scholarly journals Correlation analysis between serum neuron-specific enolase and the detection of gene mutations in lung adenocarcinoma

2021 ◽  
Vol 13 (2) ◽  
pp. 552-561
Author(s):  
Fang-Zhou Xu ◽  
Yan-Bei Zhang
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wenjie Chen ◽  
Wen Li ◽  
Zhenkun Liu ◽  
Guangzhi Ma ◽  
Yunfu Deng ◽  
...  

AbstractTo identify the prognostic biomarker of the competitive endogenous RNA (ceRNA) and explore the tumor infiltrating immune cells (TIICs) which might be the potential prognostic factors in lung adenocarcinoma. In addition, we also try to explain the crosstalk between the ceRNA and TIICs to explore the molecular mechanisms involved in lung adenocarcinoma. The transcriptome data of lung adenocarcinoma were obtained from The Cancer Genome Atlas (TCGA) database, and the hypergeometric correlation of the differently expressed miRNA-lncRNA and miRNA-mRNA were analyzed based on the starBase. In addition, the Kaplan–Meier survival and Cox regression model analysis were used to identify the prognostic ceRNA network and TIICs. Correlation analysis was performed to analysis the correlation between the ceRNA network and TIICs. In the differently expressed RNAs between tumor and normal tissue, a total of 190 miRNAs, 224 lncRNAs and 3024 mRNAs were detected, and the constructed ceRNA network contained 5 lncRNAs, 92 mRNAs and 10 miRNAs. Then, six prognostic RNAs (FKBP3, GPI, LOXL2, IL22RA1, GPR37, and has-miR-148a-3p) were viewed as the key members for constructing the prognostic prediction model in the ceRNA network, and three kinds of TIICs (Monocytes, Macrophages M1, activated mast cells) were identified to be significantly related with the prognosis in lung adenocarcinoma. Correlation analysis suggested that the FKBP3 was associated with Monocytes and Macrophages M1, and the GPI was obviously related with Monocytes and Macrophages M1. Besides, the LOXL2 was associated with Monocytes and Activated mast cells, and the IL22RA1 was significantly associated with Monocytes and Macrophages M1, while the GPR37 and Macrophages M1 was closely related. The constructed ceRNA network and identified Monocytes, Macrophages M1 and activated Mast cells are all prognostic factors for lung adenocarcinoma. Moreover, the crosstalk between the ceRNA network and TIICs might be a potential molecular mechanism involved.


The Lancet ◽  
1982 ◽  
Vol 319 (8272) ◽  
pp. 583-585 ◽  
Author(s):  
DesmondN Carney ◽  
DanielC Ihde ◽  
MartinH Cohen ◽  
PaulJ Marangos ◽  
PaulA Bunn ◽  
...  

1997 ◽  
Vol 150 (2) ◽  
pp. 173-176 ◽  
Author(s):  
Jörg Berrouschot ◽  
Kathrin Rolle ◽  
Hans-Jürgen Kühn ◽  
Dietmar Schneider

Cephalalgia ◽  
2021 ◽  
pp. 033310242110466
Author(s):  
Jaimala Kishore ◽  
Fouzia Shaikh ◽  
Adnan Mustafa Zubairi ◽  
Sana Mirza ◽  
Montaser N Alqutub ◽  
...  

Introduction Burning mouth syndrome is a painful condition of the oral cavity with ambiguous pathogenesis and diagnosis. Neuron-specific enolase is increased in several conditions including peripheral neuropathy of diabetes, ophthalmopathies, spinal cord injuries and tumors. Evidence on association of burning mouth syndrome and neuron-specific enolase is limited. Aim This study aims to evaluate neuron-specific enolase levels in primary and secondary burning mouth syndrome patients and compare the levels of neuron-specific enolase with associated conditions in secondary burning mouth syndrome. Methods One hundred and twenty-eight patients of more than 18 years of age with no gender predilection and having clinical symptoms of burning mouth syndrome and 135 healthy subjects were included. All the patients fulfilled Scala’s criteria for the diagnosis of burning mouth syndrome, including “primary” (idiopathic) and “secondary” (resulting from identified precipitating factors) burning mouth syndrome patients. Blood samples were obtained from burning mouth syndrome patients. Serum neuron-specific enolase was evaluated using enzyme-linked immunosorbent assay. To compare means and standard deviations, among primary and secondary burning mouth syndrome, data was analysed with analysis of variance and multiple comparisons test. Results The mean age of the study participants for burning mouth syndrome and healthy subjects was 53.30 and 51.6 years, respectively. Amongst the secondary burning mouth syndrome group, 32 (25%) of the patients had menopause, 15 (11.7%) had diabetes, eight (6.2%) of the patients had nutritional deficiency, seven (5.4%) had combined diabetes, menopause, and depression, six (4.6%) had combined diabetes and depression, four (3.1%) were diagnosed with Sjögren’s syndrome. A minor percentage of 2.3% (three) had gastroesophageal reflux disease, while the remaining three (2.3%) patients in the secondary burning mouth syndrome group were on anti-depressants. There was a statistically significant increase in the levels of neuron-specific enolase in primary burning mouth syndrome as compared to the secondary burning mouth syndrome and healthy groups. Among the subgroups of secondary burning mouth syndrome, diabetic individuals showed a significant increase in neuron-specific enolase level when compared with other conditions in the secondary burning mouth syndrome patients. Discussion and conclusion: The raised serum neuron-specific enolase levels in patients suffering from primary burning mouth syndrome highlight a possible neuropathic mechanism. It was also increased in the sub-group of secondary burning mouth syndrome patients having diabetes. Although it cannot be ascertained whether the deranged values in the diabetic group were due to burning mouth syndrome or due to diabetes, the raised quantity of neuron-specific enolase in the primary burning mouth syndrome group is a reliable diagnostic indicator. Future studies on the assessment of neuron-specific enolase levels as a diagnostic tool for onset and management of primary and secondary burning mouth syndrome are recommended.


2018 ◽  
Vol 46 (11) ◽  
pp. 4518-4526 ◽  
Author(s):  
Aynur Acibuca ◽  
Veysel Kutay Vurgun ◽  
Demet Menekse Gerede ◽  
Ali Timucin Altin ◽  
Inci Sule Gul ◽  
...  

Objective Catheter ablation of atrial fibrillation (AF) can lead to thromboembolic complications, especially stroke. We measured the periprocedural serum neuron-specific enolase (NSE) level, which is a biomarker of neuronal injury, after ablation of AF. Methods Forty-three patients with paroxysmal AF were prospectively enrolled before radiofrequency ablation. A neurological examination was performed before and after the procedure. The serum NSE level was determined before and at the end of the procedure and at 2, 24, and 48 h after the procedure. Results No patients developed new neurological deficits. However, the median (interquartile range) NSE level increased after ablation from 6.7 (3.87) ng/mL at baseline to 11.48 (5.3) ng/mL at 24 h postoperatively. The NSE level exceed the upper reference limit of normal (17 ng/mL) in 14 patients (33%), and these patients were found to have a larger left atrium. Conclusions Serum NSE increased in most of the patients undergoing ablation for AF, and it exceeded the normal limit in one-third of the patients. Although NSE is a biomarker of neuronal injury, the clinical importance of this increase after AF ablation and its relationship with the left atrial diameter should be evaluated in a longitudinal study.


The Lancet ◽  
1987 ◽  
Vol 329 (8524) ◽  
pp. 110 ◽  
Author(s):  
J. Pritchard ◽  
E.H. Cooper ◽  
S. Hamilton ◽  
C.C. Bailey ◽  
J. Ninane

2017 ◽  
Vol 32 (5) ◽  
pp. 475-481 ◽  
Author(s):  
Sherifa Hamed ◽  
Kotb Abbass Metwalley ◽  
Hekma Saad Farghaly ◽  
Tahra Sherief

Neuron-specific enolase is a sensitive marker of neuronal damage in various neurologic disorders. This study aimed to measure serum neuron-specific enolase levels at different time points and severities of diabetic ketoacidosis. This study included 90 children (age 9.2 ± 3.4 years) with diabetic ketoacidosis. Neuron-specific enolase was measured at 3 time points (baseline and after 12 and 24 hours of starting treatment). Among patients, 74.4% had diagnosis of new diabetes, 60% had Glasgow Coma Scale score <15, and 75.6% had moderate/severe diabetic ketoacidosis. Compared with controls (n = 30), children with diabetic ketoacidosis had higher neuron-specific enolase levels at the 3 time points ( P = .0001). In multiple regression analysis, the factors associated with higher neuron-specific enolase levels were younger age, higher glucose, lower pH, and bicarbonate values. This study indicates that serum neuron-specific enolase is elevated in diabetic ketoacidosis and correlated with the severity of hyperglycemia, ketosis, and acidosis. This study indicates that diabetic ketoacidosis may cause neuronal injury from which the patients recovered partially but not completely.


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