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PREMISE: Endophytic and mycorrhizal fungi are crucial in facilitating plant nutrition acquisition and stress tolerance. In epiphytic habitats, plants face nutrition and water stress, but their roots are mostly nonmycorrhizal and especially lacking in arbuscular mycorrhizal associations. Ophioderma pendulum is an epiphytic fern with a partially mycoheterotrophic lifestyle, likely heavily reliant on symbiotic fungi. To characterize fungal associations in the sporophyte of O. pendulum, we focused on leaves and roots of O. pendulum, seeking to reveal the fungal communities in these organs. METHODS: Roots and leaves from O. pendulum in a subtropical forest were examined microscopically to observe the morphology of fungal structures and determine the percentage of various fungal structures in host tissues. Fungal composition was profiled using metabarcoding techniques that targeted ITS2 of the nuclear ribosomal DNA. RESULTS: Roots were consistently colonized by arbuscular mycorrhizal fungi (Glomeromycota), especially Acaulospora. Unlike previous findings on epiphytic ferns, dark septate endophytes were rare in O. pendulum roots. Leaves were predominantly colonized by Ascomycota fungi, specifically the classes Dothideomycetes (46.88%), Eurotiomycetes (11.51%), Sordariomycetes (6.23%), and Leotiomycetes (6.14%). Across sampling sites, fungal community compositions were similar in the roots but differed significantly in the leaves. CONCLUSIONS: Ophioderma pendulum maintains stable, single-taxon-dominant communities in the roots, primarily featuring arbuscular mycorrhizal fungi, whereas the leaves may harbor opportunistic fungal colonizers. Our study underlines the significance of mycorrhizal fungi in the adaptation of epiphytic ferns.
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A redox-neutral copper-catalyzed cascade reaction involving alkoxyl radical-mediated ring expansion/1,4-difunctionalization of 1,3-enynes was developed, offering a straightforward approach to the tetra-substituted allenes with macrolactone, CN, and CF3 functional groups. Remarkably, incorporation of the NH2 group onto the 1,3-enyne moiety enabled further cyclization to give a unique scaffold containing a lactone and an indole moiety.
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ß-hydroxybutyrate (ß-HB), the most abundant ketone body, is produced primarily in the liver and acts as a substitute energy fuel to provide energy to extrahepatic tissues in the event of hypoglycemia or glycogen depletion. We now have an improved understanding of ß-HB as a signal molecule and epigenetic regulatory factor as a result of intensive research over the last ten years. Because ß-HB regulates various physiological and pathological processes, it may have a potential role in the treatment of metabolic diseases. The liver is the most significant metabolic organ, and the part that ß-HB plays in liver disorders is receiving increasing attention. In this review, we summarize the therapeutic effects of ß-HB on liver diseases and its underlying mechanisms of action. Moreover, we explore the prospects of exogenous supplements and endogenous ketosis including fasting, caloric restriction (CR), ketogenic diet (KD), and exercise as adjuvant nutritional therapies to protect the liver from damage and provide insights and strategies for exploring the treatment of various liver diseases.
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Dieta Cetogênica , Cetose , Hepatopatias , Humanos , Ácido 3-Hidroxibutírico/metabolismo , Corpos Cetônicos/metabolismo , Hepatopatias/tratamento farmacológicoRESUMO
Hepatectomy is currently considered the most effective option for treating patients with early and intermediate hepatocellular carcinoma (HCC). Unfortunately, the postoperative prognosis of patients with HCC remains unsatisfactory, predominantly because of high postoperative metastasis and recurrence rates. Therefore, research on the molecular mechanisms of postoperative HCC metastasis and recurrence will help develop effective intervention measures to prevent or delay HCC metastasis and recurrence and to improve the long-term survival of HCC patients. Herein, we review the latest research progress on the molecular mechanisms underlying postoperative HCC metastasis and recurrence to lay a foundation for improving the understanding of HCC metastasis and recurrence and for developing more precise prevention and intervention strategies.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/patologia , Recidiva Local de Neoplasia/prevenção & controle , Prognóstico , Hepatectomia/efeitos adversos , Estudos RetrospectivosRESUMO
Circular RNAs (circRNAs) have covalently closed loop structures at both ends, exhibiting characteristics dissimilar to those of linear RNAs. Emerging evidence suggests that aberrantly expressed circRNAs play crucial roles in hepatocellular carcinoma (HCC) by affecting the proliferation, apoptosis and invasive capacity of HCC cells. Certain circRNAs may be used as biomarkers to diagnose and predict the prognosis of HCC. Therefore, circRNAs are expected to become novel biomarkers and therapeutic targets for HCC. Herein, we briefly review the characteristics and biological functions of circRNAs, focusing on their roles in HCC to provide new insights for the early diagnosis and targeted therapy of HCC.
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INTRODUCTION: Adipose tissue deposited on the viscera is the main culprit in the development of insulin resistance (IR) and cardiometabolic diseases, whereas subcutaneous adipose tissue may have a protective role. This study aimed to propose a new predictive index - the visceral-fat area (VFA)-to-hip-circumference ratio (VHR) and explore its efficacy for prediction of IR in a Chinese population with type 2 diabetes mellitus. METHODS: A total of 643 patients with newly diagnosed diabetes were enrolled in this study. Body composition, anthropometrical, and biochemical measurements were performed. IR was defined as homeostatic model assessment of IR (HOMA-IR) > 2.69. The association between VHR and IR was analyzed. RESULTS: Regardless of gender, subjects in the IR group had higher VHR, body mass index (BMI), VFA, body fat percentage, systolic blood pressure, diastolic blood pressure (DBP), fasting blood glucose, fasting insulin, triglyceride (TG), uric acid (UA), homocysteine, and aminotransferases than those in the non-IR group. The other concomitant metabolic disorders were more common in the IR group. Further analysis showed that with the increase of VHR, the levels of HOMA-IR, BMI, VFA, DBP, TG, UA and the prevalence of nonalcoholic fatty-liver disease, hypertension, and hyperuricemia increased continuously (p trend <0.01). The linear trend test showed that VHR and IR remained closely correlated after adjusting for possible confounders (p trend <0.05). The receiver operating characteristic curve analysis showed that the area under the curve was 0.69, and the optimal cutoff of VHR was 0.89 (sensitivity 79.3%, specificity 61.5%). CONCLUSION: VHR was positively associated with IR regardless of gender, and it might be a reliable predictor for IR.
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Diabetes Mellitus Tipo 2 , Resistência à Insulina , Índice de Massa Corporal , China/epidemiologia , Humanos , Insulina , Gordura Intra-Abdominal/metabolismo , TriglicerídeosRESUMO
OBJECTIVES: To explore the prevalence and risk factors of metabolic-associated fatty liver disease (MAFLD) in Tianjin government employees of different genders. DESIGN: Cross-sectional study. SETTING: Health Management Center of Tianjin Union Medical Center. PARTICIPANTS: 16 924 government employees (59.6% male). MEASURES: Ultrasound liver examination was performed to determine whether there is fat accumulation in the organ. Participants' weight and height were measured, and body mass index (BMI) was calculated. RESULTS: The overall prevalence of MAFLD in this population was 40.76%. The rates were significantly higher in men (49.42%) than in women (27.97%). The prevalence of MAFLD was highest in men aged 40-49 years (54.04%) and women aged 60-69 years (43.44%). In all BMI groups, the prevalence was higher in men than that in women. In both genders, higher BMI was associated with the risk of MAFLD, especially for BMI ≥31.9 kg/m2. CONCLUSIONS: The prevalence of MAFLD in government employees in Tianjin was significantly higher than the average level in China. The prevalence varied by sex and age group, and those with high BMI were at the highest risk of developing MAFLD.
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Empregados do Governo , Hepatopatia Gordurosa não Alcoólica , Adulto , Idoso , China/epidemiologia , Estudos Transversais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/diagnóstico , PrevalênciaRESUMO
OBJECTIVE: To establish a radiomics signature and a nomogram model based on enhanced CT images to predict the Ki-67 index of lung cancer. METHODS: From January 2014 to December 2018, 282 patients with lung cancer who had undergone enhanced CT scans and Ki-67 examination within 2 weeks were retrospectively enrolled and analyzed. The clinical data of the patients were collected, such as age, sex, smoking history, maximum tumor diameter and serum tumor markers. Our primary cohort was randomly divided into a training group (n=197) and a validation group (n=85) at a 7:3 ratio. A Ki-67 index ≤ 40% indicated low expression, and a Ki-67 index > 40% indicated high expression. In total, 396 radiomics features were extracted using AK software. Feature reduction and selection were performed using the lasso regression model. Logistic regression analysis was used to establish a multivariate predictive model to identify high and low Ki-67 expression in lung cancer. A nomogram integrating the radiomics score was established based on multiple logistic regression analysis. Area under the curve (AUC) was used to evaluate the prediction efficiency of the radiomics signature and nomogram. RESULTS: The AUC,sensitivity, specificity and accuracy of the radiomics signature in the training and validation groups were 0.88 (95% CI: 0.82~0.93),79.2%,84.3%,81.2% and 0.86 (95% CI: 0.78~0.94),74.6%,88.1%,79.8%, respectively. A nomogram combining radiomics features and clinical risk factors (smoking history and NSE) was developed. The AUC, sensitivity, specificity and accuracy were 0.87 (95% CI: 0.80~0.95), 75.0%, 90.2% and 83.5% in the validation group, respectively. CONCLUSION: The radiomics signature and nomogram based on enhanced CT images provide a way to predict the Ki-67 expression level in lung cancer.
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Fungal members of Colletotrichum (Ascomycota) were found to be associated with Chordodesformosanus, one of the three currently known horsehair worm (Nematomorpha) species in Taiwan. The fungi were identified as Colletotrichumfructicola, which is mostly known as a plant pathogen, through the use of the nuclear ribosomal internal transcribed spacer and partial large subunit (nrITS + nrLSU) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) DNA sequences. To our knowledge, this report represents both the first records for Colletotrichum associated with hairworms and for fungi on Nematomorpha. These findings expand the knowledge on the ecological relationships of both clades.
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Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are noncoding RNAs (ncRNAs) that occupy over 90% of the human genome, and their main function is to directly or indirectly regulate messenger RNA (mRNA) expression and participate in the tumorigenesis and progression of malignances. In particular, some lncRNAs can interact with miRNAs as competing endogenous RNAs (ceRNAs) to modulate mRNA expression. Accordingly, these RNA molecules are interrelated and coordinate to form a dynamic lncRNA-mediated ceRNA regulatory network. Mounting evidence has revealed that lncRNAs that act as ceRNAs are closely related to tumorigenesis. To date, numerous studies have established many different regulatory networks in hepatocellular carcinoma (HCC), and perturbations in these ceRNA interactions may result in the initiation and progression of HCC. Herein, we emphasize recent advances concerning the biological function of lncRNAs as ceRNAs in HCC, with the aim of elucidating the molecular mechanism underlying these HCC-related RNA molecules and providing novel insights into the diagnosis and treatment of HCC.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , MicroRNAs , RNA Longo não Codificante , Carcinoma Hepatocelular/genética , Regulação Neoplásica da Expressão Gênica , Redes Reguladoras de Genes , Humanos , Neoplasias Hepáticas/genética , RNA Longo não Codificante/genéticaRESUMO
As one of the air pollution transmission channels around the beijing-Tianjin-Hebei region, Puyang frequently suffer from severe airpollution in autumn and winter. In order to study the characteristics and main sources of fine particulate matter during these periods, manual membrane sampling of PM2.5 was conducted at three national control sites from October 15, 2017, to January 13, 2018. Chemical composition analysis was conducted and, combined with a PMF receptor model, source analysis of the fine particles was also undertaken. The results show that the average mass concentration of PM2.5 in Puyang was 94.16 µg·m-3 in the autumn and winter of 2017, and Pushuihe station was the most polluted site. During the heating season, the three control stations all recorded the frequent occurrence of severe and serious pollution events, while the frequency of mild pollution events decreased. When heavy pollution events occurred, the concentrations of NO2 and CO increased significantly. The main components of PM2.5 were water-soluble ions (52.33%), OCEC (25.32%), and crustal elements (0.08%). The concentrations of NO3- were high while the concentrations of SO42- were low. When heavy pollution occurred, the concentrations of water-soluble ions, OC, EC, and K in PM2.5 increased significantly, while the concentrations of crustal elements decreased. During the sampling period, the conversion ratios of sulfur and nitrogen in Puyang were high and atmospheric oxidation was strong. The transformation of sulfur and nitrogen promoted the occurrence of heavy pollution. Emissions of NOx, CO, and VOCs were higher in Puyang in 2017, and the source apportionment results showed that the main sources of PM2.5 in autumn and winter were secondary inorganic salts (37%), industrial sources (16%), secondary organic aerosol (SOA, 14%), biomass combustion (12%), mobile sources (9%), coal burning (7%), and dust (4%). Secondary transformation played an important role in the development of heavy pollution events in Puyang. It is necessary to focus on the control of emissions from industrial sources, biomass combustion, moving source, and civil coal combustion.
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A novel modified polyoxometalate, {PMo12O40[Cu(2,2'-bpy)]}[Cu(2,2'-bpy)(en)(H2O)]2 [2,2'-bpy is 2,2'-bipyridyl (C10H8N2) and en is ethylenediamine (C2H8N2)], has been synthesized hydrothermally and structurally characterized by elemental analysis, TG, IR, XPS and single-crystal X-ray diffraction. The structural analysis reveals that the compound contains the reduced Keggin polyanion [PMo12O40]6- as the parent unit, which is monocapped by [Cu(2,2'-bpy)]2+ fragments via four bridging O atoms on an {Mo4O4} pit and bi-supported by two [Cu(2,2'-bpy)(en)(H2O)]2+ coordination cations simultaneously. There exist strong intramolecular π-π stacking between the capping and supporting units, which play a stabilizing role during the crystallization of the compound. Adjacent POM clusters are further aggregated to form a three-dimensional supramolecular network through noncovalent forces, hydrogen bonding and π-π stacking interactions. In addition, the photocatalytic properties were investigated in detail, and the results indicated that the compound can be used as a photocatalyst towards the decomposition of the organic pollutant methylene blue (MB).
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OBJECTIVE: To study the clinical features of nephrotic syndrome (NS) accompanied by eosinophilia in children. METHODS: A retrospective analysis was performed for the clinical manifestations, laboratory findings and treatment outcomes of 18 cases of eosinophilia (15 children, 3 of whom also had eosinophilia at the second recurrence) in children with NS. RESULTS: Of the 18 cases, 16 (89%) had mild eosinophilia, 1 (6%) had moderate eosinophilia, and 1 (6%) had severe eosinophilia. Twelve cases (67%) developed eosinophilia in winter and spring. Nine cases (50%) had infectious diseases: pneumonia (including 2 cases of Mycoplasma pneumonia) in 4 cases, EB virus infection in 3 cases, suspected pinworm infection in 1 case, and Streptococcal infection in 1 case. Five cases (28%) had allergic diseases: urticaria in 2 cases, allergic rhinitis in 2 cases and eczema in 1 case. There was no significant correlation between eosinophil count and the levels of urinary protein, serum albumin and cholesterol (P>0.05). In 8 cases of newly diagnosed NS, urinary protein turned negative within 4 weeks after glucocorticoid treatment. In 10 cases of recurrent NS, urinary protein turned negative in 9 cases after the adjustment of glucocorticoid treatment. In 1 case of recurrent NS (moderate eosinophilia with allergic rhinitis), symptomatic relief and negative urinary protein were achieved after anti-allergic treatment. Glucocorticoid therapy was not administered again in the patient, and the eosinophil count was reduced to a slight increase. The eosinophil counts of the other 17 cases returned to normal. CONCLUSIONS: NS with eosinophilia in children occurs mostly in winter and spring. This disorder is associated with infection or allergic diseases. There was no significant correlation between eosinophil count and the levels of urinary protein, serum albumin and cholesterol.
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Eosinofilia , Síndrome Nefrótica , Criança , Eosinófilos , Humanos , Contagem de Leucócitos , Estudos RetrospectivosRESUMO
The receptor tyrosine kinase Axl and its ligand Gas6 regulate fundamental biological processes, including cell proliferation, survival and motility, through multiple downstream signaling pathways. Evidence to date suggests that aberrant Axl expression frequently occurs in many malignancies, including hepatocellular carcinoma, and that this is critical for promoting cell proliferation, migration, angiogenesis and metastasis. Moreover, deregulated Axl expression or activation is reportedly associated with resistance to cancer drugs and targeted cancer therapies. Thus, Axl inhibitors may represent a novel therapeutic approach for cancer treatment. This Review summarizes the latest advances concerning the biological role of Axl in hepatocellular carcinoma and its potential clinical relevance.
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Carcinoma Hepatocelular/metabolismo , Neoplasias Hepáticas/metabolismo , Proteínas Proto-Oncogênicas/metabolismo , Receptores Proteína Tirosina Quinases/metabolismo , Animais , Biomarcadores Tumorais , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Suscetibilidade a Doenças , Regulação Neoplásica da Expressão Gênica , Humanos , Ligantes , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/patologia , Terapia de Alvo Molecular , Prognóstico , Ligação Proteica , Inibidores de Proteínas Quinases/farmacologia , Inibidores de Proteínas Quinases/uso terapêutico , Proteínas Proto-Oncogênicas/química , Proteínas Proto-Oncogênicas/genética , Receptores Proteína Tirosina Quinases/química , Receptores Proteína Tirosina Quinases/genética , Relação Estrutura-Atividade , Receptor Tirosina Quinase AxlRESUMO
Long non-coding RNAs (lncRNAs) are a subgroup of non-coding RNA transcripts greater than 200 nucleotides in length with little or no protein-coding potential. Emerging evidence indicates that lncRNAs may play important regulatory roles in the pathogenesis and progression of human cancers, including hepatocellular carcinoma (HCC). Certain lncRNAs may be used as diagnostic or prognostic markers for HCC, a serious malignancy with increasing morbidity and high mortality rates worldwide. Therefore, elucidating the functional roles of lncRNAs in tumors can contribute to a better understanding of the molecular mechanisms of HCC and may help in developing novel therapeutic targets. In this review, we summarize the recent progress regarding the functional roles of lncRNAs in HCC and explore their clinical implications as diagnostic or prognostic biomarkers and molecular therapeutic targets for HCC.
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Carcinoma Hepatocelular/genética , Epigênese Genética , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/genética , RNA Longo não Codificante/metabolismo , Antineoplásicos/uso terapêutico , Biomarcadores Tumorais/análise , Biomarcadores Tumorais/antagonistas & inibidores , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Carcinogênese/genética , Carcinoma Hepatocelular/diagnóstico , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/mortalidade , Progressão da Doença , Detecção Precoce de Câncer/métodos , Humanos , Neoplasias Hepáticas/diagnóstico , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/mortalidade , Terapia de Alvo Molecular/métodos , Prognóstico , RNA Longo não Codificante/análise , RNA Longo não Codificante/antagonistas & inibidores , RNA Longo não Codificante/genéticaRESUMO
The intriguing phenomenon of metal superelasticity relies on stress-induced martensitic transformation (SIMT), which is well-known to be governed by developing cooperative strain accommodation at multiple length scales. It is therefore scientifically interesting to see what happens when this natural length scale hierarchy is disrupted. One method is producing pillars that confine the sample volume to micrometer length scale. Here we apply yet another intervention, helium nanobubbles injection, which produces porosity on the order of several nanometers. While the pillar confinement suppresses superelasticity, we found the dispersion of 5-10 nm helium nanobubbles do the opposite of promoting superelasticity in a Ni53.5Fe19.5Ga27 shape memory alloy. The role of helium nanobubbles in modulating the competition between ordinary dislocation slip plasticity and SIMT is discussed.
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Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Although recent advances in therapeutic approaches for treating HCC have improved the prognoses of patients with HCC, this cancer is still associated with a poor survival rate mainly due to late diagnosis. Therefore, a diagnosis must be made sufficiently early to perform curative and effective treatments. There is a need for a deeper understanding of the molecular mechanisms underlying the initiation and progression of HCC because these mechanisms are critical for making early diagnoses and developing novel therapeutic strategies. Over the past decade, much progress has been made in elucidating the molecular mechanisms underlying hepatocarcinogenesis. In particular, recent advances in next-generation sequencing technologies have revealed numerous genetic alterations, including recurrently mutated genes and dysregulated signaling pathways in HCC. A better understanding of the genetic alterations in HCC could contribute to identifying potential driver mutations and discovering novel therapeutic targets in the future. In this article, we summarize the current advances in research on the genetic alterations, including genomic instability, single-nucleotide polymorphisms, somatic mutations and deregulated signaling pathways, implicated in the initiation and progression of HCC. We also attempt to elucidate some of the genetic mechanisms that contribute to making early diagnoses of and developing molecularly targeted therapies for HCC.
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Biomarcadores Tumorais/genética , Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , Animais , Biomarcadores Tumorais/metabolismo , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Transformação Celular Neoplásica/patologia , Regulação Neoplásica da Expressão Gênica , Predisposição Genética para Doença , Instabilidade Genômica , Humanos , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patologia , Técnicas de Diagnóstico Molecular , Terapia de Alvo Molecular , Mutação , Seleção de Pacientes , Fenótipo , Polimorfismo de Nucleotídeo Único , Medicina de Precisão , Valor Preditivo dos Testes , Transdução de SinaisRESUMO
Hepatocarcinogenesis in human chronic liver diseases is a multi-step process in which hepatic precancerous lesions progress into early hepatocellular carcinoma (HCC) and progressed HCC, and the close surveillance and treatment of these lesions will help improve the survival rates of patients with HCC. The rapid development and extensive application of imaging technology have facilitated the discovery of nodular lesions of ambiguous significance, such as dysplastic nodules. Further investigations showed that these nodules may be hepatic precancerous lesions, and they often appear in patients with liver cirrhosis. Although the morphology of these nodules is not sufficient to support a diagnosis of malignant tumor, these nodules are closely correlated with the occurrence of HCC, as indicated by long-term follow-up studies. In recent years, the rapid development and wide application of pathology, molecular genetics and imaging technology have elucidated the characteristics of precancerous lesions. Based on our extensive review of the relevant literature, this article focuses on evidence indicating that high-grade dysplastic nodules are more likely to transform into HCC than low-grade dysplastic nodules based on clinical, pathological, molecular genetic and radiological assessments. In addition, evidence supporting the precancerous nature of large cell change in hepatitis B virus-related HCC is discussed.
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Carcinoma Hepatocelular/patologia , Transformação Celular Neoplásica/patologia , Neoplasias Hepáticas/patologia , Lesões Pré-Cancerosas/patologia , Animais , Biomarcadores Tumorais/genética , Carcinoma Hepatocelular/diagnóstico por imagem , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/virologia , Transformação Celular Neoplásica/genética , Transformação Celular Viral , Hepatite B/complicações , Hepatite B/virologia , Humanos , Neoplasias Hepáticas/diagnóstico por imagem , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/virologia , Lesões Pré-Cancerosas/diagnóstico por imagem , Lesões Pré-Cancerosas/genética , Lesões Pré-Cancerosas/virologia , Prognóstico , Fatores de RiscoRESUMO
BACKGROUND: Thrombospondin-1 is a homotrimeric glycoprotein with well known functions in hemostasis and angiogenesis. Its expression was increased after experimental intracerebral hemorrhage. We determined whether increased plasma thrombospondin-1 concentrations are predictive of clinical outcomes of aneurysmal subarachnoid hemorrhage (aSAH). METHODS: Plasma thrombospondin-1 concentrations of 118 aSAH patients and 118 age- and gender-matched healthy controls were determined using enzyme-linked immunosorbent assay. Patients were followed up until death or completion of 6months after aSAH. An unfavorable outcome was defined as Glasgow Outcome Scale score of 1-3. Multivariate analyses of significant variables of univariate analyses were performed to determine independent risk factors for the clinical outcomes. RESULTS: Plasma thrombospondin-1 concentrations were significantly higher in aSAH patients than in healthy controls; plasma thrombospondin-1 concentrations were independently associated with clinical severity reflected by the World Federation of Neurological Surgeons score and Fisher score; thrombospondin-1 was identified as an independent predictor of 6-month mortality and 6-month unfavorable outcome; thrombospondin-1 had similar predictive performance compared with the World Federation of Neurological Surgeons score and Fisher score according to receiver operating characteristic curve analysis. CONCLUSION: Higher plasma thrombospondin-1 concentrations are associated with clinical severity and long-term prognosis of aSAH patients.