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Accurate measurement of sea-surface winds is critical for climate science, physical oceanography, and the rapidly expanding offshore wind energy sector. Buoy-based platforms—moored meteorological buoys, drifters, and floating LiDAR systems (FLS)—provide practical alternatives to fixed offshore structures, especially in deep water where bottom-founded installations are economically prohibitive. Yet these floating platforms are subject to continuous pitch, roll, heave, and yaw motions forced by wind, waves, and currents. Such six-degree-of-freedom dynamics introduce multiple error pathways into the measured wind signal. This paper synthesizes the current understanding of motion-induced measurement errors and the techniques developed to compensate for them. We identify four principal error mechanisms: (1) geometric biases caused by sensor tilt, which can underestimate horizontal wind speed by 0.4–3.4% depending on inclination angle; (2) contamination of the measured signal by platform translational and rotational velocities; (3) artificial inflation of turbulence intensity by 15–50% due to spectral overlap between wave-frequency buoy motions and atmospheric turbulence; and (4) beam misalignment and range-gate distortion specific to scanning LiDAR systems. Compensation strategies have progressed through four recognizable stages: fundamental coordinate-transformation and velocity-subtraction algorithms developed in the 1990s; Kalman-filter-based multi-sensor fusion emerging in the 2000s; Response Amplitude Operator modeling tailored to FLS platforms in the 2010s; and data-driven machine-learning approaches under active development today. Despite this progress, key challenges persist. Sensor reliability degrades under extreme sea states precisely when accurate data are most needed. The coupling between high-frequency platform vibrations and turbulence remains poorly characterized. No unified validation framework or benchmark dataset yet exists to compare methods across platforms and environments. We conclude by outlining research priorities: end-to-end deep-learning architectures for nonlinear error correction, adaptive algorithms capable of all-sea-state operation, standardized evaluation protocols with open datasets, and tighter integration of intelligent software with next-generation low-power sensors and actively stabilized platforms.

Insulin-like growth factor I (IGF-1) is a key regulator of tissue growth and development in response to growth hormone stimulation. In the skeletal system, IGF-1 derived from osteoblasts and chondrocytes are essential for normal bone development; however, whether bone marrow (BM)-resident cells provide distinct sources of IGF-1 in the adult skeleton remains elusive. Here, we show that BM stromal cells (BMSCs) and megakaryocytes/platelets (MKs/PLTs) express the highest levels of IGF-1 in adult long bones. Deletion of Igf1 from BMSCs by Lepr-Cre leads to decreased bone formation, impaired bone regeneration, and increased BM adipogenesis. Importantly, reduction of BMSC-derived IGF-1 contributes to fasting-induced marrow fat accumulation. In contrast, deletion of Igf1 from MKs/PLTs by Pf4-Cre leads to reduced bone formation and regeneration without affecting BM adipogenesis. To our surprise, MKs/PLTs are also an important source of systemic IGF-1. Platelet-rich plasma (PRP) from Pf4-Cre; Igf1f/f mice showed compromised osteogenic potential both in vivo and in vitro, suggesting that MK/PLT-derived IGF-1 underlies the therapeutic effects of PRP. Taken together, this study identifies BMSCs and MKs/PLTs as two important sources of IGF-1 that coordinate to maintain and regenerate the adult skeleton, highlighting reciprocal regulation between the hematopoietic and skeletal systems.

Lung adenocarcinoma (LUAD), a histological subclass of non‐small‐cell lung cancer, is globally the leading cause of cancer‐related deaths. Long noncoding RNAs (lncRNAs) are emerging as cancer regulators. Zinc finger protein multitype 2 antisense RNA 1 (ZFPM2‐AS1) is an oncogene in gastric cancer, but its functions have not been investigated in LUAD. We showed that ZFPM2‐AS1 expression is high in LUAD samples based on GEPIA database (http://gepia.cancer-pku.cn/) and validated ZFPM2‐AS1 upregulation in LUAD cell lines. Functionally, ZFPM2‐AS1 facilitated proliferation, invasion, and epithelial‐to‐mesenchymal transition of LUAD cells. Thereafter, we found that ZFPM2 was negatively regulated by ZFPM2‐AS1, and identified the suppressive effect of ZFPM2 regulation by ZFPM2‐AS1 on LUAD progression. Mechanistically, we showed that ZFPM2‐AS1 interacted with up‐frameshift 1 (UPF1) to regulate mRNA decay of ZFPM2. Rescue assays in vitro and in vivo confirmed that ZFPM2‐AS1 regulated LUAD progression and tumor growth through ZFPM2. Taken together, our findings demonstrate a role for the ZFPM2‐AS1–UPF1–ZFPM2 axis in LUAD progression, suggesting ZFPM2‐AS1 as a new potential target for LUAD treatment. The illustration of lncRNA ZFPM2‐AS1 promoted lung adenocarcinoma progression through cofunctioning with UPF1 to destabilize ZFPM2.

Oil field fouling not only causes pipelines, equipment and oil Wells to be blocked, but also brings certain security risks. In this study, the scale prediction of calcium carbonate, calcium sulfate, barium sulfate andstrontiumsulfatewascarriedouttoclarifythescalingtrendofinjected water and produced water, providing a basis for subsequent oilfield water quality treatment. The results show that: after the injection water is mixed with formation water (produced water), the larger the proportion of produced water, the slower the scaling trend of calcium carbonate; There is no scaling trend for calcium sulfate; Barium sulfate had scaling trend, and the value showed an increasing trend; Strontium sulfate showed a scaling trend and a decreasing trend in value; The mixing experiment results show that the three kinds of scale ions in any proportion of mixed water sample have different degrees of loss, the loss is mainly calcium ion, barium ion second; The prediction results of scaling trend have good correlation with the results of mixing experiment, which can be used to quickly judge the scaling situation after mixing.

Understanding human endometrial dynamics in the establishment of endometrial receptivity remains a challenge, which limits early diagnosis and treatment of endometrial-factor infertility. Here, we decode the endometrial dynamics of fertile women across the window of implantation and characterize the endometrial deficiency in women with recurrent implantation failure. A computational model capable of both temporal prediction and pattern discovery is used to analyze single-cell transcriptomic data from over 220,000 endometrial cells. The time-series atlas highlights a two-stage stromal decidualization process and a gradual transitional process of the luminal epithelial cells across the window of implantation. In addition, a time-varying gene set regulating epithelium receptivity is identified, based on which the recurrent implantation failure endometria are stratified into two classes of deficiencies. Further investigation uncovers a hyper-inflammatory microenvironment for the dysfunctional endometrial epithelial cells of recurrent implantation failure. The holistic characterization of the physiological and pathophysiological window of implantation and a computational tool trained on this temporal atlas provide a platform for future therapeutic developments. Time-series single-cell transcriptomic characterization of luteal-phase endometrium in fertile women with a variational autoencoder model uncovers the association of decreased epithelial receptivity and hyperinflammatory microenvironment in recurrent implantation failures.

Perovskite nanocrystals have shown great promise for optoelectronic applications. Understanding charge recombination under operational conditions, such as continuous-wave photoexcitation, is crucial for advancing device performance. Although time-resolved photoluminescence is widely used to study recombination kinetics, its reliance on ultrafast pulsed excitation fails to replicate the operational conditions. Here we develop an integrated spectroscopy platform that enables simultaneous acquisition of steady-state and time-resolved photoluminescence under continuous-wave illumination, with a wide range of photoexcitation intensity modulation. This approach resolves the long-standing mismatch between the typical time-resolved photoluminescence data and the actual continuous-wave operational behavior of perovskite nanocrystals. In contrast to the established Auger recombination model, which suggests accelerated recombination at high pump fluence, we demonstrate that the operando recombination kinetics is governed by the charge-carrier and trap-state interaction. This clarified recombination mechanism provides insight for designing perovskite nanocrystal films applied to efficient and stable light emission under high-power photoexcitation. Charge recombination of perovskite nanocrystals is crucial for their optoelectronic performance. Here the authors develop a continuous-wave-photoexcitation platform to study their time-resolved photoluminescence under operational conditions.

Sleep, a core circadian rhythm, maintains physiological homeostasis. Its dysfunction links to neuropsychiatric disorders. Clinically, poor sleep impairs positive emotions and enhances negative emotion susceptibility, but the mechanism remains unclear, potentially involving circadian clock genes and neuroinflammatory pathways. Divide the male C57BL/6J mice into the following five groups: Non-sleep deprivation (SD) control (CON), sleep recovery 14-day after SD 7-day (SD7R14), sleep recovery 21-day after SD 7-day (SD7R21), sleep recovery 14-day after SD 14-day (SD14R14), and sleep recovery 21-day after SD 14-day (SD14R21). Behavioral tests evaluated anxiety-like behaviors, fear and andanhedonia. Histological staining observed neuronal morphology in the medial prefrontal cortex (mPFC), and RT-qPCR was employed to measure mRNA levels of circadian clock genes, Silent information regulator 6 ( ), High mobility group box-1 ( ), and inflammatory factors. SD induces time-dependent anxiety-like behaviors (reduced exploratory activity in elevated mazes), anhedonia (decreased sucrose preference), and fear behaviors (prolonged immobility in forced swim and tail suspension tests). Histological analysis reveals reversible neuronal damage in the mPFC, with complete recovery observed after 21 days of sleep restitution. Molecular analyses show dysregulation of the muscle aryl-hydrocarbon receptor nuclear translocator-like 1 ( ) and circadian locomotor output cycles kaput ( ) circadian pathway and activation of the Sirt6/Hmgb1 inflammatory axis, leading to proinflammatory cytokine release ( ), with partial recovery after sleep restoration. SD for 7-day or 14-day may impair emotional behaviors by disrupting the RNA expression of clock genes and the Sirt6/Hmgb1 inflammatory axis, while sleep recovery for 14-day or 21-day can partially reverse this impairment.

Niraparib, a poly ADP-ribose polymerase inhibitors (PARPi), has been widely applied in the intervention of epithelial ovarian, fallopian tube, or primary peritoneal cancer. Nevertheless, as of the present moment, there are limited instances demonstrating favorable outcomes stemming from niraparib therapy in patients with clear cell renal cell carcinoma (ccRCC). Here, we report a case of a 50-year-old patient with ccRCC who subsequently developed distant metastasis. The patient received monotherapy with pazopanib and combination therapy with axitinib and tislelizumab, demonstrating limited efficacy. Liquid biopsy revealed missense mutations in the and of the homologous recombination repair (HRR) pathway, suggesting potential sensitivity to PARPi. Following niraparib treatment, the patient's condition improved, with no significant side effects. In summary, patients with ccRCC harboring HRR pathway gene mutation may potentially benefit from niraparib. This will present more options for ccRCC patients with limited response to conventional treatments.

Background Early detection of colorectal cancer (CRC) significantly enhances patient outcomes. Conventional CRC screening tools, like endoscopy and stool-based tests, have constraints due to their invasiveness or suboptimal patient adherence. Recently, liquid biopsy employing plasma cell-free DNA (cfDNA) has emerged as a potential noninvasive screening technique for various malignancies. Methods In this research, we harnessed the Mutation Capsule Plus (MCP) technology to profile an array of genomic characteristics from cfDNA procured from a single blood draw. This profiling encompassed DNA methylation, the 5’ end motif, copy number variation (CNV), and genetic mutations. An integrated model built upon selected multiomics biomarkers was trained using a cohort of 93 CRC patients and 96 healthy controls. Results This model was subsequently validated in another cohort comprising 89 CRC patients and 95 healthy controls. Remarkably, the model achieved an area under the curve (AUC) of 0.981 (95% confidence interval (CI), 0.965–0.998) in the validation set, boasting a sensitivity of 92.1% (95% CI, 84.5%-96.8%) and a specificity of 94.7% (95% CI, 88.1%-98.3%). These numbers surpassed the performance of any single genomic feature. Importantly, the sensitivities reached 80% for stage I, 89.2% for stage II, and were 100% for stages III and IV. Conclusion Our findings underscore the clinical potential of our multiomics liquid biopsy test, indicating its prospective role as a noninvasive method for early-stage CRC detection. This multiomics approach holds promise for further refinement and broader clinical application.

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal disease with poor prognosis and limited treatment options. While the majority of PDAC cases harbor KRAS mutations, approximately 8%–10% are KRAS wild‐type (KRAS‐WT). These KRAS‐WT tumors often contain actionable mutations and gene fusions, making them more suitable for precision therapies. Identifying these molecular alterations is crucial for improving outcomes in this subset of patients. This retrospective study involved 34 patients with KRAS‐WT PDAC. Genomic profiling was performed using next‐generation sequencing (NGS) and RNA sequencing to detect mutations and fusions. Comparative analysis was conducted with TCGA‐PAAD data, and immune infiltration was assessed using bioinformatic deconvolution methods. Targetable alterations were identified in multiple pathways. Key mutations included ATM (18%), PIK3CA (15%), and ROS1 (15%), while actionable gene fusions such as CCDC6‐RET and ETV6‐NTRK3 were present in 10.3% of patients. The gene mutations associated with homologous recombination deficiency (HRD) are predicted to increase sensitivity to platinum‐based chemotherapy (p = 0.047). Tumors with epigenetic regulatory genes mutations (e.g., ARID1A, KMT2C/D) exhibited enhanced immune cell infiltration, highlighting potential responsiveness to immune checkpoint inhibitors (ICIs). Kinase fusions (NTRK and RET) were linked to response to larotinib and RET‐specific inhibitors, respectively. KRAS‐WT PDAC contains actionable mutations and fusions, offering significant potential for targeted and immune‐based therapies. Further clinical studies are needed to validate these therapeutic approaches. Identifying actionable mutations and gene fusions of KRAS wild‐type pancreatic ductal adenocarcinoma offers significant potential for targeted and immune‐based therapies, by retrospective study and genomic profiling analysis, together with comparative analysis of TCGA‐PAAD data. Specifically, HRD, epigenetic regulatory gene mutations and actionable CCDC6‐RET, and NTRK3 fusions are expected to guide personalized precision therapy for KRAS‐WT PDAC and need further investigation in larger cohorts.