Disulfide bond network crosslinked flexible multifunctional chitosan coating on fabric surface prepared by the chitosan grafted with thioctic acid.

In this study, we propose a novel approach to improve the performance of chitosan coating, and thioctic acid with disulfide bonds in its molecular structure was grafted onto the side groups of chitosan macromolecules. The introduction of disulfide bond network cross-linking structure in chitosan coating weakens hydrogen bonds between chitosan macromolecules, causing the macromolecular chains to be more prone to relative motion when subjected to external forces, ultimately improving flexibility of the coating. The modified chitosan becomes more suitable for antibacterial modification in smart wearable fabrics. Subsequently, we fabricated a smart wearable fabric with excellent antibacterial properties and strong electromagnetic shielding by employing the layer-by-layer spraying technique. This involved incorporating chitosan with disulfide bonds and MXene nanoparticles. The fabric surfaces containing chitosan with disulfide bonds exhibited enhanced flexibility compared to unmodified chitosan fabric, resulting in an 8-point improvement in tactile sensation ratings. This research presents a novel approach that simultaneously enhances the electromagnetic shielding effectiveness and efficient antibacterial properties of smart wearable textiles. Consequently, it advances the application of chitosan in the field of antibacterial finishing for functional textiles.

Alteration of Thyroid Hormones in Mouse Models of Alzheimer's Disease and Aging.

INTRODUCTION: Aging is characterized by the deterioration of a wide range of functions in tissues and organs, and Alzheimer's disease (AD) is a neurodegenerative disease characterized by cognitive impairment. Hypothyroidism occurs when there is insufficient production of thyroid hormones (THs) by the thyroid. The relationship between hypothyroidism and aging as well as AD is controversial at present. METHODS: We established an animal model of AD (FAD4T) with mutations in the APP and PSEN1 genes, and we performed a thyroid function test and RNA sequencing (RNA-Seq) of the thyroid from FAD4T and naturally aging mice. We also studied gene perturbation correlation in the FAD4T mouse thyroid, bone marrow, and brain by further single-cell RNA sequencing (scRNA-seq) data of the bone marrow and brain. RESULTS: In this study, we found alterations in THs in both AD and aging mice. RNA-seq data showed significant upregulation of T-cell infiltration- and cell proliferation-related genes in FAD4T mouse thyroid. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that upregulated genes were enriched in the functional gene modules of activation of immune cells. Downregulated energy metabolism-related genes were prominent in aging thyroids, which reflected the reduction in THs. GSEA showed a similar enrichment tendency in both mouse thyroids, suggesting their analogous inflammation state. In addition, the regulation of leukocyte activation and migration was a common signature between the thyroid, brain, and bone marrow of FAD4T mice. CONCLUSIONS: Our findings identified immune cell infiltration of the thyroid as the potential underlying mechanism of the alteration of THs in AD and aging.

Resting-state EEG Microstate Features Can Quantitatively Predict Autistic Traits in Typically Developing Individuals.

Autism spectrum disorder (ASD) is not a discrete disorder and that symptoms of ASD (i.e., so-called "autistic traits") are found to varying degrees in the general population. Typically developing individuals with sub-clinical yet high-level autistic traits have similar abnormities both in behavioral performances and cortical activation patterns to individuals diagnosed with ASD. Thus it's crucial to develop objective and efficient tools that could be used in the assessment of autistic traits. Here, we proposed a novel machine learning-based assessment of the autistic traits using EEG microstate features derived from a brief resting-state EEG recording. The results showed that: (1) through the Least Absolute Shrinkage and Selection Operator (LASSO) algorithm and correlation analysis, the mean duration of microstate class D, the occurrence rate of microstate class A, the time coverage of microstate class D and the transition rate from microstate class B to D were selected to be crucial microstate features which could be used in autistic traits prediction; (2) in the support vector regression (SVR) model, which was constructed to predict the participants' autistic trait scores using these four microstate features, the out-of-sample predicted autistic trait scores showed a significant and good match with the self-reported scores. These results suggest that the resting-state EEG microstate analysis technique can be used to predict autistic trait to some extent.

Blocking Metal Nanocluster Growth through Ligand Coordination and Subsequent Polymerization: The Case of Ruthenium Nanoclusters as Robust Hydrogen Evolution Electrocatalysts.

Metal nanoclusters providing maximized atomic surface exposure offer outstanding hydrogen evolution activities but their stability is compromised as they are prone to grow and agglomerate. Herein, a possibility of blocking metal ion diffusion at the core of cluster growth and aggregation to produce highly active Ru nanoclusters supported on an N, S co-doped carbon matrix (Ru/NSC) is demonstrated. To stabilize the nanocluster dispersion, Ru species are initially coordinated through multiple Ru─N bonds with N-rich 4'-(4-aminophenyl)-2,2:6',2''-terpyridine (TPY-NH2 ) ligands that are subsequently polymerized using a Schiff base. After the pyrolysis of the hybrid composite, highly dispersed ultrafine Ru nanoclusters with an average size of 1.55 nm are obtained. The optimized Ru/NSC displays minimal overpotentials and high turnover frequencies, as well as robust durability both in alkaline and acidic electrolytes. Besides, outstanding mass activities of 3.85 A mg-1 Ru at 50 mV, i.e., 16 fold higher than 20 wt.% Pt/C are reached. Density functional theory calculations rationalize the outstanding performance by revealing that the low d-band center of Ru/NSC allows the desorption of *H intermediates, thereby enhancing the alkaline HER activity. Overall, this work provides a feasible approach to engineering cost-effective and robust electrocatalysts based on carbon-supported transition metal nanoclusters for future energy technologies.

Multifocal leukoencephalopathy in a patient medicated with etanercept and methotrexate for rheumatoid arthritis.

Methotrexate (MTX) and etanercept are commonly used in the treatment of rheumatoid arthritis (RA). Several important adverse events, including central nervous system lesions, have been reported during RA treatment. Among them, MTX-induced leukoencephalopathy is a recognized complication that is often observed following intrathecal or intravenous MTX administration. Herein, we report a case of a RA patient who was diagnosed with multifocal leukoencephalopathy during etanercept and MTX therapy. A 77-year-old Chinese woman with a 3-year history of RA had been taking subcutaneous etanercept and low-dose oral MTX since February 2021. Five months after the initial administration, she developed cognitive impairment and experienced a dropped attack. She was then admitted to our hospital in June 2021. T2-weighted magnetic resonance imaging (MRI) images revealed disseminated lesions in the white matter of the brain. Based on these MRI findings and extensive clinical investigation that excluded other possible causes of white matter lesions, she was suspected of having a demyelinating disorder. There was no evidence suggesting other neurological disorders. High-dose corticosteroid was administered, which resulted in improved cognitive impairment. This case report illustrates an important example of multifocal leukoencephalopathy induced by the combined use of etanercept and MTX, which resolved with high-dose corticosteroid. With the recent emphasis on various biologic agents for treatment of RA, our case highlights the importance of identifying leukoencephalopathy that may be induced by various biologics.

CK1δ and CK1ε Signaling Sustains Mitochondrial Metabolism and Cell Survival in Multiple Myeloma.

Multiple myeloma remains an incurable malignancy due to acquisition of intrinsic programs that drive therapy resistance. Here we report that casein kinase-1δ (CK1δ) and CK1ε are therapeutic targets in multiple myeloma that are necessary to sustain mitochondrial metabolism. Specifically, the dual CK1δ/CK1ε inhibitor SR-3029 had potent in vivo and ex vivo anti-multiple myeloma activity, including against primary multiple myeloma patient specimens. RNA sequencing (RNA-seq) and metabolic analyses revealed inhibiting CK1δ/CK1ε disables multiple myeloma metabolism by suppressing genes involved in oxidative phosphorylation (OxPhos), reducing citric acid cycle intermediates, and suppressing complexes I and IV of the electron transport chain. Finally, sensitivity of multiple myeloma patient specimens to SR-3029 correlated with elevated expression of mitochondrial genes, and RNA-seq from 687 multiple myeloma patient samples revealed that increased CSNK1D, CSNK1E, and OxPhos genes correlate with disease progression and inferior outcomes. Thus, increases in mitochondrial metabolism are a hallmark of multiple myeloma progression that can be disabled by targeting CK1δ/CK1ε. SIGNIFICANCE: CK1δ and CK1ε are attractive therapeutic targets in multiple myeloma whose expression increases with disease progression and connote poor outcomes, and that are necessary to sustain expression of genes directing OxPhos.

Modulating the polyamine/hypusine axis controls generation of CD8+ tissue-resident memory T cells.

Glutaminolysis is a hallmark of the activation and metabolic reprogramming of T cells. Isotopic tracer analyses of antigen-activated effector CD8+ T cells revealed that glutamine is the principal carbon source for the biosynthesis of polyamines putrescine, spermidine, and spermine. These metabolites play critical roles in activation-induced T cell proliferation, as well as for the production of hypusine, which is derived from spermidine and is covalently linked to the translation elongation factor eukaryotic translation initiation factor 5A (eIF5A). Here, we demonstrated that the glutamine/polyamine/hypusine axis controlled the expression of CD69, an important regulator of tissue-resident memory T cells (Trm). Inhibition of this circuit augmented the development of Trm cells ex vivo and in vivo in the BM, a well-established niche for Trm cells. Furthermore, blocking the polyamine/hypusine axis augmented CD69 expression as well as IFN-γ and TNF-α production in (a) human CD8+ T cells from peripheral blood and sarcoma tumor infiltrating lymphocytes and (b) human CD8+ CAR-T cells. Collectively, these findings support the notion that the polyamine-hypusine circuit can be exploited to modulate Trm cells for therapeutic benefit.

MoS2 @Polyaniline for Aqueous Ammonium-Ion Supercapacitors.

Ammonium-ion aqueous supercapacitors are raising notable attention owing to their cost, safety, and environmental advantages, but the development of optimized electrode materials for ammonium-ion storage still lacks behind expectations. To overcome current challenges, here, a sulfide-based composite electrode based on MoS2 and polyaniline (MoS2 @PANI) is proposed as an ammonium-ion host. The optimized composite possesses specific capacitances above 450 F g-1 at 1 A g-1 , and 86.3% capacitance retention after 5000 cycles in a three-electrode configuration. PANI not only contributes to the electrochemical performance but also plays a key role in defining the final MoS2 architecture. Symmetric supercapacitors assembled with such electrodes display energy densities above 60 Wh kg-1 at a power density of 725 W kg-1 . Compared with Li+ and K+ ions, the surface capacitive contribution in NH4 + -based devices is lower at every scan rate, which points to an effective generation/breaking of H-bonds as the mechanism controlling the rate of NH4 + insertion/de-insertion. This result is supported by density functional theory calculations, which also show that sulfur vacancies effectively enhance the NH4 + adsorption energy and improve the electrical conductivity of the whole composite. Overall, this work demonstrates the great potential of composite engineering in optimizing the performance of ammonium-ion insertion electrodes.

Programming inactive RNA-binding small molecules into bioactive degraders.

Target occupancy is often insufficient to elicit biological activity, particularly for RNA, compounded by the longstanding challenges surrounding the molecular recognition of RNA structures by small molecules. Here we studied molecular recognition patterns between a natural-product-inspired small-molecule collection and three-dimensionally folded RNA structures. Mapping these interaction landscapes across the human transcriptome defined structure-activity relationships. Although RNA-binding compounds that bind to functional sites were expected to elicit a biological response, most identified interactions were predicted to be biologically inert as they bind elsewhere. We reasoned that, for such cases, an alternative strategy to modulate RNA biology is to cleave the target through a ribonuclease-targeting chimera, where an RNA-binding molecule is appended to a heterocycle that binds to and locally activates RNase L1. Overlay of the substrate specificity for RNase L with the binding landscape of small molecules revealed many favourable candidate binders that might be bioactive when converted into degraders. We provide a proof of concept, designing selective degraders for the precursor to the disease-associated microRNA-155 (pre-miR-155), JUN mRNA and MYC mRNA. Thus, small-molecule RNA-targeted degradation can be leveraged to convert strong, yet inactive, binding interactions into potent and specific modulators of RNA function.

The Polyamine-Hypusine Circuit Controls an Oncogenic Translational Program Essential for Malignant Conversion in MYC-Driven Lymphoma.

The MYC oncoprotein is activated in a broad spectrum of human malignancies and transcriptionally reprograms the genome to drive cancer cell growth. Given this, it is unclear if targeting a single effector of MYC will have therapeutic benefit. MYC activates the polyamine-hypusine circuit, which posttranslationally modifies the eukaryotic translation factor eIF5A. The roles of this circuit in cancer are unclear. Here we report essential intrinsic roles for hypusinated eIF5A in the development and maintenance of MYC-driven lymphoma, where the loss of eIF5A hypusination abolishes malignant transformation of MYC-overexpressing B cells. Mechanistically, integrating RNA sequencing, ribosome sequencing, and proteomic analyses revealed that efficient translation of select targets is dependent upon eIF5A hypusination, including regulators of G1-S phase cell-cycle progression and DNA replication. This circuit thus controls MYC's proliferative response, and it is also activated across multiple malignancies. These findings suggest the hypusine circuit as a therapeutic target for several human tumor types. SIGNIFICANCE: Elevated EIF5A and the polyamine-hypusine circuit are manifest in many malignancies, including MYC-driven tumors, and eIF5A hypusination is necessary for MYC proliferative signaling. Not-ably, this circuit controls an oncogenic translational program essential for the development and maintenance of MYC-driven lymphoma, supporting this axis as a target for cancer prevention and treatment. See related commentary by Wilson and Klein, p. 248. This article is highlighted in the In This Issue feature, p. 247.

The Relationship Between Psychological Flexibility and Depression, Anxiety and Stress: A Latent Profile Analysis.

Purpose: To explore the potential classification of psychological flexibility (PF) among Chinese college students, analyze whether there is group heterogeneity in PF, and discuss the differences in the latent profile of PF in the negative emotions of depression, anxiety, and stress. Methods: A total of 1769 college students were investigated using the Psychological Flexibility Questionnaire and Depression-Anxiety-Stress Self-rating Scale, and heterogeneity was tested by latent profile analysis. Results: The PF of college students can be divided into three latent profiles: self-contradiction group (19.2%), high PF group (34.1%), and low PF group (46.7%). The scores of depression, anxiety, and stress are significantly different among the groups. Conclusion: There is obvious group heterogeneity in the PF of college students, and they can be divided into the self-contradiction group, the high PF group, and the low PF group. The self-contradiction and low PF groups score significantly higher on the negative emotions of depression, anxiety, and stress than the high PF group.

Comparison of Autof Ms1000 and EXS3000 MALDI-TOF MS Platforms for Routine Identification of Microorganisms.

Purpose: Matrix-assisted laser desorption-ionization-time of flight mass spectrometry (MALDI-TOF) has recently been widely used in clinical microbiology laboratories, with the advantages of being reliable, rapid, and cost-effective. Here, we reported the performance of two MALDI-TOF MS instruments, EXS3000 (Zybio, China) and Autof ms1000 (Autobio, China), which are commonly used in clinical microbiology field. Methods: A total of 209 common clinical common isolates, including 70 gram-negative bacteria strains, 58 gram-positive bacteria strains, 33 yeast strains, 15 anaerobic bacteria strains, and 33 mold strains, and 19 mycobacterial strains were tested. All strains were identified by EXS3000 (Zybio, China) and Autof ms1000 (Autobio, China). Sequence analysis of 16S rRNA or ITS regions was used to verify all strains. Results: Current study found that species-level discrimination was found to be 191 (91.39%) and 190 (90.91%) by EXS3000 and Autof ms1000, respectively. Genus-level discrimination was 205 (98.09%) by the EXS3000 and 205 (98.09%) by the Autof ms1000, respectively. The correct results at species level of the EXS3000 were 91.43% (64/70) for gram-negative bacteria, 93.1% (54/58) for gram-positive cocci, 93.94% (31/33) for yeast, 100% (15/15) for anaerobes and 81.82% (27/33) for filamentous fungi. The correct results at species level of the Autof ms1000 were 92.86% (65/70) for gram-negative bacteria, 91.38% (53/58) for gram-positive cocci, 93.94% (31/33) for yeast, 100% (15/15) for anaerobes and 78.79% (26/33) for filamentous fungi. Conclusion: Although the results show that the EXS3000 and Autof ms1000 systems are equally good choices in terms of analytical efficiency for routine procedures, the test result of EXS3000 is slightly better than Autof ms1000. It's worth mentioning that the target plate of the EXS 3000 instrument is reusable, but the target plate of the Autof ms1000 is disposable, making the EXS3000 more effective in reducing costs.

TCR-Independent Metabolic Reprogramming Precedes Lymphoma-Driven Changes in T-cell Fate.

Chronic T-cell receptor (TCR) signaling in the tumor microenvironment is known to promote T-cell dysfunction. However, we reasoned that poorly immunogenic tumors may also compromise T cells by impairing their metabolism. To address this, we assessed temporal changes in T-cell metabolism, fate, and function in models of B-cell lymphoma driven by Myc, a promoter of energetics and repressor of immunogenicity. Increases in lymphoma burden most significantly impaired CD4+ T-cell function and promoted regulatory T cell (Treg) and Th1-cell differentiation. Metabolomic analyses revealed early reprogramming of CD4+ T-cell metabolism, reduced glucose uptake, and impaired mitochondrial function, which preceded changes in T-cell fate. In contrast, B-cell lymphoma metabolism remained robust during tumor progression. Finally, mitochondrial functions were impaired in CD4+ and CD8+ T cells in lymphoma-transplanted OT-II and OT-I transgenic mice, respectively. These findings support a model, whereby early, TCR-independent, metabolic interactions with developing lymphomas limits T cell-mediated immune surveillance.

Single-cell transcriptomics identifies premature aging features of TERC-deficient mouse brain and bone marrow.

Aging is a progressive loss of physiological function and increased susceptibility to major pathologies. Degenerative diseases in both brain and bone including Alzheimer disease (AD) and osteoporosis are common in aging groups. TERC is RNA component of telomerase, and its deficiency accelerates aging-related phenotypes including impaired life span, organ failure, bone loss, and brain dysfunction. In this study, we investigated the traits of bone marrow-brain cross-tissue communications in young mice, natural aging mice, and premature aging (TERC deficient, TERC-KO) mice by single-cell transcriptome sequencing. Differentially expressed gene analysis of brain as well as bone marrow between premature aging mouse and young mouse demonstrated aging-related inflammatory response and suppression of neuron development. Further analysis of senescence-associated secretory phenotype (SASP) landscape indicated that TERC-KO perturbation was enriched in oligodendrocyte progenitor cells (OPCs) and hematopoietic stem and progenitor cells (HSPC). Series of inflammatory associated myeloid cells was activated in premature aging mice brain and bone marrow. Cross-tissue comparison of TERC-KO mice brain and bone marrow illustrated obvious ligand-receptor communications between brain glia cells, macrophages, and bone marrow myeloid cells in premature aging-induced inflammation. Enrichment of co-regulation modules between brain and bone marrow identified premature aging response genes such as Dusp1 and Ifitm3. Our study provides a rich resource for understanding premature aging-associated perturbation in brain and bone marrow and supporting myeloid cells and endothelial cells as promising therapy targeting for age-related brain-bone diseases.

Asymmetric Hydrophosphonylation of Imines to Construct Highly Stable Covalent Organic Frameworks with Efficient Intrinsic Proton Conductivity.

Imine-linked covalent organic frameworks (COFs) have received widespread attention because of their structure features such as high crystallinity and tunable pores. However, the intrinsic reversibility of the imine bond leads to the poor stability of imine-linked COFs under strong acid conditions. Also, their thermal stability is significantly lower than that of many other COFs. Herein, we report for the first time that the reversible imine bonds in the skeleton of COFs can be locked through the asymmetric hydrophosphonylation reaction of phosphite. The functionalized COFs not only retain the crystallinity and porous structure but also exhibit evidently improved chemical and thermal stabilities. In addition, the phosphorous acid groups generated by acidic hydrolysis attached to the skeleton endow the COFs with good intrinsic proton conductivity. Due to the diversity of phosphite derivatives and imine-linked COFs, this work may provide an avenue for extending the COF structures and functions through the asymmetric hydrophosphonylation reaction.

Phosphorylation of MAD2 at Ser195 Promotes Spindle Checkpoint Defects and Sensitizes Cancer Cells to Radiotherapy in ATM Deficient Cells.

The spindle assembly checkpoint (SAC) is a critical monitoring device in mitosis for the maintenance of genomic stability. Specifically, the SAC complex comprises several factors, including Mad1, Mad2, and Bub1. Ataxia-telangiectasia mutated (ATM) kinase, the crucial regulator in DNA damage response (DDR), also plays a critical role in mitosis by regulating Mad1 dimerization and SAC. Here, we further demonstrated that ATM negatively regulates the phosphorylation of Mad2, another critical component of the SAC, which is also involved in DDR. Mechanistically, we found that phosphorylation of Mad2 is aberrantly increased in ATM-deficient cells. Point-mutation analysis further revealed that Serine 195 mainly mediated Mad2 phosphorylation upon ATM ablation. Functionally, the phosphorylation of Mad2 causes decreased DNA damage repair capacity and is related to the resistance to cancer cell radiotherapy. Altogether, this study unveils the key regulatory role of Mad2 phosphorylation in checkpoint defects and DNA damage repair in ATM-deficient cells.

Disrupting the MYC-TFEB Circuit Impairs Amino Acid Homeostasis and Provokes Metabolic Anergy.

MYC family oncoproteins are regulators of metabolic reprogramming that sustains cancer cell anabolism. Normal cells adapt to nutrient-limiting conditions by activating autophagy, which is required for amino acid (AA) homeostasis. Here we report that the autophagy pathway is suppressed by Myc in normal B cells, in premalignant and neoplastic B cells of Eµ-Myc transgenic mice, and in human MYC-driven Burkitt lymphoma. Myc suppresses autophagy by antagonizing the expression and function of transcription factor EB (TFEB), a master regulator of autophagy. Mechanisms that sustained AA pools in MYC-expressing B cells include coordinated induction of the proteasome and increases in AA transport. Reactivation of the autophagy-lysosomal pathway by TFEB disabled the malignant state by disrupting mitochondrial functions, proteasome activity, AA transport, and AA and nucleotide metabolism, leading to metabolic anergy, growth arrest, and apoptosis. This phenotype provides therapeutic opportunities to disable MYC-driven malignancies, including AA restriction and treatment with proteasome inhibitors. SIGNIFICANCE: MYC suppresses TFEB and autophagy and controls amino acid homeostasis by upregulating amino acid transport and the proteasome, and reactivation of TFEB disables the metabolism of MYC-driven tumors.

Analyzing the role of family support, coping strategies and social support in improving the mental health of students: Evidence from post COVID-19.

Background: The COVID-19 pandemic and the multifaceted response strategies to curb its spread both have devastating effects on mental and emotional health. Social distancing, and self-isolation have impacted the lives of students. These impacts need to be identified, studied, and handled to ensure the well-being of the individuals, particularly the students. Aim: This study aims to analyze the role of coping strategies, family support, and social support in improving the mental health of the students by collecting evidence from post COVID-19. Methods: Data was collected from deaf students studying in Chinese universities of Henan Province, China. A survey questionnaire was designed to collect data from 210 students. Descriptive statistics were calculated using SPSS 21 while hypothesis testing was carried out using Mplus 7. Results: The results demonstrated that family support was strongly positively linked to mental health and predicted coping strategies. The direct relationship analysis showed that coping strategy strongly predicted mental health. Furthermore, coping strategies significantly mediated the relationship between family support and mental health. Additionally, the results highlighted that PSS significantly moderated the path of family support and coping strategies only. Conclusion: Family support and coping strategies positively predicted mental health, whereas, family support was also found to be positively associated with coping strategies. Coping strategies mediated the positive association between family support and mental health. However, perceived family and other support only moderated the relationship between family support and coping strategies.

Population-Based Survival Analysis of Patients With Limb Rhabdomyosarcoma and Metastasis at Diagnosis.

Purpose: Given the poor prognosis and the relative rarity of patients diagnosed with limb rhabdomyosarcoma (LRMS) and metastasis at diagnosis, we performed this study to reveal distinctive clinical features and evaluated prognostic factors of this special population in order to provide appropriate treatment. Patients and Methods: We carried out retrospective research of patients diagnosed with LRMS and metastasis from 1975 to 2016 using the Surveillance, Epidemiology, and End Results (SEER) program database. Survival curves were generated by applying the Kaplan-Meier method. In terms of evaluating and determining independent predictors of survival, we conducted univariate and multivariate survival analyses using the Cox proportional hazard regression model. Results: This retrospective analysis contained a series of 245 patients with metastatic LRMS, with male predominance (male vs. female, 1.6:1). Nearly half of the patients were diagnosed with alveolar rhabdomyosarcoma (44.9%). According to the results of the univariate and multivariate analyses, younger age, tumor subtype, and radiotherapy were found to be significantly associated with improved overall survival (OS) and cause-specific survival (CSS). Conclusions: Patients with LRMS and metastasis at diagnosis experienced a quite poor prognosis. Age at diagnosis, tumor subtype, and radiotherapy can help clinicians to better estimate the prognosis. This study indicated that local radiotherapy can provide a survival benefit.