Diagnostic applications of neonatologist-performed lung ultrasound in the delivery room in late preterm and term neonates: A systematic review of literature.

Bee sting-induced hypervirulent Klebsiella pneumoniae infection causing fulminant necrotizing fasciitis: case report and narrative review.

Advancements in sustainable bioprinting: Materials, challenges and opportunities in transition from 3D to 4D printing

The natural history of early onset scoliosis: Prognostic factors and progression risks-a review article.

Lightweight ensemble vision transformer framework for non-invasive survival prediction in glioblastoma

UCP2 protects against intracerebral hemorrhage-induced ferroptosis via suppression of TRIM21-dependent GPX4.

Integrating multi-omics data and artificial intelligence for personalized medicine in glioblastoma.

A review of evolving remote sensing and automated techniques in rock glacier mapping

Multiple sclerosis is a clinically heterogeneous disease that is driven by complex immune mechanisms. This review summarizes recent methodological advances in immunophenotyping and discusses clinical implications for diagnosis, prognosis, therapy selection, and monitoring. Methodological advances like high-dimensional flow cytometry and single-cell technologies aim to define Multiple sclerosis immunological endophenotypes associated with different disease trajectories. Novel spectral flow and mass cytometry panels reveal distinct immune cell subsets. Myeloid cell populations have been identified in aggressive disease variants and tissue-resident T cells in cerebrospinal fluid. Clinically, baseline immune signatures aim to predictdisease progression and treatment response. Patients with a highly inflammatory immune profile have been found to exhibit more rapid progression and to be prone to treatment failure. Immunophenotyping may therefore guide treatment, from identifying those at risk of Alemtuzumab-induced autoimmunity to monitoring B-cell repopulation for personalized dosing schedules. Immunophenotyping enables increasingly precise characterization of Multiple sclerosis immuno-pathogenesis. While not yet routine, these tools show promise for improving differential diagnosis, individualizing therapy initiation and monitoring. Ongoing research and standardization are paving the way towards precision immunology-approaches in clinical practice.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease with multifactorial causes, including genetic and environmental factors. This study aimed to identify environmental and lifestyle factors influencing the progression of ALS by leveraging the first and largest patient-reported ALS database in China (the AskHelpU ALS Patient Platform), addressing a critical gap in regional research. Data from 1421 patients with ALS, including detailed information on occupational exposure, lifestyle habits, dietary patterns, and medical history, were collected from the AskHelpU platform. Statistical analyses were conducted to identify associations between these factors and clinical characteristics. The associations between pre-onset factors and disease progression were analyzed using multicariable generalized linear models, adjusting for multiple comaparisons with the Bonferroni correction. Employment in the agriculture industry (p < 0.001) was associated with rapid ALS progression, whereas employment in the leasing and business services industry (p = 0.01) and education industry (p = 0.033) slowed ALS progression. Other key pre-onset prognostic factors were cigarette smoking (p = 0.043) and pre-existing hypertension (p = 0.036). By utilizing the patient-reported ALS database, this study comprehensively examined the effects of environmental, occupational, and lifestyle factors on ALS progression. These findings provide novel insights into the regional variations in ALS etiology, emphasizing the multifactorial nature of the disease.

AI-generated agents with expert personas in biotechnology: Delphi evaluation of emerging technologies and future trajectories

The co-occurrence of actionable driver alterations in non–small cell lung cancer (NSCLC) is rare. Concomitant MET exon 14 skipping ( MET ex14) and KRAS G12C mutations have been only sporadically reported, and the clinical course of the affected patients remains poorly understood. Here, we describe a rare case of advanced invasive mucinous adenocarcinoma harboring both MET ex14 and KRAS G12C mutations. A 69-year-old man was diagnosed with invasive mucinous adenocarcinoma after presenting with multifocal consolidation (cT2bN0M1a, stage IVA). Next-generation sequencing revealed concurrent MET ex14 and KRAS G12C mutations, and the programmed death ligand 1 tumor proportion score was 1%. First-line treatment with tepotinib (500 mg once daily) resulted in stable disease but no objective tumor shrinkage. Disease control was maintained for approximately 8 months before the occurrence of radiographic progression. Second-line therapy with sotorasib (960 mg once daily; later reduced to 480 mg due to edema) produced rapid radiographic progression within 1 month. To our knowledge, this is the first detailed description of the clinical course of a patient with NSCLC harboring concomitant MET ex14 and KRAS G12C mutations, who experienced limited benefit from MET inhibition and demonstrated no clinical response to KRAS inhibition. This case highlights that the coexistence of multiple actionable oncogenic drivers does not necessarily confer additive or parallel therapeutic benefit and provides clinically relevant insights for improving treatment decision-making in cases with tumors with multiple concurrent driver alterations.

Phosphaturic mesenchymal tumours (PMTs) are rare neoplasms that secrete fibroblast growth factor-23 (FGF-23), causing tumour-induced osteomalacia (TIO). Histological overlap with juvenile psammomatoid ossifying fibroma (JPOF) can lead to diagnostic difficulty, particularly outside the craniofacial skeleton. A 4-year-old girl presented with a painful forearm swelling. Radiographs demonstrated a fibro-osseous lesion in the radius and biopsy was initially non-diagnostic, leading to a presumptive diagnosis of fibrous dysplasia. Over the next 6years, the lesion enlarged, and at age 10, the patient developed genu valgum with biochemical evidence of hypophosphataemic rickets (low phosphate, raised alkaline phosphatase, elevated FGF-23). Medical therapy corrected the rickets, though deformity required guided growth surgery. At age 13, a repeat biopsy of the enlarging lesion revealed a fibro-osseous tumour with spindle stroma and psammomatoid ossicles, negative for GNAS mutation, and consistent with a phosphaturic mesenchymal tumour, connective tissue variant. This case highlights a rare radiologic presentation of PMT involving a long bone, with imaging features closely mimicking fibrous dysplasia and histological overlap with JPOF. The rapid progression of imaging findings, discordant metabolic abnormalities and markedly elevated FGF-23 levels poses a diagnostic challenge. As such, fibrous dysplasia-like lesions of the extremities in the setting of hypophosphataemic rickets should prompt consideration of PMT.

Biallelic VRK1 variants are linked to a range of neurogenic disorders, including Charcot-Marie-Tooth and related disease (CMTR), motor neuron diseases, and spinal muscular atrophy (SMA). This study aimed to characterize the genetic and clinical features of VRK1-related peripheral neuropathy in a Chinese cohort with axonal CMTR. Eight families were identified from a cohort of 351 families with axonal CMTR, including axonal CMT and distal hereditary motor neuropathies (dHMN). Clinical and genetic data were retrospectively analyzed. Haplotype analysis investigated the founder effect of the high-frequency variant, and RNA sequencing was conducted for the splice variant. A systematic literature review (PubMed/CNKI, 2009-2025) was performed to compile global cases. VRK1 was the third most common gene in our axonal recessive CMTR cohort. Ten VRK1 variants were identified, including 8 novel variants: c.7C>T, c.83T>G, c.215T>G, c.539C>T, c.879_882del, c.974T>A, c.1073_1076del, and c.1159+2T>A. The nonsense variant c.1124G>A (p.W375*) was present in 4 of 8 families with haplotype analysis supporting a founder effect. RNA sequencing confirmed c.1159+2T>A caused exon 12 skipping and frameshift (p.K357Vfs*39). The clinical phenotypes included dHMN in 7 cases and axonal recessive CMT in one case. Two patients with dHMN exhibited upper motor neuron signs. All patients presented with progressive distal lower limb weakness, without neurodevelopmental impairment. In total, 53 cases from 37 families reported to date (including the present cohort) revealed substantial clinical heterogeneity, with dHMN (28.8%) and SMA (26.9%) being most common. Early-onset cases exhibited rapid progression, whereas later-onset cases had slower courses. This study identifies 8 novel VRK1 variants and confirms the founder effect of p.W375*, expanding the genotypic and phenotypic spectrum of VRK1-related peripheral neuropathy. The clinical presentation in this cohort was predominantly motor-dominant, ranging from dHMN to axonal CMT, with notable phenotypic heterogeneity influenced by the specific protein domain involved. These findings refine the understanding of VRK1-related peripheral neuropathy and provide valuable insights for accurate diagnosis and management.

Data-driven fault detection and diagnosis in industrial process systems: A systematic review and perspective

Exploiting the immunopathogenesis of hepatitis D virus infection to develop superior treatment options.

Pseudo-Richter transformation (Pseudo-RT) in chronic lymphocytic leukemia (CLL) refers to rapid clinical progression resembling Richter transformation (RT), DLBCL - type. It presents with systemic symptoms and lymphadenopathy. Distinguishing Pseudo-Richter from true Richter transformation is challenging but clinically essential due to differences in prognosis and treatment approaches. A 69-year-old Caucasian man was diagnosed with symptomatic CLL. Treatment was initiated with ibrutinib (cycles 1-15) and venetoclax (cycles 4-15). The patient responded well, with clinical and hematological complete response. One week after the last cycle was completed, the patient developed fever, abdominal pain, and recurrent lymphadenopathy. Imaging revealed partial regression and new progression of lymph nodes, splenic infarction, and an eventual splenic rupture requiring emergency splenectomy. Histology showed a diffuse infiltrate of large cells and paraimmunoblasts with high proliferation index (~ 50%), raising suspicion of RT. However, molecular testing was negative for typical findings of high-grade lymphoma and PET-CT did not support it as well. Suspecting pseudo-RT ibrutinib was reintroduced 14 days after cessation, leading to rapid normalization of leukocyte counts and clinical improvement. We report a case of pseudo-RT in a CLL patient treated with ibrutinib/venetoclax combination therapy, contrasting prior reports involving Bruton tyrosine kinase inhibitor (BTKi) monotherapy. The rapid onset of transformation-like symptoms following recent BTKi interruption/cessation should raise suspicion for pseudo-RT, though true RT must be excluded. As BTKi use in CLL increases, this phenomenon may become more common. Prompt interdisciplinary collaboration is essential for accurate diagnosis and appropriate management. Further research is needed to develop rapid diagnostic tools to distinguish pseudo-RT from true RT.

Print, check, repeat: digital quality by design for 3D-printed medicines using OpenAI models.

ABSTRACT Quantitative analyses of offensive transitions in football have largely relied on event-based indicators and absolute pitch zones, offering limited insight into how the opponent’s defensive organisation constrains post-regain behaviour. Consequently, transition speed is often treated as inherently desirable despite its dependence on situational context. Using optical tracking data, this study proposes a context-dependent framework that models the opposition’s defensive structure at the moment of ball regain. Event and tracking data from 198 regular-season matches in the 2025 K League 1 season were analysed, yielding 26,324 in-play transitions. Defensive units were identified using a unit-based clustering approach. Transition contexts were then defined by the spatial relationship between the ball and these units. Post-regain behaviour within the first 6 s was classified into five patterns. Quick progression accounted for approximately one-third of transitions, but its likelihood varied markedly across defensive contexts and teams. Regains occurring behind the opponent’s deepest defensive unit were most conducive to rapid progression, whereas regains within or in front of organised defensive structures more often resulted in slower or disrupted outcomes. These findings demonstrate that offensive transitions are context-dependent tactical events rather than isolated speed-based actions.

Pancreatic adenocarcinoma (PAAD) is a highly aggressive malignancy characterized by rapid progression. In this study, we identify the small MAF protein, MAFF, as a critical driver of PAAD tumorigenesis and a negative regulator of the necroptotic pathway. MAFF silencing significantly suppressed malignant phenotypes in PAAD cells invitro and attenuated overall tumor growth invivo, while ectopic expression promoted tumor progression. Mechanistically, RNA-sequencing and Gene Set Enrichment Analysis (GSEA) identified necroptosis as a key pathway suppressed by MAFF. We established that MAFF acts as a direct transcriptional repressor of GATA4, which in turn serves as a transcriptional activator of the necroptotic executioner MLKL. Consequently, MAFF depletion leads to the reactivation of the GATA4-MLKL axis, triggering necroptotic cell death. The growth-inhibitory effects of MAFF silencing were effectively reversed by pharmacological inhibition of necroptosis or genetic knockdown of GATA4 or MLKL. Analysis of clinical data from TCGA and GTEx databases revealed that MAFF is significantly overexpressed in human PAAD tissues compared to normal controls, with elevated levels correlating with advanced histological grade and poor patient prognosis. Collectively, our findings demonstrate that MAFF facilitates PAAD progression by suppressing GATA4-mediated necroptosis, highlighting the MAFF-GATA4-MLKL axis as a promising therapeutic target and prognostic biomarker in pancreatic cancer.