Search Results (207)

To investigate the association between polymorphisms in the GABRA5, SOX13, and AGL genes and growth traits in Dongfeng sika deer and to identify potential molecular markers for breeding, this study was conducted based on prior genome-wide association analysis. Based on the previous GWAS analysis of 266 Dongfeng sika deer, the SNP loci of GABRA5, SOX13, and AGL genes were detected in 36 male deer samples. The genetic parameters were calculated, and an association analysis with growth traits was carried out. Phenotypic analysis indicated that body weight and chest circumference had higher coefficients of variation than other growth traits, and body weight showed a strong positive correlation with body-slant length (r = 0.743, p < 0.01) and a moderate correlation with chest circumference (r = 0.709). A total of six SNP loci were identified, including three within GABRA5 (Chr13-8442730, Chr13-9033380, and Chr13-9045819), one within SOX13 (Chr14-5681678), and two within AGL (Chr20-66603370 and Chr20-66618510). The dominant genotypes at these loci include CG (CC), AA, CG, CC (CG), AA, and GG (GC). Linkage disequilibrium analysis revealed a relatively strong association between Chr13-8442730 and Chr13-903380 on chromosome 13. Combined genotype analysis showed that diplotype CCCGGC was associated with higher body weight and larger chest circumference than other genotype combinations. Gene expression analysis showed that the relative expression levels of GABRA5, SOX13, and AGL were lower in the low-growth group than in the high-growth group, and expression variation was also observed within groups. Overall, gene expression levels appeared to be positively associated with growth traits, with higher expression associated with improved growth performance. These findings suggest that GABRA5 and AGL may serve as candidate genes for further investigation and that the identified SNP loci may contribute to the development of molecular markers for the selection of growth traits in Dongfeng sika deer. The results provide a preliminary basis for molecular breeding and genetic improvement strategies in Dongfeng sika deer bucks and serve as an important reference for genetic improvement of growth traits in Cervidae. Full article

Background. This study aimed to evaluate the efficacy and safety of low-dose neoadjuvant chemotherapy with an oral fluoropyrimidine containing tegafur, gimeracil, and oteracil (S-1) and oxaliplatin (NAC-SOX) in improving resectability and long-term outcomes in patients with advanced gastric cancer. Methods. This was a single-center, retrospective study analyzing patients with advanced gastric cancer or esophagogastric junction cancer who received NAC-SOX. (S-1: 80–120 mg/m², oxaliplatin: 100 mg/m²) followed by gastrectomy with D2 lymphadenectomy. Clinical background, chemotherapy-related adverse effects, surgical outcomes, pathological response, and survival were assessed. Results. A total of 34 patients underwent NAC-SOX, with a median age of 74 years. The most common surgical procedure was total gastrectomy (n = 16). Peripheral neuropathy was the most frequent adverse effect, but no grade 4 toxicities were observed. Postoperative complications (≥CD grade 3a) occurred in 8.8% of cases, with no treatment-related deaths. R0 resection was achieved in 85.3% of cases, and the pathological complete response rate was 20.6%. The 3-year recurrence-free and overall survival rates were 71.3% and 83.2%, respectively. Conclusions. Low-dose NAC-SOX demonstrated favorable efficacy and safety, achieving high R0 resection and pathological response rates. Further prospective studies are needed to optimize treatment strategies. Full article

Coal-fired power units remain integral to electricity supply in many regions while facing increasingly stringent environmental expectations. Bridging reliable generation with sustainability requires more than end-of-pipe controls; it demands continuous intelligence embedded in plant operations. This study introduces an industry-oriented monitoring framework that transforms historical operational records into actionable foresight, enabling on-the-fly orchestration of combustion conditions to anticipate sulfur oxide (SOx) concentrations. Leveraging 919 empirical data points collected in 2019 from Unit 8 of the Taichung Thermal Power Plant, the framework integrates robust data governance, targeted feature curation, and a neural network-based analytics core. Eight process variables—sulfur content, coal feed rate, fixed carbon, grinding rate, calorific value, excess air, air flow, and boiler efficiency—emerge as the most influential drivers through systematic selection and feature importance attribution. The resulting forecasting module exhibits near-perfect alignment with observed emissions (R² = 0.99), enabling near-real-time guidance for setpoint adjustments and facilitating compliance strategies under varying load and fuel-quality conditions. Beyond accuracy, the system is architected for scalability and portability, aligning with Industry 4.0 paradigms by coupling continuous sensing, data-driven decision support, and stakeholder transparency. By reframing emission oversight as a proactive, intelligent service rather than a static reporting function, the proposed approach advances operational resilience, regulatory compliance, and community trust, with direct implications for resource efficiency and circular economy initiatives across heavy industry. The framework reduces potential SOx emissions and improves energy utilization efficiency under varying operational conditions. This approach contributes to environmental sustainability by enabling proactive emission reduction and cleaner production practices. It supports regulatory compliance and aligns with global sustainability goals, including SDG 7 and SDG 13. Full article

Schizophrenia (SCZ) is a severe neuropsychiatric disorder characterized by a progressive clinical course and associated with a wide range of gene transcription signatures. This review examined studies retrieved from PubMed (published between 2005 and 2025) that investigated transcription factors (TFs) correlated with SCZ. Approximately 150 studies aligning with the eligibility criteria were selected. The synthesized evidence identified more than 40 TFs implicated in the pathogenesis and risk of SCZ. Based on functionality, these TFs were categorized into four groups: (1) progenitor cell TFs (TCF4, POU3F2, NKX2.1, EGR3), (2) stem cell TFs (MYC, SOX2, ASCL1, REST, NR2E1), (3) metabolic reprogramming TFs (HIF1, SREBPs, STATs, SOX9, NRF1, NRF2, p53, FOXO, ATF4, NF-κB), and (4) nuclear TFs (AhR, RXR). The discussion shed light on how these TFs in consort with hundreds of potential genes could shape the pathophysiology of SCZ. Indeed, SCZ represents a complex genomic, nuclear, metabolic, and immune disorder characterized by a diseased cellular microenvironment, with hypoxia emerging as a key feature. Although targeting TFs pharmacologically remains challenging, innovative therapeutic strategies—such as antineoplastic and antipsychotic agents that modulate the cellular microenvironment—may offer promising new directions for SCZ treatment. Full article

Chinese tongue sole (Cynoglossus semilaevis), an economically important mariculture species in China, exhibits pronounced sexual dimorphism in growth, underscoring the importance of elucidating sex regulatory mechanisms for aquaculture development. Heterogeneous nuclear ribonucleoprotein K (hnrnpk) critically regulates mammalian reproductive development, yet its role in fish sex regulation remains elusive. Here, we systematically investigated the underlying function and mechanisms of hnrnpk in C. semilaevis through integrated molecular cloning, expression profiling, upstream regulatory analysis, functional assays, and transcriptome sequencing. We found that hnrnpk was highly expressed in the gonad and liver, with female-biased expression during gonadal development. Promoter activity assays revealed that sox2 and c-Jun enhanced hnrnpk transcription, whereas foxl2 and ar suppressed it. Additionally, hnrnpk was directly targeted by miR-460a-5p in C. semilaevis, revealing multi-level transcriptional and post-transcriptional regulation. Functional analyses showed that hnrnpk regulated cyp19a1a in a cell type-dependent and dose-sensitive manner: the expression of cyp19a1a was both upregulated in hnrnpk-knockdown ovarian cells and hnrnpk-overexpression testicular cells. Interestingly, foxl2 was upregulated in hnrnpk-knockdown ovarian cells but suppressed in hnrnpk-overexpression testicular cells, which showed the distinct regulation mechanisms in the different sexual programs. Transcriptomic analyses further revealed that several sex-related genes (sox9a with downregulation, etc.) were significantly regulated, and cell development and cycle pathways were dramatically enriched in functional enrichment analyses. This might indicate that hnrnpk overexpression drives C. semilaevis testis (CSTE) toward feminization reprogramming through sox9 switching and multi-pathway perturbations. Overall, our findings might reveal that hnrnpk, a female-biased gene regulated by miR-460a-5p and transcription factors, influences sex-related gene expression through sox9 switching. This study will offer new insights for C. semilaevis hnrnpk into sex determination and also provide a potential target for monosex breeding in aquaculture. Full article

Background: Liver fibrosis arises from chronic liver injury and remains a major clinical challenge due to its progression toward cirrhosis and hepatocellular carcinoma, as well as the absence of approved antifibrotic therapies. This study aimed to characterize the transcriptomic behavior of the EGR1-FOS axis in liver fibrosis and its evolution into hepatocellular carcinoma, and to identify genes shared between liver fibrosis and cirrhosis. Methods: An integrated bioinformatics approach was applied to GEO transcriptomic datasets. Differentially expressed genes in hepatic fibrosis were identified using GSE139602, GSE84044, and GSE49541, with GSE62232 as control when needed, while GSE14323 and GSE89377 were used to detect genes common with cirrhosis. GEPIA, TIMER, and TISCH2 were used to assess the involvement of the EGR1-FOS axis in hepatocellular carcinoma. External validation of EGR1 expression dynamics and its coregulation with FOS was performed using the GSE135251 dataset. Results: Eleven hub genes were identified, with emphasis on the EGR1-FOS axis. EGR1 expression fluctuated across liver fibrosis etiologies, whereas FOS was predominantly downregulated. A strong correlation between EGR1 and FOS (r = 0.77) was observed, remaining stable across fibrosis stages (all p < 0.001) and in hepatocellular carcinoma (r = 0.698, p = 1.81 × 10⁻⁵⁵). Despite overall downregulation, both genes increased progressively with advancing fibrosis (EGR1: p = 0.0008–0.0035; FOS: p = 0.0001–0.0188). Four genes were shared between fibrosis and cirrhosis (SOX9, CD24, CXCR4, and CYP2C19). Conclusions: The EGR1-FOS axis acts as a dynamic regulator of liver fibrosis and its progression, and both this axis and the four shared genes identified may serve as valuable biomarkers and potential therapeutic targets. Full article

Uropathogenic Escherichia coli (UPEC) is a leading cause of urinary tract infections (UTIs) in companion animals. This study characterized 42 UPEC isolates recovered from dogs and cats at the University of Florida, College of Veterinary Medicine Diagnostic Laboratories between 2023 and 2024, focusing on antimicrobial resistance (AMR), virulence gene profiles, biofilm-forming ability, and phylogroup distribution of the isolates. Antimicrobial susceptibility testing (AST) showed that 40.48% of the isolates were resistant to at least one of the tested antibiotics, and 9.52% exhibited multidrug resistance (MDR). Phylogroup B2 was predominant (69.05%), and 61.90% of isolates demonstrated strong biofilm formation in artificial human urine. Virulence gene analysis revealed the presence of genes mediating adhesion (fim, pap, sfa), iron acquisition (fyuA, iro), biofilm formation (csg, bcs, pga, ycg/ymg), motility (fli, mot, flh), and stress response (oxyR, soxR/S, kat). Multiple plasmids carrying AMR and virulence determinants were also identified. The co-occurrence of the traits underscores the potential for persistent and recurrent infections, which can complicate therapeutic outcomes and facilitate horizontal gene transfer (HGT). The detection of antimicrobial-resistant, highly virulent UPEC strains possessing human UPEC traits in companion animals suggests the risk of zoonotic and reverse-zoonotic transmission, particularly in households with close pet–owner interactions. These findings emphasize the importance of judicious antimicrobial use, routine molecular surveillance, and integrated One Health strategies to mitigate the veterinary and public health threats associated with UPEC infections in companion animals. Full article

Background: Papillary Thyroid Cancer (PTC) harboring CCDC6-RET translocation is typically classified as a differentiated epithelial tumor. Although Selpercatinib, a RET-selective drug, was recently approved for use in advanced PTC, the emergence of drug resistance has already been observed. Tumor plasticity, including non-canonical Epithelial–Mesenchymal Transition (EMT) programs, is recognized as a key mechanism underlying drug resistance. The downregulation of the transcription factor Wilms’ Tumor 1 (WT1) in cancer is associated with increased motility, invasiveness, and metastatic potential. Methods: In this study, we developed a selpercatinib-resistant PTC-derived cell line, TPC-1-SelpR. Bioinformatic analyses were conducted to study the promoter of the CCDC6-RET gene and the transcriptomic landscape of PTC from RNAseq data. Subsequent real-time PCR, Western blot, and imaging techniques, such as confocal microscopy (CM) and fluorescence microscopy (FM), were employed to study the effects of WT1 loss-of-function following RNAi silencing. Results: In TPC-1-SelpR, WT1 expression appears downregulated compared to its counterpart, TPC-1. Crucially, WT1 silencing induced a context-dependent modulation of the CCDC6-RET driver: while WT1 silencing reduced CCDC6-RET expression in TPC-1, in TPC-1-SelpR, a post-transcriptional compensation of CCDC6-RET was observed. The gene expression of several factors involved in EMT, such as Twist, Vimentin, Integrin beta-1, and Profilin, was rewired in TPC-1-SelpR^{WT1-knockdown}. Although the Vimentin protein product decreased, CM and FM analyses confirmed a reorganization of residual protein: the subcellular redistribution was more dispersed in TPC-1-SelpR^{WT1-knockdown}. Further upregulation of the stemness factor Sox2 over the differentiation factor Sox17 occurred. These molecular changes were associated with higher cell motility of TPC-1-SelpR^{WT1-knockdown}. Conclusions: Collectively, these findings suggest that WT1 is a critical regulator involved in tumor plasticity, thereby supporting selpercatinib resistance. Full article

R-loops, three-stranded nucleic acid structures formed by an RNA-DNA hybrid, have emerged as important regulators of transcription and genome stability. Although advances in high-throughput sequencing have revealed widespread R-loop landscapes, platform-specific biases hinder the identification of conserved R-loops in specific cell types. Mouse embryonic stem cells, which are transcriptionally active, provide an ideal system for investigating the potential roles of stable R-loops in RNA biology. Here, we integrated 13 independent R-loop profiling datasets from four experimental platforms to define 27,950 Common R-loop regions in mouse embryonic stem cells and characterized their chromatin environment and associated biological functions. Common R-loop regions were reproducibly detected across methods and were preferentially localized to promoter-proximal and genic regions enriched in CpG islands. Genes associated with Common R-loops were highly and stably expressed, showing strong functional enrichment in RNA metabolic processes such as mRNA processing, RNA splicing, and ribonucleoprotein complex biogenesis. Chromatin state analysis revealed that Common R-loops are enriched in transcriptionally active and regulatory contexts. Sequence feature analysis further identified GC skew as a prominent signature of Common R-loops, particularly within transcribed chromatin states. Transcription factor motif analyses have identified distinct regulatory environments in Common R-loop regions, including pluripotency-associated OCT4-SOX2-TCF-NANOG motifs in enhancers, CTCF motifs in open chromatin, and YY1 motifs in promoters. Together, this study provides the first integrated analysis of conserved R-loop regions in mouse embryonic stem cells, revealing their preferential localization at regulatory loci linked to RNA metabolism and highlighting R-loops as structural and functional nodes in RNA biology. Full article

NOTCH1 is associated with various tumors, including oral squamous cell carcinoma (OSCC), with a complex role depending on cellular contexts. Our aim was to analyze the expression of NOTCH1, several stem cell markers, and selected microRNAs in preneoplastic lesion of the oral cavity, oral epithelial dysplasia (OAD). Our study included formalin-fixed paraffin-embedded biopsy samples of 36 cases of OAD and 15 cases of normal oral mucosa. Expression of NOTCH1, stem cell markers (AGR2, KLF4, NANOG, OCT4, SOX2), and miR-27a, miR-34a, miR-128, miR-145, miR-150, and miR-335 was analyzed by quantitative PCR (qPCR). Expression of NOTCH1 protein was analyzed by immunohistochemistry. In OAD compared to normal mucosa, we found a significant increase in mRNA levels of NOTCH1, stem cell markers AGR2, NANOG, OCT4, and SOX2, and miR-150 and miR-128. NOTCH1 mRNA positively correlated with all five stem cell markers’ mRNA levels and miR-150. Immunohistochemistry showed variable expression patterns of NOTCH1 in OAD and normal mucosa. Our results support the role of NOTCH1 in early phases of OSCC development, with a potential contributory role in stemness, in association with AGR2, NANOG, OCT4, and SOX2, miR-150 and miR-128. These results support a complex role of NOTCH1 in carcinoma development, i.e., from oncogenic to tumor suppressor roles and stemness maintenance, not only in invasive OSCC but also in its precursor—OED. Full article

Two sulfur-oxidizing bacterial strains, FCG-A2^T and FCG-A23^T, were isolated from coastal sediments collected in Fangchenggang, Guangxi Province, China. Phylogenetic analyses based on 16S rRNA gene and whole-genome sequences placed strain FCG-A2^T within the genus Pseudothioclava and strain FCG-A23^T within the genus Terasakiella. Genomic relatedness (ANI, AAI, dDDH, and POCP) to the closest described taxa was below the accepted species thresholds, demonstrating that both isolates represent novel species. Strain FCG-A2^T grew at 15–35 °C (optimum 25–30 °C), at pH 5.0–10.0 (optimum pH 8.0), and with 1–4% (w/v) NaCl concentrations (optimum 3%). Strain FCG-A23^T grew at 20–33 °C (optimum 25–30 °C), at pH 6.0–9.0 (optimum, pH 8.0), and with 2–6% (w/v) NaCl (optimum 2%). For both strains, ubiquinone-10 was the major respiratory quinone, and the predominant fatty acids were summed feature 3 (C_16:1ω7c and/or C_16:1ω6c) and summed feature 8 (C_18:1ω7c and/or C_18:1ω6c); strain FCG-A2^T additionally contained C_16:0 as a major fatty acid. Both strains oxidized thiosulfate to sulfate, consistent with the presence of genes encoding the Sox system and assimilatory sulfate reduction pathways. Comparative genome annotation further suggested a broader carbohydrate-degradation potential in FCG-A2^T than in FCG-A23^T, implying a wider ecological distribution and greater opportunities for FCG-A2^T to perform sulfur oxidation across habitats. The draft genomes had G + C contents of 62.09% (FCG-A2^T) and 49.06% (FCG-A23^T). Based on these results, we propose Pseudothioclava alba sp. nov. (type strain FCG-A2^T = MCCC 1K08969^T = KCTC 8462^T) and Terasakiella sediminum sp. nov. (type strain FCG-A23^T = MCCC 1K08972^T = KCTC 8464^T). Full article

Both let-7a and miR-34a have been repeatedly studied as pivotal suppressors for Hepatocellular carcinoma; however, their combined regulations remain to be fully elucidated. In the present study, we performed a comprehensive in silico analysis for let-7a and miR-34a using a wealth of updated tools: miRWalk, Genetrail and miRnet. In addition, our study is the first to quantify both miRs and their three predicted yet not experimentally validated oncogenic targets: FNDC3B, IGF2 and SOX4. This was assessed in HepG2 cell model following treatment by PEGP-vector expressing the miRs by MTT assay, florescence microscopy, qPCR and immune-florescence. Our bioinformatics analysis revealed a pool of common predicted hepatocarcinogenic targets shared by both let-7a and miR-34a. Importantly, three targets were identified as co-regulated through multiple canonical binding sites for each miR, and these had not been experimentally validated before. Furthermore, functional enrichment of these putative targets demonstrated their significant involvement in major and emerging HCC hallmarks, such as reprogramming of energy metabolism and evading immune destruction. These findings support our concept of simultaneous co-regulation of these oncogenes through the signaling networks and GO terms associated with both miRs. Consistently, our experimental results verified the significant overexpression of both miRs in HepG2 cells, leading to reduced tumor cell proliferation and decreased levels of the three oncogenic transcripts. Interestingly, miR-34a exhibited a superior suppression effect, reaching 38.7%, and SOX4 was identified as the most significantly downregulated target at both transcriptional and translational levels. Our findings provide new insights into the interconnected anti-HCC effects of let-7a and miR-34a and highlight the potential of applying their combined use to achieve the best therapeutic outcomes for this invasive tumor. Full article

There is a growing need to understand ciprofloxacin (CIP) resistance in less prevalent Salmonella serovars like Salmonella Dublin, which causes life-threatening conditions in both humans and animals. This study investigated potential factors contributing to CIP-resistance in a Salmonella Dublin isolate. The isolate was detected from an initial screening of 17 biobanked Salmonella isolates using the Kirby-Bauer disk diffusion (KBDF) method. The minimum inhibitory concentration (MIC) values of the identified CIP-resistant Salmonella Dublin isolate and a CIP-susceptible isolate of the same serovar were also obtained using the broth-dilution (BD) method. The two candidates were then challenged in 1/4 of their respective BD MICs for gene expression analysis, focusing on the acrAB efflux genes and the regulator genes marA, ramA, and soxS. Genomes of the isolates were also sequenced using the Oxford Nanopore sequencing platform, and then analyzed for mutations, antimicrobial resistance genes, and plasmids using ABRicate. The SWISS-MODEL server was used for protein modeling and comparison. For our results, the MIC values (KBDF; BD) for the CIP-resistant and CIP-susceptible Salmonella Dublin isolates were (1.5 μg/mL; 1.95 μg/mL) and (<0.125 μg/mL; 0.03 μg/mL), respectively. Both isolates had genes (mdtK, emrR, emrA, and emrB) notable for fluoroquinolone resistance, with the CIP-susceptible isolate also carrying the IncFII(S) plasmid. Expression of the acrA, acrB, ramA, and soxS genes was markedly higher in the CIP-resistant isolate, which also harbored an Asparagine (N) to Serine (S) mutation at position 868 in the GyrA protein. This mutation, however, caused no significant structural change. Despite reporting on a single CIP-resistant Salmonella Dublin isolate, our result highlights the potentially significant role of an efficient efflux system in contributing to CIP resistance in this isolate, even when no impactful mutations were identified. Full article

Background: Zika virus (ZIKV), a mosquito-borne flavivirus, is associated with congenital malformations and neuroinflammatory disorders, highlighting the need to identify host factors that shape infection outcomes. Macrophages, key targets and reservoirs of ZIKV, orchestrate both antiviral and inflammatory responses. Methods: Vitamin D (VitD) has emerged as a potent immunomodulator that enhances macrophage antimicrobial activity and regulates inflammation. To investigate how VitD shapes macrophage responses to ZIKV, we reanalyzed publicly available RNA-seq and miRNA-seq datasets from monocyte-derived macrophages (MDMs) of four donors, differentiated with or without VitD and subsequently infected with ZIKV. Results: Differential expression analysis identified long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs integrated into competing endogenous RNA (ceRNA) networks. In VitD-conditioned and ZIKV-infected MDMs, 65 lncRNAs and 23 miRNAs were significantly modulated. Notably, lncRNAs such as HSD11B1-AS1, Lnc-FOSL2, SPIRE-AS1, and PCAT7 were predicted to regulate immune and metabolic genes, including G0S2, FOSL2, PRELID3A, and FBP1. Among the miRNAs, let-7a and miR-494 were downregulated, while miR-146a, miR-708, and miR-378 were upregulated, all of which have been previously implicated in antiviral immunity. Functional enrichment analysis revealed pathways linked to metabolism, stress responses, and cell migration. ceRNA network analysis suggested that SOX2-OT and SLC9A3-AS1 may act as molecular sponges, modulating regulatory axes relevant to immune control and viral response. Conclusions: Despite limitations in sample size and experimental validation, this study provides an exploratory map of ncRNA–mRNA networks shaped by VitD during ZIKV infection, highlighting candidate molecules and pathways for further studies on host–virus interactions and VitD-mediated immune regulation. Full article

Background and Clinical Significance: Mantle cell lymphoma (MCL) frequently involves bone marrow, gastrointestinal tract, and hepatosplenomegaly, whereas pleural effusions are uncommon. Cases requiring invasive mechanical ventilation and thoracic drainage are rare. We report a case of MCL with persistent massive pleural effusions requiring invasive mechanical ventilation and bilateral continuous thoracic drainage. Case Presentation: A 71-year-old woman presented with dyspnea and was found to have bilateral pleural effusions and generalized lymphadenopathy. Shortly after admission, she developed acute respiratory failure due to pleural effusions and required invasive mechanical ventilation. Right-sided continuous thoracic drainage was initiated. Thereafter, more than 1 L of pleural fluid was drained each day. Flow cytometry of the pleural fluid showed CD5-positive B cells with kappa light-chain restriction. Bone marrow examination revealed abnormal lymphocyte infiltration. Cervical lymph node biopsy demonstrated diffuse proliferation of medium-sized, abnormal B lymphocytes with an immunophenotype of CD5⁺, CD19⁺, CD20⁺, cyclin D1⁺, SOX11⁺, and κ⁺, with a Ki-67 index of 20%, confirming MCL, stage IV. Immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) was commenced under mechanical ventilation. Shortly thereafter, left-sided continuous thoracic drainage was also initiated. However, in response to immunochemotherapy, the bilateral pleural effusions gradually subsided, enabling extubation, and there was no reaccumulation after removal of both chest tubes. Furthermore, generalized lymphadenopathy regressed, and bone marrow examination revealed resolution of lymphoma infiltration, resulting in complete remission. Conclusions: De novo MCL complicated by persistent massive pleural effusions requiring invasive mechanical ventilation and bilateral continuous thoracic drainage is rare. A thorough diagnostic workup followed by prompt initiation of immunochemotherapy can arrest pleural output, enable extubation, and be lifesaving. Clinicians should recognize that MCL rarely presents with persistent massive pleural effusions. Full article