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Background/Objectives: Static reference intervals (RIs) fail to capture the dynamic changes in bioanalytes. This study aimed to develop gender-based continuous age- and season-related RIs for neuron-specific enolase (NSE) using real-world data and to compare them with partitioned RIs. Methods: The NSE results from 4097 individuals were included after rigorous screening. Partitioned RIs were determined using the Hoffmann method. Generalized additive models for location, scale and shape (GAMLSS) were selected to develop continuous RIs. Results: The partitioned RIs are as follows: <16.4 µg/L for males aged ≥19 years; <14.47 µg/L for females aged 19–49 years; and <17.25 µg/L for females aged ≥50 years. For continuous RIs, NSE levels in males remain stable with age, while in females, NSE levels evidently increase around the age of 50. Although less impactful than age, seasonal changes still affect NSE levels. Dynamic changes and continuous RIs for NSE are visualized in this study. Conclusions: We developed gender-based continuous age- and season-integrated RIs for NSE in North China, highlighting the variation in NSE levels in females with age and season. Compared to static RIs, continuous RIs are more responsive to NSE, potentially enhancing the precision and individualization of health assessments. [ABSTRACT FROM AUTHOR]

With the aim of improving the uncertainties associated with the correct diagnosis of seronegative rheumatoid arthritis (RA) and identifying those at risk of developing interstitial lung disease (ILD), we have designed new peptide antigens bearing three post-translational modifications (PTMs) (citrulline, homocitrulline and acetyl-lysine) related to RA that could complement existing tests based on anti-citrullinated peptide/protein antibodies (ACPAs). Several chimeric peptides were synthesized and comparatively tested as antigens in ELISAs with two cohorts of sera: 178 RAs and 110 healthy blood donors. The results indicated that although chimeric peptides containing all three PTMs and vimentin and enolase domains do not significantly outperform existing ACPA tests in terms of sensitivity and specificity, they show potential to complement current assays, especially when detecting antibodies in some seronegative patients. Furthermore, the presence of these autoantibodies significantly identified patients with RA and ILD. We can conclude that the identification of specific autoantibody profiles using synthetic antigens containing peptide domains derived from proteins present in the human joint could help in the early detection of the risk of ILD in patients with RA and be useful for adapting follow-up strategies and guiding decisions during treatment. [ABSTRACT FROM AUTHOR]

Organic carbon fixed in chloroplasts through the Calvin–Benson–Bassham Cycle can be diverted toward different metabolic fates, including cytoplasmic and mitochondrial respiration, gluconeogenesis, and synthesis of diverse plastid metabolites via the pyruvate hub. In plants, pyruvate is principally produced via cytoplasmic glycolysis, although a plastid-targeted lower glycolytic pathway is known to exist in non-photosynthetic tissue. Here, we characterized a lower plastid glycolysis–gluconeogenesis pathway enabling the direct interconversion of glyceraldehyde-3-phosphate and phospho-enol-pyruvate in diatoms, ecologically important marine algae distantly related to plants. We show that two reversible enzymes required to complete diatom plastid glycolysis–gluconeogenesis, Enolase and bis-phosphoglycerate mutase (PGAM), originated through duplications of mitochondria-targeted respiratory isoforms. Through CRISPR-Cas9 mutagenesis, integrative 'omic analyses, and measured kinetics of expressed enzymes in the diatom Phaeodactylum tricornutum, we present evidence that this pathway diverts plastid glyceraldehyde-3-phosphate into the pyruvate hub, and may also function in the gluconeogenic direction. Considering experimental data, we show that this pathway has different roles dependent in particular on day length and environmental temperature, and show that the cpEnolase and cpPGAM genes are expressed at elevated levels in high-latitude oceans where diatoms are abundant. Our data provide evolutionary, meta-genomic, and functional insights into a poorly understood yet evolutionarily recurrent plastid metabolic pathway. Environmental and experimental methods reveal the importance of plastid-targeted Enolase and bis-phosphoglycerate mutase enzymes to diatoms, marine algae that contribute to global primary production. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the serum levels of neuron-specific enolase (NSE) in sepsis-associated encephalopathy (SAE) and perform a meta-analysis to assess the diagnostic and prognostic potential of serum NSE in SAE patients. Methods: We searched English and Chinese databases for studies related to SAE that reported serum NSE levels until November 2023. We extracted information from these studies including the first author and year of publication, the number of samples, the gender and age of patients, the collection time of blood samples in patients, the assay method of serum NSE, the study methods, and the levels of serum NSE with units of ng/mL. The quality assessment of diagnostic accuracy studies 2 (QUADAS-2) tool was used to evaluate the study quality. A meta-analysis was performed using Review Manager version 5.3, employing either a random effects model or a fixed effects model. Results: A total of 17 studies were included in the final meta-analysis, including 682 SAE patients and 946 NE patients. The meta-analysis demonstrated significantly higher serum NSE levels in SAE patients compared to NE patients (Z = 5.97, P < 0.001, MD = 7.79, 95%CI 5.23–10.34), irrespective of the method used for serum NSE detection (Z = 6.15, P < 0.001, mean difference [MD] = 7.75, 95%CI 5.28–10.22) and the study methods (Z = 5.97, P < 0.001, MD = 7.79, 95%CI 5.23–10.34). Furthermore, sepsis patients with a favorable outcome showed significantly lower levels of serum NSE compared to those with an unfavorable outcome (death or adverse neurological outcomes) (Z = 5.44, P < 0.001, MD = − 5.34, 95%CI − 7.26–3.42). Conclusion: The Serum level of NSE in SAE patients was significantly higher than that in septic patients without encephalopathy. The higher the serum NSE level in SAE patients, the higher their mortality rate and incidence of adverse neurological outcomes. [ABSTRACT FROM AUTHOR]

Background: Any illness that disrupts the central nervous system in the first few days of life can induce encephalopathy among neonates. This ailment can have a variety of causes. Of all the CSF neurobiochemical markers in babies with HIE, NSE has received the greatest amount of research. Up to four percent of all soluble brain proteins are NSE, a dimeric glycolytic enzyme. Neurons and neuroendocrine cells contain it primarily in their cytoplasm. When neurons suffer damage to their axons, NSE is found in high concentrations in their cytoplasm. Thus, it is sensitive for axonal injury and neuronal cell death and has a fairly high specificity for detecting axonal damage. Traditional terminology for neonatal encephalopathy (NE) has focused on hypoxic-ischemic encephalopathy, which occurs when an intrapartum incident causes perinatal hypoxia-ischemia. Objective: The purpose of this study was to review the diagnostic value of the Neuron-Specific Enolase biomarker in the evaluation of early detection and its role in prognosis of neonatal encephalopathy. Methods: In our search for information on NSE and its level in neonates with encephalopathy, we used Google Scholar, Science Direct, PubMed, and other internet databases. Additionally, the writers combed through relevant literature for references, however they only included researches that were either very recent or covering the years from 2010 to 2023. Conclusion: Serum NSE is considered to be a reliable marker for the diagnosis of different stages of NE. [ABSTRACT FROM AUTHOR]

Background: Neuron-specific enolase is a dimeric isoform of the glycolytic enzyme that is mostly present in neurons is important as a diagnostic and a prognostic value in pediatric encephalopathy which is common and is potentially life threatening, previous studies were done worldwide to detect its diagnostic and prognostic value in acute encephalopathy among adult and pediatric age groups. The current study aimed at evaluation of serum neuron specific enolase for early diagnosis of pediatric acute encephalopathy. Methods: This case control study was carried out in pediatric intensive care unit and the inpatient pediatric department, faculty of medicine, Zagazig University and was conducted on 24 patients suffering from acute encephalopathy and 24 patients presented with seizures without encephalopathy. serum neuron-specific enolase was measured. Results: Serum neuron-specific enolase level had sensitivity 95%, specificity 88.5%, PPV 94%, NPV 90% and accuracy 93% in prediction of encephalopathy. Conclusions: There was statistically significant increase in serum NSE levels in encephalopathy group more than seizures group. [ABSTRACT FROM AUTHOR]

SUMMARY: The protein‐repairing enzyme (PRE) PROTEIN L‐ISOASPARTYL METHYLTRANSFERASE (PIMT) influences seed vigor by repairing isoaspartyl‐mediated protein damage in seeds. However, PIMTs function in other seed traits, and the mechanisms by which PIMT affects such seed traits are still poorly understood. Herein, through molecular, biochemical, and genetic studies using overexpression and RNAi lines in Oryza sativa and Arabidopsis thaliana, we demonstrate that PIMT not only affects seed vigor but also affects seed size and weight by modulating enolase (ENO) activity. We have identified ENO2, a glycolytic enzyme, as a PIMT interacting protein through Y2H cDNA library screening, and this interaction was further validated by BiFC and co‐immunoprecipitation assay. We show that mutation or suppression of ENO2 expression results in reduced seed vigor, seed size, and weight. We also proved that ENO2 undergoes isoAsp modification that affects its activity in both in vivo and in vitro conditions. Further, using MS/MS analyses, amino acid residues that undergo isoAsp modification in ENO2 were identified. We also demonstrate that PIMT repairs such isoAsp modification in ENO2 protein, protecting its vital cellular functions during seed maturation and storage, and plays a vital role in regulating seed size, weight, and seed vigor. Taken together, our study identified ENO2 as a novel substrate of PIMT, and both ENO2 and PIMT in turn implicate in agronomically important seed traits. [ABSTRACT FROM AUTHOR]

The storage of serum tumor markers (STM) at −18 °C for one year has been a legal requirement in France since 1999, but has been abolished in 2022. This raises the question of the relevance of maintaining these biobanks in terms of conditions of storage. These should only be implemented after validation; in order to maintain the integrity of the biological sample and must be controlled over time according to the laboratoryʼs procedures. The aim of the study was to assess the suitability of storing 10 STMs by evaluating their stability after one year of storage at −18 °C. A new immuno-enzymatic assay (A+1) was conducted on samples that had been stored at −18 °C for one year after an initial assay (A) of one of the following STMs: carcino-embryonic antigen (CEA), alpha-fetoprotein (AFP), carbohydrate antigen 125 (CA125), carbohydrate antigen 15-3 (CA15-3), carbohydrate antigen 19-9 (CA19-9), total (TPSA), and free (FPSA) prostate-specific antigen, calcitonin (CT), thyroglobulin (TG), and neuro-specific enolase (NSE). The results were confronted to four different permissible error sources. In total, 1148 A+1 assays were performed. A strong correlation between A+1 and A values was found for all analytes, but with a statistically significant reduction in the mean A+1 concentration compared to the mean A concentration in 7/10 STMs. The bias induced by conservation seems to be technically unsustainable if we rely on the repositories closest to the current analytical performances. These results support the discontinuation of mandatory STM biobank storage at −18 °C, which requires considerable technical time and organizational effort. [ABSTRACT FROM AUTHOR]

Neuron-specific enolase (NSE) derived from neurons and peripheral neuroendocrine cells is a biomarker for neuroendocrine tumors and for prognostication in comatose cardiac arrest survivors. However, as platelets and erythrocytes contain NSE, hemolysis causes falsely elevated NSE. We used native serum and hemolysate derived from the same patients to make serial dilutions, and subsequently measured NSE (mNSE) and hemolytic index (HI) in each dilution. An algorithm suitable for the laboratory information system was developed based on the mNSE, HI and the estimated gradient of hemolytic interference from 30 patients. We estimated the associated uncertainty of the corrected NSE (cNSE) results based on the observed range of the gradient and derived an equation for cNSE for samples with limited hemolysis (i.e. 5 < HI ≤ 30): cNSE = mNSE − HI × (0.34 ± 0.23) µg/L. By semi-quantitatively grading the contribution from limited hemolysis, a texted result noting the hemolysis-associated degree of uncertainty can accompany the cNSE result. The major challenge of hemolysis when using serum NSE as a biomarker can be managed using an automated algorithm for correction of NSE results based on degree of hemolysis. However, laboratorians and clinicians should be aware of the limitations associated with in vivo hemolysis. [ABSTRACT FROM AUTHOR]

Research on prognostic factors for good outcomes in out-of-hospital cardiac arrest (OHCA) survivors is lacking. We assessed whether normal levels of normal neuron-specific enolase (NSE) value would be useful for predicting good neurological outcomes in comatose OHCA survivors treated with targeted temperature management (TTM). This registry-based observational study with consecutive adult (≥18 years) OHCA survivors with TTM who underwent NSE measurement 48 hours after cardiac arrest was conducted from October 2015 to November 2022. Normal NSE values defined as the upper limit of the normal range by the manufacturer (NSE <16.3 μg/L) and guideline-suggested (NSE < 60 μg/L) were examined for good neurologic outcomes, defined as Cerebral Performance Categories ≤2, at 6 months post-survival. Among 226 OHCA survivors with TTM, 200 patients who underwent NSE measurement were enrolled. The manufacturer-suggested normal NSE values (<16.3 μg/L) had a specificity of 99.17% for good neurological outcomes with a very low sensitivity of 12.66%. NSE <60 μg/L predicted good outcomes with a sensitivity of 87.34% and specificity of 72.73%. However, excluding 14 poor-outcome patients who died from multi-organ dysfunction excluding hypoxic brain injury, the sensitivity and specificity of normal NSE values were 12.66% and 99.07% of NSE < 16.3 μg/L, and 87.34% and 82.24% of NSE < 60 μg/L. The manufacturer-suggested normal NSE had high specificity with low sensitivity, but the guideline-suggested normal NSE value had a comparatively low specificity for good outcome prediction in OHCA survivors. Our data demonstrate normal NSE levels can be useful as a tool for multimodal appropriation of good outcome prediction. [ABSTRACT FROM AUTHOR]

Candida albicans is the predominant cause of systemic candidiasis, although other non albicans Candida species are progressively becoming more widespread nowadays. Candida auris has emerged as a deadly multidrug-resistant fungal pathogen, posing a significant threat to global public health. In the absence of effective antifungal therapies, the development of a vaccine against C. auris infections is imperative. Enolase, a key glycolytic enzyme, has emerged as a promising vaccine candidate due to its immunogenic properties and essential role in fungal virulence. Herein, full-length Enolase gene sequences from C. albicans and C. auris were cloned into suitable expression vector and transformed into Escherichia coli expression hosts. Recombinant Enolase proteins were successfully expressed and purified using affinity chromatography under native conditions, followed by SDS-PAGE characterization and Western blot analysis. CD spectroscopy verified the existence of expressed proteins in soluble native conformation. Preliminary in silico studies verified the immunogenicity of recombinant Enolase proteins isolated from both C. albicans and C. auris. Furthermore, bioinformatics analysis revealed conserved B-cell and T-cell epitopes across C. albicans and C. auris Enolase proteins, suggesting potential cross-reactivity and broad-spectrumvaccine efficacy. Our findings are anticipated to play a role in advancing therapeutic as well as diagnostic strategies against systemic candidiasis. [ABSTRACT FROM AUTHOR]

A study published in Systematic Reviews by Zhi et al. explores the use of neuron-specific enolase (NSE) as a diagnostic tool for sepsis-associated encephalopathy (SAE). The study found that SAE patients had significantly higher levels of serum NSE compared to septic patients without encephalopathy. Higher levels of serum NSE were associated with increased mortality rates and adverse neurological outcomes. While the study provides valuable insights, further research is needed to fully understand the relationship between NSE and SAE. [Extracted from the article]

Hybrid breeding is an effective approach to generate better varieties and prevent variety degradation. The present study investigated the metabolic changes underlying growth superiority in the novel Gymnocypris hybrid (GH), Gymnocypris przewalskii ♀ (GP) × G. eckloni ♂ (GE). The ranking of survival rate was GH > GE > GP, whereas the ranking of growth rate was GE > GH > GP. A proteomic analysis of G. hybrid and its parents was conducted to elucidate the metabolic changes underlying growth superiority. Identified pathways were primarily associated with amino acid, carbohydrate, energy, lipid, and nucleotide metabolism. These metabolic pathways, which are closely associated with growth, are controlled through regulation of the expression of numerous proteins, including adenosylhomocysteinase, hydroxypyruvate reductase, glutamate-cysteine ligase, L-lactate dehydrogenase, creatine kinase, GDP-L-fucose synthase, pyruvate kinase, fructose-bisphosphate aldolase, carbonic anhydrase, phosphopyruvate hydratase, phosphoglycerate kinase, S-(hydroxymethyl) glutathione dehydrogenase, and AMP deaminase. Real-time PCR assays showed that the level of mRNA expression of differentially expressed genes was positively correlated with growth. Proteins that were differentially expressed in GH exhibited fewer differences from GP and more differences from GE. These data are the first to reveal the molecular mechanism whereby growth is regulated in G. hybrid and its parents at the protein level. The study thus provides important information for genetic breeding and improvement of G. hybrid for aquaculture production. [ABSTRACT FROM AUTHOR]

[Objective]The objective of this study is to identify the genes(TaENO2s)encoding the enolase family member ENO2 in the important crop plant of wheat(Triticum aestivum L.)and to determine the alternative translation feature and protein enolase activity of TaENO2s.[Method]Wheat TaENO2s were identified by bioinformatics. One of the identified TaENO2s was selected as a representative for protoplast-based exogenous expression and characterization of alternative translation products. This selected TaENO2 was also subjected to prokaryotic expression for purification of recombinant protein. The enolase activity of the purified recombinant protein was determined with in vitro assays.[Result]The hexaploid wheat genome had three homeologous TaENO2s which sequences encoded a conserved enolase catalytic center and had a putative alternative translation start site at the internal ATG codon encoding the residue M94(ATGM94) of the enolase sequence. When exogenously expressed in protoplasts, the representative TaENO2 encoded two proteins, one full-length form of cytoplasmic and nuclear enolase protein and one N-terminal truncated form of nuclear transcriptional repressor TaMBP-1, while the variant of the same gene containing mutated ATGM94 only encoded the full-length form of enolase protein. Soluble recombinant GST-TaENO2 protein expressed in Escherichia coli was successfully purified and verified to have an in vitro enzymatic activity to catalyze the conversion from 2-phosphoglycerate (2-PGA)to phosphoenolpyruvate(PEP)[Conclusion]The wheat genome has three TaENO2 genes encoding the enolase protein ENO2. Under the condition of exogenous expression, TaENO2 encodes two protein products via mRNA alternative translation, one enolase protein translated from the first start codon and one TaMBP-1 protein translated from the internal start codon(2-PGA)to phosphoenolpyruvate(PEP).[Conclusion[The wheat genome has three TaENO2 genes encoding the enolase protein ENO2. Under the condition of exogenous expression, TaENO2 encodes two protein products via mRNA alternative translation, one enolase protein translated from the first start codon and one TaMBP-1 protein translated from the internal start codon ATGM94. The prokaryotically expressed recombinant protein GST-TaENO2 possesses in vitro enolase activity.. The prokaryotically expressed recombinant protein GST-TaENO2 possesses in vitro enolase activity. [ABSTRACT FROM AUTHOR]

Since the discovery of the neuron-specific protein by Moore and McGregor in 1965, tens of thousands of studies have investigated the basic and applied significance of neuron-specific enolase (NSE). This promising biomarker, according to many researchers, has not found widespread use in clinical practice, particularly in acute cerebrovascular accidents. Moreover, the several studies refuting the usefulness of serum NSE measurement in critically ill patients leads us to consider the reasons for such contradictory conclusions. In this article, we have analyzed the main directions in the study of NSE and expressed our perspective on the reasons for the contradictory results and the difficulties in implementing the results of these studies in clinical practice. In our opinion, the method of the enzyme-linked immunosorbent assay (ELISA) used in the majority of the studies is inappropriate for the evaluation of NSE as a marker of central nervous system damage, because it does not allow for the differentiation of heterodimers of enolases and the assessment of the enzymatic activity of this group of enzymatic proteins. Therefore, the methodological approach for the evaluation of NSE (γγ-enolase) as a biomarker needs to be elaborated and improved. Furthermore, the specificity of the applied research methods and the appropriateness of the continued use of the term "neuron-specific enolase" must be addressed. [ABSTRACT FROM AUTHOR]

Background: We compared the performance of 21 different assays performed by the Wantai Wan200+ (Wantai BioPharm, Beijing, China) with respect to other methods in use at the University Hospital of Padova (AOPD), Italy. Methods: The plasma (P) or serum (S) of 5027 leftover samples, collected from May to Sept 2023, was either analyzed or frozen at −20 °C. Beckman DXI800 (DXI), Roche Cobas 8000 e801 (RC), Snibe Maglumi 4000 plus (SM), DiaSorin Liaison XL (DL) and Binding Site Optilite (BS) equipment were used at the AOPD. P-procalcitonin (PCT), DXI; P-Troponin I (TnI), DXI; S-CA125, DXI; S-free PSA (f-PSA), DXI; S-total PSA (t-PSA), DXI; S-IL6, SM; P-Troponin T (TnT), RC; P-NT-proBNP, RC; P-Neuron-Specific Enolase (NSE), RC; S-CA15-3, DL; S-CA19-9, DL; S-AFP, DL; and S-CEA, DL were tested in fresh samples. P-Myoglobin (Myo), DXI; P-Cyfra21-1, RC; S-β2 microglobulin (B2MIC), BS; S-HE4, SM; S-PGI, SM; S-PGII, SM; S-CA72-4, SM; and S-CA50, SM were analyzed in frozen and thawed samples. Bland–Altman (BA), Passing–Bablok (PB) and Cohen's Kappa (CKa) metrics were used as statistics. Results: An excellent comparability profile was found for 11 analytes. For example, the t-PSA CKa was 0.94 (95%CI: 0.90 to 0.98), and the PB slope and intercept were 1.02 (95%CI: 0.99 to 1.03) and 0.02 (95%CI: 0.01 to 0.03), respectively; the BA bias was 2.25 (95%CI: −0.43 to 4.93). Ten tested measurands demonstrated a suboptimal comparability profile. Biological variation in EFLM (EuBIVAS) performance specifications was evaluated to assess the clinical relevance of measured biases. Conclusions: Evaluation of the Wantai Wan200+'s performance suggests that between-method differences did not exceed the calculated bias. Metrological traceability may influence the comparisons obtained for some measurands. [ABSTRACT FROM AUTHOR]

Neonatal brain injury (NBI) is a critical condition for preterm neonates with potential long-term adverse neurodevelopmental outcomes. This prospective longitudinal case–control study aimed at investigating the levels and prognostic value of serum neuron-specific enolase (NSE) during the first 3 days of life in preterm neonates (<34 weeks) that later developed brain injury in the form of either periventricular leukomalacia (PVL) or intraventricular hemorrhage (IVH) during their hospitalization. Participants were recruited from one neonatal intensive care unit, and on the basis of birth weight and gestational age, we matched each case (n = 29) with a neonate who had a normal head ultrasound scan (n = 29). We report that serum NSE levels during the first three days of life do not differ significantly between control and preterm neonates with NBI. Nevertheless, subgroup analysis revealed that neonates with IVH had significantly higher concentrations of serum NSE in comparison to controls and neonates with PVL on the third day of life (p = 0.014 and p = 0.033, respectively). The same pattern on the levels of NSE on the third day of life was also observed between (a) neonates with IVH and all other neonates (PVL and control; p = 0.003), (b) neonates with II–IV degree IVH and all other neonates (p = 0.003), and (c) between control and the five (n = 5) neonates that died from the case group (p = 0.023). We conclude that NSE could be an effective and useful biomarker on the third day of life for the identification of preterm neonates at high risk of developing severe forms of IVH. [ABSTRACT FROM AUTHOR]

Introduction COVID-19 is a relevant issue for scientists around the world. Considering the development of numerous complications due to COVID-19, the search for diagnostic approaches for the timely detection of probable lesions of the nervous system is urgent. Objectives was to determine the diagnostic and prognostic value of the NSE marker in children with COVID-19 regarding the complicated course and symptoms of nervous system damage. Materials and Methods We conducted a cohort, observational, retrospective study involving 88 children aged 1 month to 18 years with laboratory-confirmed COVID-19 by PCR. Blood serum was collected for the study to assess the level of the neurobiomarker NSE by enzyme immunoassay. We divided patients into two cohorts according to the course of the disease - the main one, which included 42 patients with a complicated course of COVID-19, and a control group - 46 patients with an uncomplicated course of the disease. The study protocol was approved by the Local Ethics Committee of the hospital. Results: In the patients of the control group, NSE was observed at the level of 12.1±1.2 µg/l, while in the children of the main one, the indicator reached 16.9±1.5 µg/l (p=0.087). Increase in the level of NSE above 15 µg/L associated with a significant increase in the risk of the appearance of clinical symptoms of damage to the nervous system and a complicated course in children with COVID-19 (p<0.05). We noted a tendency towards an increase in NSE with increased ESR indicators >10mm/h (p<0.1), a decrease in PTI <85% (p=0,03) and an increase in D-dimer >2.5mg/l (p<0.1). Conclusions We found the diagnostic and prognostic value of the NSE marker in children with COVID-19 regarding the complicated course and symptoms of nervous system damage. [ABSTRACT FROM AUTHOR]

To explore the clinical significance of dynamic monitoring of cerebrospinal fluid (CSF) and serum Lactic acid（Lac), neuron-specific enolase (NSE), and the blood–brain barrier (BBB) index in evaluating the condition and prognosis after a severe traumatic brain injury (TBI). A total of 52 severe TBI patients admitted to the Department of Neurosurgery within 24 hours after injury were dynamically monitored. CSF and serum samples were collected on the 1st, 3rd, and 7th day after a severe TBI to monitor the changes in Lac, NSE, and the BBB index. Intracranial pressure (ICP), Glasgow coma scale (GCS), and 6-month Glasgow outcome scale-extended (GOS-E) were tested. According to the results of GOS-E, the patients were divided into two groups (i.e. the poor prognosis group and good prognosis group). Statistical analysis was conducted to investigate the clinical significance of dynamic monitoring of CSF and serum Lac, NSE, and BBB index after a severe TBI. After a severe TBI, the levels of Lac, NSE, and BBB in CSF and serum were significantly higher than those in the normal range. Lac, NSE, and the BBB index did not correlate with ICP (except serum Lac) but had correlations with GCS and post-injury 6 months post-injury (except serum Lac). Moreover, the correlations between Lac, NSE, and BBB index were statistically significant (p < 0.05): CSF Lac and CSF NSE; CSF Lac and serum NSE; Lac and BBB index of CSF; Lac and BBB index of CSF; NSE and CSE of serum; CSF NSE and BBB index; and serum NSE and BBB index. Additionally, serum NSE is correlated with NSE in CSF (p < 0.05). After a severe TBI, dynamic monitoring of CSF and serum Lac, NSE, and BBB index has the potential to assess the condition, predict the prognosis, and have clinical significance. [ABSTRACT FROM AUTHOR]

This study evaluates the protective effect of Hesperidin (HES), flavanoglycone, during pre-eclampsia developed pregnancy. The pregnant rats were randomly divided into five groups as Control, L-NAME (25 mg/kg), HES (100 mg/kg), L-NAME-HES and L-NAME P-HES. After the 13th day of pregnancy, the chemicals were administrated until the 20th day. 20 days after the offspring's birth, they were separated from their mothers and all rats were sacrificed after 6 weeks' time. Serum samples were analyzed for levels of Glutathione (GSH), lipid peroxidation (LPO), and neuron-specific enolase (NSE) activity. Urine samples were analyzed for the proteinuria. While Proteinuria and LPO level increasing, GSH levels decreased in the L-NAME group when compared to the Control. As we compared L-NAME group with the L-NAMEHES and L-NAME P-HES groups, the GSH levels increased significantly while LPO levels in the HES, L-NAME-HES, L-NAME P-HES groups were decreasing. The NSE activity significantly increased in the L-NAME group compared to the Control. In contrast to the L-NAME group, its activity decreased in HES, L-NAME-HES and L-NAME P-HES groups significantly. Briefly, it can be said that HES has a significant effect on both the LPO levels and the NSE activity in the case of pre-eclampsia. [ABSTRACT FROM AUTHOR]

Lung cancer remains the leading cause of cancer mortality worldwide. Small cell lung cancer (SCLC) accounts for 10–15% of cases and has an overall 5-years survival rate of only 15%. Neuron-specific enolase (NSE) has been identified as a useful biomarker for early SCLC diagnosis and therapeutic monitoring. This work reports an electrochemical immunosensing platform based on a graphene-graphitic carbon nitride (g-C3N4) nanocomposite for ultrasensitive NSE detection. The g-C3N4 nanosheets and graphene nanosheets were synthesized via liquid exfoliation and integrated through self-assembly to form the nanocomposite. This nanocomposite was used to modify screen-printed carbon electrodes followed by covalent immobilization of anti-NSE antibodies. The unique properties of the graphene-g-C3N4 composite facilitated efficient antibody loading while also enhancing electron transfer efficiency and electrochemical response. Systematic optimization of experimental parameters was performed. The immunosensor exhibited a wide linear detection range of 10 pg/mL to 100 ng/mL and low limit of detection of 3 pg/mL for NSE along with excellent selectivity against interferences. Real serum matrix analysis validated the applicability of the developed platform for sensitive and accurate NSE quantifica-tion at clinically relevant levels. This novel graphene-g-C3N4 nanocomposite based electro-chemical immunoassay demonstrates great promise for early diagnosis of SCLC. [ABSTRACT FROM AUTHOR]

In the current study a simple and highly specific label-free impedimetric neuron specific enolase (NSE) immunosensor based on a copolymer matrix-coated disposable electrode was designed and tested. The copolymer matrix was prepared using a very conductive EDOT monomer and semi-conductive thiophene-bearing epoxy groups (ThEp), and the combination of the two monomers enhanced the conductivity and protein loading capacity of the electrode surface. The P(ThEp-co-EDOT) copolymer matrix was prepared via a drop-casting process and anti-NSE recognition biomolecules were immobilized directly on the epoxy groups of the copolymer. After the coupling of NSE molecules on the P(ThEp-co-EDOT) copolymer matrix-coated electrode surface, the charge transfer resistance (Rct) of the biosensor changed dramatically. These changes in Rct were proportional to the NSE molecule amounts captured by anti-NSE molecules. Under optimized experimental conditions, the increment in the Rct value was proportional to the NSE concentration over a range of 0.01 to 25 pg mL−1 with a detection limit (LOD) of 2.98 × 10−3 pg mL−1. This copolymer-coated electrode provided a lower LOD than the other biosensors. In addition, the suggested electrochemical immuno-platform showed good selectivity, superior reproducibility, long-term stability, and high recovery of NSE in real serum (95.64–102.20%) and saliva (95.28–105.35%) samples. These results showed that the present system had great potential for electrochemical biosensing applications. [ABSTRACT FROM AUTHOR]

Background/Aim. Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis, characterized by brain dysfunction and associated with a poor prognosis. SAE has a complex pathogenesis, and its severity is in close association with the levels of various serum factors. The aim of the study was to investigate the correlation of tumor necrosis factor (TNF)-a, monocyte chemoattractant protein (MCP)-1, and neuron-specific enolase (NSE) levels with the severity of SAE and to analyze the prognostic values of the three parameters. Methods. This prospective study enrolled 126 patients treated for SAE from June 2020 to June 2022. The levels of TNF-α, MCP-1, and NSE were measured, and the severity of SAE was evaluated using the Sequential Organ Failure Assessment (SOFA) score. Based on the SOFA score, the patients were assigned to two groups: a group with a bad prognosis and a group with a good prognosis. The correlations of TNF-α, MCP-1, and NSE levels with the severity of SAE were analyzed, and their prognostic values were evaluated during a 28-day follow-up. Results. The mean levels of TNF-α, MCP-1, and NSE and the SOFA score of the 126 patients with SAE were 6.52 ± 1.48 pg/mL, 62.53 ± 18.49 pg/mL, 8.61 ± 2.17 ng/mL, and 10.24 ± 2.86 points, respectively. Pearson's analysis demonstrated significant correlations between TNF-α, MCP-1, and NSE levels and the SOFA score of patients with SAE (r > 0, p < 0.05). Of the 126 patients, 61 (48.4%) had a poor prognosis, while 65 (51.6%) had a good prognosis. Increased serum TNF-α, MCP-1, and NSE levels were risk factors for the poor prognosis of patients with SAE [odds ratio (OR) > 1, p < 0.05]. The areas under the receiver operating characteristic (ROC) curves of serum TNF-α, MCP-1, and NSE levels were all > 0.7, suggesting high predictive values of these parameters. Conclusion. Serum TNF-α, MCP-1, and NSE levels are closely correlated with the severity of SAE and may work as valuable predictors of treatment outcome. [ABSTRACT FROM AUTHOR]

Background: The high number of accidents and traumatic brain injuries, especially in the productive age group, causes a lot of morbidity and mortality. A fast and accurate examination method is needed for the diagnosis and treatment of traumatic brain injury. Nerve damage biomarkers such as Neuron Specific Enolase, S100B, Glial Fibrillary Acidic Protein, and Myelin Basic Protein, have been used globally both for research and daily use to determine the severity of traumatic brain injury. Methods: Searches and journal searches were carried out from Science Direct, Scopus, Springer Link, and PubMed, with the keywords "Neuron Specific Enolase", "S100B", "Glial Fibrillary Acidic Protein", "Myelin Basic Protein", and "Traumatic Brain Injury ". Screening was carried out using PRISMA 2021 to look for studies that met the criteria and were of sufficient study quality according to the Newcastle-Ottawa Scale. Results: Twenty-three studies were collected and further grouped based on outcomes, both prognostic and survival outcomes. Neuron Specific Enolase, S100B, and Glial Fibrillary Acidic Protein values were higher in poor outcomes (all p values < 0.001) and poor survival (all p values < 0.001) in traumatic brain injury. Myelin Basic Protein was not significant in poor outcome (p = 0.35), but was higher in poor survival (p < 0.001) in traumatic brain injury. Conclusion: Neuron Specific Enolase, S100B, and Glial Fibrillary Acidic Protein, can be used as markers for prognostic and survival value in traumatic brain injury. Myelin Basic Protein can be used as a marker for survival value in traumatic brain injury. [ABSTRACT FROM AUTHOR]

Background: Ribosomal protein SA (RPSA) of human brain microvascular endothelial cells (HBMECs) can transfer from the cytosol to the cell surface and act as a receptor for some pathogens, including Streptococcus suis serotype 2 (SS2), a zoonotic pathogen causing meningitis in pigs and humans. We previously reported that SS2 virulence factor enolase (ENO) binds to RPSA on the cell surface of HBMECs and induces apoptosis. However, the mechanism that activates RPSA translocation to the cell surface and induces ENO-mediated HBMEC apoptosis is unclear. Results: Here, we show that RPSA localization and condensation on the host cell surface depend on its internally disordered region (IDR). ENO binds to the IDR of RPSA and promotes its interaction with RPSA and vimentin (VIM), which is significantly suppressed after 1,6-Hexanediol (1,6-Hex, a widely used tool to disrupt phase separation) treatment, indicating that ENO incorporation and thus the concentration of RPSA/VIM complexes via co-condensation. Furthermore, increasing intracellular calcium ions (Ca2+) in response to SS2 infection further facilitates the liquid-like condensation of RPSA and aggravates ENO-induced HBMEC cell apoptosis. Conclusions: Together, our study provides a previously underappreciated molecular mechanism illuminating that ENO-induced RPSA condensation activates the migration of RPSA to the bacterial cell surface and stimulates SS2-infected HBMEC death and, potentially, disease progression. This study offers a fresh avenue for investigation into the mechanism by which other harmful bacteria infect hosts via cell surfaces' RPSA. [ABSTRACT FROM AUTHOR]

Background: Ribosomal protein SA (RPSA) of human brain microvascular endothelial cells (HBMECs) can transfer from the cytosol to the cell surface and act as a receptor for some pathogens, including Streptococcus suis serotype 2 (SS2), a zoonotic pathogen causing meningitis in pigs and humans. We previously reported that SS2 virulence factor enolase (ENO) binds to RPSA on the cell surface of HBMECs and induces apoptosis. However, the mechanism that activates RPSA translocation to the cell surface and induces ENO-mediated HBMEC apoptosis is unclear. Results: Here, we show that RPSA localization and condensation on the host cell surface depend on its internally disordered region (IDR). ENO binds to the IDR of RPSA and promotes its interaction with RPSA and vimentin (VIM), which is significantly suppressed after 1,6-Hexanediol (1,6-Hex, a widely used tool to disrupt phase separation) treatment, indicating that ENO incorporation and thus the concentration of RPSA/VIM complexes via co-condensation. Furthermore, increasing intracellular calcium ions (Ca2+) in response to SS2 infection further facilitates the liquid-like condensation of RPSA and aggravates ENO-induced HBMEC cell apoptosis. Conclusions: Together, our study provides a previously underappreciated molecular mechanism illuminating that ENO-induced RPSA condensation activates the migration of RPSA to the bacterial cell surface and stimulates SS2-infected HBMEC death and, potentially, disease progression. This study offers a fresh avenue for investigation into the mechanism by which other harmful bacteria infect hosts via cell surfaces’ RPSA. [ABSTRACT FROM AUTHOR]

A photoelectrochemical (PEC) immunosensor was designed based on MgIn2S4-decorated inorganic halide perovskite CsPbBr3 combined with the signal polarity conversion strategy for neuron-specific enolase (NSE) detection. CsPbBr3 was applied as the basic photoactive material owing to its excellent optical and electronic properties, which provide a good PEC performance for sensor construction. In order to improve the stability of this perovskite, the three-dimensional flower-like MgIn2S4 with a desirable direct band gap was applied to enhance the PEC response. Also, the excellent structure of MgIn2S4 provides large surface-active sites for CsPbBr3 loaded. For enhancing the detection sensitivity of PEC immunosensor, p-type CuInS2 was used as a signal probe which fixed on detection antibody (Ab2). When the target NSE was present, the photogenerated electrons produced by CuInS2 were transferred to the test solution, and the polarity of PEC signal changes. Based on the above photosensitive materials and signal conversion strategy, the proposed PEC immunosensor showed favorable detection performance, and the linear detection range is 0.0001 ~ 100 ng/mL with a 38 fg/mL of detection limit. The proposed strategy improved the adhibition of CsPbBr3 in the analytical chemistry field as well as provided a reference method for other protein detections. [ABSTRACT FROM AUTHOR]

Here, we employ coelution experiments and far‐western blotting to identify stable interactions between the main components of the B. subtilis degradosome and the small proteins SR1P and SR7P. Our data indicate that B. subtilis has a degradosome comprising at least RNases Y and PnpA, enolase, phosphofructokinase, glycerol‐3‐phosphate dehydrogenase GapA, and helicase CshA that can be co‐purified without cross‐linking. All interactions were corroborated by far‐western blotting with proteins purified from E. coli. Previously, we discovered that stress‐induced SR7P binds enolase to enhance its interaction with and activity of enolase‐bound RNase Y (RnY), while SR1P transcribed under gluconeogenic conditions interacts with GapA to stimulate its interaction with and the activity of RnjA (RnjA). We show that SR1P can directly bind RnjA, RnY, and PnpA independently of GapA, whereas SR7P only interacts with enolase. Northern blotting suggests that the degradation of individual RNAs in B. subtilis under gluconeogenic or stress conditions depends on either RnjA or RnY alone or on RnjA‐SR1P, RnY‐SR1P, or RnY‐Eno. In vitro degradation assays with RnY or RnjA substrates corroborate the in vivo role of SR1P. Currently, it is unknown which substrate property is decisive for the utilization of one of the complexes. [ABSTRACT FROM AUTHOR]

The prediction of outcomes following cardiac arrest continues to provide significant difficulties. A preferred strategy involves adopting a multimodal approach, which encompasses the careful evaluation of the biomarker neuron-specific enolase (NSE). This systematic review and meta-analysis aimed to gather and summarize new and existing evidence on the prediction effect of neuron-specific enolase for survival to hospital discharge among adult patients with cardiac arrest. We searched PubMed Central, Scopus, EMBASE databases, and the Cochrane Library without language restrictions from their inceptions until 30 October 2023 and checked the reference lists of the included studies. Pooled results were reported as standardized mean differences (SMDs) and were presented with corresponding 95% confidence intervals (CIs). The primary outcome was survival to hospital discharge (SHD). Eighty-six articles with 10,845 participants were included. NSE showed a notable degree of specificity in its ability to predict mortality as well as neurological status among individuals who experienced cardiac arrest (p < 0.05). This study demonstrates the ability to predict fatality rates and neurological outcomes, both during the time of admission and at various time intervals after cardiac arrest. The use of NSE in a multimodal neuroprognostication algorithm has promise in improving the accuracy of prognoses for persons who have undergone cardiac arrest. [ABSTRACT FROM AUTHOR]

Neuron-specific enolase (NSE), which is a highly specific marker for neurons, could be a predictor for prognosis in patients with symptomatic intracranial hemorrhage (sICH) with acute ischemic stroke who are receiving endovascular treatment (EVT). This study aimed to investigate the relationship between NSE and sICH in patients with acute anterior circulation stroke undergoing EVT. A total of 215 consecutive patients with acute stroke treated with EVT were included. Patients with stroke and acute anterior circulation occlusion, receiving EVT treated at our hospital, were enrolled between January 2017 and August 2021. NSE level was measured on arrival at the neurology intensive care unit after EVT. The patients were divided into 2 groups according to whether sICH was present. Univariate and multivariate analyses were performed. NSE level was also incorporated into the TAG score (modified Thrombolysis in Cerebral Infarction score, Alberta Stroke Program Early CT Score, and glucose level), which was developed as a scoring system to predict sICH, and the prediction capability was compared with the TAG score alone. Causal inference was performed using the package DoWhy in Python to evaluate the causal relationship between NSE and sICH. The area under the curve (AUC) value of NSE showed moderate accuracy, with an AUC value of 0.729 (95% confidence interval, 0.655–0.795; P < 0.001). The NSE cutoff value was set at 23.88 ng/mL. When the NSE level ≥23.88 ng/mL, the sensitivity was 58.33% and the specificity was 78.72% (P < 0.001). The AUC for the TAG + NSE score was 0.801 compared with an AUC of 0.632 for the TAG score (Z = 2.034; P = 0.042). A causal inference model using the DoWhy library shows a proportional relationship between NSE and the diagnosis of sICH. This study is the first to show that increased NSE level is an independent predictor of sICH in patients with acute anterior circulation stroke who are undergoing endovascular treatment. [ABSTRACT FROM AUTHOR]

The early stages of diabetic peripheral neuropathy (DPN) are symptomless. A reliable dependable and sensitive biomarker is needed for the purpose of early identification of diabetic peripheral neuropathy. The main objective of the study was to evaluate the accuracy of serum neuron-specific enolase (NSE) as a biomarker for early identification of diabetic peripheral neuropathy. Patient samples were collected from the National Diabetes Center, Mustansiriyah University; a case control study was done from April 2022 to November 2022, in Baghdad, Iraq. One hundred sixty individuals between 30 to 60 years-old were included. Participants were divided into three groups: group one included 40 type 2 diabetic patients with peripheral neuropathy, group two consisted of 40 type 2 diabetic patients without peripheral neuropathy and group three included 80 apparently in good health as the control. Toronto Clinical Neuropathy Scoring System (TCSS) was used for clinical evaluation of peripheral neuropathy. Glycated hemoglobin (HbA1c) was measured by the CLOVER A1c system. In addition, serum NSE levels were measured by Enzyme Linked Immunosorbent Assay (ELISA) technique. Age, sex, and other standard variables were used as a basis for comparisons between groups. Statistically, diabetic patients with peripheral neuropathy demonstrated higher level of NSE (28.42±6.93 ng/ml) than did either diabetic patients without peripheral neuropathy (21.07±2.0 ng/ml) or controls (12.54±2.34 ng/ml) with a high degree of significance (p <0.001). In the context of Discrimination between DPN patients and diabetic patients without neuropathy, the area under curve for neuron-specific enolase was 0.812, 95% confidence interval [CI] = 0.716-0.909, p <0.001. Cut-off value of serum neuron-specific enolase was 22.53 ng/ml, sensitivity and specificity were 70% and 77%, respectively. In the context of discrimination between DPN and controls, the area under curve for neuron-specific enolase was 1.00, 95% confidence interval was 1.0-1.0, p <0.001. At a cut-off value of serum neuron-specific enolase = 18.3 ng/ml, both the sensitivity and specificity were 100%. Neuron-specific enolase could potentially be used as a biomarker to detect early diabetic peripheral neuropathy and prevent it from developing to an advanced state. [ABSTRACT FROM AUTHOR]

Objective To explore the clinical significance of monitoring neuron specific enolase (NSE), carbohydrate antigen 125 (CA125), and carbohydrate antigen 199 (CA199) in patients with pneumoconiosis. Methods A retrospective analysis was conducted among 222 patients with pneumoconiosis admitted to this hospital from January 2018 to December 2022. The patients were divided into three groups according to the stage of pneumoconiosis (stage I, II, and III). The serum levels and abnormal rates of NSE, CA125, and CA199 among these groups were compared. Results Among the 222 patients with pneumoconiosis, 51 (22.97%) were in stage I, 52 (23.42%) were in stage II, and 119 (53.61%) were in stage III. There were statistically significant differences in serum NSE and CA125 levels among pneumoconiosis patients at different stages (P < 0.001), and serum NSE and CA125 levels in patients at stage III were higher than those in stage I and stage II (P < 0.001). There was no statistically significant difference in serum CA199 level among pneumoconiosis patients at different stages (P = 0.163). The abnormal rates of serum NSE, CA125, and CA199 levels among 222 patients were 45.05%, 27.93%, and 2.70%, respectively. There were statistically significant differences in serum NSE and CA125 abnormal rates among pneumoconiosis patients at different stages (both P < 0.001), and both showed an increasing trend with the increase of stage. Conclusions Monitoring serum NSE and CA125 in patients with pneumoconiosis can indicate the progression of their condition and provide references for the treatment plan. [ABSTRACT FROM AUTHOR]

Objective: To explore the application value of magnetic resonance imaging(MRI) diffusion tensor imaging(DTI)parameters combined with serum neuron specific enolase(NSE) and lipoprotein-associated phospholipase A2(Lp-PLA2) in the diagnosis and risk assessment of poor prognosis of patients with cerebral infarction. Methods: 106 patients with cerebral infarction who were admitted to China Japan Friendship Hospital of Jilin University from March 2021 to September 2022 were selected as cerebral infarction group, another 62 healthy volunteers who were underwent physical examinations during the same period were selected as control group,the DTI parameters, serum NSE and Lp-PLA2 levels were compared between two groups. 90d after discharge from cerebral infarction group, the assessment of prognosis by the modified Rankin scale(m RS), they were divided into good prognosis group and poor prognosis group, and the above indicators levels were compared between two groups. The value of DTI parameters combined with serum NSE and Lp-PLA2 for diagnosed cerebral infarction and predicted the prognosis of patients with cerebral infarction was analyzed by the receiver operating characteristic(ROC) curve. Results: The apparent diffusion coefficient (ADC) value and fractional anisotropy index(FA) value of cerebral infarction group were lower than those of control group (P＜0.05), and the serum NSE and Lp-PLA2 levels were higher than those of control group(P＜0.05). The FA value and ADC value of poor prognosis group were lower than those of good prognosis group(P＜0.05), and the serum NSE and Lp-PLA2 levels were higher than those of good prognosis group(P＜0.05). The area under the curve(AUC) for diagnosed cerebral infarction and predicted poor prognosis of patients with cerebral infarction by combined with FA value,ADC value, NSE and Lp-PLA2 were 0.852 and 0.874, respectively, and which were higher than individual diagnosed and predicted of each factor. Conclusion: The DTI parameters FA value and ADC value of cerebral infarction decrease, while serum NSE and Lp-PLA2levels increase, combine with DTI parameters and serum NSE and Lp-PLA2 detection has high value for the diagnosis and prognosis predict of cerebral infarction [ABSTRACT FROM AUTHOR]

Mycobacterium tuberculosis enolase is an essential glycolytic enzyme that catalyzes the conversion of 2, phosphoglycerate (PGA) to phosphoenol pyruvate (PEP). It is also a crucial link between glycolysis and the tricarboxylic acid (TCA) pathway. The depletion of PEP has recently been associated with the emergence of non-replicating drug resistant bacteria. Enolase is also known to exhibit multiple alternate functions, such as promoting tissue invasion via its role as a plasminogen (Plg) receptor. In addition, proteomic studies have identified the presence of enolase in the Mtb degradosome and in biofilms. However, the precise role in these processes has not been elaborated. The enzyme was recently identified as a target for 2-amino thiazoles - a novel class of anti-mycobacterials. In vitro assays and characterization of this enzyme were unsuccessful due to the inability to obtain functional recombinant protein. In the present study, we report the expression and characterization of enolase using Mtb H37Ra as a host strain. Our study demonstrates that the enzyme activity and alternate functions of this protein are significantly impacted by the choice of expression host (Mtb H37Ra or E. coli). Detailed analysis of the protein from each source revealed subtle differences in the post-translational modifications. Lastly, our study confirms the role of enolase in Mtb biofilm formation and describes the potential for inhibiting this process. • Mycobacterium tuberculosis Enolase is a key enzyme linking the glycolytic and TCA pathways. • Here we demonstrate the successful expression of functional Mtb Enolase using Mtb H37Ra as a surrogate. • Recombinant protein obtained from Mtb H37Ra demonstrated increased yield and functionality as compared to the E.coli host. • The enzymes differed in their activity, alternate functions and post-translational modifications. • Lastly, we confirmed the role of Mtb Enolase in biofilm formation. [ABSTRACT FROM AUTHOR]

Enolase proteins play a significant role as moonlighting proteins. In their role as surface-associated enolase, they have multiple functions as they interact with extracellular matrix proteins. Type I and III collagens are the major constituents of this extracellular matrix, and collagen is one of the targets of interaction with the enolase of many pathogens, thereby helping the colonization process and promoting the subsequent invasion of the host. This work aimed to determine the participation of non-typeable H. influenzae enolase as a collagen-binding protein. In this study, through the use of in vitro tests it was demonstrated that recombinant enolase of non-typeable H. influenzae (rNTHiENO) strongly binds to type I collagen. Using molecular docking, the residues that could take part in the interaction of non-typeable H. influenzae enolase-type I collagen (NTHiENO-Cln I) and non-typeable H. influenzae enolase-type III collagen (NTHiENO-Cln III) were identified. However, in vitro assays show that NTHiENO has a better affinity to interact with Cln I, concerning type Cln III. The interaction of NTHiENO with collagen could play a significant role in the colonization process; this would allow H. influenzae to increase its virulence factors and strengthen its pathogenesis. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDA) has been found to have a high mortality rate. Despite continuous efforts, current histopathological classification is insufficient to guide individualized therapies of PDA. We first define the molecular subtypes of PDA (MSOP) based on a meta-cohort of 845 samples from 11 PDA datasets. We then performed functional analyses involving immunity, fibrosis and metabolism. We recognized six molecular subtypes with different survival statistics and molecular composition. The squamous basal-like (SBL) subtype had a poor prognosis and high infiltration of ENO1+ (Enolase 1)/ADM+ (Adrenomedullin) cancer-associated fibroblasts (CAFs). The immune mesenchymal-like (IML) subtype and the normal mesenchymal-like (NML) subtype were characterized by genes associated with extracellular matrix (ECM) activities and immune responses, having favorable prognoses. IML was featured by elevated exhausted immune signaling and inflammatory CAFs infiltration, whereas NML was featured with myofibroblastic CAFs infiltration. The exocrine-like (EL) subtype was high in exocrine signals, while the pure classical-like (PCL) subtype lacked immunocytes infiltration. The quiescent-like (QL) subtype had diminished metabolic signaling and high infiltration of NK cells. SBL, IML and NML were enriched in innate anti-PD-1 resistance signatures. In sum, this MSOP depicts a vivid cell-to-molecular atlas of the tumor microenvironment of PDA and might facilitate to design a precise combination of therapies that target immunity, metabolism and stroma. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder characterized by amyloid plaques, neurofibrillary tangles, and cerebral amyloid angiopathy (CAA). CAA is a condition manifesting as amyloid deposits in the cerebral vasculature, eventually leading to microhemorrhage. Here, we have treated the CRND8 mouse model with the C5a agonist (EP67) in order to observe the effects on cerebral amyloidosis, CAA, and hyperphosphorylated tau. EP67 attaches to the C5a receptor on phagocytes and stimulates the engulfment and digestion of fibrillar and prefibrillar amyloid while exhibiting minimal inflammation. Older CRND8 mice and their respective controls were treated with EP67 for a prolonged period of time. Following treatment, the CRND8 mice displayed improved spatial memory, while both amyloid deposition and tau hyperphosphorylation were found to be diminished. • EP67 C5aR agonist ameliorates cognitive impairment and decrease amyloid deposition in CAA mouse model. • Application of the agonist molecule decreases tau hyperphosphorylation. • EP67 treatment in CAA increases the levels of VEGF and NSE which both have positive impact in memory and cognition. [ABSTRACT FROM AUTHOR]

The aim of this study is to investigate whether serum neuron-specific enolase (NSE) and pentraxin-3 (PTX-3) values are effective in the diagnosis and prognosis of acute pulmonary embolism. In addition, in the light of significant results, we aimed to determine a cut-off value for NSE and PTX-3 in acute pulmonary embolism and to try to determine the sensitivity - specificity in the diagnosis of pulmonary embolism according to these values. In this prospective study, patients who applied to the Emergency Department of Manisa Celal Bayar University School of Medicine between September 2019 and January 2021 and were diagnosed with acute pulmonary embolism constituted the study group and healthy volunteers without any chronic disease or drug use constituted the control group. Serum NSE and PTX-3 values of the patient and control groups were compared. In addition, demographic data, vital signs, laboratory findings, PESI (pulmonary embolism severity index) scores and prognoses of the patients were investigated. In this study 70 patients diagnosed with pulmonary embolism were included to the patient group. 36 (51.4%) of them were women and the mean age was 67.01 ± 14. 74 healthy volunteers were included to the control group; 45 of them (60.8%) were women and the mean age was 44.99 ± 12.85. In patient group the mean PTX-3 value of the was 1.753±1.91 ng/ml, the mean NSE value was 182.13±14.99 ng/ml. In control group, the mean PTX-3 value was 0.429±0.035 ng/ml, the mean NSE value was 166.51±5.14 ng/ml. While there was a statistical difference between two groups in terms of pentraxin-3 value, there was no difference in terms of NSE value. When the cut-off value of 1.115 ng/ml for serum pentraxin-3 in the ROC analysis in order to distinguish the patients with pulmonary embolism from the control group, sensitivity was found to be 58.6% and specificity to be 96%. In our study, we found that serum PTX-3 level is a powerful biomarker with high specificity in the diagnosis of acute pulmonary embolism and is positively associated with the severity and prognosis of the disease. Therefore, we believe that serum PTX-3 may be a guiding biomarker in the diagnosis and prognosis of acute pulmonary embolism in clinical practice. [ABSTRACT FROM AUTHOR]

An efficient photo-to-electrical signal is pivotal to photoelectrochemical (PEC) biosensors. In our work, a novel PEC biosensor was fabricated for the detection of neuron-specific enolase (NSE) based on a ZnIn2S4/Ag2CO3 Z-scheme heterostructure. Due to the overlapping band potentials of the ZnIn2S4 and Ag2CO3, the formed Z-scheme heterostructure can promote the charge separation and photoelectric conversion efficiency. And the concomitant Ag nanoparticles in Ag2CO3 provided multiple functions to enhance the PEC response of the Z-scheme heterostructure. It acts not only as a bridge for the transfer of carriers between ZnIn2S4 and Ag2CO3, promoting the constructed Z-scheme heterostructure, but also as electron mediators to accelerate the transfer of photogenerated carriers and improve the capture of visible light of the Z-scheme heterostructure by surface plasmon resonance (SPR). Compared with single Ag2CO3 and ZnIn2S4, the photocurrent of the designed Z-scheme heterostructure increased more than 20 and 60 times respectively. The fabricated PEC biosensor based on a ZnIn2S4/Ag2CO3 Z-scheme heterostructure exhibits sensitive detection to NSE, and presents a linear range of 50 fg·mL−1 ~ 200 ng·mL−1 with a limit of detection of 4.86 fg·mL−1. The proposed PEC biosensor provides a potential approach for clinical diagnosis. [ABSTRACT FROM AUTHOR]

The construction of advanced systems capable of accurately detecting neuron-specific enolase (NSE) is essential for rapidly diagnosing small-cell lung cancer. In this study, an electrochemiluminescence (ECL) resonance energy transfer immunosensor was proposed for the ultra-sensitive detection of NSE. The co-reactants C2O42− and Ru(bpy)32+ were integrated to form a self-enhanced ECL luminophore (Ru-ZnMOF) as the ECL donor. The abundant carboxyl functional groups of Ru-ZnMOF supported antibody 1 via an amidation reaction. Polydopamine-modified zinc dioxide nanoflowers, as ECL acceptors, inhibited Ru-ZnMOF ECL signaling. The linear range of NSE was 10 fg mL−1 to 100 ng mL−1 with a detection limit of 3.3 fg mL−1 (S/N = 3), which is suitably low for determining NSE in real samples. [ABSTRACT FROM AUTHOR]

Malignant tumors have become a major social health problem that seriously threatens human health, among which pancreatic cancer has a high degree of malignancy, difficult diagnosis and treatment, short survival time, and high mortality. More and more attention has been paid to abnormal lipid metabolism as a momentous carcinogenesis mechanism. Here, we explored the relationship between abnormal lipid metabolism, enolase, and pancreatic cancer by clinical data analysis. A high-fat mouse model was constructed, and then, a subcutaneous tumorigenesis mouse model of carcinoma of pancreatic cells and a metastatic neoplasm mouse pattern of pancreatic carcinoma cells injected through the tail vein were constructed to explore whether abnormal lipid metabolism affects the progression of pancreatic cancer in mice. We constructed a high-lipid model of pancreatic carcinoma cell lines and knockdown and overexpressed enolase in pancreatic carcinoma cell lines and investigated whether high lipid regulates epithelial-mesenchymal transition (EMT) by upregulating enolase (ENO), thereby promoting the cells of pancreatic carcinoma to invade and migrate. Triglycerides, total cholesterol, free cholesterin, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and neuron-specific enolase (NSE) from pancreatic cancer patients and nonpancreatic cancer patients were tested. The differences in blood lipids between patients with and without pancreatic carcinoma were compared, and the correlation between blood lipids and neuron-specific enolase was analyzed. We confirmed that the serum triglyceride level of pancreatic cancer patients at initial diagnosis is overtopping nonpancreatic cancer patients, and the neuron-specific enolase level of patients with pancreatic carcinoma is better than nonpancreatic carcinoma sufferers. Triglyceride level is positively correlated with neuron-specific enolase level, and serum triglyceride level has predictive value for pancreatic cancer. Hyperlipidemia can promote tumor growth and increase the expression levels of ENO1, ENO2, and ENO3 in subcutaneous tumor formation of pancreatic cancer in mice. Additional hyperlipidemia promoted pancreatic carcinoma metastasis in the lung in mice injected through the tail vein, which confirmed that hyperlipidemia accelerated the process of EMT by increasing the expression of ENO1, ENO2, and ENO3, therefore promoting the pancreatic cancer cell metastasis. [ABSTRACT FROM AUTHOR]

Protein methylation is mainly observed in lysine, arginine and histidine residues. Histidine methylation occurs at one of two different nitrogen atoms of the imidazole ring, producing N τ-methylhistidine and N π-methylhistidine, and it has recently attracted attention with the identification of SETD3, METTL18 and METTL9 as catalytic enzymes in mammals. Although accumulating evidence had suggested the presence of more than 100 proteins containing methylated histidine residues in cells, much less information has been known regarding histidine-methylated proteins than lysine- and arginine-methylated ones, because no method has been developed to identify substrates for histidine methylation. Here, we established a method to screen novel target proteins for histidine methylation, using biochemical protein fractionation combined with the quantification of methylhistidine by LC-MS/MS. Interestingly, the differential distribution pattern of N τ-methylated proteins was found between the brain and skeletal muscle, and identified γ-enolase where the His-190 at the N τ position is methylated in mouse brain. Finally, in silico structural prediction and biochemical analysis showed that the His-190 in γ-enolase is involved in the intermolecular homodimeric formation and enzymatic activity. In the present study, we provide a new methodology to find histidine-methylated proteins in vivo and suggest an insight into the importance of histidine methylation. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of anti-cancer drug POMHEX on sperm function in mature mice. Methods Mouse epididymal sperm were exposed to POMHEX (0. 1-100 juumol/L) in vitro. Total and progressive motility of sperms were assessed using computer-as sis ted semen analysis system (CASA), and their viability was evaluated by Eosin-nigrosine staining. ATP level of sperm was detected by luciferin-luciferase system. Western blot analysis was performed to assess protein phosphorylation, and Coomassie brilliant blue G250 staining was used to estimate acrosome integrity. Results POMHEX with concentrations of 0. 1 |xmol/L significantly attenuated total and progressive motility of sperms (P < 0. 05), exhibiting a dose-dependent effect, but no effect on sperm viability. Additionally, POMHEX with concentrations of M 1 |xmol/L significantly inhibited ATP level in sperms and protein tyrosine phosphorylation during sperm capacitation in mice (Pc 0. 01). Although there was no effect on the spontaneous acrosome reaction of mouse sperm, POMHEX with concentrations of P5 pjnol/L inhibited Ca2+ ionophore A23187-induced acrosome reaction (P < 0. 01). Conclusion Our results reveal that the POMHEX can impede sperm motility and capacitation in vitro, and then potentially result in reproductive toxicity in mouse sperm. Our findings suggest that patients undergoing POMHEX treatment should consider fertility preservation options in advance. [ABSTRACT FROM AUTHOR]

Autistic spectrum disease (ASD) is an increasingly common diagnosis nowadays with a prevalence of 1–2% in most countries. Its complex causality—a combination of genetic, immune, metabolic, and environmental factors—is translated into pleiomorphic developmental disorders of various severity, which have two main aspects in common: repetitive, restrictive behaviors and difficulties in social interaction varying from awkward habits and verbalization to a complete lack of interest for the outside world. The wide variety of ASD causes also makes it very difficult to find a common denominator—a disease biomarker and medication—and currently, there is no commonly used diagnostic and therapeutic strategy besides clinical evaluation and psychotherapy. In the CORDUS clinical study, we have administered autologous cord blood to ASD kids who had little or no improvement after other treatments and searched for a biomarker which could help predict the degree of improvement in each patient. We have found that the neuron-specific enolase (NSE) was elevated above the normal clinical range (less than 16.3 ng/mL) in the vast majority of ASD kids tested in our study (40 of 41, or 97.5%). This finding opens up a new direction for diagnostic confirmation, dynamic evaluation, and therapeutic intervention for ASD kids. [ABSTRACT FROM AUTHOR]

Under hypoxia, Saccharomyces cerevisiae forms cytoplasmic condensates composed of proteins, including glycolytic enzymes, that are thought to regulate cellular metabolism. However, the hypoxic conditions required for condensate formation remain unclear. In this study, we developed a 300-mL-scale culture method to produce condensate-forming cells by precisely controlling the dissolved oxygen (DO) level in the media. Using enolase as a model, a foci formation rate of more than 50% was achieved at ∼0.1% DO, and the results showed that the DO level affected the foci formation rate. The foci formation rates of the previously reported foci-deficient strains and strains with single amino acid substitutions in the endogenous enolase were examined, and the effect of these amino acid substitutions on glucose consumption and ethanol and glycerol production under hypoxia was evaluated. The results of this study contribute to the investigation of the mechanisms that regulate biomacromolecular condensates under hypoxia. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of remifentanil combined with sevoflurane on awakening quality, stress response, serum neuron specific enolase (NSE) and S-100β protein in elderly patients with total hip arthroplasty (THA). Methods: 85 elderly patients with THA who were admitted to the Third Affiliated Hospital of Bengbu Medical College from April 2020 to May 2022 were selected, and they were divided into observation group (sevoflurane and remifentanil combined anesthesia, n=43) and control group (remifentanil anesthesia, n=42) according to random number table method. The awakening quality, sedation, analgesia, stress response indexes, serum NSE and S-100茁 protein levels, postoperative cognitive dysfunction (POCD) and perioperative adverse reactions were observed and compared between the two groups. Results: Compared with the control group, the observation group had shorter periods of consciousness disappearance, extubation, and awakening (P<0.05). Epinephrine (E), norepinephrine (NE) and cortisol (Cor) in the observation group at postoperative 12 h were lower than those in the control group at the same time point (P<0.05). Visual pain simulation scores (VAS) in the observation group at postoperative 12 h were lower than those in the control group at the same time point (P<0.05). Ramsay sedation score was higher than that in the control group at the same time point (P<0.05). The NSE and S-100茁 protein in the observation group at postoperative 12 h were lower than those in the control group at the same time point (P<0.05). The incidence of POCD in the observation group was lower than that in the control group (P<0.05). There was no significant difference in the incidence of adverse reactions between the two groups (P>0.05). Conclusion: Remifentanil combined with sevoflurane has better sedative and analgesic effect in elderly patients with THA, which can improve the awakening quality, reduce the degree of stress response, reduce the incidence of POCD, regulate the serum NSE and S-100茁 protein levels. [ABSTRACT FROM AUTHOR]

• The relationship between EEG and neuron specific enolase (NSE) has been previously described, but without considering the influence of EEG background. • NSE is higher in patients with repetitive epileptiform discharges on continuous, discontinuous, and burst-suppression. • NSE is however lower with epileptiform features on suppression, likely reflecting the need of viable neurons to generate them. Electroencephalogram (EEG) and serum neuron specific enolase (NSE) are frequently used prognosticators after cardiac arrest (CA). This study explored the association between NSE and EEG, considering the role of EEG timing, its background continuity, reactivity, occurrence of epileptiform discharges, and pre-defined malignancy degree. Retrospective analysis including 445 consecutive adults from a prospective registry, surviving the first 24 hours after CA and undergoing multimodal evaluation. EEG were interpreted blinded to NSE results. Higher NSE was associated with poor EEG prognosticators, such as increasing malignancy, repetitive epileptiform discharges and lack of background reactivity, independently of EEG timing (including sedation and temperature). When stratified for background continuity, NSE was higher with repetitive epileptiform discharges, except in the case of suppressed EEGs. This relationship showed some variation according to the recording time. Neuronal injury after CA, reflected by NSE, correlates with several EEG features: increasing EEG malignancy, lack of background reactivity, and presence of repetitive epileptiform discharges. The correlation between epileptiform discharges and NSE is influenced by underlying EEG background and timing. This study, describing the complex interplay between serum NSE and epileptiform features, suggests that epileptiform discharges reflect neuronal injury particularly in non-suppressed EEG. [ABSTRACT FROM AUTHOR]

The development of infections caused by pathogenic bacteria is largely related to the specific properties of the bacterial cell surface and extracellular hydrolytic activity. Furthermore, a significant role of hijacking of host proteolytic cascades by pathogens during invasion should not be disregarded during consideration of the mechanisms of bacterial virulence. This is the key factor for the pathogen evasion of the host immune response, tissue damage, and pathogen invasiveness at secondary infection sites after initial penetration through tissue barriers. In this review, the mechanisms of bacterial impact on host plasminogen—the precursor of the important plasma serine proteinase, plasmin—are characterized, principally focusing on cell surface exposition of various proteins, responsible for binding of this host (pro)enzyme and its activators or inhibitors, as well as the fibrinolytic system activation tactics exploited by different bacterial species, not only pathogenic, but also selected harmless residents of the human microbiome. Additionally, the involvement of bacterial factors that modulate the process of plasminogen activation and fibrinolysis during periodontitis is also described, providing a remarkable example of a dual use of this host system in the development of chronic diseases. [ABSTRACT FROM AUTHOR]

The current diagnostics of fish allergy lack sufficient accuracy such that more reliable tests such as component-resolved diagnosis (CRD) are urgently needed. This study aimed at identifying fish allergens of salmon and grass carp and evaluating the sensitization pattern in fish allergic subjects from two distinct populations in Asia. One hundred and three fish allergic subjects were recruited from Hong Kong (67 subjects) and Japan (46 subjects). Western blot and mass spectrometry were used to identify allergens from salmon and grass carp. Fish allergens were purified and tested against 96 sera on ELISA to analyze patients' sensitization pattern. The protein profiles of salmon meat prepared under different cooking methods until core temperature reached 80 °C were evaluated by SDS-PAGE and mass spectrometry. Three common allergens between salmon and grass carp, namely enolase, glycerldehyde-3-phosphate dehydrogenase (GAPDH) and parvalbumin, and two salmon-specific allergens collagen and aldolase were identified. Parvalbumin was the major allergen for both fishes showing an overall sensitization rate of 74.7%, followed by collagen (38.9%), aldolase (38.5%) and enolase (17.8%). Japanese subjects showed more diverse allergen sensitization pattern and more frequent IgE-binding to heat-labile salmon allergens. Compared with steaming and boiling, cooking by baking and frying retained more fish proteins inclusive of heat-labile allergens. Fish allergic patients from different Asian populations show varying fish allergen sensitization profiles. The relevant extracts and components for diagnosis are population-dependent but parvalbumin and collagen are important biomarkers. Cooking methods modify allergen composition of salmon and appear to influence patients' allergic manifestations. [ABSTRACT FROM AUTHOR]