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Neuron-specific enolase (NSE) is considered a biomarker for the severity of nervous system diseases. We sought to explore whether serum NSE concentration in ischemic stroke patients undergoing mechanical thrombectomy (MT) is related to 3-month functional outcome and symptomatic intracranial hemorrhage (sICH). We retrospectively collected the data of acute ischemic stroke patients with anterior circulation infarction receiving MT within 6 h in our stroke center. Favorable outcome and poor outcome at 3 months were defined as modified Rankin Scale (mRS) score 0-2 and 3-6, respectively. sICH was defined according to the Heidelberg bleeding classification. We used multivariate logistic regression model and receiver operating characteristic curves to investigate the correlation between NSE and clinical outcomes. Among the 426 patients enrolled, 40 (9.4%) patients developed sICH. Three-month favorable outcome in 160 (37.6%) and poor outcome in 266 (62.4%) patients were observed. Serum NSE levels was significantly correlated with 3-month mRS score ( = 0.473, < 0.001). A cutoff value of 15.29 and 23.12 ng/mL for serum NSE was detected in discriminating 3-month poor outcome (area under the curve, 0.724) and sICH (area under the curve, 0.716), respectively. Multivariate analysis showed that high serum NSE levels were independently associated with 3-month poor outcome (odds ratio [OR] 5.049, 95% confidence interval [CI] 2.933-8.689, <0.001) and sICH (OR 5.111, 95% CI 2.210-11.820, < 0.001). Our study demonstrated that high serum NSE levels after receiving MT were independently associated with 3-month poor outcome and sICH in acute ischemic stroke patients. Serum NSE levels could be a good predictor of clinical outcomes for patients receiving MT.

Background The aim of this study was to explore the diagnostic and prognostic value of serum tumor M2‐pyruvate kinase (TuM2‐PK), neuron‐specific enolase (NSE), and progastrin‐releasing peptide (ProGRP) levels in patients with small cell lung cancer (SCLC). Methods The levels of serum TuM2‐PK, NSE, and ProGRP in 102 patients with SCLC, 60 patients with benign lung disease (BLD), and 90 healthy controls were detected. Results The serum TuM2‐PK, NSE, and ProGRP levels in the SCLC group were higher than those in BLD group (p < 0.05) and healthy control group (p < 0.05). The sensitivity of TuM2‐PK, NSE, and ProGRP detection in SCLC was 82.35%, 60.78%, and 77.45% respectively, and specificity was 91.11%, 81.11%, and 86.67%, respectively. The area under the curve (AUC) of SCLC resulting from TuM2‐PK was significantly better than that of NSE and ProGRP. The application of TuM2‐PK combined with NSE and ProGRP improved the diagnostic yield of SCLC patients and had better diagnostic value than TuM2‐PK alone. Univariate and multivariate analysis indicated that an elevated TuM2‐PK level was an independent prognostic factor for shorter survival in SCLC. Conclusions These results suggest that TuM2‐PK levels in the serum could be an effective biomarker for the diagnosis and prognosis of SCLC. To explore the diagnostic and prognostic value of serum TuM2‐PK, NSE, and ProGRP levels in SCLC patients. Serum TuM2‐PK, NSE, and ProGRP levels were higher in the SCLC group than the controls group. Univariate and multivariate analysis indicated that an elevated TuM2‐PK level was an independent prognostic factor for shorter overall survival in SCLC. These results suggest that TuM2‐PK levels in the serum could be a new effective biomarker for the diagnosis and prognosis of SCLC.

Background This study aimed to investigate the clinical application of combined detection of serum calcitonin (Ctn), carcinoembryonic antigen (CEA), and neuron‐specific enolase (NSE) in predicting lateral lymph node metastasis (LLNM) in medullary thyroid carcinoma (MTC). Methods Seventy‐four consecutive patients with MTC were enrolled. The relationship between serum Ctn, CEA, and NSE and LLNM was retrospectively analyzed by univariate analysis and logistic regression analysis. Furthermore, the clinical application of serum Ctn, CEA, and NSE combined detection in prediction of LLNM in MTC was also evaluated. Results The rate of LLNM in this study was 48.64% (36/74).The expression levels of serum Ctn, CEA, and NSE in MTC with LLNM were significantly higher than those without LLNM (all P < .01). The area under the curve (AUC) predicted by serum Ctn, CEA, and NSE for LLNM in MTC patients was 0.867, 0.831, and 0.726, respectively, and the AUC of serum Ctn, CEA, and NSE combined detection was up to 0.890, higher than using a single biomarker. The sensitivity and specificity of serum Ctn, CEA, and NSE combined detection in prediction of LLNM were 88.89% and 81.57%, respectively. Conclusions The concentrations of serum Ctn, CEA, and NSE are closely related to LLNM in MTC, and the combined detection of all three biomarkers has a higher clinical value in the evaluation of MTC patients with LLNM. With more perspective study in the future, it would be an indicator of influencing personalized surgical strategy for different MTC patients.

Introduction Serum neuron‐specific enolase (NSE) is an important tumor marker for small cell lung cancer and neuroblastoma. However, the test of serum NSE compromised by specimen hemolysis is presented as a falsely higher result, which seriously disturbs clinical decision. This study aimed to establish a solution integrated with laboratory information system to clear the bias from hemolysis on serum NSE test. Methods The reference range of serum hemolysis index (HI) was first established, and specimen hemolysis rate was compared between HI test and visual observation. NSE concentration in serum pool with normal HI was spiked with serial diluted lysates from red blood cells to deduce individual corrective equation. The agreement between individual corrective equation and original NSE test was assayed by Bland and Altman plots. Results The high HI existed in 32.6% of specimens from patients. The NSE median of hemolyzed specimens was significant higher than the baseline (p = 0.038), while the corrected NSE median had no difference compared with the baseline (p = 0.757). The mean difference of corrected NSE and initial NSE was 1.92%, the SD of difference was 5.23%, and furthermore, the difference was independent of tendency of HI (Spearman r = −0.069, p = 0.640). The 95% confidence interval of mean difference (from −8.33% to 12.17%) was less than the acceptable bias range (±20%). Conclusion The agreement between individual correction equation and NSE assay was satisfied. Our automated processing algorithm for serum NSE could provide efficient management of posttest data and correct positive bias from specimen hemolysis. The automated processing algorithm for serum NSE influenced by specimen hemolysis. We recommend estimation for clinical needs when a NSE result is above 16.3 μg/L and is also influenced by specimen hemolysis. If the result is used for tendency supervision of tumor marker, level variation more than 25% compared to last test, which is warning clinical importance, will reminder the need of the individual corrected equation. And so it is if the result is used for auxiliary diagnosis of SCLC or NB.

Background Neuron‐specific enolase (NSE) is an important tumor marker in the serum of patients with lung cancer. Elevated serum NSE levels are also associated with many other diseases. However, there is no unified population reference interval for serum NSE. This study aimed to investigate the distribution of serum NSE in healthy Chinese adults aged 20‐79 years and to establish its reference interval in Chinese population. Methods A total of 10 575 healthy subjects were in line with the requirements of this study. The concentration of serum NSE was detected by a fully automated Cobas e602 analyzer with matching reagents. The population reference interval for serum NSE was established using the unilateral 95th percentile (P95) according to standard guidelines. Results The distributions of serum NSE were not significantly different between males and females (P > 0.05) and also did not differ by age (P > 0.05). Therefore, the population reference interval for serum NSE was established as upper limit 25.4 ng/mL (90% confidence interval: 24.5‐26.2 ng/mL). Conclusions We established the first population reference interval for serum NSE in a large healthy Chinese adult cohort, which was higher than that recommended by Roche Diagnostics GmbH. This new reference interval is more practical and applicable in Chinese adults.

Neural stem cells have great potential for the development of novel therapies for nervous system diseases. However, the proliferation of endogenous neural stem cells following brain ischemia is insufficient for central nervous system self-repair. Ginkgolide B has a robust neuroprotective effect. In this study, we investigated the cell and molecular mechanisms underlying the neuroprotective effect of ginkgolide B on focal cerebral ischemia/reperfusion injury in vitro and in vivo. Neural stem cells were treated with 20, 40 and 60 mg/L ginkgolide B in vitro. Immunofluorescence staining was used to assess cellular expression of neuron-specific enolase, glial fibrillary acid protein and suppressor of cytokine signaling 2. After treatment with 40 and 60 mg/L ginkgolide B, cells were large, with long processes. Moreover, the proportions of neuron-specific enolase-, glial fibrillary acid protein- and suppressor of cytokine signaling 2-positive cells increased. A rat model of cerebral ischemia/reperfusion injury was established by middle cerebral artery occlusion. Six hours after ischemia, ginkgolide B (20 mg/kg) was intraperitoneally injected, once a day. Zea Longa's method was used to assess neurological function. Immunohistochemistry was performed to evaluate the proportion of nestin-, neuron-specific enolase- and glial fibrillary acid protein-positive cells. Real-time quantitative polymerase chain reaction was used to measure mRNA expression of brain-derived neurotrophic factor and epidermal growth factor. Western blot assay was used to analyze the expression levels of brain-derived neurotrophic factor and suppressor of cytokine signaling 2. Ginkgolide B decreased the neurological deficit score, increased the proportion of nestin-, neuron-specific enolase- and glial fibrillary acid protein-positive cells, increased the mRNA expression of brain-derived neurotrophic factor and epidermal growth factor, and increased the expression levels of brain-derived neurotrophic factor and suppressor of cytokine signaling 2 in the ischemic penumbra. Together, the in vivo and in vitro findings suggest that ginkgolide B improves neurological function by promoting the proliferation and differentiation of neural stem cells in rats with cerebral ischemia/reperfusion injury.

The optimal tumor marker for predicting the prognosis of advanced thymic carcinoma (ATC) remains unclear. We conducted a multi-institutional retrospective study of patients with ATC. A total of 286 patients were treated with chemotherapy. Clinicopathological information, including serum tumor markers, was evaluated to determine the overall survival (OS) and progression-free survival (PFS). The carcinoembryonic antigen, cytokeratin-19 fragment, squamous cell carcinoma (SCC) antigen, progastrin-releasing peptide, neuron-specific enolase (NSE), and alpha-fetoprotein levels were evaluated. In the Kaplan–Meier analysis, the OS was significantly shorter in the patients with elevated NSE levels than in those with normal NSE levels (median, 20.3 vs. 36.8 months; log-rank test p = 0.029; hazard ratio (HR), 1.55; 95% confidence interval (CI), 1.05–2.31 (Cox proportional hazard model)); a similar tendency regarding the PFS was observed (median, 6.4 vs. 11.0 months; log-rank test p = 0.001; HR, 2.04; 95% CI, 1.31–3.18). No significant differences in the OS and PFS were observed among the other tumor markers. In both univariate and multivariate analyses of the patients with SCC only, the NSE level was associated with the OS and PFS. Thus, the NSE level may be a prognostic tumor marker for thymic carcinoma, regardless of histology.

Neuropathy is one of most common complications in diabetic patients. Diagnosis of diabetic neuropathy is essential for decreasing the rate of the disability and death. Neuron-specific enolase (NSE) is released from damaged neuronal cells and enters the blood circulation through an injured blood brain barrier. Therefore, serum NSE can reflect the damage of neurons and brain tissue. To evaluate peripheral polyneuropathy and cognitive function in Type 2 Diabetes Mellitus (T2DM) and correlate them with NSE level as a possible biomarker of diabetic neuropathy. Forty five T2DM patients with polyneuropathy were randomly recruited in this study compared to 45 healthy age and sex matched subjects as a control. Patients group were divided into two subgroups, 24 diabetic patients with painful peripheral neuropathy and 21 with painless peripheral neuropathy. All were subjected to clinical assessment by diabetic neuropathy symptom score, Dyck neuropathy grading, Mini-Mental State Examination (MMSE), assessment of HbA1c, NSE biomarker and neurophysiological assessment (nerve conduction study (NCS), event related potential (P300wave) and somatosensory evoked potential (SSEP) of the right median nerve). There were significant decrease in cognitive functions in diabetic patients compared to controls and a significant increase in NSE in diabetic patients. There were no significant difference between patients with painless and painful diabetic neuropathy as regard MMSE, HbA1c and NSE. There were significant correlation of P300 in diabetic patients with HbA1c and NSE. Neurophysiological assessment of diabetic patients by NCS, SSEP and P300 have well evaluation of cognitive functions, painless, and painful diabetic polyneuropathy. NSE is a beneficial biomarker in diabetic patients to pick up neurological complications.

Diffuse large B-cell lymphoma (DLBCL) is a highly common type of malignant and heterogeneous non-Hodgkin's lymphoma. Tumor-associated macrophages, specially the M2-type, promote tumor progression and drug resistance. The clinical outcome of patients with high neuron-specific enolase (NSE) expression is worse than that with low NSE expression. The tumor-promoting mechanism of NSE, however, remains unclear. This study explored the role of NSE in macrophage polarization associated with the immune microenvironment of DLBCL. Our results showed that NSE protein expression was higher in lymphoma cell lines than in the B lymphocytes. Functional studies demonstrated that upregulation of NSE in lymphoma cells could promote M2 polarization and migration ability of macrophage, thereby consequently promoting the progression of lymphoma in vitro and in vivo. Further mechanism studies revealed that lymphoma-derived exosomes could mediate NSE into macrophages, NSE enhanced nuclear p50 translocation with subsequent defective classical nuclear factor-κB activity in macrophages. These results indicate that NSE may be a potential target for lymphoma therapy and a prognosis marker for lymphoma.

The utility of serum progastrin-releasing peptide (ProGRP) and neuron-specific enolase (NSE) as biomarkers for treatment monitoring and as prognostic factors was investigated in small cell lung cancer (SCLC) patients. Patients were first diagnosed pathologically at the First Affiliated Hospital of the University of Science and Technology of China and had their serum ProGRP and NSE levels measured using an electrochemiluminescence immunoassay. A total of 120 SCLC patients were enrolled. In responsive patients, ProGRP levels decreased significantly following two cycles of chemotherapy and continued to decline over the course of treatment. However, this decrease in ProGRP levels was not observed in non-responsive patients. Changes in ProGRP levels were more accurate than changes in NSE levels for monitoring the effects of chemotherapy in patients with SCLC. Following two treatment cycles or after the occurrence of drug resistance, changes in ProGRP levels in patients with low ProGRP levels at the time of diagnosis were not notably, regardless of whether or not patients were responders. The area under the receiver operating characteristic curve of the decline in ProGRP levels as a therapeutic biomarker of SCLC was 0.9643, and the cut-off value was 55.02%. A decline in ProGRP levels maybe a good predictor of objective response to chemotherapy in patients with SCLC with higher ProGRP levels at diagnosis. This model is expected to replace or be combined with imaging to predict chemotherapeutic treatment effects in patients with SCLC.