Spinal epidural angiolipomas (SEALs) are rare, benign extradural lesions accounting for 0.04 to 1.2% of all spinal axis tumors. They are typically noninfiltrating, located dorsally in the thoracic canal, and present with progressive myelopathy. Histologically, spinal epidural angiolipomas consist of mature adipose tissue interspersed with abnormal vascular channels, which may be capillary or cavernous based on vessel size. Cavernous-type spinal epidural angiolipomas are extremely rare, with only isolated reports in the literature. Surgical decompression with tumor excision is the treatment of choice in symptomatic patients, and diagnosis is confirmed on histopathological examination. We report three patients (two males, one female; age range, 28-60 years) with cavernous-type spinal epidural angiolipoma with varying presentations. MRI demonstrated dorsally located thoracic extradural lesions causing significant cord compression, and in one patient the tumor was extending into the left neural foramina. All patients underwent posterior decompression (open-door laminoplasty, or hemilaminectomy) and piecemeal gross total resection of a well-defined, noninfiltrative, highly vascular epidural mass. Histopathology in all cases confirmed a cavernous variant, composed of congested, thin-walled, dilated vessels admixed with mature adipose tissue. All patients experienced significant postoperative symptomatic improvement, without neurological deterioration or intraoperative neuromonitoring changes. Cavernous-type spinal epidural angiolipomas belong to an extremely rare subtype of spinal epidural angiolipoma that should be considered in the differential diagnosis of enhancing dorsal thoracic extradural lesions. Surgical decompression with gross-total excision offers excellent early neurological recovery in most patients, and histopathological examination remains essential for definitive diagnosis and prognostication.

Acute lung injury (ALI) is a respiratory disease with a high mortality rate. Shionone, derived from the Chinese herbal medicine Aster tataricus, has anti-inflammatory and antioxidant effects. However, its protective effect on ALI remains unclear. In this study, we aimed to assess the protective effect of shionone on lipopolysaccharide (LPS)-induced ALI and to elucidate its underlying mechanisms. In this study, male C57BL/6 mice aged 8-10 weeks were randomly divided into five groups (10 mice per group) including control group, LPS group, LPS + shionone (50 mg/kg) group, LPS + shionone (100 mg/kg) group, and LPS + Dexamethasone (1 mg/kg) group. In mice with LPS-induced ALI, shionone significantly reduced lung index, lung wet/dry weight ratio, production of inflammatory cytokines, nitric oxide (NO) content, malondialdehyde (MDA) production, and increased superoxide dismutase (SOD) activity and nicotinamide adenine dinucleotide phosphate (NADPH) level. Shionone improved lung histopathological injury by inhibiting inflammatory cell infiltration and edema in LPS-induced ALI in mice. In vitro, shionone inhibited oxidative stress and inflammation in LPS-induced BEAS-2B cells. Shionone improved the protein expression of anti-ferroptosis proteins, including glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), in mice lung tissues and BEAS-2B cells. Additionally, GC-MS-based metabolomic analysis showed that shionone increased the levels of various metabolites, such as fructose, glucose, and lactic acid. Shionone ameliorated LPS-induced ALI by downregulating Kelch-like ECH-associated protein 1 (Keap1) and upregulating Nuclear factor erythroid 2-related factor 2 (Nrf2), Heme oxygenase-1 (HO-1), and quinone oxidoreductase 1 (NQO1) in both in vivo and in vitro study. In conclusion, this study demonstrated that shionone mitigated LPS-induced ALI by inhibiting ferroptosis through regulation of Keap1/Nrf2/SLC7A11/GPX4 pathway, indicating that shionone may be a promising agent for ALI.

The "Karakoram Anomaly" - the atypical stability of glaciers in a warming climate-has introduced considerable uncertainty into projections of regional water resources. However, the resilience of this anomaly under sustained climate forcing remains poorly quantified. In this study, multi-source geodetic data (ASTER, NASA DEM, ICESat‑2) were integrated to reassess glacier mass balance across the Karakoram and its sub‑regions between 2000 and 2024. Our results indicate a region‑wide specific mass balance of -0.0386 ± 0.0032 m w.e. a - [1], with strong spatio-temporal heterogeneity. We document a progressive decay of the Karakoram Anomaly: it was region‑wide before 2010, contracted to the northern and central Karakoram during 2010-2020, and has largely weakened since 2020, persisting only in isolated basins. This evolution is closely associated with summer warming and changes in precipitation. Topography exerts a key control on spatial variability. These findings improve our understanding of the Karakoram anomaly and are of great significance for regional water resources management and disaster prevention under climate change.

Early animal embryos undergo rapid cleavages that partition cytoplasmic volumes orders of magnitude larger than those of somatic cells [1] . Each division must reposition nuclei and centrosomes and distribute organelles within minutes, over distances up to hundreds of micrometers [2] . Cleavage furrows are positioned by microtubule asters [3,4] , but the mechanical mechanism for long-range transport of cytoplasmic components before cytokinesis was unknown. Here, we show that cytoplasm behaves as a locally switchable active material. Fluidization at the midplane allows bulk actomyosin to convert a local mechanical asymmetry into directed global flows of all components as a composite material. Using an actin-intact cycling Xenopus egg extract together with Xenopus and medaka embryos, we find that F-actin mechanically couples microtubule asters, organelles, nuclei and centrosomes into a gel-like composite that propagates forces over hundreds of micrometers. After mitosis, Aurora B kinase patterns a locally fluidized midplane, from which myosin-II contractility drives coherent cytoplasmic flows. A fluid dynamics model accounts for the observed flow geometry and rates. Our results reveal how local control of the material state of cytoplasm converts mitotic symmetry breaking into long-range intracellular transport and identify bulk actomyosin as the active stress generator that partitions embryonic cytoplasm as a composite gel.

Individuals with schizophrenia consistently show thinning retinal layers, which can potentially serve as neural biomarkers. The association between retinal morphology and core symptom domains like cognitive functioning, however, has not been systematically synthesized. We hypothesize that deficits in retinal structure are associated with cognitive dysfunction in schizophrenia. This systematic review and meta-analysis looks at studies available from inception to June 9, 2026. Outcome measures include correlation coefficients between cognition scores and retinal thickness values (both macular and peripapillary-total and sector-wise) assessed using optical coherence tomography in patients with schizophrenia and related disorders. We assessed risk of bias with the Joanna Briggs Institute critical appraisal tool. Meta-analysis was conducted using the restricted maximum-likelihood method and Fisher's r-to-z transformation. Data from 16 studies (n=1,475 eyes; 847 patients) were included in a series of 88 pooled analyses. Overall cognitive ability correlated with thickness of the macular-retinal nerve fiber layer (mRNFL) (pooled-r=0.180; p=.002; k=7) and the superior-quadrant of the peripapillary RNFL (pRNFL) (pooled-r=0.214; p=.026; k=7). Attention correlated with mRNFL (pooled-r=0.210; p<.001; k=6), macular-inner plexiform layer (mIPL) (pooled-r=0.142; p=.012; k=8), and pRNFL (pooled-r=0.207; p<.001; k=9) thicknesses. Processing speed correlated with foveal thickness (FT) (pooled-r=0.206; p=.008; k=7), mIPL (pooled-r=0.194; p=.001; k=6), and pRNFL (pooled-r=0.211; p<.001; k=5) thicknesses. Executive function correlated with macular thickness (pooled-r=0.099; p=.018; k=10) and mRNFL (pooled-r=0.159; p=.009; k=6). Age, sex, cardiometabolic comorbidities, and smoking moderated these correlations. We provide evidence suggesting that retinal layer thickness is associated with poorer cognitive functioning in schizophrenia, supporting retinal changes as indicators of disease-related neural processes. The small number of available studies limits these conclusions.

Cytoskeletal network architecture is crucial in determining emergent morphology and dynamics, particularly in processes like stress fiber nucleation, where cells respond to mechanical cues. However, a clear understanding of the connection between architecture, dynamics, and mechanical response remains lacking. In this study, we investigate how self-assembled cytoskeletal structures respond to external mechanical perturbations, focusing on filament and crosslinker mixtures in two dimensions. Using agent-based models complemented by coarse-grained thermodynamic analysis, we reveal how molecular motor activity enables cytoskeletal structures to robustly adapt to changing mechanical conditions. Our simulations demonstrate that under tensile forces, self-assembled active asters transform into bundle-like structures, reminiscent of de novo stress fiber formation in living cells, while pre-existing active bundles elongate further in a reproducible and regulated manner. In contrast, passive assemblies exhibit no such qualitative morphological reorganization, highlighting the critical role of activity in mechanical adaptation. We derive a simple relation approximating active stress as a function of average relative motor alignment, a measure of mesoscopic architecture, which allows us to predict changes in stress characteristics in response to mechanical perturbations with or without morphological reorganization. Our results demonstrate how mesoscopic architecture and motor activity work in tandem to enable robust morphological and mechanical adaptation in cytoskeletal structures, providing insight into cellular mechanosensing and stress fiber formation.

In France, nearly one third of breast cancers occur after the age of 70, yet these patients have long been underrepresented in the clinical trials that inform treatment decisions. This exclusion, rarely made explicit, became embedded in clinical practice. The ASTER 70s trial, published in The Lancet in 2025, provides new evidence. It shows that adjuvant chemotherapy does not improve overall survival in women aged 70 and older, while exposing them to significant toxicity and potential loss of autonomy. This seemingly negative result constitutes a decisive finding: it demonstrates that it is both possible and necessary to generate evidence for populations long excluded from clinical research. It calls for a rethinking of health equity.