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In size, weight, and power (SWaP)-constrained optical systems, such as spaceborne LiDAR, high-precision centroid localization often relies on focal-plane measurements without dedicated wavefront sensors. Under such conditions, the nonlinear coupling between optical aberrations and sensor noise introduces systematic bias that is difficult to mitigate using conventional centroiding methods. To address this issue, we propose a physics-conditioned feature correction framework based on an aberration-conditioned attention mechanism. A hybrid CNN–Transformer architecture is employed to predict and compensate for systematic centroid bias. Specifically, convolutional layers encode the degraded spot morphology, while a multi-head attention mechanism leverages Seidel aberration coefficients to adaptively modulate spatial features for precise regression. Given the unavailability of absolute ground-truth coordinates in empirical scenarios, a physics-consistent simulation framework based on scalar diffraction theory is constructed to generate synthetic data for supervised learning. Simulation results indicate that the proposed method objectively reduces anisotropic systematic bias, achieving a localization root-mean-square error (RMSE) of 0.011 to 0.021 pixels, and maintains stable sub-pixel accuracy even under a 10% empirical prior perturbation. To evaluate generalization performance and engineering reliability, a wedge-based double-spot platform is developed to verify physical consistency via geometric invariance. Experimental results demonstrate a measured spacing standard deviation (SD) of 0.015 to 0.039 pixels. This validates the framework’s transferability from theoretical simulation to controlled physical measurements, providing an algorithmic foundation for precision optical metrology in hardware-constrained environments.

In this retrospective analysis, we explored the clinical characteristics and risk factors of secondary infections in patients with severe heatstroke with the aim to gain epidemiological insights and identify risk factors for secondary infections. The study included 129 patients with severe heatstroke admitted to the General Hospital of the Southern Theater Command of the PLA between January 1, 2011, and December 31, 2021. Patients were divided into an infection group (n = 24) and a non-infection group (n = 105) based on infection occurrence within 48 h of intensive care unit (ICU) admission. Clinical indicators, infection indicators, and clinical outcomes within 24 h of ICU admission were collected and compared between the groups. Independent risk factors for infection in patients with severe heatstroke were analyzed using univariate and multivariate analyses. A nomogram model was constructed, evaluated, and validated. Among the 129 patients with heatstroke, 24 developed secondary infections. Infections occurred between days 3 and 10 post-ICU admission, primarily affecting the lungs. Multivariate analysis identified vasopressor use, serum creatinine level, and gastrointestinal dysfunction at admission as independent risk factors, while elevated lymphocyte count (odds ratio [OR] = 0.167; 95% confidence interval [CI] 0.049-0.572; P = 0.004) was protective against severe heatstroke. Infected patients required longer durations of mechanical ventilation (OR = 2.764; 95% CI, 1.735-4.405; P = 0.044) and total hospital stay than those in the non-infection group. The nomogram model demonstrated clinical feasibility. Increased lymphocyte count is an independent protective factor against infections in patients with severe heatstroke. Vasopressor use, gastrointestinal dysfunction, and elevated serum creatinine levels are independent risk factors. These indicators can aid clinicians in assessing infection risk in patients with severe heatstroke.

Background To examine the microbial profiles in parenchyma tissues in bladder cancer. Methods Tissue samples of cancerous bladder mucosa were collected from patients diagnosed with bladder cancer (22 carcinoma tissues and 12 adjacent normal tissues). The V3‐V4 region of the bacterial 16S rRNA gene was PCR amplified, followed by sequencing on an Illumina MiSeq platform. Bioinformatics analysis for microbial classification and functional assessment was performed to assess bladder microbiome diversity and variations. Results The predominant phylum in both tissues was Proteobacteria. The cancerous tissues exhibited lower species richness and diversity. Beta diversity significantly differed between the cancerous and normal tissues. Lower relative abundances of the microbial genera Lactobacillus, Prevotella_9, as well as Ruminococcaceae were observed, whereas those of Cupriavidus spp., an unknown genus of family Brucellaceae, and Acinetobacter, Anoxybacillus, Escherichia‐Shigella, Geobacillus, Pelomonas, Ralstonia, and Sphingomonas were higher in the cancerous tissues. These findings indicate that these genera may be potentially utilized as biomarkers for bladder cancer. PICRUSt analysis revealed that several pathways involved in the metabolism of harmful chemical compounds were enriched in the cancer tissues, thereby providing evidence that environmental factors are strongly associated with bladder cancer etiology. Conclusion This is the first study that has described and analyzed the dysbiotic motifs of urinary microbiota in the parenchymatous tissues of bladder cancer via 16S rRNA gene sequencing. Our results suggest that changes in the bladder microbiome may serve as biomarkers for bladder cancer, possibly assisting in disease screening and monitoring. This is the first study describing and analyzing the dysbiosis signatures of urinary microbiota within the parenchyma in bladder cancer using a 16S rRNA gene sequencing method. The study reveals previously undescribed bacterial diversity present in human bladder. The bladder microbiome changes could be a biomarker of bladder cancer that could be used to help in screening for the disease. Analysis of the inferred bladder cancer metagenome identified the strongest association with the harmful chemical products that may be metabolized.

Background The prognosis of bladder urothelial carcinoma (BLCA) varies greatly among patients, and conventional pathological predictors are generally inadequate and often inaccurate to predict the heterogeneous behavior of BLCA. This study aims to investigate the prognostic value and function of TOP2A in BLCA. Methods TOP2A expression level was examined by RNA-sequencing, quantitative real time polymerase chain reaction and immunohistochemistry from 10, 40 and 209 BLCA samples, respectively. Public databases were analyzed for validation. Cell proliferation, migration, invasion assays were performed to explore potential functions of TOP2A in BLCA. Flow cytometry was performed for cell cycle and apoptosis analysis. Univariable and multivariable Cox regression models were performed to identify independent risk factors for the prognosis of BLCA. Results We found TOP2A was significantly upregulated in BLCA samples, especially for high-grade and advanced stage tumors, compared with matched normal epithelial tissue. Univariable COX regression analysis revealed high TOP2A expression was significantly associated with poorer cancer-specific, progression-free and recurrence-free survival, but not independently of clinical characteristics in the multivariable models. Knockdown of TOP2A remarkably inhibited the proliferation of BLCA cells and non-cancerous urothelial cells. Furthermore, migration and invasion capacity of BLCA cells were strongly suppressed after TOP2A knockdown. Moreover, flow cytometry suggested TOP2A had anti-apoptotic function, and knockdown of TOP2A could induce resistance to doxorubicin in J82 cells. Conclusions In our study, TOP2A was overexpressed in BLCA and could serve as a prognostic biomarker for BLCA. Moreover, TOP2A is functionally important for the proliferation, invasion and survival of BLCA cells.

Cisplatin-based chemotherapy is the first-line treatment for patients with advanced bladder cancer. However, as more than 50% of patients are ineligible for cisplatin-based chemotherapy, there is an urgent need to develop new drugs. Cuprous oxide nanoparticles (CONPs), as a new nano-therapeutic agent, have been proved to be effective in many kinds of tumors. In the present study, CONPs showed dose-dependent and time-dependent inhibitory effects on various bladder cancer cell lines (T24, J82, 5637, and UMUC3) and weak inhibitory effects on non-cancerous epithelial cells (SVHUCs). We found that CONPs induced cell cycle arrest and apoptosis in bladder cancer cells. We further demonstrated that the potential mechanisms of CONP-induced cytotoxicity were apoptosis, which was triggered by reactive oxygen species through activation of ERK signaling pathway, and autophagy. Moreover, the cytotoxic effect of CONPs on bladder cancer was confirmed both in orthotopic xenografts and subcutaneous nude mouse models, indicating that CONPs could significantly suppress the growth of bladder cancer in vivo. In further drug combination experiments, we showed that CONPs had a synergistic drug–drug interaction with cisplatin and gemcitabine in vitro, both of which are commonly used chemotherapy agents for bladder cancer. We further proved that CONPs potentiated the antitumor activity of gemcitabine in vivo without exacerbating the adverse effects, suggesting that CONPs and gemcitabine can be used for combination intravesical chemotherapy. In conclusion, our preclinical data demonstrate that CONPs are a promising nanomedicine against bladder cancer and provide good insights into the application of CONPs and gemcitabine in combination for intravesical bladder cancer treatment.

Snow cover has significant impacts on the global water cycle, ecosystem, and climate change. At present, satellite remote sensing is regarded as the most efficient approach to detect long-term and multiscale observations of snow cover extent. The Visible Infrared Imaging Radiometer Suite (VIIRS) sensor onboard Joint Polar Satellite System (JPSS) satellites will replace the Moderate-Resolution Imaging Spectroradiometer (MODIS) to prolong data recording in the future. Therefore, it is a fundamental task to analyze and evaluate the consistency of the snow cover products retrieved from these two sensors. In this study, we performed comparisons and a consistency evaluation between the MODIS and VIIRS snow cover products in three major snow distribution regions in China: Northeast China (NE), Northwest China (NW) and the Qinghai–Tibet Plateau (QT). The results demonstrated that (1) the normalized difference snow index (NDSI)-derived snow cover products showed suitable consistency between VIIRS and MODIS under clear sky conditions, with a mean difference value of less than 5%; (2) the VIIRS snow cover product presented much more snow and fewer clouds than that of MODIS in the snow season due to the differences in cloud-masking algorithms; (3) cloud mask strongly affects the potential of snow cover observation, and presents seasonal pattern in the test regions; and (4) VIIRS is able to distinguish clouds from snow with greater accuracy. The comparisons indicated that the greater the difference in cloud cover, the poorer the agreement in snow cover. This evaluation implies that perfecting the cloud-masking algorithm of VIIRS to update the MODIS would be the best solution to achieve better consistency for long-term and high-quality snow cover products.

Hepatic portal venous gas is often referred to as the “sign of death” because it signifies a very poor prognosis if appropriate treatments are not promptly administered. The etiologies of hepatic portal venous gas are diverse and include severe complex abdominal infections, mesenteric ischemia, diving, and complications of endoscopic surgery, and the clinical manifestations are inconsistent among individual patients. Thus, whether emergency surgery should be performed remains controversial. In this report, we present three cases of hepatic portal venous gas. The patients initially exhibited symptoms consistent with severe shock of unknown etiology and were treated in the intensive care unit upon admission. We rapidly identified the cause of each individual patient’s condition and selected problem-directed intervention measures based on active organ support, antishock support, and anti-infection treatments. Two patients recovered and were discharged without sequelae, whereas one patient died of refractory infection and multiple organ failure. We hope that this report will serve as a valuable reference for decision-making when critical care physicians encounter similar patients.

Purpose: Acute lung injury (ALI) is a common clinical syndrome with high mortality. The chemokine ligand 25 (CCL25) is involved in inflammation, leukocyte trafficking and immunoregulation. However, the role and mechanism of CCL25 in ALI are not fully understood yet. The aim of this study was to explore the relationship between acute lung injury and CCL25. Patients and Methods: In this study, we first examined chemokine expression in sepsis patients and found that serum CCL25 expression levels were relatively high in sepsis patients compared to healthy individuals. Based on this, we designed in vitro and in vivo experiments to verify the validity of the theory. In vitro, we used lipopolysaccharide-stimulated human pulmonary microvascular endothelial cells (HPMECs). In vivo, we established male C57BL/6 mice cecal ligation puncture (CLP) model of sepsis. Results: In vitro, we used lipopolysaccharide-stimulated human pulmonary microvascular endothelial cells (HPMECs) and found significantly higher expression of CCL25 by enzyme-linked immunosorbent assay. Inhibition of CCL25 resulted in a significant decrease in the expression of inflammatory cytokines in HPMECs. In addition, we found that CCL25 promoted increased endothelial permeability by reducing the expression of tight junction proteins and was associated with activation of the P38 MAPK pathway by measuring the transepithelial electrical resistance and fluorescence intensity of fluorescein isothiocyanate. Results from luciferase assays and chromatin immunoprecipitation assays showed that inhibition of NF-[kappa]B activity in HPMECs decreased CCL25 expression, but addition of recombinant CCL25 increased cell permeability and inflammatory cytokine expression. In vivo, we established male C57BL/6 mice cecal ligation puncture (CLP) model of sepsis. We found that inhibition of CCL25 significantly reduced inflammatory cytokine expression in a CLP-induced sepsis model, thereby alleviating lung tissue damage in mice. Conclusion: Our study suggests that CCL25 contributed to the development of ALI by modulating the functions of microvascular endothelial cells. Keywords: CCL25/CCR11, inflammatory cytokines, cell permeability, acute lung injury, P38, NF-[kappa]B

Background: Heat stroke (HS), a potentially fatal heat-related illness, is often accompanied by disseminated intravascular coagulation (DIC) early, resulting in a poorer prognosis. Unfortunately, diagnosis by current DIC scores is often too late to identify DIC. This study aims to investigate the predictors and predictive model of DIC in HS to identify DIC early. Methods: This retrospective study analyzed clinical data of patients with HS in a tertiary hospital from January 1, 2008 to December 31, 2020. Univariate and multivariate logistic regression analyses were employed to identify the risk factors for DIC in HS. The predictive models based on these risk factors were constructed and externally validated, and their predictive efficacy was evaluated using receiver operating characteristic curves. Results: A total of 219 HS patients, including 49 with DIC, were included. The independent risk factors for DIC were identified as follows: neutrophil percentage (Neu%), lymphocyte count, lymphocyte percentage (Lym%), creatine kinase-MB (CKMB), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), neutrophil–lymphocyte ratio (NLR), monocyte–lymphocyte ratio (MLR), and rhabdomyolysis (RM). After logarithmization, the final predictive model based on the logarithm of lactate dehydrogenase (InLDH; odds ratio (OR) = 9.266, 95% confidence interval (95%CI; 4.379–19.607), p < 0.0001) and the logarithm of neutrophil–lymphocyte ratio (InNLR; OR = 3.393, 95%CI (1.834–6.277), p < 0.0001) was constructed with the largest area under the curve (0.928). A nomogram incorporating InLDH and InNLR was developed and showed excellent discrimination and calibration capabilities. Conclusion: Nine independent risk factors were identified for the occurrence of DIC in HS patients. The predictive model based on InLDH and InNLR can effectively predict the incidence of DIC. A nomogram based on InLDH and InNLR was developed to facilitate early identification and timely treatment of DIC in HS patients.

Methylation of tumor suppressor gene promoter leads to transcription inactivation and is involved in tumorigenesis. Several studies demonstrate a potential association between the Death-Associated Protein Kinase (DAPK) gene promoter methylation and bladder cancer risk, tumor stage and histological grade. Due to inconsistent results of these studies, we performed this meta-analysis to ascertain the association. Studies were retrieved from the PubMed, Embase, Web of Science and the Cochrane Library databases. Study selection and data extraction were executed by two reviewers independently. Meta-analysis was performed using Stata 13.0 and Review Manager 5.3 software. A total of 21 articles involving 15 case control and 8 case series studies were included in this meta-analysis. DAPK promoter methylation was associated with bladder cancer risk (OR: 5.81; 95%CI = 3.83-8.82, P<0.00001). The frequency of DAPK promoter methylation was equal in bladder cancer tissue and paired adjacent normal tissue (OR: 0.87; 95%CI = 0.31-2.48, P = 0.794). Furthermore, DAPK promoter methylation was associated with higher histological grade (OR: 1.52; 95%CI = 1.10-2.09, P = 0.011) but not associated with tumor stage (OR: 1.12; 95%CI = 0.67-1.87, P = 0.668). The result suggests that DAPK promoter methylation is significantly increased in bladder cancer patients compared to normal controls. DAPK promoter methylation could serve as a biomarker for bladder cancer detection and management.