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HOXC13 antisense RNA (HOXC13-AS, also known as HOXC-AS5) is a long non-coding RNA that is expressed abnormally in various types of tumors and is closely related to clinical staging, clinical pathological features, and patient survival. HOXC13-AS is involved in the occurrence and development of tumors, affecting cell proliferation, migration, invasion, epithelial–mesenchymal transition, and tumor growth. This review summarizes the clinical significance of HOXC13-AS as a biomarker for human tumor diagnosis and prognosis and outlines the function and molecular regulation mechanism of HOXC13-AS in various types of cancer, including nasopharyngeal carcinoma, breast cancer, oral squamous cell carcinoma, glioma, and cervical cancer. Overall, this review emphasizes the potential of HOXC13-AS as a human tumor predictive biomarker and therapeutic target, paving the way for its clinical application.

Long non-coding RNAs (lncRNAs) are crucial regulatory molecules that participate in numerous cellular development processes, and they have gathered much interest recently. HOXA10 antisense RNA (HOXA10-AS, also known as HOXA-AS4) is a novel lncRNA that was identified to be dysregulated in some prevalent malignancies. In this review, the clinical significance of HOXA10-AS for the prognosis of various cancers is analyzed. In addition, the major advances in our understanding of the cellular biological functions and mechanisms of HOXA10-AS in different human cancers are summarized. These cancers include esophageal carcinoma (ESCA), gastric cancer (GC), glioma, laryngeal squamous cell carcinoma (LSCC), acute myeloid leukemia (AML), lung adenocarcinoma (LUAD), nasopharyngeal carcinoma (NPC), oral squamous cell carcinoma (OSCC), and pancreatic cancer. We also note that the aberrant expression of HOXA10-AS promotes malignant progression through various underlying mechanisms. In conclusion, HOXA10-AS is expected to serve as an ideal clinical biomarker and an effective cancer therapy target.

In this article, a partially isolated dual work function (PIDWF) gate In-Ga-Zn-O (IGZO) thin-film transistor (TFT) is proposed to reduce the off-state current (Ioff) obviously, which also provides a feasible integration method for stacking IGZO TFT on Si-based devices. It is found that compared with the general back gate IGZO TFT structure, the Ioff of the proposed IGZO TFT reduces from $2.57\times 10{^{-}14 }$ A/ $\mu $ m to $7.57\times 10{^{-}16 }$ A/ $\mu $ m, achieving two orders of magnitude improvement. This breakthrough has the potential to increase the retention time of DRAM applications by nearly 100 times. Moreover, the pronounced novel structure has mitigated parasitic capacitance, thereby leading to a notable 47.7% reduction in write latency within dynamic-random-access-memory (DRAM) circuits. The relevant operation mechanism is carefully demonstrated and verified by the simulation of the electric field and potential barrier results by technical computer-aided design (TCAD). Furthermore, the impacts of the dual gate work function level, the length, and the type of isolation dielectric between dual work function gates are systematically investigated. The results show that the off-state leakage is further reduced by increasing the difference of the work function levels between in dual gates, the dielectric length (LD) and using the isolation layer with a lower dielectric constant. The PIDWF gate IGZO TFT exhibits scalability and is capable of achieving an 84.6% reduction in leakage current even with ultra-short channel lengths, which offers a promising application for future 3D DRAM applications with little extra cost.

The public health level in a country is closely related to national development and quality of life. In order to appraise the level of health services in the western region of China, panel data of 124 prefecture-level units covering the period 2011 to 2021 was used together with a health evaluation index system based on four dimensions: quality of life, environmental situation, the level of health services and longevity. To assess this, we used entropy weights, standard deviation and coefficient of variation together with the geographical detector model that measures the stratified spatial heterogeneity. The results show that although public health services have improved overall, the various dimensions are still not balanced as longevity did not match up everywhere. While the developmental level of the various health dimensions presents a pattern of a relatively smooth increasing gradient in the west-central- east direction, the situation with respect to the north-centralsouth is more uneven with both ups and downs. However, a trend of continuous enhancement of all health dimensions was found with a significant positive correlation of spatial clustering, with hotspots and ‘sub-hotspots’ contracting from north to south, while coldspots and ‘sub-coldspots’ expanded from west to east. This can be seen as the result of multiple factors, with the level of urbanization and economic level as the dominant factors and government guidance, agglomeration capacity and industrial structure being auxiliary.

Homeobox (HOX) genes encode highly conserved transcription factors that play vital roles in embryonic development. DNA methylation is a pivotal regulatory epigenetic signaling mark responsible for regulating gene expression. Abnormal DNA methylation is largely associated with the aberrant expression of HOX genes, which is implicated in a broad range of human diseases, including cancer. Numerous studies have clarified the mechanisms of DNA methylation in both physiological and pathological processes. In this review, we focus on how DNA methylation regulates HOX genes and briefly discuss drug development approaches targeting these mechanisms.

Interactions between the monsoon and decadal oscillations in the Pacific and Atlantic have influenced the multidecadal variability of precipitation in eastern China over the past 1150 years, according to stable oxygen isotope records from three stalagmites.

Persistent inflammation and associated pain significantly impact individuals’ quality of life, posing substantial healthcare challenges. Proinflammatory cytokines, released by activated macrophages, play crucial roles in the development of chronic inflammatory conditions such as rheumatoid arthritis. To identify and evaluate potential therapeutic interventions targeting this process for mitigating inflammation and pain, we created myeloid cell-specific knockout of Vamp3 (vesicle-associated membrane protein 3) mice (Vamp3Δmyel) by crossing LysM-Cre mice with newly engineered Vamp3flox/flox mice. Bone marrow-derived macrophages and peritoneal resident macrophages from Vamp3Δmyel mice exhibited a significant reduction in TNF-α and IL-6 release compared to control mice. Moreover, Vamp3 deficiency led to decreased paw edema and ankle joint swelling induced by intraplantar injection of complete Freund’s adjuvant (CFA). Furthermore, Vamp3 depletion also mitigated CFA-induced mechanical allodynia and thermal hyperalgesia. Mechanistically, Vamp3 loss ameliorated the infiltration of macrophages in peripheral sites of the hind paw and resulted in reduced levels of TNF-α and IL-6 in the CFA-injected paw and serum. RT-qPCR analysis demonstrated downregulation of various inflammation-associated genes, including TNF-α, IL-6, IL-1β, CXCL11, TIMP-1, COX-2, CD68, and CD54 in the injected paw at the test day 14 following CFA administration. These findings highlight the novel role of Vamp3 in regulating inflammatory responses and suggest it as a potential therapeutic target for the development of novel Vamp-inactivating therapeutics, with potential applications in the management of inflammatory diseases.

BackgroundCalcium and magnesium are essential minerals that have significant roles in nerve function and regulation. There may be a correlation between dietary calcium and magnesium intake and peripheral neuropathy. However, this relationship remains unclear and requires further study.MethodsData from 7,726 participants in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2004 were analyzed in this study. The relationship between total dietary calcium and magnesium intake, as well as each quantile, and peripheral neuropathy was analyzed using a multifactor logistic regression model. To illustrate the dose–response relationship between calcium and magnesium intake and peripheral neuropathy, we utilized a restricted cubic spline (RCS) plot.ResultsOur analysis found a positive correlation between dietary intake of calcium and magnesium and peripheral neuropathy (calcium: OR 1.000, 95% CI 1.000–1.000; magnesium: OR 1.001, 95% CI 1.00–1.002). Participants in the first and third quantiles of dietary calcium intake had a significantly higher incidence of peripheral neuropathy than those in the second quantile (OR 1.333, 95% CI 1.034–1.719, OR 1.497, 95% CI 1.155–1.941). Those in the first and third quantiles of dietary magnesium intake also had a significantly higher incidence of peripheral neuropathy than those in the second quantile (OR 1.275, 95% CI 1.064–1.528, OR 1.525, 95% CI 1.231–1.890). The restricted cubic spline analysis revealed a U-shaped nonlinear relationship between dietary intake of calcium and magnesium and peripheral neuropathy.ConclusionThe study found a U-shaped non-linear relationship between dietary calcium and magnesium intake levels and peripheral neuropathy, indicating that both excessive and insufficient intake of calcium and magnesium can increase the incidence of peripheral neuropathy.

The common two-dimensional boron doped diamond flat plate electrode in the practical wastewater treatment application shows the disadvantages of small reactive area and low degradation efficiency. In order to realize excellent degradation efficiency towards wastewater, it is expected that boron doped diamond electrode has high specific surface area so as to enhance the reactive area and has special surface structure so as to enhance its oxidative and catalytic ability. However, there still exists problems such as the complexity of preparation process and expensive equipment for such boron-doped diamond electrode. In order to address above problem, this article focuses on the preparation methods of the boron doped diamond electrode, analyze the merits and demerit of these methods, and discusses its industrial application prospect in wastewater treatment.

Objective. To observe the effects of chimeric antigen receptor T (CAR-T) cell immunotherapy on immune cells and related toxic side effects in patients with refractory acute lymphoblastic leukemia (ALL). Methods. A retrospective study was conducted in 35 patients with refractory ALL. The patients were treated with CAR-T cell therapy in our hospital from January 2020 to January 2021. The efficacy was evaluated at one and three months post treatments. The venous blood of the patients was collected before treatment, 1 month after treatment, and 3 months after treatment. The percentage of regulatory T cells (Treg cells), natural killer (NK) cells, and T lymphocyte subsets (CD3+, CD4+, and CD8+ T cells) was detected by flow cytometry. The ratio of CD4+/CD8+ was calculated. Patient’s toxic side effects such as fever, chills, gastrointestinal bleeding, nervous system symptoms, digestive system symptoms, abnormal liver function, and blood coagulation dysfunction were monitored and recorded. The incidence of toxic and side effects was calculated, and the incidence of infection was recorded. Results. After one month of CAR-T cell therapy in 35 patients with ALL, the efficacy evaluation showed that complete response (CR) patients accounted for 68.57%, CR with incomplete hematological recovery (CRi) patients accounted for 22.86%, and partial disease (PD) patients accounted for 8.57%, and the total effective rate was 91.43%. In addition, compared with that before treatment, the Treg cell level in CR+CRi patients treated for 1 month and 3 months decreased prominently, and the NK cell level increased dramatically (P0.05). Conclusion. CAR-T cell therapy had a good effect on patients with refractory ALL by regulating the immune function of the body via mediating the content of immune cells. CAR-T cell therapy may have therapeutic effect on refractory ALL patients with mild side effects and high safety.

MiR-873/CDK3 has been shown to play a critical role in ERα signaling and tamoxifen resistance. Thus, targeting this pathway may be a potential therapeutic approach for the treatment of ER positive breast cancer especially tamoxifen resistant subtype. Here we report that Norcantharidin (NCTD), currently used clinically as an ani-cancer drug in China, regulates miR-873/CDK3 axis in breast cancer cells. NCTD decreases the transcriptional activity of ERα but not ERβ through the modulation of miR-873/CDK3 axis. We also found that NCTD inhibits cell proliferation and tumor growth and miR-873/CDK3 axis mediates cell proliferation suppression of NCTD. More important, we found that NCTD sensitizes resistant cells to tamoxifen. NCTD inhibits tamoxifen induced the transcriptional activity as well ERα downstream gene expressions in tamoxifen resistant breast cancer cells. In addition, we found that NCTD restores tamoxifen induced recruitments of ERα co-repressors N-CoR and SMRT. Knockdown of miR-873 and overexpression of CDK3 diminish the effect of NCTD on tamoxifen resistance. Our data shows that NCTD regulates ERα signaling and tamoxifen resistance by targeting miR-873/CDK3 axis in breast cancer cells. This study may provide an alternative therapy strategy for tamoxifen resistant breast cancer.

In this study, phenylalanine ammonia lyase (PAL) is used as model, and the cross-linked enzyme aggregates of PAL with crude-pored microspherical silica core (NH-PAL-CLEAs) are prepared. The conditions for the preparation of NH-PAL-CLEAs are optimized. Moreover, some characteristics of the NH-PAL-CLEAs are examined. The optimized conditions for preparing NH-PAL-CLEAs are as follows: 117.75 mg silica, 0.2% (v/v) glutaraldehyde and 1 mL free PAL solution (2 U). Under optimized conditions, the maximum activity recovery of NH-PAL-CLEAs reaches 25%. Compared with PAL-CLEAs, the resulting NH-PAL-CLEAs can be easily separated from the reaction mixture by natural precipitation without centrifugation and filtration treatments. Moreover, NH-PAL-CLEAs show superior operational stability. This technique not only overcomes the difficulty to recover CLEAs due to their small particle sizes and soft for many industrial applications, but also reduces production cycle and energy consumption. As a result, this technique shows superior application prospect for enzyme immobilization.

Proliposomes were used to improve the solubility and oral bioavailability of nifedipine. Nifedipine proliposomes were prepared by methanol injection-spray drying method. The response surface method was used to optimize formulation to enhance the encapsulation efficiency (EE%) of nifedipine. The particle size of nifedipine proliposomes after rehydration was 114 nm. Surface morphology of nifedipine proliposomes was observed by a scanning electron microscope (SEM) and interaction of formulation ingredients was assessed by differential scanning calorimetry (DSC). The solubility of nifedipine is improved 24.8 times after forming proliposomes. In vitro release experiment, nifedipine proliposomes had a control release effect, especially in simulated gastric fluid. In vivo, nifedipine proliposomes significantly improved the bioavailability of nifedipine. The area under the concentration-time curve (AUC0−∞) of nifedipine proliposomes was about 10 times than nifedipine after oral administration. The elimination half-life (T1/2β) of nifedipine was increased from 1.6 h to 6.6 h. In conclusion, proliposomes was a promising system to deliver nifedipine through oral route and warranted further investigation.

Vitamin D3 is an effective skin protective substance to prevent photoaging. Liposomes were used as a carrier to deliver vitamin D3 to improve the stability and to enhance the treatment effect of vitamin D3. The stability of vitamin D3 liposomes, average cumulative penetration, and retention of vitamin D3 in the skin were then evaluated and compared with free vitamin D3. Finally, the treatment effect of vitamin D3 liposomes in a rat photoaging model was appraised and Haematoxylin-Eosin (H&E) staining was used to assess the histology changes of the skin after vitamin D3 liposome treatment. The results indicated that liposomes could significantly improve the stability of vitamin D3. The average skin retention of vitamin D3 liposomes was 1.65 times that of the vitamin D3 solution. Vitamin D3 liposomes could repair the surface morphology of skin in the photoaging model and promote the production of new collagen fibers. Vitamin D3 liposomes as a potential skin care agent could significantly improve skin appearance and repair damage in the histology of photoaging.

A series of 1,2-dihydroquinoline derivatives were synthesized and evaluated for cytotoxicity in HeLa, Hep G2 and 6HEK-293T cell lines. EEDQ2 was identified as a promising anti-cancer agent with low IC50 in HeLa (18.55μg/ml) and Hep G2 (14.53μg/ml) cells. For improving the antitumor activity and tumor selectivity of EEDQ2, we prepared transferrin (Tf)-modified liposomes (LPs) to deliver EEDQ2. When HeLa and Hep G2 cells were treated with LP-delivered EEDQ2, the ROS level was significantly enhanced, and mitochondrial membrane potential was reversed. Tf-LPs improved cell uptake of EEDQ2 by about 3.7 times compared with non-targeted LPs. These data suggest that Tf-LPs delivering EEDQ2 is a promising strategy to treat cancer.

FOXP1 is a member of FOXP subfamily transcription factors. Mutations in FOXP1 gene have been found in various development-related cognitive disorders. However, little is known about the etiology of these symptoms, and specifically the function of FOXP1 in neuronal development. Here, we report that suppression of Foxp1 expression in mouse cerebral cortex led to a neuronal migration defect, which was rescued by overexpression of Foxp1. Mice with Foxp1 knockdown exhibited ectopic neurons in deep layers of the cortex postnatally. The neuronal differentiation of Foxp1-downregulated cells was normal. However, morphological analysis showed that the neurons with Foxp1 deficiency had an inhibited axonal growth in vitro and a weakened transition from multipolar to bipolar in vivo. Moreover, we found that the expression of Foxp1 modulated the dendritic maturation of neurons at a late postnatal date. Our results demonstrate critical roles of Foxp1 in the radial migration and morphogenesis of cortical neurons during development. This study may shed light on the complex relationship between neuronal development and the related cognitive disorders.

People's health is the basis for the progress of social civilization and an important symbol of national prosperity and national strength. Using the entropy method, spatial autocorrelation, spatio-temporal geographic weighted regression and other methods, we conducted a comprehensive evaluation of the high-quality development level of public health in Guizhou Province from 2011 to 2020 and an evolutionary analysis of the spatio-temporal divergence. The results revealed four key aspects of the state of public health in Guizhou Province. (1) The overall level of public health is constantly improving, but structural imbalance is prominent. (2) From the spatial dimension, the spatial differences in the level of public health have gradually moved from significant to a state of equilibrium. The northeastern cities were more strongly driven by the radiation of the peripheral cities, while this effect was weaker in the southwestern cities. From the time dimension, the spatial pattern shows a clear gradient, with a faster vertical growth rate. (3) The overall spatial correlation of the level of public health is weak, with more cold spots than hot spots, showing a distribution pattern of "strong in the northeast and weak in the southwest". (4) The new rural cooperative medical care participation rate, (rural) per capita health expenditure, and the electronic health record creation rate have become the most important drivers affecting the high-quality development of public health in Guizhou Province. [ABSTRACT FROM AUTHOR]

Abstract In the vascular system, angiotensin II (Ang II) mediated vasoconstriction by inducing the production of 20-hydroxyeicosatetraenoic acid (20-HETE). However, the role of 20-HETE in Ang II-induced cardiac dysfunction had yet to be fully elucidated. This study investigated the effects of Ang II on CYP4A expression and 20-HETE production in H9c2 cells using RT-qPCR, Western blot, and ELISA. The role of 20-HETE in Ang II-induced cardiac hypertrophy was examined using DHE, MitoSOX, and JC-1 staining to evaluate reactive oxygen species (ROS) generation and mitochondrial membrane potential changes. The ERK/Akt and CaN/NFAT3 signaling pathways were analyzed through Western blot. Ang II was found to promote CYP4A expression and 20-HETE production in H9c2 cells via an AT1 receptor-dependent mechanism. Additionally, the upregulation of AT1 receptor expression by 20-HETE further confirms its facilitatory effect on the Ang II signaling pathway. Inhibition of 20-HETE synthesis or blockade of its receptor, G-protein-coupled receptor 75 (GPR75), significantly reversed Ang II-induced cardiac hypertrophy. This reversal was closely associated with 20-HETE-induced ROS production, oxidative stress, and activation of the Ca2+/CaN/NFAT3 signaling pathway. This study demonstrated that 20-HETE mediated Ang II-induced cardiac hypertrophy and, for the first time, highlighted the significant role of the GPR75 receptor in this process. These findings suggested that targeting 20-HETE reduction or blocking its receptor action could offer a novel therapeutic approach for cardiovascular diseases associated with Ang II.

Cervical cancer, ranking as the fourth most common cancer in women globally, is closely linked to chronic inflammation resulting from persistent human papillomavirus (HPV) infection. Chronic inflammation mediated by cyclooxygenase (COX) has been identified as a factor in cancer onset and progression, with HPV oncoproteins E6 and E7 inducing COX activation. Nonsteroidal anti-inflammatory drugs (NSAIDs) have demonstrated the capability to significantly inhibit COX activity, playing a crucial preventive and therapeutic role in various tumors. This paper explores the therapeutic value and potential clinical applications of NSAIDs in cervical cancer by examining the mechanistic interactions between HPV and COX and the carcinogenic effects of COX in cervical cancer.

Placental development is a multifaceted process critical for a fruitful pregnancy, reinforced by a complex network of molecular pathways that synchronize trophoblast migration, differentiation, and overall placental function. This review provides an in-depth analysis of the key signaling pathways, such as Wnt, Notch, TGF-β, and VEGF, which play fundamental roles in trophoblast proliferation, invasion, and the complicated process of placental vascular development. For instance, the Wnt signaling pathway is essential to balance trophoblast stem cell proliferation and differentiation, while Notch signaling stimulates cell fate decisions and invasive behavior. TGF-β signaling plays a critical role in trophoblast invasion and differentiation, predominantly in response to the low oxygen environment of early pregnancy, regulated by hypoxia-inducible factors (HIFs). These factors promote trophoblast adaptation, ensure proper placental attachment and vascularization, and facilitate adequate fetal-maternal exchange. Further, we explore the epigenetic and post-transcriptional regulatory mechanisms that regulate trophoblast function, including DNA methylation and the contribution of non-coding RNAs, which contribute to the fine-tuning of gene expression during placental development. Dysregulation of these pathways is associated with severe pregnancy complications, such as preeclampsia, intrauterine growth restriction, and recurrent miscarriage, emphasizing the critical need for targeted therapeutic strategies. Finally, emerging technologies like trophoblast organoids, single-cell RNA sequencing, and placenta-on-chip models are discussed as innovative tools that hold promise for advancing our understanding of placental biology and developing novel interventions to improve pregnancy outcomes. This review emphasizes the importance of understanding these molecular mechanisms to better address placental dysfunctions and associated pregnancy disorders.

Background/Objectives: Head and neck squamous cell carcinoma (HNSCC) is a prevalent and aggressive cancer with high rates of metastasis and poor prognosis. Recent research highlights the role of 5-methylcytosine (m5C) in cancer progression. NSUN2, an m5C methyltransferase, has been implicated in various cancers, but its role in HNSCC remains elusive. Methods: NSUN2 expression and its impact on HNSCC were analyzed by using clinical samples and bioinformatic analysis. m5C-Bis-Seq was used to assess changes in mRNA m5C modification and identify downstream targets. Both in vitro and vivo studies were performed to evaluate the impact of NSUN2 manipulation on tumor growth and metastasis. Results: Results indicated that NSUN2 was significantly upregulated in HNSCC tissues compared to normal tissues and was associated with poor prognosis. NSUN2 knockdown led to decreased cell proliferation, migration, and invasion in vitro and reduced tumorigenicity and lymph node metastasis in vivo. m5C-Bis-Seq revealed altered m5C-modification patterns upon NSUN2 knockdown, with LAMC2 identified as a key downstream target. Conclusions: NSUN2-mediated m5C-modification enhanced LAMC2 stability, promoting epithelial–mesenchymal transition (EMT) signaling pathways. These findings demonstrate that NSUN2 promotes the initiation and progression of HNSCC by stabilizing the LAMC2 transcript through m5C-dependent mechanisms, offering a promising epitranscriptomic-targeted therapeutic approach for HNSCC.

Abstract The optimal selection of pinning nodes for multi-agent flocking is a challenging NP-hard problem. Current pinning node selection strategies mainly rely on centrality measures of complex networks, which lack rigorous mathematical proof for effective flocking control. This paper proposes a pinning node selection strategy based on matrix eigenvalue theory. First, the effect of the pinning node on the eigenvalue of the Laplacian matrix is analyzed. Then, a synchronization index representing the topology uniformity of the multi-agent system is proposed to exert maximum influence on the system synchronizability. A practical optimal pinning node selection method based on the synchronization index is proposed and analyzed using the eigenvalue perturbation method. Finally, simulations demonstrate that the convergence rate of the system obtained using the optimal synchronizability pinning node selection method is better than that achieved with the maximum degree centrality node selection strategy.

Plant glycoside hydrolase family 9 genes (GH9s) are widely distributed in plants and involved in a variety of cellular and physiological processes. In the current study, nine GH9 genes were identified in the mulberry and were divided into two subfamilies based on the phylogenetic analysis. Conserved motifs and gene structure analysis suggested that the evolution of the two subfamilies is relatively conserved and the glycoside hydrolase domain almost occupy the entire coding region of the GH9s gene. Only segmental duplication has played a role in the expansion of gene family. Collinearity analysis showed that mulberry GH9s had the closest relationship with poplar GH9s. MaGH9B1, MaGH9B6, MaGH9B5, and MaGH9B3 were detected to have transcript accumulation in the stalk of easy-to drop mature fruit drop, suggesting that these could play a role in mulberry fruit drop. Multiple cis-acting elements related to plant hormones and abiotic stress responses were found in the mulberry GH9 promoter regions and showed different activities under exogenous abscisic acid (ABA) and 2,4- dichlorophenoxyacetic acid (2,4-D) stresses. We found that the lignin content in the fruit stalk decreased with the formation of the abscission zone (AZ), which could indirectly reflect the formation process of the AZ. These results provide a theoretical basis for further research on the role of GH9s in mulberry abscission.

BackgroundAlthough malnutrition has been shown to influence the clinical outcomes of Stroke Patients with Bulbar Paralysis (SPBP), the prevalence and influencing factors have yet to be uncovered.ObjectiveThis study aims to assess the current prevalence and factors associated with malnutrition in SPBP.MethodsA multicenter cross-sectional investigation was conducted among SPBP in China from 2019 to 2021. Information was collected on basic information, health condition, diagnosis, treatment, neurological function, activities of daily living, swallowing function, and nutritional status. A multivariable logistic regression model was used to identify the factors that influenced nutritional status. ROC analysis was used to assess the predictive value of each independent influencing factor and the logit model.ResultsIn total, 774 SPBP were enrolled, and the prevalence of malnutrition was 60.59%. Pulmonary infection [aOR:2.849, 95%CI: (1.426, 5.691)], hemoglobin [aOR: 0.932, 95%CI: (0.875, 0.982)], serum albumin [aOR: 0.904, 95%CI: (0.871, 0.938)], total protein [aOR: 0.891, 95%CI: (0.819, 0.969)], prealbumin [aOR: 0.962, 95%CI: (0.932, 0.993)], and National Institute of Health Stroke Scale (NIHSS) scores [aOR: 1.228, 95%CI: (1.054, 1.431)] were independent factors associated with malnutrition in SPBP. ROC analysis revealed that the logit model had the best predictive value [area under the curve: 0.874, 95% CI: (0.812, 0.936); specificity: 83.4%; sensitivity: 79.3%; p

Summary: Emerging studies have demonstrated the link between RNA modifications and various cancers, while the predictive value and functional mechanisms of RNA modification-related genes (RMGs) in esophageal squamous cell carcinoma (ESCC) remain unclear. Here we established a prognostic signature for ESCC based on five RMGs. The analysis of ESCC clinical samples further verified the prognostic power of the prognostic signature. Moreover, we found that the knockdown of NSUN6 promotes ESCC progression in vitro and in vivo, whereas the overexpression of NSUN6 inhibits the malignant phenotype of ESCC cells. Mechanically, NSUN6 mediated tRNA m5C modifications selectively enhance the translation efficiency of CDH1 mRNA in a codon dependent manner. Rescue assays revealed that E-cadherin is an essential downstream target that mediates NSUN6’s function in the regulation of ESCC progression. These findings offer additional insights into the link between ESCC and RMGs, as well as provide potential strategies for ESCC management and therapy.