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A bstract Quantifying complexity in quantum systems has witnessed a surge of interest in recent years, with Krylov-based measures such as Krylov complexity ( C K ) and Spread complexity ( C S ) gaining prominence. In this study, we investigate their interplay by considering the complexity of states represented by density matrix operators . After setting up the problem, we analyze a handful of analytical and numerical examples spanning generic two-dimensional Hilbert spaces, qubit states, quantum harmonic oscillators, and random matrix theories, uncovering insightful relationships. For generic pure states, our analysis reveals two key findings: (I) a correspondence between moment-generating functions (of Lanczos coefficients) and survival amplitudes, and (II) an early-time equivalence between C K and 2 C S . Furthermore, for maximally entangled pure states, we find that the moment-generating function of C K becomes the Spectral Form Factor and, at late-times, C K is simply related to NC S for N ≥ 2 within the N -dimensional Hilbert space. Notably, we confirm that C K = 2 C S holds across all times when N = 2. Through the lens of random matrix theories, we also discuss deviations between complexities at intermediate times and highlight subtleties in the averaging approach at the level of the survival amplitude.

A bstract We conduct an exhaustive study of the interior geometry of a family of asymptotically AdS d +1 hairy black holes in an analytically controllable setup. The black holes are exact solutions to an Einstein-Maxwell-Dilaton theory and include the well-known Gubser-Rocha model. After reviewing the setup, we scrutinize the geometry beyond the horizon, finding that these backgrounds can exhibit timelike or Kasner singularities. We generalize the no inner-horizon theorem for hairy black holes to accommodate these findings. We then consider observables sensitive to the geometry behind the horizon, such as Complexity = Anything and the thermal a -function. In the Kasner case, we propose a new variant of complexity that characterizes the late-time rate by the Kasner exponents, extending previous work by Jørstad, Myers and Ruan. Additionally, we elucidate the power-law behavior of the thermal a -function near the singularity, directly relating it to the Kasner exponents. Finally, we introduce axion-like fields in the Gubser-Rocha model to study the impact of translational symmetry breaking on the black hole interior. We show that Kasner singularities occur for both explicit and spontaneous symmetry breaking, with the Kasner exponents depending on the strength of broken translations only in the latter case.

Cuticular waxes are complex mixtures of very-long-chain fatty acids (VLCFAs) and their derivatives, forming a natural barrier on aerial surfaces of terrestrial plants against biotic and abiotic stresses. In VLCFA biosynthesis, β-ketoacyl-CoA synthase (KCS) is the key enzyme, catalyzing the first reaction in fatty acid elongation and determining substrate specificity. We isolated a rice (Oryza sativa) wax crystal-sparse leaf 4 (WSL4) gene using a map-based cloning strategy. WSL4 is predicted to encode a KCS, a homolog of Arabidopsis (Arabidopsis thaliana) CER6. Complementation of the mutant wsl4-1 with WSL4 genomic DNA rescued the cuticular wax-deficient phenotype, confirming the function of WSL4. The load of wax components longer than 30 carbons (C30) and C28 were reduced markedly in wsl4-1 and wsl4-2 mutants, respectively. Overexpression of WSL4 increased the cuticular wax load in rice leaves. We further isolated a cofactor of WSL4, OsCER2, a homolog of Arabidopsis CER2, by coimmunoprecipitation and confirmed their physical interaction by split-ubiquitin yeast two-hybrid experiments. Expression of WSL4 alone in elo3 yeast cells resulted in increased C24 but did not produce VLCFAs of greater length, whereas expressing OsCER2 alone showed no effect. Coexpression of WSL4 and OsCER2 in elo3 yeast cells yielded fatty acids up to C30. OsCER2 with a mutated HxxxD motif (H172E, D176A, and D176H) interrupted its interaction with WSL4 and failed to elongate VLCFAs past C24 when expressed with WSL4 in elo3 yeast cells. These results demonstrated that WSL4 was involved in VLCFA elongation beyond C22 and that elongation beyond C24 required the participation of OsCER2.

A bstract We establish a direct correspondence between the Lanczos approach and the orthogonal polynomials approach in random matrix theory. In the large- N and continuum limits, the average Lanczos coefficients and the recursion coefficients become equivalent, with the precise mapping b (1 – x ) = R x and a (1 – x ) = S ( x ). As a result, the two formalisms yield identical expressions for the leading density of states. We further analyze the Krylov dynamics associated with the recursion coefficients and show that the orthogonal polynomials admit a natural interpretation as Krylov polynomials. This picture is realized explicitly in the Gaussian Unitary Ensemble, where all quantities can be computed analytically.

This retrospective study aimed to investigate the clinical characteristics, management, and prognosis of pediatric malignancy-associated hemophagocytic lymphohistiocytosis (M-HLH). This was a retrospective, single-center cohort study, pediatric patients diagnosed with M-HLH diagnosed from January 2003 to December 2024 in our center were enrolled. Clinical characteristics, treatment regimens, overall response rate (ORR), and overall survival (OS) were evaluated. Univariate and multivariate analyses of potential factors were performed to identify prognostic factors. Of the 44 patients, the median age at M-HLH diagnosis was 6.63 years (range: 0.33-15.58). Most patients (79.5%) developed HLH induced by tumors. Lymphoma was the most common malignancy (56.8%), predominantly of the T/NK - cell subtype (36.4%), followed by acute leukemia (27.3%) and Langerhans cell histiocytosis (15.9%). Marked elevations were observed in IL - 2R, IFN - γ, TNF - α, IL - 6, and IL - 10. Pathogenic variants in HLH - associated genes ( , , and were identified in three cases. Patients with the HLH at malignancy diagnosis were significantly older and had lower platelet and albumin levels compared to those with HLH after malignancy chemotherapy(  < 0.05). The ORR at the 4 week HLH diagnosis and at the final follow-up was 63.6% and 68.2%, respectively. The 6-month, 1-year, and 2-year OS rates were 79%, 69%, and 67%, respectively. Elevated serum ferritin (> 5000 ng/mL), age (> 10 years), lactate dehydrogenase (> 500 U/L), and failure to achieve CR were all associated with lower OS (  < 0.05). Achieving CR significantly enhanced OS in malignancy-induced HLH (  < 0.01), but not in chemotherapy-induced HLH. Failure to achieve CR by the final follow-up was an independent risk factor for a poor prognosis. The prognosis of pediatric M - HLH patients is poor. Remission of HLH is critical to the prognosis of M - HLH. Personalized and intensive treatment regimens are necessary for pediatric M - HLH.

A bstract We examine the multifold complexity and Loschmidt echo for an inverted harmonic oscillator. We give analytic expressions for any number of precursors, implementing multiple backward and forward time evolutions of the quantum state, at the leading order in the perturbation. We prove that complexity is dominated by the longest permutation of the given time combination in an alternating “zig-zag” order, the exact same result obtained with holography. We conjecture that the general structure for multifold complexity should hold true universally for generic quantum systems, in the limit of a large number of precursors.

Senescence of vascular smooth muscle cells (VSMCs) contributes to aging-related cardiovascular diseases by promoting arterial remodelling and stiffness. Ferroptosis is a novel type of regulated cell death associated with lipid oxidation. Here, we show that pro-ferroptosis signaling drives VSMCs senescence to accelerate vascular NAD + loss, remodelling and aging. Pro-ferroptotic signaling is triggered in senescent VSMCs and arteries of aged mice. Furthermore, the activation of pro-ferroptotic signaling in VSMCs not only induces NAD + loss and senescence but also promotes the release of a pro-senescent secretome. Pharmacological or genetic inhibition of pro-ferroptosis signaling, ameliorates VSMCs senescence, reduces vascular stiffness and retards the progression of abdominal aortic aneurysm in mice. Mechanistically, we revealed that inhibition of pro-ferroptotic signaling facilitates the nuclear-cytoplasmic shuttling of proliferator-activated receptor-γ and, thereby impeding nuclear receptor coactivator 4-ferrtin complex-centric ferritinophagy. Finally, the activated pro-ferroptotic signaling correlates with arterial stiffness in a human proof-of-concept study. These findings have significant implications for future therapeutic strategies aiming to eliminate vascular ferroptosis in senescence- or aging-associated cardiovascular diseases. Ferroptosis is a novel form of regulated cell death associated with lipid oxidation. Here, the authors demonstrate that the proferroptosis signal is activated and drives vascular aging by inducing senescence in vascular smooth muscle cells.

In this study, novel composite titanium-based metal-organic framework (MOF) beads were synthesized from titanium based metal organic framework MIL-125 and chitosan (CS) and used to remove Pb(II) from wastewater. The MIL-125-CS beads were prepared by combining the titanium-based MIL-125 MOF and chitosan using a template-free solvothermal approach under ambient conditions. The surface and elemental properties of these beads were analyzed using scanning electron microscopy, Fourier transform infrared and X-ray photoelectron spectroscopies, as well as thermal gravimetric analysis. Moreover, a series of experiments designed to determine the influences of factors such as initial Pb(II) concentration, pH, reaction time and adsorption temperature was conducted. Notably, it was found that the adsorption of Pb(II) onto the MIL-125-CS beads reached equilibrium in 180 min to a level of 407.50 mg/g at ambient temperature. In addition, kinetic and equilibrium experiments provided data that were fit to the Langmuir isotherm model and pseudo-second-order kinetics. Furthermore, reusability tests showed that MIL-125-CS retained 85% of its Pb(II)-removal capacity after five reuse cycles. All in all, we believe that the developed MIL-125-CS beads are a promising adsorbent material for the remediation of environmental water polluted by heavy metal ions.

Aims N‐methyl‐D‐aspartic acid (NMDA) receptors play subunit‐specific role in central neuronal development. However, insights into the pharmacological modulation of NMDA receptors were mainly lack of subunit and synaptic selectivity. The purpose of the present study was to develop a novel strategy to rapidly recognize NMDA subunit 2A (NMDA‐2A) ligands from natural products and provide subunit‐selective drug candidates for Alzheimer's disease (AD). Methods The recombinant NMDA‐2A containing a tag of epidermal growth factor receptor (EGFR) was expressed in Escherichia coli cells and immobilized on ibrutinib‐modified microspheres based on the specific reaction between EGFR and its inhibitor ibrutinib. A novel affinity stationary phase was synthesized to screen NMDA‐2A ligands from Gardenia jasminoides Ellis. Results The immobilized receptor column exhibited excellent receptor selectivity and ligand‐binding activity. Crocetin was screened by using this method. In a cellular model of AD, the protein level of NMDA‐2A was significantly decreased compared with the control group, while treatment with crocetin significantly increased NMDA‐2A level in a concentration‐dependent manner, confirming that crocetin could bind to NMDA‐2A in vitro. Conclusion In the present study, we developed a reliable method for the rapid identification of NMDA‐2A ligands from natural products, which may be used as a platform for new drug discovery to generate high‐quality drug candidates. (i) The modification of ibrutinib; (ii) the preparation of NMDA‐2A column and its application in bioactive compound identification from Gardenia jasminoides Ellis; and (iii) the reaction between ibrutinib‐modified microspheres and EGFR‐tagged NMDA‐2A.

Long noncoding RNAs (lncRNAs) are implicated in renal cell carcinoma (RCC), but remain largely unclear. Using publicly available transcriptome sequencing data from renal cancer ( n  = 703) and integrating bioinformatics analyses, we screened and identified a valuable lncRNA, EGFR-AS1. In our validation cohort ( n  = 204), EGFR-AS1 was significantly upregulated in RCC tissues ( P   <  0.001). Gain-of-function and loss-of-function studies showed that EGFR-AS1 promoted cell proliferation and invasion in vitro and in vivo. Based on previous studies and sequence complementarity of EGFR with EGFR-AS1, we demonstrated that EGFR-AS1 directly bound to EGFR mRNA and inhibited its degradation. Furthermore, RNA pull-down and mass spectrometry analyses showed that EGFR-AS1 interacted with HuR, which was responsible for the mRNA stability of EGFR. Multivariate analysis suggested that higher EGFR-AS1 expression predicted a poor prognosis in RCC patients (high vs low: P  = 0.018, HR = 2.204, 95% CI: 1.145–4.241). In conclusion, EGFR-AS1 enhances the malignant phenotype of RCC cells by enhancing HuR-mediated mRNA stability of EGFR. Our data also provide biological rationales for EGFR-AS1 as a prognostic biomarker and a potential therapeutic target for RCC.