👤 Chao Yan

SLC35B4, a nucleotide sugar transporter that mediates the transport of UDP-GlcNAc and UDP-xylose, was found to be required for the replication of influenza A virus (IAV) of the H5N1 subtype in our genome-wide siRNA library screen. We found that defective IAV replication in SLC35B4-deficient A549 cells was independent of virus strain specificity, and the virulence of IAV in Slc35b4 knockdown mice was also decreased. By examining the individual stages of the IAV replication cycle, we discovered that the amount of internalized IAV was significantly reduced in SLC35B4-knockout A549 cells. Mechanistically, SLC35B4 facilitated IAV replication by transporting UDP-xylose, which attaches to the serine residue of heparan sulfate proteoglycans (HSPGs) in the heparan sulfate (HS) biosynthesis pathway. Knockdown of associated host factors (i.e., XYLT2, B4GALT7, EXT1, and EXT2) in the HS biosynthesis pathway also impaired IAV replication. Furthermore, we revealed that AGRN, a unique HSPG family member, was important for the endocytosis of IAV in A549 cells. Moreover, we found that the homeostasis of the AGRN protein was regulated by HS modification mediated by the initial UDP-xylose transporter SLC35B4, thereby affecting the expression level of endocytic adapter AP2B1 to influence IAV internalization. Collectively, these findings establish that SLC35B4 is an important regulator of IAV replication and uncover the underlying mechanisms by which SLC35B4 employs UDP-xylose transport activity to promote IAV internalization.IMPORTANCEThe entry process of IAV represents a favorable target for drug development. In this study, we identified SLC35B4 as an important host factor for the efficient replication of different subtypes of IAV Show less

Microcystin-LR (MC-LR) is a toxin that causes hepatic steatosis. Our previous study found that exposure to 60 μg/L MC-LR for 9 months resulted in liver lipid accumulation, but the underlying mechanisms remain elusive. Herein, for the first time, fatty acid-targeted metabolome and RNA-seq were combined to probe the effect and mechanism of chronic (12-month) MC-LR treatment on mice lipid metabolism at environmental-related levels (1, 60, and 120 μg/L). It was found that MC-LR dose-dependently raised serum and liver lipid levels. The total cholesterol (TC) levels in the liver were significantly increased following treatment with 1 μg/L MC-LR (equivalent to 0.004 μ/L in human). Treatment with 60 and 120 μg/L MC-LR significantly elevated TC and triglyceride (TG) levels in both serum and liver. Serum fatty acid-targeted metabolome analysis demonstrated that exposure to 1, 60, and 120 μg/L MC-LR caused significant alterations in the fatty acid profile. Chronic 1, 60, and 120 μg/L MC-LR treatment significantly increased serum polyunsaturated fatty acids (PUFAs), including conjugated linoleic acid and eicosapentaenoic acid, which positively correlated with serum or liver TG levels. Chronic exposure to 120 μg/L MC-LR led to a significant decrease in the accumulation of saturated fatty acids, including citramalic acid, pentadecanoic acid, and docosanoic acid, which were negatively correlated with serum or liver lipid levels. These findings suggested that 1 μg/L MC-LR exposure caused mild lipid metabolism disruption, while 60 and 120 μg/L MC-LR treatment resulted in pronounced hepatic steatosis in mice. Transcriptome analysis revealed that chronic environmental MC-LR treatment regulated the expression of genes involved in the phosphatidylinositol 3-kinase (PI3K) complex and fatty acid metabolism. Western blotting and RT-qPCR confirmed that chronic environmental MC-LR exposure activated the PI3K/AKT/mTOR signaling pathway, the downstream of Show less

RNA interference (RNAi) holds promise as a gene-silencing therapy for liver cancer but faces challenges related to siRNA instability, short half-life, and inefficient cellular uptake. In this study, we designed a self-assembling RNA nanoparticle targeting three oncogenes- Show less

Bats are natural reservoirs for diverse viruses, yet they rarely develop disease, suggesting unique antiviral adaptations. In this study, we performed a comprehensive genome-wide analysis in the common vampire bat ( Show less

Aberrant activation of fibroblast growth factor receptors (FGFRs) plays a critical role in tumorigenesis across multiple cancer types, driving the development of various FGFR inhibitors. Despite clinical advances, therapeutic efficacy remains limited by the emergence of drug resistance, primarily mediated by gatekeeper mutations in FGFRs. To overcome this challenge, we designed and synthesized a novel series of 7-(1-methyl-1 Show less

The selective inhibition of fibroblast growth factor receptors (FGFR) presents a significant challenge due to the high degree of sequence and the close structural similarity of the subtypes. Herein, we designed selective dual FGFR2/3 inhibitors based on the in-depth understanding of protein-ligand interaction contributions. We efficiently identified ISM7594 ( Show less

Parkinson's disease (PD), as a neurodegenerative disorder, is characterized primarily by damage to the central nervous system, accompanied by astrocyte dysfunction and the activation of ferroptosis. Recent studies have shown that oligodendrocytes also exhibit functional abnormalities in the brains of PD patients and are involved in the ferroptotic process. However, it remains unclear whether there is an interaction between oligodendrocytes and astrocytes and how they induce neuronal ferroptosis. Here, we employed single-nucleus sequencing and spatial transcriptomics to characterize the intercellular communication network between oligodendrocytes and astrocytes in the PD environment. Among these, astrocytes are the primary recipients of signals sent by oligodendrocytes in the FGF (Fibroblast growth factors) signaling pathway. In PD, the communication intensity is weakened, involving FGF1 and FGF9 and their receptors FGFR1, FGFR2, and FGFR3. Subsequently, we further validated the significant activation of mitochondrial oxidative phosphorylation processes within oligodendrocytes and astrocytes in PD mice, and that astrocytes might also involve the interaction of Mt1 and Ca Show less

Surufatinib is a novel, China-developed small-molecule tyrosine kinase inhibitor that demonstrates high selectivity for VEGFR, FGFR1, and CSF1R. Surufatinib has been approved for the treatment of neuroendcrine tumors, including pancreatic neuroendocrine tumors (PNEN) and non-pancreatic neuroendocrine tumors (N-pNEN). The purpose of this retrospective study is to assess Surufatinib's safety and effectiveness in patients with various advanced solid malignancies. The general clinical statistics and follow-up data of patients treated with Surufatinib for advanced solid tumors at Zhejiang Provincial People's Hospital between January 2021 and April 2024 were gathered. Enhanced CT was used to assess the effectiveness during that time, and cases side effects were gathered. Survival rates of different diseases were analyzed using the Kaplan-Meier method. A total of 28 eligible patients were enrolled in this study. At the end of follow-up, treatment with Surufatinib resulted in the following outcomes: Complete response (CR) in 0 cases (0.0%), Partial response (PR) in 5 cases (17.9%), Stable disease (SD) in 7 cases (25.0%), and Progressive disease (PD) in 16 cases (57.1%). Objective response rate (ORR) and Disease control rate (DCR) were 17.9% and 42.9%, respectively. In the PNEN group, ORR was 33.3%, DCR was 66.7%, median progression-free survival (mPFS) was 11 months, while median overall survival (mOS) was 17 months. In the N-pNEN group, ORR was 14.3%, DCR was 42.3%, mPFS was 6 months and mOS was 7 months. ORR was 8.3%, DCR was 25%, mPFS was 2 months, and mOS was 2 months. The most common adverse reactions included hypoproteinemia, proteinuria, bone marrow suppression and gastrointestinal toxicity, and which of them were grade 1 to grade 2. In advanced solid tumors beyond PNEN, Surufatinib demonstrates clinically meaningful survival benefits for patients refractory to standard therapies, with a generally manageable safety profile. Show less

Fibroblast growth factor receptors (FGFRs) play a critical role in the regulation of cancer cell proliferation, differentiation, and migration. However, the development of acquired resistance to FGFR inhibitors remains a major challenge in treating non-small cell lung cancer (NSCLC), particularly due to mutations at the gatekeeper residue. In this study, we report the discovery of a series of irreversible FGFR inhibitors targeting gatekeeper mutations in FGFR1-3, utilizing a 2,4,5-trisubstituted pyrimidine scaffold. Through rational design, structure-activity relationship optimization, and pharmacokinetic evaluation, compound ng Show less

Fibroblast growth factor receptors (FGFRs) are established oncogenic drivers in various solid tumors. However, the approved FGFR inhibitors face challenges with acquired resistance and dose-limiting adverse effects associated with FGFR1/4 inhibition, limiting therapeutic efficacy. Herein, we systematically explored linker and electrophile moieties based on the pyrrolopyrazine carboxamide core and identified aniline α-fluoroacrylamide as an effective covalent warhead. Compound Show less

Approaches of promoting a neural milieu permissive for plasticity and resilience against neuronal injury are important strategies for the treatment of a range of neurological disorders. Fibroblast growth factor 21 (FGF21) which is known for its role as a potent regulator of glucose and energy metabolism has also proved to be neuroprotective against various mental diseases. However, the underlying molecular mechanisms remain elusive. Here, we report a study of the neuroprotective effects of FGF21 by promoting 5-HT Show less

Post traumatic stress disorder (PTSD) is a serious and persistent mental diseases. Nowadays, Treatment of PTSD patients in clinical practice is mainly based on drug therapy accompanied by psychological therapy. However, the therapeutic effect is unsatisfactory. It is urgent to detect how to treat PTSD patients. Here, we found that ginsenoside can significantly relieve PTSD symptoms in mice model. Rg3, one of the main pharmacological components of ginsenoside, prevents PTSD by promoting alternatively activated M2 phenotype microglia while inhibiting classically activated inflammatory M1 phenotype microglia. Mechanistically, Rg3 up-regulates fibroblast growth factor receptor 1 (FGFR1) expression in microglia to suppress excessive activation of microglia and reduce neuronal apoptosis. Importantly, knocking down FGFR1 expression in BV2 cells promoted a pro-inflammatory phenotype of BV2 cells, while over-expressing FGFR1 reversed this effect. In vivo PTSD mice model results showed that knockdown FGFR1 prevents the therapeutic effect of Rg3, which indicates that FGFR1 is an essential target of PTSD. Our results reveal that Rg3 may be a potential drug to treat PTSD patients. Show less

Pheochromocytomas and paragangliomas (PPGLs) exhibit the highest degree of heritability among all human tumors, yet the genetics of urinary bladder paragangliomas (UBPGLs) remains poorly understood. The present study aims to examine the characteristics of a cohort of Chinese patients with UBPGLs, focusing particularly on genetics. The study included 70 Chinese patients with UBPGLs from 15 centers in China, 240 patients with non-head and neck PGLs (non-HNPGLs) outside the urine bladder, and 16 Caucasian patients with UBPGLs. Tumor DNA samples were sequenced by next generation sequencing. All identified pathogenic variants (PVs) were confirmed by Sanger sequencing. Among the 70 Chinese patients, PVs were identified in 38 cases: 23 in cluster 1 A (13 SDHB, 1 SDHD, 1 SDHA, 4 IDH1, 2 SLC25A11, and 2 FH), 4 in cluster 1B (3 EPAS1 and 1 EGLN1), and 11 in cluster 2 genes (7 HRAS, 1 FGFR1, 2 NF1, and 1 H3F3A). Compared with other non-HNPGLs, UBPGLs had more PVs in cluster 1 A genes (32.9% vs. 14.2%, p < 0.001), but fewer in cluster 1B (5.7% vs. 19.2%, p = 0.002) and cluster 2 genes (15.7% vs. 42.5%, p < 0.001). PVs in SDHB (18.6%) was the most common in Chinese patients with UBPGLs, followed by HRAS (10.0%). No PVs was found in 45.7% of all UBPGLs. PVs in HRAS, SLC25A11, EPAS1, and FH were also identified in Caucasians with UBPGLs. Chinese patients with UBPGLs have a diverse genetic profile. PVs in cluster 1 A genes underlie nearly 1/3 of patients, highlighting the importance of genetic testing. Diverse germline and somatic PVs are also present in Caucasian patients with UBPGLs. Show less

Mammalian scent glands mediate species-specific chemical communication, yet the mechanistic basis for convergent musk production remain incompletely understood. Forest musk deer and muskrat have independently evolved specialized musk-secreting glands, representing a striking case of convergent evolution. Through an integrated multi-omics approach, this study identified cyclopentadecanone as a shared key metabolic precursor in musk from both forest musk deer and muskrat, although downstream metabolite profiles diverged between the two lineages. Single-cell RNA sequencing revealed that these specialized apocrine glands possessed unique secretory architecture and exhibited transcriptional profiles associated with periodic musk production, distinct from those in conventional apocrine glands. Convergent features were evident at the cellular level, where acinar, ductal, and basal epithelial subtypes showed parallel molecular signatures across both taxa. Notably, acinar cells in both species expressed common genes involved in fatty acid and glycerolipid metabolism (e.g., Show less

Neonatal necrotizing enterocolitis (NEC) is a life-threatening gastrointestinal disease of premature infants, characterized by immune dysregulation and compromised intestinal barrier integrity. Interleukin-27 receptor α (IL-27Ra), a critical component of the JAK-STAT signaling pathway, exhibits dual pro- and anti-inflammatory roles in various inflammatory conditions. However, its role in NEC pathogenesis remains unclear. To elucidate the functional role of IL-27Ra in NEC development and assess its potential as a therapeutic target. A multi-tiered approach was employed, including integrative analysis of clinical NEC specimens by single-cell and bulk RNA sequencing, and a neonatal mouse NEC model. NEC was induced in mice via hyperosmolar formula feeding combined with LPS gavage, intermittent hypoxia, and cold stress. Additional experiments included immunofluorescence staining for IL-27Ra, cytokine profiling (ELISA, quantitative real-time PCR (qPCR)), use of IL-27Ra knockout (IL-27Ra Show less

Oxymatrine is an alkaloid with the property of immunomodulation. Recent studies have demonstrated that oxymatrine inhibits experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by promoting the production of interferon-β (IFN-β). However, the mechanism through which oxymatrine regulates the production of IFN-β remains unclear. The aim of this study was to investigate the pharmacological effects and related molecular mechanisms of oxymatrine in the treatment of EAE through in vivo and in vitro experiments. Oxymatrine alleviated neurological dysfunction, demyelination, and inflammation in EAE mice. It reduced microglia/macrophage infiltration and polarization, lowered pro-inflammatory cytokine levels (iNOS, TNF-α), and enhanced the expression of IL-10 and IL-27. Additionally, oxymatrine upregulated the STING/TBK1/IRF3 signaling pathway in EAE mice, promoting IFN-β production by microglia. Similarly, in LPS-induced BV2 cells, oxymatrine suppressed inflammatory factors and activated the STING/TBK1/IRF3 pathway to enhance IFN-β production. Notably, treatment with the STING inhibitor, C176, reversed these effects in both EAE mice and LPS-induced BV2 cells, confirming the pathway's critical role in the mechanism of oxymatrine therapy. Oxymatrine promotes IFN-β production in microglia by upregulating the STING/TBK1/IRF3 signaling pathway, thereby alleviating the neurological dysfunction of EAE and reducing pathological and inflammatory events. This study identifies a novel anti-EAE mechanism of oxymatrine: promoting IFN-β production in microglia by activating the STING/TBK1/IRF3 pathway. However, it lacks clinical sample verification. If validated later, oxymatrine may provide a more economical, convenient endogenous IFN-β induction regimen for MS patients. Show less

B cells express many protein ligands, yet their regulatory functions are incompletely understood. We profiled ligand expression across murine B sublineage cells, including those activated by defined receptor signals, and assessed their regulatory capacities and specificities through in silico analysis of ligand-receptor interactions. Consequently, we identified a B cell subset that expressed cytokine interleukin-27 (IL-27) and chemokine CXCL10. Through the IL-27-IL-27 receptor interaction, these IL-27/CXCL10-producing B cells targeted CD40-activated B cells in vitro and, upon induction by immunization and viral infection, optimized antibody responses and antiviral immunity in vivo. Also present in breast cancer tumors and retained there through CXCL10-CXCR3 interaction-mediated self-targeting, these cells promoted B cell PD-L1 expression and immune evasion. Mechanistically, Show less

Ionizable lipids are critical for determining the potency of mRNA lipid nanoparticles (LNPs). Various mRNA therapies require LNPs that achieve efficient delivery while maintaining appropriate immunogenicity in vivo. While research has largely focused on screening the amine headgroups, linkers and hydrophobic tails of ionizable lipids, the role of tail unsaturation in influencing mRNA delivery and immunogenicity of LNPs has received less attention. Here, we utilized a four-component Ugi reaction (Ugi-4CR) system to synthesize a small library of 17 ionizable lipids with identical backbones but varying in degrees, positions, and types of unsaturation in hydrophobic tails. We systemically investigated structure-activity relationships and elucidated the influence of tail unsaturation on physicochemical properties, endosomal escape, mRNA delivery efficiency and immunogenicity of LNPs. The findings indicate that optimization of tail unsaturation could serve as a promising strategy to improve mRNA encapsulation and delivery efficacy while modulating LNP immunogenicity in vivo. Using interleukin-27 (IL-27)-encoded mRNA as a model, we demonstrated the potential of selected LNPs for protein supplementation therapies. These insights provide a foundation for the rational design of ionizable lipids, advancing the development of more efficient and safer mRNA delivery systems. Show less

Pancreatic cancer has a complex immunosuppressive tumor microenvironment (TME), which is highly resistant to conventional therapies and emerging cancer immunotherapies. Oncolytic viruses are multifaceted killers of malignant tumors, which can selectively infect, replicate in and lyse tumor cells, release tumor-associated antigens to stimulate specific antitumor immune responses, and recruit immune cells into the TME, turning "cold" tumors "hot". Here, we report a novel A novel oncolytic VV with deletion of the TK, N1L, and A41L genes, and expression of the red fluorescent protein (RFP) gene (VVL-TD-RFP) was constructed using CRISPR-Cas9-based homologous recombination. This virus was armed with IL-27, creating VVL-TD-IL-27. The characteristics of these viruses were evaluated VVL-TD-RFP cured 71.4% of tumor-bearing mice, compared with 14.3% of animals treated with VVLΔTKΔN1L that does not have an A41L gene deletion. Efficacy was mainly dependent on elevated dendritic cell (DC) populations, activation of DC, CD86 VVL-TD-mIL-27 is a potential immunotherapy agent for the treatment of pancreatic cancer, and a clinical study of this virus is warranted. Show less

Recipients' age has emerged as a key factor that impacts on acute renal allograft rejection and graft survival. Age-related functional and structural changes in the immune system have been observed, yet the precise influence of aged immunity on kidney transplant remains unclear. In an initial retrospective analysis of clinical data gathered from two major centers in China and Germany, we found a correlation between aging and mitigated rejection outcomes in kidney recipients. To study the mechanism, we performed kidney transplantation on mice and observed attenuated allograft rejection in senescent recipients. Single-cell transcriptome analysis of allograft kidneys indicated a protective role of p21 Show less

Tuberculous pleural effusion (TPE) diagnosis still faces many difficulties and challenges. Some studies have shown that pleural interleukin -27 (IL-27) had a diagnostic potential for TPE. However, their findings are not always consistent. This study aimed to investigate the diagnostic accuracy of pleural IL-27 for TPE. We prospectively enrolled 211 patients with undiagnosed pleural effusion. Effusion Mycobacterium tuberculosis (Mtb) culture, Ziehl-Neelsen staining, biopsy, and response to antituberculosis therapy were used to define TPE. The pleural IL-27 levels were determined by enzyme-linked immunosorbent assay (ELISA). A receiver operating characteristic curve (ROC) with the area under the curve (AUC) was used to evaluate the diagnostic accuracy of IL-27 for TPE. In addition, we investigated the influence of age on the diagnostic performance of IL-27 by resampling patients with different upper age limits in the inclusion criteria. Among the 211 enrolled participants, 33 were TPE and 178 were non-TPE. The mean concentration of IL-27 in TPE patients was significantly higher than that of non-TPE patients. The AUC of IL-27 was 0.76 (95 %CI: 0.67-0.86). At the threshold of 500 pg/mL, the sensitivity and specificity of IL-27 were 0.26 (95 %CI: 0.20-0.33) and 0.91 (95 %CI:0.76-0.97), respectively. The AUC of IL-27 is 0.84 in patients with an upper age limit of 70. Still, it decreased to 0.76 in patients with an upper age limit of 75. Age can affect the diagnostic performance of IL-27 for TPE. Show less

Reverse Potts shunt is a promising yet high-risk therapy for pediatric pulmonary arterial hypertension. Postoperative hemodynamics is critically influenced by shunt configuration but is difficult to predict. This study aimed to quantify the effects of shunt size and location on hemodynamics to guide surgical planning. Based on a patient-specific model, four postoperative models with two different shunt locations [left pulmonary artery (LPA)-descending aorta (DAO) and pulmonary artery bifurcation-aortic arch] and three conduit sizes (4, 5, and 6 mm) were created. The direct Potts shunt model was created by a direct side-to-side anastomosis between the LPA and DAO with a 6-mm circular opening. Quantitative parameters including the shunt ratio (SR), which was defined as the percentage of the shunt flow rates to the total pulmonary inflow rate, lower limb oxygen saturation, and pressure were analyzed. Increasing the shunt size from 4 mm to 6 mm elevated the SR from 6.01% to 9.80%, concurrently reducing lower limb oxygen saturation from 89.57% to 86.52%. When taking 11,000 Pa as the threshold, this increased SR resulted in a reduction of the high-pressure area from 17.32% of the total pulmonary artery area to almost zero. Meanwhile, the high-pressure area on the aorta expanded from 8.72% of the total aortic area to 14.94%. These results indicated a reduction in the right ventricular afterload and an increase in the left ventricular afterload. Notably, a 6-mm shunt at the pulmonary artery bifurcation yielded a significantly larger SR than at the LPA (9.80% vs. 2.68%), which is attributed to a higher pressure gradient at the pulmonary artery bifurcation (1,201 Pa vs. 162 Pa). The shunt location had a greater impact on the SR than shunt size within the 4 mm-6 mm range in this specific case. A 6-mm shunt at the pulmonary artery bifurcation yielded a significantly larger SR than at the LPA, which is attributed to the higher preoperative pressure gradient at the bifurcation site. Left heart function is as critical as right heart function in maintaining pressure balance and determining outcomes, as the shunt flow increases the left ventricular afterload. Show less

Mental health among college students represents a significant and growing public health concern. Negative bias in prospection is closely related to depression and anxiety. Prospection bias (PB) encompasses increased negativity, reduced positivity and overgeneralization, which exhibit intricate co-occurrence patterns and exert a complex influence on mental health. However, the presence of distinct patterns of PB and their impact on mental health remain unknown. We recruited 1,030 Chinese college students to complete assessments of PB, depression, anxiety, stress and resilience. Latent profile analysis (LPA) was used to identify distinct PB profiles. Linear regression was then applied to examine their effects on mental health outcomes. The results suggested six profiles: (1) high levels of increased negativity and overgeneralization but a low level of reduced positivity (contradictory overgeneralizers), (2) low PB, (3) moderate low PB, (4) a high level of increased negativity but low levels of reduced positivity and overgeneralization (simple contradictory), (5) high PB, and (6) moderate high PB. Regression analyses demonstrated that high prospection bias predicted more severe stress, depressive and anxious symptoms, as well as lower resilience. Additionally, the results implied that handling increased negativity and reduced positivity of prospection might be potential ways to improve mental health. These findings may facilitate the early detection of mental health issues among college students and contribute to the refinement of future interventions. The online version contains supplementary material available at 10.1186/s12888-025-07732-0. Show less

Robotic technology is transforming healthcare by delivering more precision, convenience, and efficiency, as seen in applications like blood collection robots. However, the full potential of such innovations hinges critically on patient acceptance. To systematically understand the drivers of intention to use, the concept of technological readiness-an individual's stable propensity to embrace new technologies-provides a valuable lens. Nevertheless, the demographic profile of technological readiness and its specific relationship with the intention to use nursing robots remain underexplored. This study aimed to identify profiles of technology readiness among patients, analyze the factors influencing these profiles, and investigate the relationship between different profiles and the intention to use blood collection robots. In this study, data on technology readiness and intention to use were collected from 331 patients between December 2024 and February 2025 through a cross-sectional survey. Latent profile analysis (LPA) was employed to assess population heterogeneity in patients' technology readiness, whereas logistic regression analysis was applied to identify factors associated with the intention to use blood collection robots. Potential profiling revealed three distinct technology readiness populations: conservative avoiders (47.7%), ambivalent adopters (18.5%), and active adopters (33.8%). The results of the three-profile classification are related to the intention to use blood collection robots. The results clearly show that the intention to use the blood collection robot by patients belonging to conservative avoiders (profile 1) was weaker and statistically significant than both active adopters (profile 3) and ambivalent adopters (profile 2). While profile 2 has a high intention to use, it also has a high level of insecurity and discomfort. Interestingly, the group of patients with low education levels is more likely to be attributed to active adopters. The results of the multiple regression analysis on patients' intention to use revealed significant differences in education level, experience with robots, and potential profiles. This study reveals the complex psychological characteristics of patient groups when encountering new technologies and their potential relationship with intention to use nursing robots. This suggests that clinical practice should account for patient heterogeneity from standardized procedures to a patient-centered approach. Targeted measures should be proposed to enhance the efficiency of technology implementation and improve patient experience. Show less

To explore the dynamic evolution of symptom clusters in patients with gynecologic malignancies during the early postoperative period and identify key transition points and influencing factors, providing evidence for precision symptom management in clinical nursing. A longitudinal study was conducted among 324 patients using the MDASI-PeriOp-GYN on postoperative days 1 (T1), 5 (T2), and 7 (T3). Exploratory factor analysis identified symptom clusters at each time point, and growth mixture modeling (GMM) was applied to examine trajectory patterns. Latent profile analysis (LPA) and network analysis were performed at T2 to identify patient subgroups, influencing factors, and core symptoms. Five symptom clusters were identified: disease behavior, gastrointestinal, endocrine, neurological, and emotional. The emotional cluster, independent at T1 and T3, merged with the disease behavior cluster at T2. GMM indicated that all clusters declined from T1 to T2, followed by divergence after T2. LPA identified high- and low-symptom subgroups. Patients with ovarian cancer and those with KPS₁ were more likely to belong to the high-symptom group. Network analysis revealed "poor appetite" as the most central symptom at T2. Postoperative day 5 (T2) represents a critical transition point in symptom evolution. Ovarian and KPS₁ are at higher risk for severe symptoms, and "poor appetite" plays a key driving role. Targeted assessment and intervention at T2 may reduce symptom burden and improve recovery outcomes in patients with gynecologic malignancies. Show less

To elucidate the accurate roles of dysfunctional sleep beliefs in modulating cancer-related fatigue (CRF), identify distinct sleep hygiene profiles, and assess whether and how these profiles serve as mediators in lung cancer patients undergoing chemotherapy. This study recruited 396 lung cancer patients receiving chemotherapy between May and December 2023. Participants completed the Sleep Hygiene Index, Brief Fatigue Inventory, and Dysfunctional Beliefs and Attitudes about Sleep Scale. Latent profile analysis (LPA) was conducted to identify profiles of sleep hygiene, and mediation analysis was performed to explore the impacts of sleep hygiene profiles and dysfunctional sleep beliefs on CRF. LPA revealed three distinct sleep hygiene profiles: normal (33.3%), excellent (50.3%), and poor (16.4%). Family monthly disposable income, radiotherapy, and performance status were identified as influential factors distinguishing these profiles. Additionally, the dimensions of dysfunctional sleep beliefs and sleep hygiene profiles showed different correlations with CRF. With the normal sleep hygiene group as reference, mediation analysis revealed that poor sleep hygiene serves as a mediator between sleep worry of dysfunctional sleep beliefs and CRF (SE = 0.010, 95% CI [0.006, 0.047]). This study contributes to understanding the heterogeneity in sleep hygiene in lung cancer patients undergoing chemotherapy and elucidates the underlying mechanisms of the relationship between sleep worry of dysfunctional cognitions and CRF. Clinical healthcare providers developing targeted interventions in terms of sleep beliefs and sleep hygiene might be helpful to alleviate CRF in this population. Show less

Low physical activity (LPA) significantly heightens the susceptibility of both type 2 diabetes mellitus (T2DM) and chronic renal disease. Nearly half of population diagnosed with T2DM globally worsen into diabetic kidney disease (DKD). Focusing on physically inactive populations, we aimed to comprehensively evaluate the trends over time and regional changes in T2DM-associated DKD attributable to LPA burden. We utilized data of the 2021 Global Burden of Disease (GBD) Study to initially assess the worldwide effects of T2DM-associated DKD attributable to LPA by computing the numbers and age-standardized rates (ASRs) of death, disability-adjusted life years (DALYs), years of life lost (YLLs), and years lived with disability (YLDs), categorized by subtypes in 2021. Linear regression model was applied to analyze the illness burden from 1990 to 2021. Furthermore, cluster analysis was performed to assess the regional differences in disease burden across GBD regions. Lastly, to forecast the illness burden for the next 25 years, we utilized the autoregressive Integrated Moving Average (ARIMA) and Excess Risk (ER) models. In 2021, the fatalities attributed to T2DM-related DKD attributable to LPA amounted to 30835 (95%UI: 12346-51646) cases, with 698484 (95%UI: 275039-1158032) DALYs. The ASRs of death and DALYs were 0.38 (95%UI: 0.15-0.63) and 8.19 (95%UI: 3.21-13.6) per 100000 individuals, respectively. Between 1990 and 2021, there was a notable escalation in deaths, DALYs, YLDs, and YLLs, as well as their ASRs. The highest burden was observed among males, older adults (aged 70 years and above), and middle Socio-demographic Index (SDI). Significant differences were noted in the disease burden among various regions and countries as defined by the GBD study. Predictive analyses indicate a continued escalation of this burden by the year 2050. The global impact of DKD attributable to LPA remains considerable, with significant disparities noted across different genders, ages, and regions. To mitigate this burden, it is crucial to implement effective interventions aimed at addressing physical inactivity, specifically designed for targeted demographic groups. Show less