NSE Protein Research Articles

Matrix Metalloproteinase-9, Neuron-specific Enolase, S100 B and Tau Protein Levels in the Patients with Carbon monoxide Poisoning

Background: S100B, NSE, MMP-9, and Tau protein levels increase in cases causing hypoxic cell damage. The diagnosis of the severity of carbon monoxide (CO) poisoning in the early period of these parameters was studied. Material and Method: COHb level measurement was made using a signal capture CO-pulse oximeter (Masimo's SET Rainbow, Masimo's Co, USA) at the first admission of the patients. Then, COHb levels were confirmed by arterial blood gas(ABG) analysis. The patients were divided into two groups as mild and moderate-severe, according to their Glasgow coma scores (GCS) [Mild (14–15); Moderate (9–13) or Severe (3–8)]. The control group was composed of 16 healthy and non-smoking volunteers. Results: The serum S100B protein and MMP-9 values at 0 hr of admission in the hospital and 3hr of treatment were not significantly different in the patient group as compared to the control group. Tau protein levels were significantly higher in the patient group at 0 and 3 hours (p> 0.05) as compared to healthy person. Conclusion: There was no relationship between CO poisoning and MMP-9 and S100B protein levels. NSE and Tau protein were significantly higher in the patient group than the control group. Tau protein may be more useful marker as compared to neuron-specific enolase.

Enrofloxacin hydrochloride toxicological effects on crucian carp reflected by serological changes and neurotoxicity

Due to its water solubility and wide applicability, enrofloxacin hydrochloride (EH) may enter aquatic ecosystems and cause negative effects on aquatic organisms. This study aimed to explore toxicological effects via serological changes and neurotoxicity, which were induced by EH exposure in crucian carp (Carassius auratus var. Pengze). The drug residues in brain tissue and protein content in serum were determined to analyze serological changes. Alterations in brain tissue structure and function, cerebral microvessels permeability, and the expressions of gene and protein regarding blood-brain barrier (BBB) were studied to reflect the neurotoxicity. Employing a validated high-performance liquid chromatography (HPLC) method, EH residues could be detected at various time-points throughout the experiment. Enzyme-linked immunosorbent assay (ELISA) showed that EH increased the levels of S100B, NSE and GFAP proteins in serum. Additionally, there was a significant positive correlation between serum S100B, NSE protein contents and EH residues (P < 0.05). Hematoxylin and eosin (H&E) staining revealed brain damage from EH exposure by the formation of vacuoles in brain glial cells, pyknosis of the nucleus, and a decrease in cell population density. Transmission electron microscope (TEM) revealed morphological changes in microvessels and condensation of astrocyte nucleus. Evans blue (EB) permeability test visualized an obvious increase in cerebral microvessels leakage. The real-time quantitative PCR (qPCR) results indicated that EH up-regulated the mRNA expression levels of S100B, NSE and GFAP, down-regulated the mRNA expression levels of P-gp, ZO-1, Occludin and Claudin-5. The Western blot (WB) results demonstrated increased NSE and GFAP protein expressions, decreased P-gp and Occludin protein expressions following EH exposure in brain, in consistent with the gene expressions, respectively. In conclusion, these findings indicated that EH brought about marked rise in serum biomarker levels and disrupted the central nervous system (CNS) of crucian carp. These data would help elucidate the mechanism underlying EH-induced neurotoxicological effects.

Биомаркеры ишемии органа зрения как предикторы ишемического инсульта головного мозга

Purpose. To study biomarkers of ischemia of the organ of vision in patients with acute disorders of the arterial circulation of the retina and optic nerve. Material and methods. We observed 38 patients (38 eyes). The patients were divided into two groups, the first group consisted of 26 patients (26 eyes) with acute circulatory disorders of the optic nerve (anterior ischemic neuropathy), the second group consisted of 12 patients (12 eyes) with acute circulatory disorders of the retina (occlusion of the central artery retina and its branches). The control group consisted of 12 practically healthy individuals. Results. In a biochemical study in patients with anterior ischemic neuropathy (1st group), the level of NSE in the lacrimal fluid was increased compared to the control group and averaged 32.3 ± 0.85 ng/ml, although in the blood serum it remained within the normal range , which reflects the beginning of destructive processes in the nervous tissue. In patients with acute circulatory disorders of the retina (2nd group), the content of NSE in the lacrimal fluid was increased by 1.7 times compared with the control group. Conclusion. The NSE study can be used in a comprehensive examination of patients with acute circulatory disorders of the optic disc and retina as an additional marker of the neurodegenerative process. Since data from traditional methods of research do not always show the degree of damage to the visual pathways, the study of the level of NSE helps to make assumptions about the severity of the disease and predict the outcome. Keywords: visual organ ischemia, occlusion, anterior ischemic neuropathy, central retinal artery, diagnostics, NSE protein

Brain injury biomarkers do not predict delirium in acutely ill older patients: a prospective cohort study

Delirium is a common, serious, and often preventable neuropsychiatric emergency mostly characterized by a disturbance in attention and awareness. Systemic insult and inflammation causing blood–brain-barrier (BBB) damage and glial and neuronal activation leading to more inflammation and cell death is the most accepted theory behind delirium's pathophysiology. This study aims to evaluate the relationship between brain injury biomarkers on admission and delirium in acutely ill older patients. We performed a prospective cohort study which analyzed plasma S100B levels at admission in elderly patients. Our primary outcome was delirium diagnosis. Secondary outcomes were association between S100B, NSE and Tau protein and delirium diagnosis and patients’ outcomes (admissions to intensive care, length of hospital stay, and in-hospital mortality). We analyzed 194 patients, and 46 (24%) developed delirium, 25 on admission and 21 during hospital stay. Median of S100B at admission in patients who developed delirium was 0.16 and median was 0.16 in patients who didn’t develop delirium (p: 0.69). Levels S100B on admission did not predict delirium in acutely ill elderly patients.Trial registration: The study was approved by the local institutional review board (CAPPESq, no. 77169716.2.0000.0068, October 11, 2017) and registered in Brazilian Clinical Trials Registry (ReBEC, no. RBR-233bct).

Abrikossof’s Tumor: Report of a Case

The granular cell tumor of the breast is a rare tumor and a usually benign disease that appears clinically and radiologically like a malign tumor. We report a case of GCT in a woman of 41 years, who present a clinically and radiologically suspect later. The anatomopathological examination showed the benign tumor proliferation and a large tumorectomy was realized. The immunostaining with PS100 and NSE protein confirm the nature of the tumor.

Clinic and diagnosis of encephalopathy of critical conditions in children with infectious diseases

Purpose: to assess the functional state of the brain in critically ill encephalopathy in children with infectious diseases.Materials and methods: 75 patients aged from 1 month to 17 years 11 months with infectious diseases, who were in the intensive care unit of the clinic, were examined, divided into two groups: the main group and the comparison group. Exclusion criteria: patients with cerebral palsy, organic lesions of the central nervous system, neuroinfections and epilepsy. Conducted daily clinical and neurological examination; study of the level of neurospecific proteins (NSE, protein S100) in blood serum; electroencephalography; study of evoked potentials of various modalities; ultrasound examination of the optic nerves, neuroimaging.Results: All patients had general infectious manifestations, the development of sepsis syndrome, cerebral systemic disorders with impaired consciousness, as well as convulsive syndrome. In the acute period of the disease in the main group, NSE values in 87.5% of children were within the upper limit of normal, S100 protein levels were many times higher than those in the comparison group. In dynamics, all patients showed an increase in the level of NSE, which correlated with persistent neurological symptoms in the form of irritability, weakness, and cognitive decline. In the comparison group, an increase in NSE occurred in 53% of children, an increase in S100 - in 83%. By the time of discharge, 47% of patients had an increase NSE and S100 protein. Visual evoked potentials in 84% of the children of the main group in the acute period, had a decrease the amplitude of the N2-P2 cortical response was revealed without significant dynamics in the future, which was accompanied by pronounced clinical manifestations, which made it possible to substantiate the expediency of dispensary observation of children who underwent a critical condition against the background of severe infectious pathology.Conclusion: in infectious diseases in children that are not accompanied by inflammatory processes in the nervous system, but proceed with the development of a critical condition, there is a neuropsychiatric deficit in the outcomes, which necessitates follow-up follow-up of such patients in the future.

Inhibition of ROCK2 kinase activity improved behavioral deficits and reduced neuron damage in a DEACMP rat model

The main pathological changes that occur in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) are extensive demyelination of brain white matter and neuron damage. Previous studies suggested that demyelination and neuron injury are related to activating the Rho/ROCK signaling pathway. Inhibition of the Rho/ROCK signaling pathway can alleviate neuron injury and promote myelin repair. This study utilized a DEACMP model in which rats were prepared by space injection of CO gas intraperitoneally (CO group), and the association between the Rho/ROCK signaling pathway and DEACMP was investigated. The ROCK2 kinase inhibitor Y-27632 was used to prevent the effects of the DEACMP model to elucidate its protective mechanism. The results demonstrated that the cognitive and motor functions were significantly impaired, and the GFAP, NSE, RhoA, and ROCK2 protein levels were significantly increased in the CO group within three weeks after the model was established. After Y-27632 intervention, the cognitive and motor functions of the CO+Y-27632 group were significantly improved within three weeks after the model was established. In the CO+Y-27632 group, the RhoA, ROCK2, GFAP, and NSE (indicating neuron injury) protein levels decreased significantly, and the MBP protein levels (indicating myelin repair) increased significantly within three weeks after the model was established. These results suggested that the pathogenesis of DEACMP was associated with activation of the Rho/ROCK pathway and that Y-27632 inhibited ROCK2 kinase activity in the CO exposed rats, resulting in improved behavioral deficits, reduced neuron damage, and promotion of myelin repair. Therefore, Y-27632 might be a potentially effective drug for the treatment of DEACMP-induced brain damage.

Markers of brain damage in full-term newborns with intrauterine growth retardation

The increase in the number of newborns with intrauterine growth retardation, who are characterized not only by high perinatal morbidity and mortality, but also by neurodevelopmental disorders in later life, has determined a wide search for diagnostic markers of prenatal hypoxia for a timely objective assessment of brain damage and a justification of neuroprotection methods. This article presents literature data on biomarkers and methods of instrumental diagnosis of brain damage that have received evidence of the effectiveness of their use in early neonatal life of newborns with intrauterine growth retardation. It is emphasized that such biomarkers as S100B, NSE, and BDNF proteins are the most reliable and easy to determine non-invasively. However, for their wide application in clinical practice, it is necessary to establish reference values in umbilical cord blood and urine, while taking into account the gestational age, sex, and method of giving birth, and to unify the use of laboratory analysis systems and diagnostic tests for this purpose. The comparison of biomarker indicators with cerebral oximetry, electroencephalogram and magnetic resonance imaging data will allow for developing new approaches to the treatment of perinatal pathology and, largely, preventing adverse consequences in those born with intrauterine growth retardation.

Determination of factors affecting cognitive function in patients with chronic kidney disease stage 5

Objective. Patients with stage 5 chronic kidney disease.Study objective. Determination of factors affecting cognitive function in patients with CKD-5.Design and methods. The study included young and middle-aged patients (18 to 60 years old) (n = 40), there is a terminal stage of chronic kidney disease (CKD). Exclusion criteria: history of diseases of the central nervous system, brain injury, episodes of cerebrovascular accident with severity, coronary artery disease, chronic heart failure, pregnancy, abuse of alcohol, refusal to participate in the study. In a previous work, patient examination data were obtained on the Status PF hardware complex. Neurodynamic indicators were estimated, including the determination of the time of a simple visual-motor reaction (MTCM) and a complex visual-motor reaction (MPSM), reaction to a moving object (RDO), memory and attention. Using Spearman’s correlation analysis, we evaluated the impact on cognitive functions of a number of factors, presumably related to neurodynamics. The following factors were selected: age, creatinine level, NSE and S100 proteins, hemoglobin level, Beck’s depression points, indicators of personal and situational anxiety.Results. All patients examined on the Status PF software package had mild cognitive impairment in terms of neurodynamics, attention, and memory. The average positive relationship between the level of depression and various indicators of RDO was established: with RDO_average (ρ = 0.405; p = 0.018), with RDO_total delay (ρ = 0.540; p &lt; 0.001), with RDO_average delay (ρ = 0.421; p = 0.007), as well as weak positive – with CEMR average exposure (ρ = 0.358; p = 0.023). An average positive relationship of creatinine level with RDO_O (ρ = 0.438; p = 0.005) is noted. A weak positive relationship between the level of personal anxiety and RDO_total delay (ρ = 0.334; p = 0.035) was revealed. The average negative relationship between hemoglobin level and RDO_total delay (ρ = –0.535; p &lt; 0.001) was revealed. A weak positive relationship between situational anxiety and SEMR is determined by the number of errors (ρ = 0.364; p = 0.021), as well as a weak negative one with the attention volume (ρ = –0.357; p = 0.024). A weak negative relationship of age with visual memory per word was revealed (ρ = –0.362; p = 0.022).Domain of usage. Outpatient and hospital treatment stages of patients with chronic kidney disease case management

Gualou Guizhi Granule Protects against OGD/R-Induced Injury by Inhibiting Cell Pyroptosis via the PI3K/Akt Signaling Pathway.

Pyroptosis is a proinflammatory form of regulated cell death that plays an important role in ischemic stroke. Gualou Guizhi granule (GLGZG) is a classic prescription that has been shown to exert neuroprotective effects against cerebral ischemia reperfusion injury. In the present study, we examined the involvement of pyroptosis and its associated mechanism in protecting nerve function. Methods. Primary neurons were exposed to oxygen-glucose deprivation and reperfusion (OGD/R) conditions in the presence or absence of GLGZG. Cellular viability was measured by the 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazoliumbromide (MTT) assay. The number of apoptoic cells was detected by NeuN and NSE protein expression. The expression levels of the pyroptosis markers, namely, NOD-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, interleukin-18 (IL-18), and IL-1β were determined by quantitative real-time PCR analysis, western blot, and ELISA analyses as appropriate. Moreover, the expression levels of the PI3K/Akt pathway key proteins were determined by quantitative real-time PCR analysis and western blot assays. To determine the PI3K/Akt pathway involvement in GLGZG-mediated neuroprotection, the PI3K inhibitor LY294002 (LY, 10 μM) was added. The expression levels of NeuN, Akt, and p-Akt were evaluated. Results. It was found that GLGZG could inhibit OGD/R-induced cell apoptosis, increase neuronal cell viability, decrease the production of IL-18 and IL-1β, and downregulate the expression levels of pyroptosis markers (NLRP3, ASC, and caspase-1). Furthermore, GLGZG could modulate the PI3K/Akt signaling pathway. Pharmacological inhibition of the PI3K pathway not only abrogated the effects of GLGZG on Akt but also neutralized its prosurvival and antipyroptotic actions. Conclusions. The findings indicated that GLGZG pretreatment effectively reduced OGD/R-induced injury by inhibiting cell pyroptosis and activating the PI3K/Akt pathway. These data provide important evidence for the therapeutic applications of this regimen in ischemic stroke.

Порівняльна характеристика впливу препарату на основі амантадину гідрохлорид на зміни показників титрів нейромаркерів при експериментальному ятрогенному компресійно-токсичному ураженні нижнього альвеолярного нерва у нормоглікемічних кролів та на тлі алоксанового цукрового діабету

Resume. Under the conditions of an experimental study of normoglycemic animals and the creation of aloxan sugar diabetes (ASD) as a premorbital background, iatrogenic damage to the lower alveolar nerve by filling materials based on resorcinol-formalin and epoxy resin causes destructive - degenerative changes, as evidenced by an increase in neuromarker titers NSE and S100 protein. After a 30-day therapy with a drug based on amantadine hydrochloride at a dose of 10 mg / kg, both indicators in both study groups significantly decreased. The titers of NSE and S100 protein in the group with ASD in both subgroups were 1.94 times, and 1.87 times less, which indicates the effectiveness of its use in this pathology, but compared with the group of normoglycemic animals, these indicators were 1.1 times and 1.72 times less, which occurred against the background of a parallel decrease in S 100 protein titers by 1.99 and 2.04 times, which indicates the presence of neuroprotective activity in this drug. This, in turn, is conducive to its further clinical research and the involvement of a drug based on amantadine hydrochloride in the main protocol for the treatment of patients with diabetes. Key words: iatrogenic compression-toxic lesion of the lower alveolar nerve, aloxan sugar diabetes, neuron-specific enolase, S 100 protein, amantadne hydrochloride, neuroprotection.

The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer.

The prostate stem cell antigen (PSCA), as a predominantly prostate-specific marker, is overexpressed in most prostate cancer specimens, is positively correlated with prostate cancer androgen independence, and has the potential to be treated with castration-resistant prostate cancer (CRPC) as a gene therapy target. Using the typical androgen deprivation therapy, most tumors will progress to CRPC, as well as develop into neuroendocrine prostate cancer (NEPC) characterized by the expression of neuroendocrine markers such as enolase 2 (NSE). Our study was aimed at investigating the expressions of PSCA and NSE and the relationship between the two markers, as well as the correlation between the PSCA and NSE expressions and the clinicopathological parameters in prostate cancer specimens from 118 patients by using immunohistochemistry. Our results demonstrated that the PSCA and NSE protein expressions did not correlate with the prostate cancer patients' age or the hormone therapy but showed a significant correlation with the pathological tumor stage of prostate cancer, the Gleason score, and the presence of metastasis. There is a positive association between PSCA and NSE but a negative one between the prostate-specific antigen (PSA) and PSCA or between PSA and NSE. High PSCA and NSE expressions correlated with a poor prognosis in prostate cancer patients. PSCA may play an important role in the progression of neuroendocrine prostate cancer (NEPC).

Analysis of serum S-100 beta protein, NSE and neurological deficits in patients with cerebral infarction and reperfusion treated with butylphthalide

Objective To investigate the effects of butylphthalide on serum S-100 beta protein, NSE and neurological deficits in patients with cerebral infarction and reperfusion. Methods From January 2016 to January 2018, 104 patients with early cerebral infarction admitted to the People's Hospital of Feicheng were divided into two groups according to different treatment methods.The control group (n=52) was given routine treatment, while the observation group (n=52) was given butylphthalide treatment on the basis of the control group.The degree of neurological deficit, serum NSE and S-100 beta protein levels were compared between the two groups before and after thrombolysis. Results The NIHSS scores of the two groups before thrombolysis were (10.27±1.32)points and (10.28±1.30)points, respectively, the difference between the two groups was no statistically significant(t=0.038, P>0.05). The NIHSS scores of the two groups were decreased at 24h and 7d after thrombolysis, which of the observation group at 24h and 7d after thrombolysis were (8.32±1.37)points and (4.25±1.54)points, respectively, which were significantly lower than those of the control group [(9.24±1.40)points and (9.50±1.24)points], the differences were statistically significant (t=3.396, 19.147, all P 0.05). At 24h and 7d after thrombolysis, the serum NSE levels of the two groups were decreased.The serum NSE levels of the observation group at 24h and 7d after thrombolysis were (15.08±9.35)U/mL and (13.25±6.47)U/mL, respectively, which were significantly lower than those in the control group [(18.96±10.14)U/mL and (16.98±7.11) U/mL], the differences were statistically significant (t=2.028, 2.79, all P 0.05). At 24h and 7d after thrombolysis, the serum S-100β protein levels were decreased in both two groups, which in the observation group were (1.13±0.62 )μg/L and (0.53±0.48)μg/L, respectively, which were significantly lower than those in the control group [(1.40±0.64)μg/L, (0.87±0.32)μg/L], the differences were statistically significant (t=2.185, 4.25, all P<0.05). Conclusion Butylphthalide injection for patients with cerebral infarction and reperfusion can effectively promote the recovery of neurological function, improve the levels of serum NSE and S-100 beta protein, and help patients recover as soon as possible. Key words: Infarction, middle cerebral artery; Reperfusion; Serum S-100 beta protein; NSE; Neurological deficit; Butylphthalide

Diagnostic Algorithm in Hirschsprung's Disease: Focus on Immunohistochemistry Markers.

Hirschsprung disease (HD) is caused by the congenital absence of ganglion cells in the distal bowel (aganglionosis). Rectal biopsy is considered important for its diagnosis. The aim of this study was to apply immunohistochemical staining using a minimal set of antibodies and develop an algorithm that will assist in the diagnosis of HD. Rectal or colonic biopsies were performed in patients with HD (n=26) or patients treated for other bowel diseases (n=34). Immunohistochemical staining was performed for MAP1b, peripherin, S-100, calretinin, NSE, bcl-2 and CD56 proteins. Staining for CD56, S-100, peripherin and calretinin facilitated the identification of ganglion cells. The use of CD56 and S-100 antibodies together resulted in the highest rate of ganglion cell staining intensity (94%). We propose a practical diagnostic algorithm with the application of CD56 and S-100 antibodies that can be used in clinical practice in children suspected of Hirschsprung's disease.

NSE & S100B protein blood level assessment during a long-distance trail race.

Blood samples were collected from 4 athletes before, during and at the end of one of two races: Grand Raid de la Réunion 2017 (GRR: 165 km, elevation gain: 9529 m, 2 runners) and Trail de la Bourbon 2017 (TB: 111 km, elevation gain: 6433 m, 2 runners). Serum S100B and NSE levels were measured for each runner before, during and after the race. Serum S100B levels (normal range: < 0.15 μg/L) increased early during the race and remained high up to the end of the race in all 4 runners (range: 0.17-0.59 μg/L). NSE level (normal range: < 15 μg/L) increased in 3 of the 4 runners (range: 16.8-39.2 μg/L). This preliminary study shows the potential interest of S100B and NSE serum assessment during long-distance races. Further studies are needed to confirm these results and to investigate the origins and significance of this increase in brain injury markers.

Electroacupuncture improves neurobehavioral function and brain injury in rat model of intracerebral hemorrhage.

Acupuncture has been widely used as a treatment for stroke in China for a long time. Recently, studies have demonstrated that electroacupuncture (EA) can accelerate intracerebral hemorrhage (ICH)-induced angiogenesis in rats. In the present study, we investigated the effect of EA on neurobehavioral function and brain injury in ICH rats. ICH was induced by stereotactic injection of collagenase type I and heparin into the right caudate putamen. Adult ICH rats were randomly divided into the following three groups: model control group (MC), EA at non-acupoint points group (non-acupoint EA) and EA at Baihui and Dazhui acupoints group (EA). The neurobehavioral deficits of ICH rats were assessed by modified neurological severity score (mNSS) and gait analysis. The hemorrhage volume and glucose metabolism of hemorrhagic foci were detected by PET/CT. The expression levels of MBP, NSE and S100-B proteins in serum were tested by ELISA. The histopathological features were examined by haematoxylin-eosin (H&E) staining. Apoptosis-associated proteins in the perihematomal region were observed by immunohistochemistry. EA treatment significantly promoted the recovery of neurobehavioral function in ICH rats. Hemorrhage volume reduced in EA group at day 14 when compared with MC and non-acupoint EA groups. ELISA showed that the levels of MBP, NSE and S100-B in serum were all down-regulated by EA treatment. The brain tissue of ICH rat in the EA group was more intact and compact than that in the MC and non-acupoint groups. In the perihematomal regions, the expression of Bcl-2 protein increased and expressions of Caspase-3 and Bax proteins decreased in the EA group vs MC and non-acupoint EA groups. Our data suggest that EA treatment can improve neurobehavioral function and brain injury, which were likely connected with the absorption of hematoma and regulation of apoptosis-related proteins.

The prognostic value of cerebral oxygenation and retrograde pressure during carotid endarterectomy

&lt;p&gt;&lt;strong&gt;Aim:&lt;/strong&gt; The study aimed to determine the predictive value of retrograde pressure (RP) indicators and cerebral oxygenation in the evaluation of ischemic brain damage during carotid endarterectomy (CEA).&lt;br /&gt;&lt;strong&gt;Methods:&lt;/strong&gt; This nonrandomized, prospective pilot study included 87 patients with asymptomatic stenosis greater than 70% who underwent carotid endarterectomy under general anesthesia. Brain tolerance to ischemia was determined by measuring and evaluating RP (∆rSO2) and cerebral oxygenation (rSO2) during a trial clamping of the carotid artery. Depending on the degree of reduction of cerebral oxygenation from the baseline (∆rSO2) during a trial clamping of the carotid artery, patients were divided into 3 groups: the first group (n = 35) - ∆rSO2 &amp;lt;9.9%, the second group (n = 35) - ∆rSO2 from 10 to 19.9%, the third group (n = 14) - ∆rSO2 ≥ 20%. The primary end-point of the study was to obtain the AUC value exceeding 0.70, which could mean a high predictive quality of research methods. &lt;br /&gt;&lt;strong&gt;Results:&lt;/strong&gt; There were no perioperative strokes or myocardial infarctions during the study. Average time of carotid artery clamping was 28 (26-30) minutes. 3 patients who received temporary shunts were excluded from the study because of a simultaneous decrease in the rSO2 and ∆rSO2 indicators. It was found out that S-100 and NSE protein concentration in all groups did not significantly differ at different stages (p&amp;gt; 0.05). A temporary shutdown of blood flow in the carotid artery during CEA is accompanied by significant elevation of cerebral damage markers (S100, NSE) concentration with their subsequent restoration at 3 days after surgery. ROC - analysis revealed that none of the methods for assessing cerebral ischemic tolerance (RP, ∆rSO2 and rSO2) is precise enough (AUC &amp;gt; 0.7) to predict brain injury during carotid endarterectomy. Satisfactory, but a poor quality (AUC&amp;lt; 0.7) of predicting an increase in the reference values of S-100 protein neuromarkers was demonstrated by retrograde pressure, while the other indicators (∆rSO2 and rSO2) did not exceed the area under the curve (AUC) over 0.60. &lt;br /&gt;&lt;strong&gt;Conclusion:&lt;/strong&gt; Methods of measuring retrograde pressure and cerebral oxygenation are merely a reflection of the collateral blood flow and the cerebral oxygenation level due to their close relationship, but they cannot be used as predictors of ischemic neuronal damage during carotid endarterectomy because of poor predictive quality.&lt;/p&gt;

Mechanism research and effect of ulinastatin in the brain tissue injury of acute hydrogen sulfide intoxicated rats

To observe the effect of Ulinastatin (UTI) in the dynamic changes of aquaporin 4 (AQP4) and cyclooxygenase-2 (COX-2) in the brain tissue injury of acute hydrogen sulfide (H2S) intoxicated, to explore the Mechanism of brain tissue injury of acute H2S-intoxicated and the protection effect of UTI. A total of 96 SD rats of clean grade were divided randomly into four groups: normal control group (NS group, n=8) , UTI control group (UTI group, n=8) , H2S-intoxicated model group (H2S group, n=40) , UTI treatment group (H2S+UTI group, n=40). The H2S group and H2S+UTI group were exposed to H2S (284 mg/m(3)) by inhalation for 1 h, then H2S+UTI group was intraperitoneally exposed to UTI at the dose of 10(5) U/kg for 2 h, H2S group and H2S+UTI group were sacrificed at 2, 6, 12, 24 and 48 h after exposure, respectively. Remove the brain tissue, observe the rats behavioral changes at each time points. The mRNA expression of AQP4、COX-2 and NSE in the brain tissue were measured by RT-PCR method, and the protein expression of AQP4、COX-2 and NSE in the brain tissue were detected by immunohistochemical Streptavidin-perosidase method. Pathological changes of brain tissue were observed by lightmicroscope. 1、Nerve cells in the H2S group rats had edema, degeneration, focal inflammatory cell infiltrate, capillary hyperplasia, expansion. Compared with NS group, the cerebral NSE mRNA and protein expression at each time point in H2S group after exposure were significantly increased (P<0.01). 2、Compared with NS group, the cerebral AQP4 and COX-2 mRNA and protein expression at each time point in H2S group after exposure were significantly increased (P<0.01). 3、The degree of brain damage was significantly decreased in H2S+UTI group than that in H2S group. Compared with H2S group, the cerebral NSE mRNA and protein expression at 6, 12, 24 and 48 h in H2S+UTI group after exposure were significantly decreased (P<0.01) , no significantly difference at 2h (P>0.05). 4、Compared with the H2S group, the cerebral AQP4 and COX-2 mRNA and protein expression at 6, 12, 24 and 48 h in H2S+UTI group after exposure were significantly decreased (P<0.01) , slightly decreased at 2 h. The mechanism of brain injury of acute hydrogen sulfide intoxicated associated with abnormal expression of the cerebral AQP4, COX-2 levels. Intervention of UTI can reduce the cerebral AQP4 and COX-2 levels after hydrogen sulfide intoxicated, reduce the degree of brain injury.

Changes in symptom severity and biochemical markers of brain injury in patients with treatment-resistant schizophrenia

One of the major problems of the methodology of translational research is to find biomarkers that serve as indicators of treatment response. The aim was to study the dynamics of biochemical markers in the process of combined antipsychotics and electroconvulsive therapy. Material and methods Present study was conducted in 34 patients with treatment-resistant schizophrenia (31.6±9.4 years old) that underwent combined ECT (10 ECTs on average) and pharmacological treatment. The assessment included PANSS and determination of NSE and S100B protein concentrations using automated immunochemical analyzer Elecsys 2010. Blood samples were obtained before the beginning of ECT, 24 hours after the third and sixth ECTs. Results Average reduction of PANSS score was 29,1%, >20% for 85% of patients. There were no significant differences in NSE and S100B concentrations at different stages of treatment. This result is consistent with data on the safety of ECT from the point of view of the integrity of cells. There were found statistically significant differences between S100B concentration in women and men (60±18 and 43±23 ng/L, respectively, P =0.029) and a trend of increase in S100 levels with the increase of disease duration ( r =0.372, P =0.062). Serum S100B concentrations at baseline negatively correlated with positive and negative symptoms severity and with PANSS composite score. No correlation between treatment efficiency and biochemical markers' levels was found. Conclusion Combined antipsychotic and electroconvulsive therapy was effective for treatment-resistant schizophrenic patients and did not induce nerve cells damage. Initial symptom severity was correlated with S100B levels.

The potential clinic value of the changes of BAEP and S-100 in the serum as early diagnosis of the bilirubin encephalopathy of newborns

Objective To explore the potential clinic value of NSE and S-100 in the serum as early diagnosis in the Bilirubin Encephalopathy(BE) of newborns. Methods 46 neborns were choosed as group A with TSB≥342μmol/L;48 with TSB(256-342)μmol/L as group B;and 30 full term deliveries newborns as normal control group C.Their TSB,NSE and S-100 in the serum were measured.Meanwhile,the BAEP scores were carried out. Results The concentrations of NSE,S-100 and the BAEP scores in newborns of group A and B had significant differences as compared with group C(P< 0.05).Correlation analysis showed that there was a significant positive correlation between serum NSE,S-100 protein and TSB(P< 0.05),while there was a negative correlation between serum NSE,S-100 protein and BAEP scores(P< 0.05). Conclusion Serum NSE and S-100 protein can use as early diagnosis targets for the the Bilirubin Encephalopathy(BE)of newborns clinically. Key words: Hyperbilirubinemia; Neonatal; Neuron specific enolase; S-100