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The addition of Co to Ni-based alloys can reduce the stacking fault energy. In this study, a novel Ni-26.6Co-18.4Cr-4.1Mo-2.3Al-0.3Ti-5.4Nb alloy was developed by increasing the Co addition to 26.6 wt.%. A new strategy to break the trade-off between strength and ductility is proposed by introducing dense nanosized precipitations, stacking faults, and nanoscale twins in the as-prepared alloys. The typical characteristics of the deformed alloy include dense dislocations tangles, nanotwins, stacking faults, and Lomer-Cottrell locks. In addition to the pinning effect of the bulky δ precipitates to the grain boundaries, the nanosized γ' particles with a coherent interface with the matrix show significant precipitation strengthening. As a result, the alloy exhibits a superior combination of yield strength of 1093 MPa and ductility of 29%. At 700 °C, the alloy has a high yield strength of 833 MPa and an ultimate tensile strength of 1024 MPa, while retaining a ductility of 6.3%.
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Dual-ion battery is a new type of battery in which both anions and cations participate in the energy storage process. However, this unique battery configuration imposes high requirements on the cathode, which typically presents a poor rate performance due to the sluggish diffusion dynamics and intercalation reaction kinetics of anions. Herein, we report petroleum coke-based soft carbon as the cathode for dual-ion batteries, exhibiting a superior rate performance with a specific capacity of 96â mAh g-1 at a rate of 2 C and 72â mAh g-1 remained even at 50 C. In situ XRD and Raman demonstrate that the anions can directly form lower-stage graphite intercalation compounds during the charge process owing to the surface effect, skipping the long evolutionary process from higher to lower stage, thus significantly improving the rate performance. This study highlights the impact of the surface effect and provides a promising perspective for dual-ion batteries.
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A medium-carbon low-alloy steel was prepared via the asymmetric rolling process with different ratios of upper and down roll velocities. Subsequently, the microstructure and mechanical properties were explored by using SEM, EBSD, TEM, tensile tests and nanoindentation. The results show that asymmetrical rolling (ASR) can significantly improve strength while retaining good ductility compared with conventional symmetrical rolling. The yield strength and tensile strength of the ASR-steel are 1292 ± 10 MPa and 1357 ± 10 MPa, respectively, which are higher than the values of 1113 ± 10 MPa and 1185 ± 10 MPa for the SR-steel. The ASR-steel retains good ductility of 16.5 ± 0.5%. The significant increase in strength is related to the joint actions of the ultrafine grains, dense dislocations and a large number of nanosized precipitates. This is mainly because of the introduction of extra shear stress on the edge under asymmetric rolling, which induces gradient structural changes hence increasing the density of geometrically necessary dislocations.
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It has been widely reported that glioma stem-like cells (GSCs) serve a crucial role in the malignant progression of glioma. In particular, recent studies have reported that long non-coding RNAs (lncRNAs) are closely associated with glioma development. However, the underlying molecular regulatory mechanistic role of GSCs remains poorly understood. The present study established two highly malignant glioma stem-like cell lines from clinical surgical specimens. In these, it was found that the lncRNA growth arrest-specific 5 (GAS5) expression was downregulated in GSCs and high-grade glioma tissues, compared with normal human astrocyte cells (NHAs) and normal brain tissues, respectively, which also showed a positive correlation with patient survival. Functional assays revealed that knocking down GAS5 expression promoted the proliferation, invasion, migration, stemness, and tumorigenicity of GSGs, while suppressing their apoptosis. Mechanistically, GAS5 directly sponged miR-23a, which in turn functioned as an oncogene by inhibiting E-cadherin, through the assays of reverse transcription-quantitative PCR (RT-qPCR) and luciferase reports. In addition, rescue experiments demonstrated that GAS5 could promote the expression and function of E-cadherin in a miR-23a-dependent manner. Collectively, these data suggest that GAS5 functions as a suppressor in GSCs by targeting the miR-23a/E-cadherin axis, which may be a promising therapeutic target against glioma.
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Glioma , RNA Longo não Codificante , Humanos , Linhagem Celular Tumoral , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Glioma/patologia , MicroRNAs/genética , MicroRNAs/metabolismo , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neoplásicas/patologia , Caderinas/metabolismoRESUMO
Objective: To investigate the efficacy of modified percutaneous balloon compression for simple third branch pain and its postoperative complications. Methods: Clinical data and surgical records of 132 patients with third branch pain treated with percutaneous balloon compression from March 2015 to May 2019 were retrospectively analyzed, of which 81 cases were in the modified group and 51 cases were in the classic group. The modified technique was to compress again at the foramen ovale to enhance the compression in V3 after compression of the Gasserian ganglion. Results: In the modified group, the overall therapeutic efficiency was 96.3%, with 77 patients (95.1%) having immediate postoperative pain relief and one patient (1.2%) having occasional pain without the need for medication. In the classic group, immediate postoperative pain relief was seen in 43 cases (84.3%), and two patients (3.9%) had occasional pain with no need for medication. The rate of complete pain relief was significantly higher in the modified group than in the classic group (P < 0.05). Postoperative follow-up ranged from 14 to 48 months. The pain-free rates were 77.8 and 54.9% in the modified and classic groups, respectively. The incidence of facial numbness in the region of the first branch was significantly lower than in the classic group (P < 0.001). Conclusion: The modified procedure has significant advantages over the classic procedure in improving surgical efficacy, reducing postoperative recurrence rate, and decreasing postoperative numbness in the region, and can be used to treat simple trigeminal neuralgia in the third branch.
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BACKGROUND: Subarachnoid hemorrhage (SAH) is a severe neurological emergency, resulting in cognitive impairments and threatening human's health. Currently, SAH has no effective treatment. It is urgent to search for an effective therapy for SAH. OBJECTIVE: To explore the expression of Omi protein after subarachnoid hemorrhage in rats. METHODS: SAH rat model was established by injecting blood into the prechiasmatic cistern. Neurological deficit was assessed by detecting neurological deficit scores and brain tissue water contents. Apoptotic cells were evaluated by TUNEL staining and IHC staining. Omi and Cleaved caspase 3 expressions in nerve cells were determined by double staining using IF. Apoptosis-related proteins were measured by Western blotting assay. RESULTS: SAH rat model was successfully established, showing more apoptotic cells and high neurological deficit scores in SAH rat. In SAH rat model, Omi expression in nerve cells was elevated and the upregulation of Omi mainly occurred in cytoplasm, accompanied by the degradation of XIAP and the increased cleaved caspase 3/9 and cleaved PARP. Once treated with UCF-101, a specific inhibitor of Omi, the increased cell apoptosis, left/right brain moisture contents and neurological deficits were notably reversed in SAH rat brain. Of note, SAH-induced the increases of apoptosis-related protein in nerve cells were also rescued by the administration of UCF-101. CONCLUSIONS: UCF-101-mediated Omi inhibition decreased the degradation of XIAP and subsequently inhibited the activation of apoptosis-related proteins, decreased nerve cell apoptosis, leading to the improvement on early brain injury in SAH rat. UCF-101-based Omi inhibition may be used to treat SAH with great potential application.
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Proteínas do Tecido Nervoso/metabolismo , Fatores de Processamento de Serina-Arginina/metabolismo , Hemorragia Subaracnóidea/metabolismo , Animais , Apoptose , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Caspase 3/metabolismo , Proteínas Inibidoras de Apoptose/metabolismo , Masculino , Proteínas do Tecido Nervoso/antagonistas & inibidores , Pirimidinonas/farmacologia , Ratos , Ratos Sprague-Dawley , Inibidores de Serina Proteinase/farmacologia , Fatores de Processamento de Serina-Arginina/antagonistas & inibidores , Tionas/farmacologiaRESUMO
BACKGROUND: Subarachnoid hemorrhage (SAH) is a life-threatening disease worldwide, and effective pharmaceutical treatment is still lacking. Celastrol is a plant-derived triterpene which showed neuroprotective potential in several types of brain insults. This study aimed to investigate the effects of celastrol on early brain injury (EBI) after SAH. METHODS: A total of sixty-one male Sprague-Dawley rats were used in this study. Rat SAH endovascular perforation model was established to mimic the pathological changes of EBI after SAH. Multiple methods such as 3.0T MRI scanning, immunohistochemistry, western blotting and propidium iodide (PI) labeling were used to explore the therapeutic effects of celastrol on SAH. RESULTS: Celastrol treatment attenuated SAH-caused brain swelling, reduced T2 lesion volume and ventricular volume in MRI scanning, and improved overall neurological score. Albumin leakage and the degradation of tight junction proteins were also ameliorated after celastrol administration. Celastrol protected blood-brain bairrer integrity through inhibiting MMP-9 expression and anti-neuroinflammatory effects. Additionally, necroptosis-related proteins RIP3 and MLKL were down-regulated and PI-positive cells in the basal cortex were less in the celastrol-treated SAH group than that in untreated SAH group. CONCLUSIONS: Celastrol exhibits neuroprotective effects on EBI after SAH and deserves to be further investigated as an add-on pharmaceutical therapy.
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Barreira Hematoencefálica/patologia , Lesões Encefálicas/tratamento farmacológico , Lesões Encefálicas/etiologia , Necroptose/efeitos dos fármacos , Fármacos Neuroprotetores/uso terapêutico , Triterpenos Pentacíclicos/uso terapêutico , Hemorragia Subaracnóidea/complicações , Albuminas/metabolismo , Animais , Barreira Hematoencefálica/diagnóstico por imagem , Barreira Hematoencefálica/efeitos dos fármacos , Edema Encefálico/complicações , Edema Encefálico/diagnóstico por imagem , Edema Encefálico/tratamento farmacológico , Lesões Encefálicas/diagnóstico por imagem , Ventrículos Cerebrais/efeitos dos fármacos , Ventrículos Cerebrais/patologia , Regulação para Baixo/efeitos dos fármacos , Inflamação/patologia , Masculino , Metaloproteinase 9 da Matriz/metabolismo , Fármacos Neuroprotetores/farmacologia , Tamanho do Órgão/efeitos dos fármacos , Triterpenos Pentacíclicos/farmacologia , Proteínas Quinases/metabolismo , Ratos Sprague-Dawley , Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo , Transdução de Sinais/efeitos dos fármacos , Hemorragia Subaracnóidea/diagnóstico por imagem , Análise de Sobrevida , Junções Íntimas/efeitos dos fármacos , Junções Íntimas/metabolismo , Regulação para Cima/efeitos dos fármacosRESUMO
The NLR family pyrin domain-containing 3 (NLRP3) multiprotein complex is associated with neuroinflammation and poor prognosis after subarachnoid hemorrhage (SAH). Accumulating evidence shows that Mer tyrosine kinase (MerTK) alleviates inflammatory responses via a negative feedback mechanism. However, the contribution and function of MerTK in SAH remain to be determined. In this study, we explored the role of MerTK during microglial NLRP3 inflammasome activation and evaluated its contribution to the outcome of SAH in mice. Activating MerTK with growth arrest-specific 6 (Gas6) alleviated brain edema, neuronal degeneration and neurological deficits after SAH by regulating neuroinflammation. Gas6 did not change the mRNA levels of Nlrp3 or Casp1 but decreased the protein expression of NLRP3, cleaved caspase1 (p20), interleukin-1ß and interleukin-18. Furthermore, Gas6 increased the expression of Beclin1, the ratio of LC3-II/LC3-I and the level of autophagic flux. Inhibiting autophagy with 3-MA reversed the inhibition of NLRP3 inflammasome activation and diminished the neuroprotective effects of Gas6. Thus, MerTK activation may exert protective effects by limiting neuroinflammation and promoting neurological recovery after SAH via autophagy induction.
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Autofagia/fisiologia , Encéfalo/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Hemorragia Subaracnóidea/metabolismo , c-Mer Tirosina Quinase/metabolismo , Animais , Autofagia/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Linhagem Celular , Cicloexanóis/farmacologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Microglia/efeitos dos fármacos , Microglia/metabolismo , Pirimidinas/farmacologia , Hemorragia Subaracnóidea/prevenção & controle , c-Mer Tirosina Quinase/antagonistas & inibidoresRESUMO
SEM, TEM characterizations, in combination with tensile tests, provided an intriguing observation that ultra-high-strength and good ductility could be achieved simultaneously by changing the ratio of large and small precipitates in high-carbon steel (1.0C-1.5Cr-0.31Mn-0.20Si, wt %). The high yield strength of 670 MPa, tensile-stress of 740 MPa, and good ductility (elongation of 26%) were obtained by adopting spheroidization annealing, cold rolling, recrystallization annealing, and cold drawing. This led to nanosized precipitates with a large ratio of big size to the small size of 0.28, promoting high dislocation storage of 1.39 × 1014 m-2. In addition, the finite element (FE) method was used to simulate the cold-rolling process, and the largest stress and strain were 830 MPa and 0.6 at a depth of 3 mm after the fourth pass of the 0.10C-1.50Cr steel, respectively. The stress and strain accumulation in the top layer was potentially caused by severe plastic deformation, as well as attrition rendered by the rollers. This explained the emergence of dense low-angle grain boundaries in the region close to the surface of the cold rolled steel.
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BACKGROUND: Increased plasma copeptin concentrations are related to poor prognosis after aneurysmal subarachnoid hemorrhage (aSAH). The aim of this study was to assess prognostic significance of plasma copeptin detection compared with glial fibrillary astrocyte protein, myelin basic protein, S100B, phosphorylated axonal neurofilament subunit H, neuron-specific enolase, tau and ubiquitin carboxyl-terminal hydrolase L1 in aSAH. METHODS: We detected plasma concentrations of the aforementioned biomarkers in 105 healthy controls using ELISA. Their predictive ability for symptomatic cerebral vasospasm and 6-month poor outcome (Glasgow Outcome Scale score of 1-3) were compared. RESULTS: Plasma concentrations of the preceding biomarkers were highly correlated with World Federation of Neurological Surgeons subarachnoid hemorrhage scale (WFNS) scores as well as were significantly higher in patients with symptomatic cerebral vasospasm than in those without symptomatic cerebral vasospasm and in patients with poor outcome than in those with good outcome. In terms of area under receiver operating characteristic curve, their predictive value for symptomatic cerebral vasospasm and 6-month poor outcome was in the range of WFNS scores. Plasma copeptin concentration, but not plasma concentrations of other biomarkers, statistically significantly improved the predictive performance of WFNS scores. CONCLUSIONS: Copeptin in plasma might have the potential to be a useful prognostic biomarker for aSAH.
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Glicopeptídeos/sangue , Aneurisma Intracraniano/diagnóstico , Hemorragia Subaracnóidea/diagnóstico , Vasoespasmo Intracraniano/diagnóstico , Adulto , Idoso , Biomarcadores/sangue , Estudos de Casos e Controles , Feminino , Expressão Gênica , Proteína Glial Fibrilar Ácida/sangue , Proteína Glial Fibrilar Ácida/genética , Glicopeptídeos/genética , Humanos , Aneurisma Intracraniano/sangue , Aneurisma Intracraniano/patologia , Masculino , Pessoa de Meia-Idade , Proteína Básica da Mielina/sangue , Proteína Básica da Mielina/genética , Proteínas de Neurofilamentos/sangue , Proteínas de Neurofilamentos/genética , Fosfopiruvato Hidratase/sangue , Fosfopiruvato Hidratase/genética , Valor Preditivo dos Testes , Prognóstico , Estudos Prospectivos , Subunidade beta da Proteína Ligante de Cálcio S100/sangue , Subunidade beta da Proteína Ligante de Cálcio S100/genética , Hemorragia Subaracnóidea/sangue , Hemorragia Subaracnóidea/patologia , Ubiquitina Tiolesterase/sangue , Ubiquitina Tiolesterase/genética , Vasoespasmo Intracraniano/sangue , Vasoespasmo Intracraniano/patologia , Proteínas tau/sangue , Proteínas tau/genéticaRESUMO
BACKGROUND: Periostin, a neurite outgrowth-promoting factor, is increasingly expressed in rat brain tissues after cerebral ischemia or subarachnoid hemorrhage. However, periostin concentrations are undetermined in peripheral blood from patients with traumatic brain injury (TBI). METHODS: In this prospective, observational study, serum periostin concentrations were measured in 130 controls and 130 severe TBI patients. We investigated its association with trauma severity reflected by Glasgow Coma Scale (GCS) score and prognosis (i.e., 30-day mortality and 30-day overall survival). RESULTS: As compared with the controls, serum periostin concentrations were significantly increased in the patients [(median, 246.5ng/ml; interquartile range, 164.5-328.6ng/ml) vs. (median, 61.8ng/ml; interquartile range, 37.9-77.9ng/ml), P<0.001]. Periostin concentrations independently correlated with GCS scores (t=-6.199, P<0.001). Serum periostin concentrations higher than 308.2ng/ml predicted 30-day mortality with a sensitivity of 72.4% and a specificity of 78.2% [area under curve, 815; 95% confidence interval (CI), 0.737-0.878]. Periostin concentrations higher than 246.5ng/ml were independently related to 30-day mortality and 30-day overall survival with odds ratio value of 3.829 (95% CI, 1.104-13.281) and hazard ratio value of 5.667 (95% CI, 1.953-16.443) respectively. CONCLUSIONS: Increased serum periostin concentrations clearly reflect trauma severity and mortality following TBI.
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Lesões Encefálicas Traumáticas/sangue , Moléculas de Adesão Celular/sangue , Adolescente , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Adulto JovemRESUMO
Subarachnoid hemorrhage (SAH) is a serious medical problem with few effective pharmacotherapies available, and neuroinflammation has been identified as an important pathological process in early brain injury (EBI) after SAH. Methylene blue (MB) is an older drug that has been recently proven to exert extraordinary neuroprotective effects in several brain insults. However, no study has reported the beneficial effects of MB in SAH. In the current investigation, we studied the neuroprotective effects of MB in EBI after SAH and focused on its anti-inflammatory role. A total of 303 rats were subjected to an endovascular perforation process to produce an SAH model. We found that MB could significantly ameliorate brain edema secondary to BBB disruption and alleviate neurological dysfunction after SAH. MB administration also promoted the phosphorylation of Akt and GSK-3ß, leading to an increased concentration of MEF2D in the nucleus. The cytokine IL-10 was up-regulated, and IL-1ß, IL-6 and TNF-α were down-regulated after MB administration. MB administration could also alleviate neutrophil infiltration and microglia activation after SAH. MK2206, a selective inhibitor of Akt, abolished the neuroprotective effects of MB, inhibited the phosphorylation of Akt and prevented the nuclear localization of MEF2D. MK2206 also reduced the expression of IL-10 and increased the expression of pro-inflammatory cytokines. In conclusion, these data suggested that MB could ameliorate neuroinflammatory responses after SAH, and its anti-inflammatory effects might be exerted via activation of the Akt/GSK-3ß/MEF2D pathway.
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Azul de Metileno/farmacologia , Hemorragia Subaracnóidea/tratamento farmacológico , Animais , Anti-Inflamatórios/farmacologia , Barreira Hematoencefálica/efeitos dos fármacos , Encéfalo/metabolismo , Edema Encefálico/tratamento farmacológico , Lesões Encefálicas/metabolismo , Citocinas/metabolismo , Glicogênio Sintase Quinase 3 beta/metabolismo , Interleucina-10/metabolismo , Interleucina-6/metabolismo , Fatores de Transcrição MEF2/metabolismo , Masculino , Neuroimunomodulação/efeitos dos fármacos , Fármacos Neuroprotetores/uso terapêutico , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos , Ratos Sprague-Dawley , Transdução de Sinais , Hemorragia Subaracnóidea/fisiopatologia , Fator de Necrose Tumoral alfa/metabolismoRESUMO
BACKGROUND: Macrophage migration inhibitory factor (MIF) is a well-known pro-inflammatory cytokine. Serum MIF concentrations are associated with the severity and prognosis of ischemic stroke. METHODS: In this prospective, observational study, white blood cell (WBC) count and serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and MIF among 108 severe traumatic brain injury (TBI) patients and 108 controls were measured. We determined whether serum MIF concentrations are associated with inflammation, severity, in-hospital major adverse events (IMAEs) (i.e., in-hospital mortality, acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction) and long-term clinical outcome (i.e., 6-month functional outcome) after TBI. RESULTS: As compared to the controls, serum CRP, IL-6, TNF-α and MIF concentrations were significantly increased. MIF concentrations correlated with WBC count, CRP, IL-6 and TNF-α concentrations and Glasgow coma scale (GCS) scores. MIF in serum was independently associated with IMAEs and long-term clinical outcome. Area under receiver operating characteristic curve of MIF concentrations was similar to GCS scores'. Moreover, MIF concentrations markedly improved the predictive value of GCS scores for 6-month unfavorable outcome. CONCLUSION: Increased serum MIF concentrations have close relation to inflammation, trauma severity and clinical outcomes, substantializing MIF as a good prognostic biomarker after TBI.
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Lesões Encefálicas Traumáticas/sangue , Lesões Encefálicas Traumáticas/diagnóstico , Fatores Inibidores da Migração de Macrófagos/sangue , Adolescente , Adulto , Idoso , Feminino , Humanos , Pessoa de Meia-Idade , Prognóstico , Adulto JovemRESUMO
BACKGROUND: In-hospital major adverse events (IMAEs), mainly including acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, are associated with poor prognosis after traumatic brain injury (TBI). Thioredoxin, a potent anti-oxidant, has been identified as an oxidative stress marker. This study was designed to explore the association of serum thioredoxin concentrations with IMAEs of patients with severe TBI. METHODS: This prospective, observational study recruited a total of 108 healthy controls and 108 patients with severe TBI. We investigated the possible relation of serum thioredoxin concentrations to IMAEs and trauma severity (reflected by Glasgow coma scale scores) following TBI using a multivariate analysis. RESULTS: Serum thioredoxin concentrations were higher in the patients than in the controls. Serum concentrations of thioredoxin significantly correlated with admission Glasgow coma scale scores. Thioredoxin in serum independently predicted any IMAEs. As compared to admission Glasgow coma scale scores, thioredoxin concentrations had similar areas under receiver operating characteristic curve for any IMAEs. CONCLUSION: Increased serum thioredoxin concentrations are highly associated with trauma severity and IMAEs, indicating thioredoxin might be a potential prognostic biomarker after TBI.
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Lesões Encefálicas Traumáticas/sangue , Lesões Encefálicas Traumáticas/complicações , Hospitais , Tiorredoxinas/sangue , Adolescente , Adulto , Idoso , Lesões Encefálicas Traumáticas/diagnóstico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Adulto JovemRESUMO
BACKGROUND: Nesfatin-1 is related to inflammation. Its increased circulating concentrations are associated with the severity and prognosis of subarachnoid hemorrhage. In-hospital major adverse events (IMAEs), including acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, are correlated with mortality after traumatic brain injury (TBI). The present study was designed to investigate the changes of plasma nesfatin-1 concentrations and further assess its association with inflammation, trauma severity, in-hospital mortality and IMAEs following TBI. METHODS: We measured plasma nesfatin-1 concentrations of 100 severe TBI patients and 100 controls. Progressive hemorrhagic injury and posttraumatic cerebral infarction were diagnosed based on a follow-up computerized tomography scan. Acute traumatic coagulopathy was identified according to a coagulation test. RESULTS: Plasma nesfatin-1 concentrations were significantly higher in patients than in controls and associated highly with Glasgow coma scale (GCS) scores and plasma C-reactive protein concentrations. Nesfatin-1 was indicated as an independent predictor for in-hospital mortality and IMAEs. In accordance with area under receiver operating characteristic curve, its predictive value was similar to GCS scores. CONCLUSION: Increased plasma nesfatin-1 concentrations are associated closely with inflammation, trauma severity and clinical outcomes, indicating that nesfatin-1 might be involved in inflammation and become a good prognostic biomarker following TBI.
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Lesões Encefálicas Traumáticas/sangue , Lesões Encefálicas Traumáticas/diagnóstico , Proteínas de Ligação ao Cálcio/sangue , Proteínas de Ligação a DNA/sangue , Proteínas do Tecido Nervoso/sangue , Adolescente , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Nucleobindinas , Prognóstico , Adulto JovemRESUMO
BACKGROUND: Galectin-3 plays a significant role in microglia activation. Its increased circulating concentration has been associated with some inflammatory diseases. In-hospital major adverse events (IMAEs), including acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, have high prevalence and are strong predictors of mortality after severe traumatic brain injury (STBI). The present study was designed to investigate the relationships between plasma galectin-3 concentrations and trauma severity, in-hospital mortality and IMAEs following STBI. METHODS: Plasma galectin-3 concentrations of 100 STBI patients and 100 controls were determined. Diagnosis of progressive hemorrhagic injury and posttraumatic cerebral infarction was made on the follow-up computerized tomography scan. Acute traumatic coagulopathy was defined based on coagulation test. RESULTS: Plasma galectin-3 concentrations were significantly higher in patients as compared to controls and also associated highly with Glasgow Coma Scale scores and plasma C-reactive protein concentrations. Galectin-3 emerged as an independent predictor for in-hospital mortality and IMAEs. Areas under receiver operating characteristic curve of plasma galectin-3 concentrations were similar to those of Glasgow Coma Scale scores for prediction of in-hospital morality and IMAEs. CONCLUSIONS: Plasma galectin-3 concentrations have close relation to inflammation, trauma severity and clinical outcome, suggesting that galectin-3 should have the potential to be a good prognostic biomarker after STBI.
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Lesões Encefálicas Traumáticas/sangue , Galectina 3/sangue , Adulto , Idoso , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/diagnóstico , Lesões Encefálicas Traumáticas/mortalidade , Feminino , Hospitais , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Adulto JovemRESUMO
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.
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Hemorragia Subaracnóidea/sangue , Hemorragia Subaracnóidea/diagnóstico , Trombospondina 1/sangue , Adulto , Ensaio de Imunoadsorção Enzimática , Feminino , Humanos , Masculino , Análise Multivariada , Prognóstico , Estudos Prospectivos , Fatores de RiscoRESUMO
BACKGROUND: Higher plasma 8-iso-Prostaglandin F2α concentrations have been associated with poor outcome of severe traumatic brain injury. We further investigated the relationships between plasma 8-iso-Prostaglandin F2α concentrations and clinical outcomes in patients with acute intracerebral hemorrhage. METHODS: Plasma 8-iso-Prostaglandin F2α concentrations of 128 consecutive patients and 128 sex- and gender-matched healthy subjects were measured by enzyme-linked immunosorbent assay. We assessed their relationships with disease severity and clinical outcomes including 1-week mortality, 6-month mortality and unfavorable outcome (modified Rankin Scale score>2). RESULTS: Plasma 8-iso-Prostaglandin F2α concentrations were substantially higher in patients than in healthy controls. Plasma 8-iso-Prostaglandin F2α concentrations were positively associated with National Institutes of Health Stroke Scale (NIHSS) scores and hematoma volume using a multivariate linear regression. It emerged as an independent predictor for clinical outcomes of patients using a forward stepwise logistic regression. ROC curves identified the predictive values of plasma 8-iso-Prostaglandin F2α concentrations, and found its predictive value was similar to NIHSS scores and hematoma volumes. However, it just numerically added the predictive values of NIHSS score and hematoma volume. CONCLUSIONS: Increased plasma 8-iso-Prostaglandin F2α concentrations are associated with disease severity and clinical outcome after acute intracerebral hemorrhage.
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Hemorragia Cerebral/sangue , Hemorragia Cerebral/mortalidade , Dinoprosta/análogos & derivados , Acidente Vascular Cerebral/sangue , Acidente Vascular Cerebral/mortalidade , Doença Aguda , Idoso , Biomarcadores/sangue , Hemorragia Cerebral/diagnóstico , Dinoprosta/sangue , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Mortalidade/tendências , Acidente Vascular Cerebral/diagnóstico , Resultado do TratamentoRESUMO
Enhanced blood levels of copeptin correlate with poor clinical outcomes after acute critical illness. This study aimed to compare the prognostic performances of plasma concentrations of copeptin and other biomarkers like myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1 in severe traumatic brain injury. We recruited 102 healthy controls and 102 acute patients with severe traumatic brain injury. Plasma concentrations of these biomarkers were determined using enzyme-linked immunosorbent assay. Their prognostic predictive performances of 6-month mortality and unfavorable outcome (Glasgow Outcome Scale score of 1-3) were compared. Plasma concentrations of these biomarkers were statistically significantly higher in all patients than in healthy controls, in non-survivors than in survivors and in patients with unfavorable outcome than with favorable outcome. Areas under receiver operating characteristic curves of plasma concentrations of these biomarkers were similar to those of Glasgow Coma Scale score for prognostic prediction. Except plasma copeptin concentration, other biomarkers concentrations in plasma did not statistically significantly improve prognostic predictive value of Glasgow Coma Scale score. Copeptin levels may be a useful tool to predict long-term clinical outcomes after severe traumatic brain injury and have a potential to assist clinicians.
Assuntos
Lesões Encefálicas/sangue , Lesões Encefálicas/diagnóstico , Glicopeptídeos/sangue , Adolescente , Adulto , Idoso , Biomarcadores/sangue , Feminino , Humanos , Escala de Gravidade do Ferimento , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Prospectivos , Adulto JovemRESUMO
Higher plasma copeptin levels correlate with poor clinical outcomes after traumatic brain injury. Nevertheless, their links with acute traumatic coagulopathy and progressive hemorrhagic injury are unknown. Therefore, we aimed to investigate the relationship between plasma copeptin levels, acute traumatic coagulopathy and progressive hemorrhagic injury in patients with severe traumatic brain injury. We prospectively studied 100 consecutive patients presenting within 6h from head trauma. Progressive hemorrhagic injury was present when the follow-up computerized tomography scan reported any increase in size or number of the hemorrhagic lesion, including newly developed ones. Acute traumatic coagulopathy was defined as an activated partial thromboplastic time greater than 40s and/or international normalized ratio greater than 1.2 and/or a platelet count less than 120×10(9)/L. We measured plasma copeptin levels on admission using an enzyme-linked immunosorbent assay in a blinded fashion. In multivariate logistic regression analysis, plasma copeptin level emerged as an independent predictor of progressive hemorrhagic injury and acute traumatic coagulopathy. Using receiver operating characteristic curves, we calculated areas under the curve for progressive hemorrhagic injury and acute traumatic coagulopathy. The predictive performance of copeptin was similar to that of Glasgow Coma Scale score. However, copeptin did not obviously improve the predictive value of Glasgow Coma Scale score. Thus, copeptin may help in the prediction of progressive hemorrhagic injury and acute traumatic coagulopathy after traumatic brain injury.