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Comprehensive assessment of fragmented fiber shedding from recycled cotton textiles part i structural changes in woven fabrics and mass loss quantification during laundering
How I treat plasma cell leukemia
Abstract Plasma cell leukemia (PCL) represents an exceptionally aggressive plasma cell malignancy defined by ≥5% circulating plasma cells in the peripheral blood of patients otherwise meeting the diagnostic criteria for multiple myeloma (MM), per the International Myeloma Working Group consensus. This ultrahigh-risk disease exhibits distinctive clinical features including frequent extramedullary involvement, severe cytopenias, hypercalcemia, renal insufficiency, and/or significantly elevated β2-microglobulin and lactate dehydrogenase levels. The molecular landscape includes high-risk cytogenetic abnormalities and mutations that promote accelerated proliferation, apoptotic resistance, immune evasion, and bone marrow microenvironmental independence through dysregulated adhesion molecule and chemokine receptor expression. Although autologous stem cell transplantation, proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies improved historical outcomes, the therapeutic paradigm continues to evolve. Novel therapeutic approaches including B-cell maturation antigen–directed therapies (bispecific antibodies and chimeric antigen receptor T-cell therapy), G protein-coupled receptor class C group 5 member D (GPRC5D)-targeted therapy, and B-cell lymphoma 2 (BCL-2) inhibition demonstrate promise in treating both primary and secondary PCL. Despite these advances, PCL remains inadequately studied, with treatment approaches predominantly extrapolated from MM trials in which patients with PCL have largely been excluded. This review synthesizes current evidence and presents illustrative clinical cases demonstrating practical treatment approaches, while highlighting critical knowledge gaps requiring dedicated prospective clinical trials to meaningfully improve outcomes in this challenging disease entity.
Multi-scale contextual modeling and fine-grained adaptive fusion for real-time surface defect detection
Abstract Surface defect detection in steel strips requires both accurate recognition and efficient inference under complex industrial backgrounds. Existing methods still encounter difficulties in modeling scale-varied defects, preserving fine-grained defect cues, and aligning multi-level features efficiently. To address these issues, we propose CDF-YOLO, a real-time detection framework that integrates multi-scale contextual modeling and fine-grained adaptive fusion on the YOLOv12 baseline. Specifically, a Dilated Context Pyramid Bottleneck (C2f_DCPB) is introduced to enhance contextual representation through parallel dilated branches; a Fine-grained Adaptive Fusion module (FAN_Block) is embedded into the high-resolution path to strengthen local texture and structural-detail representation; and DySample is adopted to improve content-adaptive upsampling for multi-scale feature fusion. Experiments on the NEU-DET dataset show that CDF-YOLO achieves an mAP50 of 95.4% and 101.3 FPS under the adopted test protocol, while cross-dataset evaluation on DeepPCB further indicates improved generalization performance. These results suggest that CDF-YOLO provides a favorable accuracy-efficiency trade-off on public industrial defect datasets. Nevertheless, validation on larger-scale production-line data and further optimization for edge deployment remain necessary for practical industrial application.
Phospho-Drp1: rewiring platelet function testing
“The feasibility of free septal mucosal grafts in preventing postoperative middle meatus synechia after endoscopic sinus surgery”
Abstract This study aimed to evaluate the feasibility and safety of using a free septal mucosal graft to prevent middle meatal synechiae following endoscopic sinus surgery (ESS). This prospective observational study was conducted at a tertiary referral center between March 2022 and February 2024. Adult patients with chronic rhinosinusitis without nasal polyps (CRSsNP) who were refractory to medical therapy were included. All patients underwent unilateral ESS followed by placement of a free septal mucosal graft over exposed bone in the middle meatus. Postoperative outcomes were assessed using the Sinonasal Outcome Test-22 (SNOT-22), Lund–Kennedy Endoscopic Score (LKES), and Perioperative Sinus Endoscopy (POSE) score. A total of 116 patients completed the study. Significant improvement in SNOT-22 scores was observed at 6 months postoperatively ( p < 0.001). Significant improvement was also noted in endoscopic findings (LKES, p < 0.001). Stable middle turbinate position without lateralization was achieved in 91 (78%) of cases. Free septal mucosal grafting appears to be a feasible, biocompatible, and technically straightforward method to reduce middle meatal synechiae following ESS.
Extended HLA haplotypes and transplant survival
Abstract The benefit of extended phased (∼) HLA class I∼class III∼class II haplotypes in reducing the mortality after hematopoietic cell transplantation is unknown and requires information on functional class III variation. We identified a robust class III single-nucleotide polymorphism (SNP), rs915654, informative for mortality and relapse in 1436 patients and their haploidentical related donors through multivariable regression analysis of 26 candidate class III SNPs. Three-marker haplotypes, as defined by 1 class I locus, 1 class II locus, and rs915654 were determined in patients separately from donors. Inclusion of rs915654 into relapse and mortality models already containing patient HLA-E∼DRB1 and donor HLA-B∼DRB1 improved each model (likelihood ratio test P = .06 and P = .004, respectively, for relapse; P = .10 and P = .01, respectively, for mortality). The risks of mortality and relapse increased with decreasing numbers of favorable patient and donor markers. Retesting in an independent cohort of 1141 haploidentical transplants yielded similar results. The number of unfavorable markers additionally increased nonrelapse mortality. HLA-A∼C∼B∼DRB1∼DQB1 haplotypes were defined according to their expected numbers of favorable markers, and the theoretical utility for selecting donors was explored. In summary, extended HLA class I∼class III∼class II haplotypes influence the success of transplantation and inform the biology of the major histocompatibility complex in health and disease. The selection of haploidentical donors for future patients may be optimized with knowledge of donor HLA haplotypes.
Exploring the associations among physical activity, social adaptation, and emotional intelligence in adolescents: a network analysis study
First ‘true sugar’ molecule found in space — offering hints to life’s origins
Digesting FPN1 (SLC40A1) in intestinal iron absorption
Exploring electrophysiology as a biomarker for human red blood cell monitoring in extracorporeal membrane oxygenation
CHORUS line: a leg up for HHT
Deep reinforcement learning-based resource recommendation system for ideological and political education
Take yourself on ASHOPing spree
Refraction centile curves for Caucasian and Chinese children and adolescents from simulated data cohorts
Clinical spectrum of hereditary hemorrhagic telangiectasia: data from the Comprehensive HHT Outcomes Registry of the US (CHORUS)
Abstract Hereditary hemorrhagic telangiectasia (HHT), an autosomal dominant vasculopathy affecting 1 in 5000 individuals, is the second most common inherited bleeding disorder worldwide. Despite this prevalence, comprehensive data on disease manifestations and complications remain limited. To address this gap, the US Congress allocated funding leading to the Comprehensive HHT Outcomes Registry of the United States (CHORUS), a prospective, 15-center longitudinal registry enrolling unselected patients with confirmed HHT. In this initial report, we describe findings from the first 600 participants, with a median age of 53 (range, 0-88) years and 60% female. Despite most participants developing typical HHT manifestations by age 13 years, the majority (63%) were not diagnosed until mid-to-late adulthood. Recurrent spontaneous epistaxis occurred in 95% of participants, chronic gastrointestinal bleeding in 30%, and heavy menstrual bleeding in 35% of postmenarche females, together resulting in moderate-to-severe mucosal bleeding in 76%. Iron deficiency and/or anemia were diagnosed in 68%, with 41% requiring IV iron and 25% requiring red cell transfusions. Serious complications of solid-organ arteriovenous malformations were frequent, including intracranial hemorrhage (3%), pulmonary hemorrhage (2%), venous thromboembolism (7%), arterial thromboembolism (11%), heart failure (7%), and pulmonary hypertension (7%). These data from CHORUS, the first national US registry of its kind, provide reliable, real-world estimates of the incidence, prevalence, and severity of numerous HHT manifestations and complications. HHT has a high burden of moderate-to-severe bleeding, anemia, thrombosis, and major neurologic and cardiopulmonary complications. There is a mean interval between first symptoms and diagnosis of &gt;2 decades, during which substantial, serious, and preventable HHT morbidity, including early intracranial hemorrhage, may occur. This trial was registered at clinicaltrials.gov as NCT06259292.
Changes in physical fitness in Chinese primary schools following the “double reduction” policy based on Policy Instrument Theory
Polycomb repressive complex 2 insufficiency underlies myeloid leukemia in Down syndrome
Abstract Children with Down syndrome (DS) have an elevated risk of developing myeloid leukemia (ML; ML in DS [ML-DS]). In addition to mutations in GATA1, which generate the truncated isoform GATA1-short (GATA1s), ML-DS requires additional somatic gene mutations, most frequently in cohesion and Polycomb repressive complex 2 (PRC2) genes. Here, we show that PRC2 insufficiency underlies ML-DS pathogenesis. Transplantation of Gata1s fetal liver cells followed by deletion of the cohesion subunit Stag2 and/or the PRC2 component Ezh2 induced megakaryocyte-biased differentiation and expansion of megakaryocytic progenitors, culminating in lethal myelofibrosis. Mechanistically, loss of Stag2 or Ezh2 reinforced Gata1s-driven reduced chromatin accessibility at erythroid transcription factor target loci in premegakaryocyte/erythroid progenitors (pre-MegEs), thereby promoting megakaryocytic skewing. Ezh2 loss attenuated the Gata1s-mediated global elevation of H3K27 trimethylation in pre-MegEs, resulting in derepression of a broad set of PRC2 target genes and establishing a functionally PRC2-insufficient state. Similarly, Stag2 loss induced a moderate but significant degree of PRC2-insufficient state in Gata1s progenitors. Furthermore, chromosome 21–encoded miR-125b blocked megakaryocytic differentiation of Gata1s progenitors lacking either Stag2 or Ezh2 alone but drove full transformation and expansion of CD150+Sca-1+c-Kit+ leukemic stem cell–like populations only upon concurrent loss of both Stag2 and Ezh2, leading to acute megakaryoblastic leukemia in mice. These findings reveal that cohesin and PRC2 insufficiencies converge on PRC2 dysfunction while exerting distinct epigenetic effects and synergize with trisomy 21 and GATA1s to remodel the epigenetic landscape, driving progression from a preleukemic state to overt leukemia.
Static-dynamic-thermal characteristic analysis and experimental study of motorized spindle
Creatinine assay interferences compromises MELD accuracy and may bias liver allocation
Abstract The Model for End-Stage Liver Disease (MELD) score is widely used to prioritize patients for liver transplantation and to estimate short-term mortality in end-stage liver disease. Inaccuracies in serum creatinine measurements, particularly interference from bilirubin, both key components of the MELD, may influence clinical decision-making. However, standardized approaches to address such analytical bias are lacking. Here we show that bilirubin-related interference leads to clinically relevant MELD distortions and associated outcomes. We developed a correction model using controlled in vitro matrices and validated it against representative patient samples. The model was applied to a large cohort from registry data and a separate clinical population. After correction, clinically meaningful score shifts occurred in a substantial proportion of patients, with lower corrected scores associated with altered transplantation probability and mortality estimates. These findings highlight the importance of harmonized, interference-resistant creatinine assays to improve fairness and accuracy in liver transplant allocation.