Explore the vast range of titles available.

Background As part of China’s medical insurance-related grouping payment reform, public hospitals, which are the primary providers of medical insurance services, face remarkable pressure to control costs. This study examined uvulopalatopharyngoplasty (UPPP) surgery for patients with obstructive sleep apnea (OSA) at Hospital C to identify factors influencing inpatient costs and assess the impact of payment reform on treatment practices. Methods Using data from 251 OSA patients undergoing UPPP at Hospital C, the study evaluated changes in cost reduction, cost structure, patient disease severity, and medical quality before and after the payment reform. Results Inpatient costs for OSA patients undergoing UPPP surgery significantly decreased following the trial implementation of CHS-DRG, with notable reductions in medication and consumable expenses, as well as a shorter length of hospitalization. The CHS-DRG reform did not affect illness severity, patient safety during hospitalization, or long-term surgical outcomes for OSA patients. Conclusion After the CHS-DRG reform, Hospital C proactively adjusted clinical pathways to manage costs and improve inpatient turnover efficiency without resorting to cost-shifting, patient refusal, or staged surgeries. Despite the financial pressures, hospitals should aim to establish a win-win mechanism between hospitals, physicians, and patients, enhance internal management, and improve financial performance. Additionally, medical security authorities should explore more precise DRG payments and value-based payment models to promote high-quality hospital development rather than impose constraints. Study approval This study was approved by the Ethics Committee of Beijing Tsinghua Changgung Hospital (Approval No. 23418-0-02).

Background Glioma is the most common and malignant tumor of central nervous system. The tumor initiation, self-renewal, and multi-lineage differentiation abilities of glioma stem cells (GSCs) are responsible for glioma proliferation and recurrence. Although circular RNAs (circRNAs) play vital roles in the progression of glioma, the detailed mechanisms remain unknown. Methods qRT-PCR, western blotting, immunohistochemistry, and bioinformatic analysis were performed to detect the expression of circATP5B, miR-185-5p, HOXB5, and SRSF1. Patient-derived GSCs were established, and MTS, EDU, neurosphere formation, and limiting dilution assays were used to detect the proliferation of GSCs. RNA-binding protein immunoprecipitation, RNA pull-down, luciferase reporter assays, and chromatin immunoprecipitation assays were used to detect these molecules’ regulation mechanisms. Results We found circATP5B expression was significantly upregulated in GSCs and promoted the proliferation of GSCs. Mechanistically, circATP5B acted as miR-185-5p sponge to upregulate HOXB5 expression. HOXB5 was overexpressed in glioma and transcriptionally regulated IL6 expression and promoted the proliferation of GSCs via JAK2/STAT3 signaling. Moreover, RNA binding protein SRSF1 could bind to and promote circATP5B expression and regulate the proliferation of GSCs, while HOXB5 also transcriptionally regulated SRSF1 expression. Conclusions Our study identified the SRSF1/circATP5B/miR-185-5p/HOXB5 feedback loop in GSCs. This provides an effective biomarker for glioma diagnosis and prognostic evaluation.

Glioblastoma multiforme (GBM) is the most lethal type of craniocerebral gliomas. Glioma stem cells (GSCs) are fundamental reasons for the malignancy and recurrence of GBM. Revealing the critical mechanism within GSCs’ self-renewal ability is essential. Our study found a novel circular RNA (circRPPH1) that was up-regulated in GSCs and correlated with poor survival. The effect of circRPPH1 on the malignant phenotype and self-renewal of GSCs was detected in vitro and in vivo. Mechanistically, UPF1 can bind to circRPPH1 and maintain its stability. Therefore, more existing circRPPH1 can interact with transcription factor ATF3 to further transcribe UPF1 and Nestin expression. It formed a feedback loop to keep a stable stream for stemness biomarker Nestin to strengthen tumorigenesis of GSCs continually. Besides, ATF3 can activate the TGF-β signaling to drive GSCs for tumorigenesis. Knocking down the expression of circRPPH1 significantly inhibited the proliferation and clonogenicity of GSCs both in vitro and in vivo. The overexpression of circRPPH1 enhanced the self-renewal of GSCs. Our findings suggest that UPF1/circRPPH1/ATF3 maintains the potential self-renewal of GSCs through interacting with RNA-binding protein and activating the TGF-β signal pathway. Breaking the feedback loop against self-renewing GSCs may represent a novel therapeutic target in GBM treatment.

Unmanned Aerial Vehicles (UAVs) have emerged as efficient tools in disaster-stricken areas, facilitating efficient data dissemination for post-disaster rescue operations. However, the limited onboard energy of UAVs imposes significant constraints on their operational lifespan, thereby presenting substantial challenges for efficient data dissemination. Therefore, this work investigates a data dissemination scheme to enhance the UAVs’ bandwidth efficiency in multi-UAV-enabled Internet of Vehicles, thereby reducing UAVs’ energy consumption and improving overall system performance when UAVs hover along designated flight trajectories for data dissemination. Specifically, first, we present a software-defined network-based framework for data dissemination in multi-UAV-enabled IoV. According to this framework, we formulate a problem called C2BS (Coding-based Cooperative Broadcast Scheduling) that focuses on optimizing the UAVs’ bandwidth efficiency by leveraging the combined benefits of coding and caching. Furthermore, we demonstrate the NP-hardness of the C2BS problem by employing a polynomial time reduction technique on the simultaneous matrix completion problem. Then, inspired by the benefits offered by genetic algorithms, we propose a novel approach called the Genetic algorithm-based Cooperative Scheduling (GCS) algorithm to address the C2BS problem. This approach encompasses a coding scheme for representing individuals, a fitness function for assessing individuals, operators (i.e., crossover and mutation) for generating offspring, a local search technique to enhance search performance, and a repair operator employed to rectify infeasible solutions. Additionally, we present an analysis of the time complexity for the GCS algorithm. Finally, we present a simulation model to evaluate the performance. Experimental findings provide evidence of the excellence of the proposed scheme.

Glioma is the most aggressive and common malignant neoplasms in human brain tumors. Numerous studies have showed that glioma stem cells (GSCs)drive the malignant progression of gliomas. Recent studies have revealed that circRNAs can maintain stemness and promote malignant progression of glioma stem cells. We used bioinformatics analysis to identify circRNAs and potential RNA-binding proteins (RBPs) in glioma. qRT-PCR, western blotting, RNA FISH, RNA pull-down, RNA immunoprecipitation assay, ChIP, immunohistochemistry, and immunofluorescence methods were used to quantified the expression of circNCAPG, U2AF65, RREB1 and TGF-β1, and the underlying mechanisms between them. MTS, EDU, neurosphere formation, limiting dilution neurosphere formation and transwell assays examined the proliferation and invasive capability of GSCs, respectively. We identified a novel circRNA named circNCAPG was overexpressed and indicated the poor prognosis in glioma patients. Upregulating circNCAPG promoted the malignant progression of GSCs. RNA binding protein U2AF65 could stabilize circNCAPG by direct binding. Mechanically, circNCAPG interacted with and stabilized RREB1, as well as stimulated RREB1 nuclear translocation to activate TGF-β1 signaling pathway. Furthermore, RREB1 transcriptionally upregulated U2AF65 expression to improve the stability of circNCAPG in GSCs, which established a feedback loop involving U2AF65, circNCAPG and RREB1. Since circRNA is more stable than mRNA and can execute its function continuously, targeting circNCAPG in glioma may be a novel promising therapeutic.

Background Temporal lobe epilepsy (TLE) is among the most common types of epilepsy and often leads to cognitive, emotional, and psychiatric issues due to the frequent seizures. A notable pathological change related to TLE is hippocampal sclerosis (HS), which is characterized by neuronal loss, gliosis, and an increased neuron fibre density. The mechanisms underlying TLE-HS development remain unclear, but the reactive transcriptomic changes in glial cells and neurons of the hippocampus post-epileptogenesis may provide insights. Methods To induce TLE, 200 nl of kainic acid (KA) was stereotactically injected into the hippocampal CA1 region of mice, followed by a 7-day postinjection period. Single-cell RNA sequencing (ScRNA-seq), single-nucleus RNA sequencing (SnRNA-seq), and Xenium-based spatial transcriptomics analyses were employed to evaluate the changes in mRNA expression in glial cells and neurons. Results From the ScRNA-seq and SnRNA-seq data, 31,390 glial cells and 48,221 neuronal nuclei were identified. Analysis of the differentially expressed genes (DEGs) revealed significant transcriptomic alterations in the hippocampal cells of mice with TLE, affecting hundreds to thousands of mRNAs and their signalling pathways. Enrichment analysis indicated notable activation of stress and inflammatory pathways in the TLE hippocampus, while pathways related to axonal development and neural support were suppressed. Xenium analysis demonstrated the expression of all 247 genes across mouse brain sections, revealing the spatial distributions of their expression in 27 cell types. Integrated analysis of the DEGs identified via the three sequencing techniques revealed that Spp1 , Trem2 , and Cd68 were upregulated in all glial cell types and in the Xenium data; Penk , Sorcs3 , and Plekha2 were upregulated in all neuronal cell types and in the Xenium data; and Tle4 and Sipa1l3 were downregulated in all glial cell types and in the Xenium data. Conclusion In this study, a high-resolution single-cell transcriptomic atlas of the hippocampus in mice with TLE was established, revealing potential intrinsic mechanisms driving TLE-associated inflammatory activation and altered cell interactions. These findings provide valuable insights for further exploration of HS development and epileptogenesis.

Glioma is the most common and aggressive primary malignant brain tumor. Circular RNAs (circRNAs) and RNA-binding proteins (RBPs) have been verified to mediate diverse biological behaviors in various human cancers. Therefore, the aim of this study was to explore a novel circRNA termed circGNB1 and elucidate relative molecular mechanism in functional phenotypes, which might be a potential prognostic biomarker and therapeutic approach for glioma. CircGNB1 was upregulated in glioma and closely associated with the low poor prognosis. Functional assays demonstrated that circGNB1 overexpression promoted glioma stem cells (GSCs) viability proliferation, invasion, and neurosphere formation. Mechanistically, circGNB1 upregulated the expression of oncogene XPR1 via sponging miR-515-5p and miR-582-3p. The following experiments proved XPR1 could promote the malignant phenotype of GSCs via upregulating IL6 expression and activating JAK2/STAT3 signaling. Moreover, the RNA binding protein IGF2BP3 could bind to and maintain the stability of circGNB1, thus promoting the effects of circGNB1 on GSCs. Our study reveals that circGNB1 plays a crucial role in promoting tumorigenesis and malignant progression in glioma, which provides a promising cancer biomarker.

Recanalization intervention has improved patient outcomes in ischemic stroke, but severe ischemia‐reperfusion injury remains a major challenge, necessitating effective pharmacotherapy to reverse neuronal damage and recover neurofunctions. Traditional neuroprotection strategies aim to inhibit neuronal death, and are still insufficient to recover long‐term neurological dysfunctions. In this work, it is found that carbon monoxide (CO) as a neuromodulator exerts a new role in promoting neurogenesis via the crosstalk between brain endothelial cells and neural stem cells, which is beyond its recognized roles in anti‐inflammation and anti‐oxidation. This reveals a new possibility to address the above challenge. Furthermore, this work develops a biomimetic and reactive oxygen species‐activated CO nanogenerator to effectively penetrate blood‐brain barrier, arrive in stroke‐affected regions, and release CO in a controlled manner for an innovative dual‐channel therapy strategy via co‐driving neuroprotection and neurogenesis. This strategy further demonstrates its therapeutic effects on reversing brain injury and recovering neurofunctions in a mouse ischemic stroke model. This work reveals an important new role of CO, and further offers an advanced pharmacotherapy for long‐term neurological dysfunctions in ischemic stroke. This work develops a biomimetic and reactive oxygen species‐activated carbon monoxide (CO) nanogenerator to penetrate blood‐brain barrier, arrive in stroke‐affected regions, and release CO in a controlled manner for an innovative dual‐channel therapy strategy via co‐driving neuroprotection and neurogenesis.