Serum neuron specific enolase could predict subclinical brain damage and the subsequent occurrence of brain related vascular events during follow up in essential hypertension

2016 ◽  
Vol 363 ◽  
pp. 158-163 ◽  
Author(s):  
Alina González-Quevedo ◽  
Sergio González-García ◽  
Zenaida Hernández-Díaz ◽  
Otman Fernández Concepción ◽  
Luis Quevedo Sotolongo ◽  
...  
Shock ◽  
1995 ◽  
Vol 4 (Supplement) ◽  
pp. 58
Author(s):  
Hitoshi Imaizumi ◽  
Masashi Yoshida ◽  
Morihito Satoh ◽  
Yasuo Shichinohe ◽  
Tomoyuki Kawamata ◽  
...  

2007 ◽  
Vol 29 (2) ◽  
pp. 134-139 ◽  
Author(s):  
Felix Henrique Paim Kessler ◽  
George Woody ◽  
Luís Valmor Cruz Portela ◽  
Adriano Bretanha Lopes Tort ◽  
Raquel De Boni ◽  
...  

OBJECTIVE: Studies have shown signs of brain damage caused by different mechanisms in cocaine users. The serum neuron specific enolase and S100B protein are considered specific biochemical markers of neuronal and glial cell injury. This study aimed at comparing blood levels of S100B and NSE in chronic cocaine users and in volunteers who did not use cocaine or other illicit drugs. METHOD: Twenty subjects dependent on cocaine but not on alcohol or marijuana, and 20 non-substance using controls were recruited. Subjects were selected by consecutive and non-probabilistic sampling. Neuron specific enolase and S100B levels were determined by luminescence assay. RESULTS: Cocaine users had significantly higher scores than controls in all psychiatric dimensions of the SCL-90 and had cognitive deficits in the subtest cubes of WAIS and the word span. Mean serum S100B level was 0.09 ± 0.04 µg/l among cocaine users and 0.08 ± 0.04 µg/l among controls. Mean serum neuron specific enolase level was 9.7 ± 3.5 ng/l among cocaine users and 8.3 ± 2.6 ng/l among controls. CONCLUSIONS: In this first study using these specific brain damage markers in cocaine users, serum levels of S100B and neuron specific enolase were not statistically different between cocaine dependent subjects and controls.


Tumor Biology ◽  
1992 ◽  
Vol 13 (5-6) ◽  
pp. 352-357 ◽  
Author(s):  
Mariadomenica D’Alessandro ◽  
Paola Mariani ◽  
Davide Lomanto ◽  
Francesco Carlei ◽  
Emanuele Lezoche ◽  
...  

1971 ◽  
Vol 10 (01) ◽  
pp. 39-46
Author(s):  
C. Alexandrou ◽  
E. Papadakis ◽  
E. Gyftaki ◽  
J. Darsinos

SummaryRadioisotope renograms were obtained in the upright and prone position in 9 normal subjects, in 5 patients with untreated essential hypertension and in 21 hypertensives under treatment, showing moderate postural hypotension.No significant renographic change were seen in the two positions in normal subjects and untreated hypertensives. Treated hypertensives with postural hypotension showed significant impairment of renal function in the upright position in 15 cases and no change in 6. Renal creatinine clearance was lower in the group that showed renographic changes. Renography in the upright position is suggested as a convenient test for early diagnosis and follow-up of the adverse effects of antihypertensive treatment.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 453-P
Author(s):  
MONIA GAROFOLO ◽  
ELISA GUALDANI ◽  
DANIELA LUCCHESI ◽  
LAURA GIUSTI ◽  
VERONICA SANCHO-BORNEZ ◽  
...  

2017 ◽  
Vol 38 (suppl_1) ◽  
Author(s):  
D. Konstantinidis ◽  
C. Tsioufis ◽  
K. Dimitriadis ◽  
T. Kalos ◽  
E. Andrikou ◽  
...  

2021 ◽  
Vol 10 (15) ◽  
pp. 3400
Author(s):  
Cathy Degroote ◽  
Roland von Känel ◽  
Livia Thomas ◽  
Claudia Zuccarella-Hackl ◽  
Jens C. Pruessner ◽  
...  

Hyperreactivity to stress may be one explanation for the increased risk of cardiovascular disease (CVD) in individuals with essential hypertension. We investigated blood lipid reactivity to the Montreal Imaging Stress Task (MIST), a psychosocial stressor, in hypertensive and normotensive men and tested for prospective associations with biological risk factors. Fifty-six otherwise healthy and medication-free hypertensive and normotensive men underwent the MIST. We repeatedly measured cortisol and blood lipid profiles (total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG)) immediately before and up to 1 h after stress. Lipid levels were corrected for stress hemoconcentration. Thirty-five participants completed follow-up assessment 2.9 ± 0.12 (SEM) years later. CVD risk was assessed by prospective changes in TC/HDL-C ratio, IL-6, D-dimer, and HbA1c from baseline to follow-up. The MIST induced significant changes in all parameters except TC (p-values ≤ 0.043). Compared with normotensives, hypertensives had higher TC/HDL-C-ratio and TG (p-values ≤ 0.049) stress responses. Blood lipid stress reactivity predicted future cardiovascular risk (p = 0.036) with increases in HbA1c (ß = 0.34, p = 0.046), IL-6 (ß = 0.31, p = 0.075), and D-dimer (ß = 0.33, p = 0.050). Our results suggest that the greater blood lipid reactivity to psychosocial stress in hypertensives, the greater their future biological CVD risk. This points to lipid stress reactivity as a potential mechanism through which stress might increase CVD risk in essential hypertension.


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