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Tumor cells require high levels of cholesterol for membrane biogenesis for rapid proliferation during development. Beyond the acquired cholesterol from low-density lipoprotein (LDL) taken up from circulation, tumor cells can also biosynthesize cholesterol. The molecular mechanism underlying cholesterol anabolism in esophageal squamous cell carcinoma (ESCC) and its effect on patient prognosis are unclear. Dysregulation of lipid metabolism is common in cancer. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) has been implicated in various cancer types; however, its role in esophageal squamous cell carcinoma (ESCC) remains unclear. In this study, we identified that LPCAT1 is highly expressed in ESCC and that LPCAT1 reprograms cholesterol metabolism in ESCC. LPCAT1 expression was negatively correlated with patient prognosis. Cholesterol synthesis in ESCC cells was significantly inhibited following LPCAT1 knockdown; cell proliferation, invasion, and migration were significantly reduced, along with the growth of xenograft subcutaneous tumors. LPCAT1 could regulate the expression of the cholesterol synthesis enzyme, SQLE, by promoting the activation of PI3K, thereby regulating the entry of SP1/SREBPF2 into the nucleus. LPCAT1 also activates EGFR leading to the downregulation of INSIG-1 expression, facilitating the entry of SREBP-1 into the nucleus to promote cholesterol synthesis. Taken together, LPCAT1 reprograms tumor cell cholesterol metabolism in ESCC and can be used as a potential treatment target against ESCC.

The increasing momentum of agricultural digital transformation and green development necessitates investigations into how farmers’ digital literacy influences their engagement in green production behaviours, which is critical for achieving the high-quality development of modern agriculture. Utilising primary survey data collected from farmers in rural areas of Guizhou Province, China, this study investigated how digital literacy affects farmers’ green production behaviours. The findings are as follows: (1) Digital literacy exerts a significant positive impact on farmers’ adoption of green production behaviours. Regarding the hierarchical effect, the order of influence is as follows: digital security awareness > basic digital skills > digital application and innovation. (2) The facilitating effect of digital literacy is primarily achieved through two pathways: the peer effect and the guidance effect. (3) Farmers with higher education levels are more impacted by digital literacy than farmers with lower education levels. (4) The impact of digital literacy is more positively significant for young and older farmers than for middle-aged groups. Based on these research findings, it is recommended that future policy formulation and technology extension efforts should prioritise support for specific regions and groups, such as mountainous areas, small-scale operations, low-education backgrounds, and the elderly. Such targeted approaches are crucial for encouraging wider adoption of green production behaviours among farmers.

ObjectivesEsophageal cancer is one of the malignant tumor with poor survival. The 5-year survival rate of esophageal cancer patients remains poor due to limited therapeutic options and the development of drug-resistance. Recent evidence suggests that long non-coding RNAs (lncRNAs) are involved in occurrence and development of tumor, however, the molecular mechanisms of lncRNA taurine-upregulated gene 1 (TUG1) in esophageal cancer remain unknown.ResultsTUG1 was overexpressed in esophageal cancer tissues and cells. The knockdown of TUG1 repressed proliferation and invasion, while promoted apoptosis of esophageal cancer cells by negatively regulating miR-1294 expression. Furthermore, PLK1 was a target mRNA of miR-1294 in esophageal cancer cells. Therefore, the effects of PLK1 silencing on proliferation, apoptosis, and invasion of esophageal cancer cells could be overturned by silencing miR-1294. Additionally, TUG1 silencing inhibited growth of tumor cells in vivo.ConclusionsTUG1 was found as oncogenic gene in esophageal cancer. Mechanically, TUG1 attributed to esophageal cancer process by regulating miR-1294/ PLK1 axis.

This paper investigates bisimulation relations of delayed switched Boolean control networks (DSBCNs), using the semi‐tensor product (STP) approach. Firstly, the notion of bisimulation in DSBCNs is formalized. Subsequently, based on the skeleton matrix of DSBCN, two necessary and sufficient conditions are derived for checking this notion. Moreover, as an application of bisimulation relations, this paper explores the propagation of controllability for DSBCNs through a bisimulation relation. It shows the possibility that the controllability of a DSBCN can be inferred by studying a potentially simpler DSBCN. At last, two examples are proposed to illustrate the efficiency of the obtained results. (i)The notion of bisimulation of DSBCNs are given, which extends the corresponding bisimulations notion of Boolean control networks and switching linear systems to DSBCNs. (ii)Two necessary and sufficient conditions are derived for checking this notion, which characterizes the bisimulation relations of DSBCNs from two different aspects. (iii)The propagation of controllability for DSBCNs is esxplored through a bisimulation relation.

Background Although 15-hydroxyprostaglandin dehydrogenase (HPGD) is known to regulate the metabolism of prostaglandins and lipoxin A4, and its dysregulation has been implicated in various cancers, its role in esophageal squamous cell carcinoma (ESCC) has not been determined. This study is the first to comprehensively characterize HPGD expression in ESCC and establish its clinical relevance in predicting patient outcomes. Furthermore, we elucidated the previously unrecognized molecular mechanisms through which HPGD suppresses ESCC progression and its potential as a novel therapeutic target. Methods Transcriptome sequencing was performed on paired tumor and adjacent normal tissues from deceased patients with ESCC to identify differentially expressed genes. The differential expression of the HPGD gene was subsequently validated in two independent, large-scale ESCC patient cohorts, and its prognostic significance was evaluated. To evaluate the functional role of HPGD in ESCC, the enzyme was overexpressed in ESCC cell lines, and a series of in vitro assays were conducted to assess its effects on proliferation, apoptosis, invasion, and migration. To elucidate the molecular mechanisms underlying the effects of HPGD, we performed transcriptomic sequencing to profile gene expression changes in ESCC cells. Through multiple analyses, including measurements of lipid peroxidation, intracellular ferrous ion and reactive oxygen species (ROS) levels, dual-fluorescence flow cytometry for autophagy, phosphoprotein microarrays, biotin pull-down assays, and chromatin immunoprecipitation (ChIP), we demonstrated that HPGD regulates the malignant phenotype of ESCC cells primarily by inducing ferroptosis and autophagy. Finally, the impact of HPGD on ESCC tumor growth was validated in vivo using a subcutaneous xenograft model in nude mice. Results HPGD expression was significantly lower in ESCC tissues than in normal tissues and was negatively correlated with tumor cell differentiation and patient outcomes. HPGD overexpression inhibited ESCC cell proliferation, invasion, and migration in vitro and in xenograft tumor growth in vivo. In vitro experiments demonstrated that HPGD suppresses ERK1/2 activation by facilitating lipoxin A4 (LXA4) degradation. This inhibition facilitates binding of the RNA-binding protein U2AF2 to the promoter region of the transferrin receptor (TFRC), thereby increasing TFRC expression. Consequently, these alterations lead to intracellular iron accumulation and initiate ferroptosis. Excessive generation of ROS during ferroptosis results in hyperactivation of autophagy via the AMPK/mTOR signaling pathway. Mitigating the HPGD-induced upregulation of TFRC or reducing ROS production effectively reverses ferroptosis, prevents excessive autophagy, and ameliorates malignant cell phenotypes. Conclusions HPGD exerts its antitumor effects by promoting ferroptosis through the LXA4-ERK1/2-U2AF2 signaling axis, which in turn induces autophagy hyperactivation via the AMPK-mTOR pathway. These findings suggest that HPGD is a promising therapeutic target for esophageal squamous cell carcinoma (ESCC) and reveal the nonclassic role of the RNA-binding protein U2AF2 in regulating the expression of TFRC by acting like a transcription factor.

This paper discusses the problem of global state regulation via output feedback for a class of feedforward nonlinear time-delay systems with unknown measurement sensitivity. Different from previous works, the nonlinear terms are dominated by upper triangular linear unmeasured (delayed) states multiplied by unknown growth rate. The unknown growth rate is composed of an unknown constant, a power function of output, and an input function. Furthermore, due to the measurement uncertainty of the system output, it is more difficult to solve this problem. It is proved that the presented output feedback controller can globally regulate all states of the nonlinear systems using the dynamic gain scaling technique and choosing the appropriate Lyapunov–Krasovskii functionals.

Objective The insula, as a critical hub for multimodal information integration, plays a pivotal role in post-stroke dysphagia(PSD). However, the mechanisms underlying its structural and functional network reorganization remain elusive. This study aims to systematically investigate the alterations in gray matter volume and functional connectivity patterns of the insula in patients with dysphagia after cerebral infarction using multimodal neuroimaging techniques, and to untangle their clinical associations with swallowing function impairments. Methods Three groups of subjects were recruited: healthy controls (HC, n = 15), cerebral infarction patients without dysphagia (ND, n = 13), and cerebral infarction patients with dysphagia (DYS, n = 11). Resting-state functional magnetic resonance imaging (rs-fMRI) and high-resolution T1-weighted structural imaging data were acquired. Seed-based analysis (using the CONN FC toolbox) was employed to quantify the whole-brain functional connectivity (FC) of the insula, and voxel-based morphometry (VBM) was used to assess gray matter volume changes. Swallowing function was standardized using the Fiberoptic Endoscopic Evaluation of Swallowing (FEES) and the Penetration/Aspiration Scale (PAS). Results The DYS, ND, and HC groups showed significant differences in grey matter volume in the left insula ( p FDR =0.041). Compared to the HC group, both cerebral infarction groups (ND and DYS) demonstrated increased functional connectivity between the left insula and the left lateral occipital cortex (superior division), left precuneus, and left cerebellum. In contrast, functional connectivity with the right insula cortex, right frontal operculum cortex, left anterior cingulate, and right frontal pole was decreased. Among these differences, compared to the ND group, the DYS group showed a more significant reduction in functional connectivity within the right frontal operculum cortex and a more pronounced increase in functional connectivity within the left lateral occipital cortex superior division and left cerebellum. Compared to the HC group, patients in both cerebral infarction groups (ND and DYS) showed significantly enhanced functional connectivity between the right insula and the right posterior cingulate gyrus, left lateral occipital cortex (superior division), right precuneus, left frontal pole and right frontal pole. Conversely, functional connectivity with the left insula cortex and left anterior cingulate gyrus was significantly reduced. Moreover, compared to the ND group, the DYS group demonstrated more pronounced increases in functional connectivity within the right posterior cingulate gyrus and right superior cerebellar peduncle, along with a more significant decrease in functional connectivity within the right insula cortex. Enhanced FC between the left insula and the left lateral occipital cortex (superior division) correlated positively with PAS, while enhanced FC between the right insula and the right cerebellum correlated negatively with PAS. Conclusion Our study found left insular gray matter atrophy underlies the pathology of PSD, and abnormal insular functional connectivity is key to its development. The severity of post-stroke dysphagia can affect the functional connectivity between the insula and the right cerebellum as well as the left occipital lobe. These results reveal potential neural compensation mechanisms in PSD and offer new directions for clinical prognostic biomarker development.

Using the method of static game analysis, the potential risk and responsibility across the entire pork supply chain are discussed from the perspective of all stakeholders involved. Included in the analysis are pig suppliers, slaughterers, pork processors, pork sellers and consumers. The results indicate the following: firstly, the lower the probability of inspections on downstream businesses and the higher the single inspection fee, the greater the probability of harmful substances used by upstream businesses and the higher the costs. Secondly, businesses that actively manufacture and transfer harmful substances in the supply chain cannot add extra costs. Finally, the quality and risk factors in pork production may not follow a strictly linear growth. This study might explain the unique problems that occur in pork supply chain management in large developing countries such as China.

Compared to healthy controls, spinal cord injury (SCI) patients demonstrate white matter (WM) abnormalities in the brain. However, little progress has been made in comparing cerebral WM differences between SCI-subgroups. The purpose of this study was to investigate WM microstructure differences between paraplegia and quadriplegia using tract-based spatial statistics (TBSS) and atlas-based analysis methods. Twenty-two SCI patients (11 cervical SCI and 11 thoracic SCI) and 22 age- and sex-matched healthy controls were included in this study. TBSS and atlas-based analyses were performed between SCI and control groups and between SCI-subgroups using multiple diffusion metrics, including fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD). Compared to controls, SCI patients had decreased FA and increased MD and RD in the corpus callosum (CC; genu and splenium), superior longitudinal fasciculus (SLF), corona radiata (CR), posterior thalamic radiation (PTR), right cingulum (cingulate gyrus; CCG) and right superior fronto-occipital fasciculus (SFOF). Cervical SCI patients had lower FA and higher RD in the left PTR than thoracic SCI patients. Time since injury had a negative correlation with FA within the right SFOF ( = -0.452, = 0.046) and a positive association between the FA of left PTR and the American Spinal Injury Association (ASIA) sensory score ( = 0.428, = 0.047). In conclusion, our study suggests that multiple cerebral WM tracts are damaged in SCI patients, and WM disruption in cervical SCI is worse than thoracic injury level, especially in the PTR region.

Objective This study investigated how the injury completeness, level, and duration of spinal cord injury (SCI) affect cortical morphometric changes in humans. Methods T1‐weighted images were acquired from 59 SCI patients and 37 healthy controls. Voxel‐based morphometry analyses of the gray matter volume (GMV) were performed between SCI patients and healthy controls, complete SCI and incomplete SCI, and tetraplegia and paraplegia. Correlation analyses were performed to explore the associations between GMV and clinical variables in SCI patients. Results Compared to healthy controls, SCI patients showed decreased GMV in bilateral middle frontal gyrus, left superior frontal gyrus (SFG), left medial frontal gyrus in the whole‐brain analysis, while increased GMV in right supplementary motor area and right pallidum in ROI analysis. The complete SCI had lower GMV in left primary somatosensory cortex (S1) and higher GMV in left primary motor cortex compared with incomplete SCI. Lower GMV was identified in left thalamus and SFG in tetraplegia than that in paraplegia. Moreover, time since injury was positive with the GMV in right pallidum, positive correlations were observed between the GMV in bilateral S1 and total motor and sensory scores, whereas the GMV in left cuneus was negatively correlated with total motor and sensory scores in SCI patients. Conclusions The study provided imaging evidence for identifying cerebral structural abnormalities in SCI patients and significant differences in complete/incomplete and paraplegia/tetraplegia subgroups. These results suggested brain structural changes occur after SCI and these changes may depend on the injury completeness, level, and duration. Our study provided imaging evidence for identifying cerebral structural abnormalities in patients with SCI and significant differences in complete/incomplete and paraplegia/tetraplegia subgroups.