggregate reaction. These findings offer valuable guidance for controlling AAR.

Abstract Small nucleolar RNAs (snoRNAs) were previously regarded as a class of functionally conserved housekeeping genes, primarily involved in the regulation of ribosome biogenesis by ribosomal RNA (rRNA) modification. However, some of them are involved in several biological processes via complex molecular mechanisms. DNA damage response (DDR) is a conserved mechanism for maintaining genomic stability to prevent the occurrence of various human diseases. It has recently been revealed that snoRNAs are involved in DDR at multiple levels, indicating their relevant theoretical and clinical significance in this field. The present review systematically addresses four main points, including the biosynthesis and classification of snoRNAs, the mechanisms through which snoRNAs regulate target molecules, snoRNAs in the process of DDR, and the significance of snoRNA in disease diagnosis and treatment. It focuses on the potential functions of snoRNAs in DDR to help in the discovery of the roles of snoRNAs in maintaining genome stability and pathological processes.

Objective To determine the efficacy and safety of Astragalus combined with renin-angiotensin-aldosterone system (RAAS) blockers in treating stage III diabetic nephropathy (DN) by meta-analysis.Methods PubMed, Embase, Cochrane Library, Wiley, and Web of Science databases were searched for articles published between August 2007 and August 2022. Clinical studies on Astragalus combined with RAAS blockers for the treatment of stage III DN were included. Meta-analysis was performed by RevMan 5.1 and Stata 14.3 software.Results A total of 32 papers were included in this meta-analysis, containing 2462 patients from randomized controlled trials, with 1244 receiving the combination treatment and 1218 solely receiving RAAS blockers. Astragalus combined with RAAS blockers yielded a significantly higher total effective rate (TER) (mean difference [MD] 3.63, 95% confidence interval [CI] 2.59–5.09) and significantly reduced urinary protein excretion rate (UPER), serum creatinine (Scr), blood urine nitrogen (BUN) and glycosylated hemoglobin (HbAlc) levels. In subgroup analysis, combining astragalus and angiotensin receptor blocker significantly lowered fasting plasma glucose (FPG) and 24 h urinary protein (24hUTP) levels, compared with the combined astragalus and angiotensin-converting enzyme inhibitor treatment. Meanwhile, the latter significantly decreased the urinary microprotein (β2-MG). Importantly, the sensitivity analysis confirmed the study’s stability, and publication bias was not detected for UPER, BUN, HbAlc, FPG, or β2-MG. However, the TER, SCr, and 24hUTP results suggested possible publication bias.Conclusions The astragalus-RAAS blocker combination treatment is safe and improves outcomes; however, rigorous randomized, large-scale, multi-center, double-blind trials are needed to evaluate its efficacy and safety in stage III DN.

Purpose In this first-in-human dose escalation study, the safety and efficacy of IO-108, a fully human monoclonal antibody targeting leukocyte immunoglobulin-like receptor B2 (LILRB2), was investigated in patients with advanced solid tumors as monotherapy and in combination with pembrolizumab, an anti-programmed cell death protein 1 (PD-1) antibody.Methods The study included patients with histologically or cytologically confirmed advanced and relapsed solid tumors, with measurable disease by Response Evaluation Criteria In Solid Tumors (RECIST) V.1.1. Patients were treated with escalating doses of IO-108 every 3 weeks (Q3W) as monotherapy and in combination with pembrolizumab. Safety and tolerability were the primary objectives. Secondary and exploratory objectives included: pharmacokinetics, clinical efficacy, immunogenicity and biomarkers.Results Of 25 patients enrolled, 12 were treated with IO-108 monotherapy and 13 received combination therapy. IO-108 was well-tolerated up to the maximally administered dose of 1,800 mg every 3 weeks (Q3W) as monotherapy and in combination with pembrolizumab. No dose-limiting toxicity was observed, and a maximum tolerated dose was not reached. Treatment-related adverse events (TRAEs) occurred in 6 (50.0%) patients treated with IO-108 monotherapy and 6 (46.2%) patients treated with IO-108+pembrolizumab. All TRAEs were mild or moderate (Grade 1 or 2), and no TRAEs led to treatment discontinuation or death. IO-108 exhibited a dose-proportional increase in exposure. Full receptor occupancy (RO) in peripheral blood was achieved at doses ≥600 mg. The overall response rate was 9% (1/11) in the monotherapy and 23% (3/13) in the combination therapy. A patient with treatment-refractory Merkel cell carcinoma treated with IO-108 monotherapy achieved a durable complete response (CR) for more than 2 years. Pharmacodynamic gene expression changes reflecting increased tumor infiltration of T cells were associated with clinical benefits in both monotherapy and combination therapy. Additionally, baseline tumor inflammation gene signature (TIS) scores correlated with clinical benefit.Conclusion IO-108 is well tolerated and has led to objective response as monotherapy and in combination with pembrolizumab. The complete response and the pharmacodynamic changes in the monotherapy cohort demonstrate single agent activity of IO-108 and provide proof of concept that targeting myeloid-suppressive pathways through LILRB2 inhibition may potentiate the clinical efficacy of anti-PD-1 immune checkpoint inhibitors.Trial registration number NCT05054348.

Abstract Polatuzumab vedotin is a CD79b‐directed antibody–drug conjugate that targets B cells and delivers the cytotoxic payload monomethyl auristatin E (MMAE). The phase III POLARIX study (NCT03274492) evaluated polatuzumab vedotin in combination with rituximab, cyclophosphamide, doxorubicin, and prednisone (R‐CHP) as first‐line treatment of diffuse large B‐cell lymphoma (DLBCL). To examine dosing decisions for this regimen, population pharmacokinetic (popPK) analysis, using a previously developed popPK model, and exposure–response (ER) analysis, were performed. The popPK analysis showed no clinically meaningful relationship between cycle 6 (C6) antibody‐conjugated (acMMAE)/unconjugated MMAE area under the concentration–time curve (AUC) or maximum concentration, and weight, sex, ethnicity, region, mild or moderate renal impairment, mild hepatic impairment, or other patient and disease characteristics. In the ER analysis, C6 acMMAE AUC was significantly associated with longer progression‐free and event‐free survival (both p = 0.01). An increase of

Objectives: Providing satisfactory healthcare services for breast cancer survivors can effectively reduce their burden and the pressure on medical resources. The aim of this study was to explore health care service demands for community-dwelling breast cancer survivors using the Kano model. Methods: A cross-sectional survey was conducted from January to March 2023 among breast cancer survivors discharged from a tertiary cancer hospital. Participants were asked to fill out a self-designed questionnaire involving the Kano model, which helped to categorize and prioritize the attributes of healthcare services. The questionnaire included 30 health care services. Additionally, their social demographic characteristics were collected during the survey. Results: A total of 296 valid questionnaires were collected, and demand attributes of the 30 health care services were evaluated. The findings revealed that one of 30 services was classified as “must-be attributes” (body image management), 13 as “one-dimensional attributes” (focused on medical security support, health management, and health counseling), 3 as “attractive attributes” (focused on communication needs and telehealth services), and 11 as “indifferent attributes” (mainly in the area of psycho-social services). Conclusions: Breast cancer survivors in the community have different levels of need for various health care services. It’s crucial for healthcare providers to identify these needs and devise effective strategies to deliver the appropriate services. Services with must-be and one-dimensional attributes should be given priority, and efforts should be made to provide services with attractive attributes, hence improving the quality of life of breast cancer survivors.

Abstract Endocrine‐resistant ER+HER2– breast cancer (BC) is particularly aggressive and leads to poor clinical outcomes. Effective therapeutic strategies against endocrine‐resistant BC remain elusive. Here, analysis of the RNA‐sequencing data from ER+HER2– BC patients receiving neoadjuvant endocrine therapy and spatial transcriptomics analysis both show the downregulation of innate immune signaling sensing cytosolic DNA, which primarily occurs in endocrine‐resistant BC cells, not immune cells. Indeed, compared with endocrine‐sensitive BC cells, the activity of sensing cytosolic DNA through the cGAS‐STING pathway is attenuated in endocrine‐resistant BC cells. Screening of kinase inhibitor library show that this effect is mainly mediated by hyperactivation of AKT1 kinase, which binds to kinase domain of TBK1, preventing the formation of a trimeric complex TBK1/STING/IRF3. Notably, inactivation of cGAS–STING signaling forms a positive feedback loop with hyperactivated AKT1 to promote endocrine resistance, which is physiologically important and clinically relevant in patients with ER+HER2– BC. Blocking the positive feedback loop using the combination of an AKT1 inhibitor with a STING agonist results in the engagement of innate and adaptive immune signaling and impairs the growth of endocrine‐resistant tumors in humanized mice models, providing a potential strategy for treating patients with endocrine‐resistant BC.

Homologous recombination (HR) repair for DNA double‐strand breaks (DSBs) is critical for maintaining genome stability and conferring the resistance of tumor cells to chemotherapy. Nuclear PTEN which contains both phosphatidylinositol 3,4,5‐trisphosphate 3‐phosphatase and protein phosphatase plays a key role in HR repair, but the underlying mechanism remains largely elusive. We find that SUMOylated PTEN promotes HR repair but represses nonhomologous end joining (NHEJ) repair by directly dephosphorylating TP53‐binding protein 1 (53BP1). During DNA damage responses (DDR), tumor suppressor ARF (p14ARF) was phosphorylated and then interacted efficiently with PTEN, thus promoting PTEN SUMOylation as an atypical SUMO E3 ligase. Interestingly, SUMOylated PTEN was subsequently recruited to the chromatin at DSB sites. This was because SUMO1 that was conjugated to PTEN was recognized and bound by the SUMO‐interacting motif (SIM) of breast cancer type 1 susceptibility protein (BRCA1), which has been located to the core of 53BP1 foci on chromatin during S/G2 stage. Furthermore, these chromatin‐loaded PTEN directly and specifically dephosphorylated phosphothreonine‐543 (pT543) of 53BP1, resulting in the dissociation of the 53BP1 complex, which facilitated DNA end resection and ongoing HR repair. SUMOylation‐site‐mutated PTENK254R mice also showed decreased DNA damage repair in vivo. Blocking the PTEN SUMOylation pathway with either a SUMOylation inhibitor or a p14ARF(2‐13) peptide sensitized tumor cells to chemotherapy. Our study therefore provides a new mechanistic understanding of PTEN in HR repair and clinical intervention of chemoresistant tumors.

Abstract Mosunetuzumab is a CD3/CD20 bispecific antibody. As an on‐target effect, transient elevation of interleukin‐6 (IL‐6) occurs in early treatment cycles. A physiologically‐based pharmacokinetic (PBPK) model was developed to assess potential drug interaction caused by IL‐6 enzyme suppression on cytochrome P450 3A (CYP3A) during mosunetuzumab treatment. The model's performance in predicting IL‐6 CYP3A suppression and subsequent drug–drug interactions (DDIs) was verified using existing clinical data of DDIs caused by chronic and transient IL‐6 elevation. Sensitivity analyses were performed for a complete DDI risk assessment. The IL‐6 concentration‐ and time‐dependent CYP3A suppression during mosunetuzumab treatment was simulated using PBPK model with incorporation of in vitro IL‐6 inhibition data. At clinically approved doses/regimens, the DDI at maximum CYP3A suppression was predicted to be a midazolam maximum drug concentration in plasma (Cmax) and area under the plasma drug concentration–time curve (AUC) ratio of 1.17 and 1.37, respectively. At the 95th percentile of IL‐6 concentration level or when gut CYP3A suppression was considered, the predicted DDI risk for mosunetuzumab remained low (

Objectives: Early identification of sarcopenia in patients with chronic liver disease is crucial for patient management and prevention of severe complications. We aimed to assess the effectiveness of Ishii score, Strength, Assistance with Walking, Rise from a Chair, Climb Stairs and Falls (SARC-F), SARC-F and Calf Circumference (SARC-CalF), and Mini Sarcopenia Risk Assessment-7 (MSRA-7) to screen sarcopenia in patients with chronic liver disease. Methods: This prospective study included patients with chronic liver disease in the infectious department of a tertiary hospital in Sichuan, China. Ishii score, SARC-F, SARC-CalF, and MSRA-7 were used to screen for sarcopenia risk. Sarcopenia was diagnosed according to the Asian Myometriosis Working Group (AWGS) 2019, which was used as the gold standard to compare the performance of the four screening tools. We completed clinical registration on the Chinese Clinical Trial Registration website (ChiCTR2100043910). Results: A total of 366 patients with chronic liver disease (22.4% women, mean age 48.96 ± 11.88 years) were evaluated. Based on the AWGS 2019 standard, the prevalence of sarcopenia in patients with chronic liver disease was 17.5%. Among all participants, receiver operating characteristic (ROC) produced an area under the curve (AUC) of 0.82 for Ishii score (sensitivity 85.94%, specificity 78.15%), 0.53 for SARC-F (sensitivity 6.25%, specificity 99.34%), 0.64 for SARC-CalF (sensitivity 45.31%, specificity 83.11%), and 0.55 for MSRA-7 (sensitivity 87.50%, specificity 22.85%). Based on AUC, decision curve analysis, and calibration curves, we concluded that Ishii score was the most accurate screening tool and was superior to the other tools. Conclusions: Ishii score is more suitable for screening sarcopenia in patients with chronic liver disease than the SARC-F, SARC-CalF, and MSRA-7, based on the AWGS 2019 criteria. Nursing professionals can use Ishii score as a clinical tool to screen for sarcopenia in patients with chronic liver disease, providing an indication cue for the final diagnosis of sarcopenia, improving diagnostic efficiency, and enabling early identification and prevention of complications resulting from sarcopenia.

Abstract Mosunetuzumab (Mosun) is a CD20xCD3 T‐cell engaging bispecific antibody that redirects T cells to eliminate malignant B cells. The approved step‐up dose regimen of 1/2/60/30 mg IV is designed to mitigate cytokine release syndrome (CRS) and maximize efficacy in early cycles. A population pharmacokinetic (popPK) model was developed from 439 patients with relapsed/refractory B‐Cell Non‐Hodgkin lymphoma receiving Mosun IV monotherapy, including fixed dosing (0.05–2.8 mg IV every 3 weeks (q3w)) and Cycle 1 step‐up dosing groups (0.4/1/2.8–1/2/60/30 mg IV q3w). Prior to Mosun treatment, ~50% of patients had residual levels of anti‐CD20 drugs (e.g., rituximab or obinutuzumab) from prior treatment. CD20 receptor binding dynamics and rituximab/obinutuzumab PK were incorporated into the model to calculate the Mosun CD20 receptor occupancy percentage (RO%) over time. A two‐compartment model with time‐dependent clearance (CL) best described the data. The typical patient had an initial CL of 1.08 L/day, transitioning to a steady‐state CL of 0.584 L/day. Statistically relevant covariates on PK parameters included body weight, albumin, sex, tumor burden, and baseline anti‐CD20 drug concentration; no covariate was found to have a clinically relevant impact on exposure at the approved dose. Mosun CD20 RO% was highly variable, attributed to the large variability in residual baseline anti‐CD20 drug concentration (median = 10 μg/mL). The 60 mg loading doses increased Mosun CD20 RO% in Cycle 1, providing efficacious exposures in the presence of the competing anti‐CD20 drugs. PopPK model simulations, investigating Mosun dose delays, informed treatment resumption protocols to ensure CRS mitigation.

Abstract Background Mitochondrial outer membrane permeabilisation (MOMP) plays a pivotal role in cellular death and immune activation. A deeper understanding of the impact of tumour MOMP on immunity will aid in guiding more effective immunotherapeutic strategies. Methods A comprehensive pan‐cancer dataset comprising 30 cancer‐type transcriptomic cohorts, 20 immunotherapy transcriptomic cohorts and three immunotherapy scRNA‐seq datasets was collected and analysed to determine the influence of tumour MOMP activity on clinical prognosis, immune infiltration and immunotherapy effectiveness. Leveraging 65 scRNA‐Seq datasets, the MOMP signature (MOMP.Sig) was developed to accurately reflect tumour MOMP activity. The clinical predictive value of MOMP.Sig was explored through machine learning models. Integration of the MOMP.Sig model and a pan‐cancer immunotherapy CRISPR screen further investigated potential targets to overcome immunotherapy resistance, which subsequently underwent clinical validation. Results Our research revealed that elevated MOMP activity reduces mortality risk in cancer patients, drives the formation of an anti‐tumour immune environment and enhances the response to immunotherapy. This finding emphasises the potential clinical application value of MOMP activity in immunotherapy. MOMP.Sig, offering a more precise indicator of tumour cell MOMP activity, demonstrated outstanding predictive efficacy in machine‐learning models. Moreover, with the assistance of the MOMP.Sig model, FOXO1 was identified as a core modulator that promotes immune resistance. Finally, these findings were successfully validated in clinical immunotherapy cohorts of skin cutaneous melanoma and triple‐negative breast cancer patients. Conclusions This study enhances our understanding of MOMP activity in immune modulation, providing valuable insights for more effective immunotherapeutic strategies across diverse tumours.

Objective: The treatment of breast cancer still faces great challenges, and it is necessary to continuously explore effective drugs and targets to promote immune precision medicine. This study aims to investigate the immune-related regulatory mechanism of cordycepin in breast cancer. Methods: Network pharmacology was employed to discovery the action of cordyceps on breast cancer targets, molecular docking was employed to analyze the interaction pattern between core components and targets, and biological information analysis was used to explore the target-related immune mechanism and verified in vitro experiments. Results: The results of this study indicate that cordycepin can effectively inhibit breast cancer. The roles of cordycepin's active component and its target gene ALB were elucidated through the combined use of network pharmacology and molecular docking. Bioinformatics analysis revealed convincing associations between ALB and many immune pathway marker genes. ALB was inhibited in tumor expression, and cordycepin was found to enhance the expression of ALB in vitro to play an anti-tumor role. Conclusion: Cordycepin regulates immune suppression of tumor, which is expected to open a new chapter of breast cancer immunotherapy.

Objective To investigate the prognostic impact of initial lung cancer (LC) on second primary breast cancer after LC (LC-BC) and further develop a nomogram for predicting the survival of patients.Methods All patients diagnosed with LC-BC and first primary BC (BC-1) during 2000–2017 were collected from Surveillance, Epidemiology, and End Results database. Pathological features, treatment strategies and survival outcomes were compared between LC-BC and BC-1 before and after propensity score matching (PSM). Cox regression analysis was performed to identify the prognostic factors associated with LC in patients with LC-BC. Additionally, least absolute shrinkage and selection operator regression analysis was used to select clinical characteristics for nomogram construction, which were subsequently evaluated using the concordance index (C-index), calibration curve and decision curve analysis (DCA).Results 827 429 patients with BC-1 and 1445 patients with LC-BC were included in the analysis. Before and after PSM, patients with BC-1 had a better prognosis than individuals with LC-BC in terms of both overall survival (OS) and breast cancer-specific survival (BCSS). Furthermore, characteristics such as more regional lymph node dissection, earlier stage and the lack of chemotherapy and radiation for LC were found to have a stronger predictive influence on LC-BC. The C-index values (OS, 0.748; BCSS, 0.818), calibration curves and DCA consistently demonstrated excellent predictive accuracy of the nomogram.Conclusion In conclusion, patients with LC-BC have a poorer prognosis than those with BC-1, and LC traits can assist clinicians estimate survival of patients with LC-BC more accurately.

Bacterial aromatic polyketides are mainly biosynthesized by type II polyketide synthases (PKSs). The PKSs cannot be functional unless their acyl carrier proteins (ACPs) are phosphopantetheinylated by phosphopantetheinyl transferases (PPTases). Gra-ORF32 was identified as an in-cluster PPTase dedicated for granaticin biosynthesis in Streptomyces vietnamensis and the Arg- and Pro-rich N terminus was found to be crucial for catalytic activity. Overexpression of the encoding genes of the holo-ACP synthases of fatty acid synthases (FAS ACPSs) of both E. coli and S. vietnamensis could efficiently activate the production of granaticins in the Δgra-orf32 mutant, suggesting the ACP of granaticin (graACP) is an efficient substrate for FAS ACPSs. However, Gra-ORF32, the cognate PPTase of the graACP, could not compensate the conditional deficiency of ACPS in E. coli HT253, indicating that it has evolved to be functionally segregated from fatty acid biosynthesis. Nine out of eleven endogenous and all the tested exogenous non-cognate PPTases could activate the production of granaticins to varied extents when overexpressed in the Δgraorf32 mutant, indicating that ACPs of type II PKSs could also be widely recognized as effective substrates by the Sfp-type PPTases. The exogenous PPTases of type II PKSs activated the production of granaticins with much higher efficiency, suggesting that the phylogenetically distant in-cluster PPTases of type II PKSs could share substrate preferences for the ACPs of type II PKSs. A significantly elevated production of granaticins was observed when the mutant Δgra-orf32 was cultivated on ISP2 plates, which was a consequence of crosstalk between the granaticin pathway and a kinamycinlike pathway as revealed by transcriptome analysis and pathway inactivations. Although the host FAS ACPS could efficiently activate the production of granaticins when overexpressed, only Gra-ORF32 activated the efficient production of granaticins under natural physiological conditions, indicating that the activity of the host FAS ACPS was strictly regulated, possibly by binding the FAS holo-ACP product with high affinity. Our findings would contribute to a more comprehensive understanding of how the ACPs of type II PKSs are activated and facilitate the future functional reconstitutions of type II PKSs in E. coli. [ABSTRACT FROM AUTHOR]

Background: To investigate the effect of flavaspidic acid BB (BB) on biofilms and quorumsensing-related genes of drug-resistant Staphylococcus epidermidis (SE) and to provideatheoretical basis for the development of BB as a new type of quorumsensing inhibitor. Methods: The microdilution method was applied to screen 15 clinical isolates of S. epidermidis for drug-resistant S. epidermidis to be used as the test strain. The effects of BBonthe biofilms of drug-resistant S. epidermidis at different growth stages were studied usingthecell counting kit-8 assay and scanning electron microscopy. The gene expression of sigB, sarA, and luxS, regulators involved in quorum sensing of biofilm formation, was measuredby PCR. Results: The minimum inhibitory concentrations of BB against 15 clinical strains of S. epidermidis ranged 11.67–66.67 µg/mL. BB significantly inhibited biofilmformationbydrug-resistant SE06 in the aggregation and maturation stages, with an activity superior tothose of mupirocin and fusidic acid (P < 0.05). At 40 µg/mL, BB reduced the secretionof extracellular polymers and promoted the disruption of biofilm structure. At 80 µg/mL, BBspecifically interfered with the quorum sensing system of drug-resistant SE06bydownregulating sarA and luxS, thereby inhibiting this microbe’s biofilmformation. Conclusion: BB exhibited strong inhibitory activity against SE06 by suppressing biofilmformation and downregulating quorum sensing-related genes and was identified as anewpotential quorum sensing inhibitor against S. epidermidis. [ABSTRACT FROM AUTHOR]