• Clinical and Experimental Pediatrics
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• v.60 no.9
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• pp.302-306
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• 2017

Purpose: This study aimed to investigate whether serum neuron-specific enolase (NSE) was expressed in acute encephalitis syndrome (AES) that causes neuronal damage in children. Methods: This prospective observational study was conducted in the pediatric neurology ward of Soetomo Hospital. Cases of AES with ages ranging from 1 month to 12 years were included. Cases that were categorized as simple and complex febrile seizures constituted the non-AES group. Blood was collected for the measurement of NSE within 24 hours of hemodynamic stabilization. The median NSE values of both groups were compared by using the Mann-Whitney U test. All statistical analyses were performed with SPSS version 12 for Windows. Results: In the study period, 30 patients were enrolled. Glasgow Coma Scale mostly decreased in the AES group by about 40% in the level ${\leq}8$. All patients in the AES group suffered from status epilepticus and 46.67% of them had body temperature >$40^{\circ}C$. Most of the cases in the AES group had longer duration of stay in the hospital. The median serum NSE level in the AES group was 157.86 ng/mL, and this value was significantly higher than that of the non-AES group (10.96 ng/mL; P<0.05). Conclusion: AES cases showed higher levels of serum NSE. These results indicate that serum NSE is a good indicator of neuronal brain injury.

• 대한핵의학회:학술대회논문집
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• 1985.05a
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• pp.155.1-155.1
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• 1985

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.1
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• pp.49-56
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• 2018

Purpose: Glufosinate ammonium poisoning can cause seizures, even after a symptom-free period. This study was conducted to evaluate the relationship between serum neuron specific enolase (NSE) level and the occurrence of seizures in patients with acute glufosinate ammonium poisoning. Methods: For this retrospective observational study, data from patients diagnosed with acute glufosinate ammonium poisoning were collected between January 2016 and June 2016. Serum NSE was measured within 2 hours of arrival at the emergency department. The patients were divided into a seizure group and a non-seizure group. Results: The seizure group included eight of the 15 total patients (53.3%). The serum NSE level was significantly higher in the seizure group than in the non-seizure group ($32.4{\pm}11.9ng/mL$ vs. $19.5{\pm}5ng/mL$, p=0.019). The amount of glufosinate ingested and initial and peak serum ammonia levels were significantly higher in the seizure group than in the non-seizure group. There was no significant difference in the area under the curve of the serum NSE level or the initial and peak serum ammonia levels in terms of predicting the occurrence of seizures. Conclusion: In acute glufosinate poisoning, initial serum NSE levels may help in prediction of seizures.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.3
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• pp.193-198
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• 2012

Changes in the expression profiles of specific proteins leads to serious human diseases, including colitis. The proteomic changes related to colitis and the differential expression between tuberculous (TC) and ulcerative colitis (UC) in colon tissue from colitis patients has not been defined. We therefore performed a proteomic analysis of human TC and UC mucosal tissue. Total protein was obtained from the colon mucosal tissue of normal, TC, and UC patients, and resolved by 2-dimensional electrophoresis (2-DE). The results were analyzed with PDQuest using silver staining. We used matrix-assisted laser desorption ionization time-of-flight/time-of-flight spectrometry (MALDI TOF/TOF) to identify proteins differentially expressed in TC and UC. Of the over 1,000 proteins isolated, three in TC tissue and two in UC tissue displayed altered expression when compared to normal tissue. Moreover, two proteins were differentially expressed in a comparative analysis between TC and UC. These were identified as mutant ${\beta}$-actin, ${\alpha}$-enolase and Charcot-Leyden crystal protein. In particular, the expression of ${\alpha}$-enolase was significantly greater in TC compared with normal tissue, but decreased in comparison to UC, implying that ${\alpha}$-enolase may represent a biomarker for differential diagnosis of TC and UC. This study therefore provides a valuable resource for the molecular and diagnostic analysis of human colitis.

• Journal of Veterinary Clinics
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• v.28 no.5
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• pp.522-525
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• 2011

A 14 year old female Siberian tiger presented for postmortem examination. A large mass attached to sublumbar area was found to be circumscribing aorta with metastases to mesenteric lymph nodes, uterus, kidney, adrenal gland, lung and thymus. The tumor cells were arranged in clusters or nests separated by well-developed fibrovascular stroma. The individual cells were plump and polygonal with granular eosinophilic cytoplasms and had distinct cell borders. The tumor cells were positive for synaptophysin, chromogranin A and neuron-specific enolase, and negative for cytokeratins, S100 and glial fibrillary acidic protein. The primary tumor was diagnosed as a malignant retroperitoneal paraganglioma.

• Journal of Gastric Cancer
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• v.17 no.3
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• pp.228-236
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• 2017

Purpose: Enolase is a cytoplasmic enzyme that catalyzes the conversion of 2-phosphoglycerate to phosphoenolpyruvate in the glycolytic pathway. The aim of this study was to investigate whether the overexpression of neuron-specific enolase (NSE) can serve as a prognostic factor in patients with gastric cancer (GC). Materials and Methods: To assess its prognostic value in GC, NSE expression was measured by immunohistochemistry in a clinically annotated tissue microarray comprising of 327 human GC specimens. Cytoplasmic NSE expression was scored from 0 to 4, reflecting the percentage of NSE-positive cells. Results: In terms of histology as per the World Health Organization criteria (P=0.34), there were no differences between the NSE overexpression (NSE-OE) and NSE underexpression (NSE-UE) groups. The NSE-OE group showed a significantly lower rate of advanced GC (P<0.01), lymph node metastasis (P=0.01), advanced stage group (P<0.01), cancer-related death (P<0.01), and cancer recurrence (P<0.01). Additionally, a Kaplan-Meier survival analysis revealed that the NSE-OE group had longer cumulative survival times than the NSE-UE group (log-rank test, P<0.01). However, there were no significant differences in the serum levels of NSE expression in patients with GC and healthy volunteers (P=0.28). Conclusions: Patients with NSE overexpressing GC tissues showed better prognostic results, implying that NSE could be a candidate biomarker of GC.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2002.11a
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• pp.97.1-97
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• 2002

• Proceedings of the Zoological Society Korea Conference
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• 1995.10b
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• pp.81-81
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• 1995

No Abstract, See Full Text

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.4
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• pp.2541-2544
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• 2013

Background: The aim of the present study was to evaluate the serum neuron-specific enolase (NSE) levels in patients with prostate cancer, Hodgkin lymphoma, lung cancer and peripheral nerve tumors. Materials and Methods: NSE levels were determined by ELISA in the sera of 100 prostate cancer, 47 Hodgkin lymphoma, 35 lung cancer and 35 peripheral nerve tumor patients and also in 132 healthy controls. Results: The median levels of serum NSE were elevated in patients with lung cancer (p=0.018) and peripheral nerve tumors (p=0.008). NSE levels in prostate cancer and Hodgkin lymphoma patients were higher than the controls but there was no statistically significant difference (p>0.05). Conclusions: We conclude that NSE may be applied in routine to gain insight about the clinical statuses of various cancer patients, but more studies are needed to determine the organ specificity.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.502-510
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• 1992

Background: Neuron specific enolase (NSE) is a neuronal form of the glycolytic enzyme enolase which was first found in extracts of brain tissue, and later in a variety of APUD cells and neurons of the diffuse endocrine system. SCLC shares many APUD properties with normal neuroendocrine cells. NSE immunostaining and serum NSE measurement may be a useful marker of neuroendocrine differentiation in lung tumors and diagnosis of small cell carcinoma. Methods: NSE immunohistochemical staining was done and at the same time serum NSE levels were measured in 22 small cell lung cancer and 21 non small cell lung cancer which were confirmed histologically. Results: 1) NSE immunoreactivity was detected in 9 of the 18 (50%) small cell lung cancer, in 5 of the 16 non small cell lung cancer. 2) Whereas the mean value in non-small cell lung cancer group was $11.79{\pm}4.47\;ng/ml$, the mean level of serum NSE in small cell lung cancer increased up to $59.3{\pm}77.8\;ng/ml$. In small cell lung cancer patients, mean value of limited disease group was $20.19{\pm}12.91\;ng/ml$, while mean value of extended disease group was $91.9{\pm}94.2\;ng/ml$ showing statistically significant difference. If serum levels above 20 ng/ml were tentatively defined as positive, 16 of 22 (73%) patients with SCLC had positive serum NSE level, but only one patient with NSCLC did. There was no correlation between serum NSE level and immunoreactivity of NSE. Conclusion: These studies indicate that serum NSE measurement may be a useful marker for the diagnosis and disease extent and NSE immunostaining can be used to demonstrate the neuroendocrine components of lung tumor.