A possible role of cyclooxygenase-2 in the relationship between sleep and sudden unexpected death in epilepsy

Epilepsia ◽  
2012 ◽  
Vol 53 (10) ◽  
pp. 1846-1848 ◽  
Author(s):  
Gabriela Matos ◽  
Laura Bennedsen ◽  
Vanessa A. Garcia ◽  
Fulvio A. Scorza ◽  
Esper A. Cavalheiro ◽  
...  
2010 ◽  
Vol 70 (3) ◽  
pp. 665-670 ◽  
Author(s):  
FA. Scorza ◽  
RM. Cysneiros ◽  
RM. Arida ◽  
VC. Terra ◽  
HR. Machado ◽  
...  

People with epilepsy have an increased risk of dying prematurely and the most common epilepsy-related category of death is sudden unexpected death in epilepsy (SUDEP). SUDEP is mainly a problem for patients with chronic uncontrolled epilepsy. The ultimate goal of research in SUDEP is to develop new methods to prevent it and actions other than medical and surgical therapies that could be very useful. Nutritional aspects, i.e., omega-3 fatty acids deficiency, could have an interesting role in this scenario. Some animal and clinical studies have suggested that omega-3 fatty acids could be useful in the prevention and treatment of epilepsy and hence SUDEP. It has been ascertained that the only foods that provide large amounts of omega-3 are seafood (fish and shellfish); however, some fish are contaminated with methylmercury, which may counteract the positive effects of omega-3 fatty acids. Our update review summarises the knowledge of the role of fish consumption on epilepsy research.


Metabolites ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 6 ◽  
Author(s):  
Kobchai Santisukwongchote ◽  
Yutti Amornlertwatana ◽  
Thanapat Sastraruji ◽  
Churdsak Jaikang

Coronary heart disease (CHD) is the major cause of death in sudden unexpected death (SUD) cases. Tryptophan (TRP) and its metabolites are correlated with the CHD patient but less studies in the SUD. The aim of this study was to evaluate the relationship of TRP and its metabolites with the CHD in the SUD cases. Blood samples and heart tissues were collected from CHD subjects (n = 31) and the control group (n = 72). Levels of kynurenine (KYN), kynurenic acid (KYA), xanthurenic acid (XAN), 3-hydroxyanthranillic acid (HAA), quinolinic acid (QA), picolinic acid (PA) and 5-hydroxyindoleacetic acid (HIAA) were determined by HPLC-DAD. A severity of heart occlusion was categorized into four groups, and the relationship was measured with the TRP metabolites. The HIAA and The KYN levels significantly differed (p < 0.01) between the CHD group and the control group. Lower levels of QA/XAN, PA/KA, HAA/XAN, KYN/XAN and KYN/TRP were found in the CHD group. However, PA/HAA, PA/HIAA, PA/KYN and XAN/KA values in the CHD group were higher than the control group (p < 0.05). This study revealed that the values of PA/KA and PA/HAA provided better choices for a CHD biomarker in postmortem bodies.


1988 ◽  
Vol 6 (2) ◽  
pp. 176-187 ◽  
Author(s):  
William C. Wadland ◽  
Bert Keller ◽  
William Jones ◽  
James Chapados

2008 ◽  
Vol 12 (1) ◽  
pp. 208-209 ◽  
Author(s):  
Fulvio A. Scorza ◽  
Ricardo M. Arida ◽  
Marly de Albuquerque ◽  
Esper A. Cavalheiro

2017 ◽  
Vol 1 (1) ◽  
pp. 1-8
Author(s):  
Liping Zou ◽  
Ye Zhang ◽  
Rong Zhu

Status thymico-lymphaticus had ever been explained as a cause of sudden death usually in children, but few cases were reported in adults. We sought to determine the relationship between thymic hypertrophy and sudden unexpected death in adult (SUDA), and associated macroscopic and microscopic findings. Adult post mortems from 1984 to 2014 were reviewed and 23 thymic hypertrophy patients without SUDA, 33 thymic hypertrophy patients with SUDA and 172 SUDAs without thymic hypertrophy entered. The data of thymus, lymph nodes, spleen, heart, aorta, and adrenal glands were collected for macroscopic and histological analysis. Ten antibodies were used and applied to 3 children and 46 adult thymus specimens. We found, as an independent factor, thymic hypertrophy increased significantly the risk of SUDA (6.9 folds) in both male and female. What’s more, SUDAs associated with thymic hypertrophy were quite younger (22.5 years) than those without it. A majority of patients with hypertrophic thymus had a variable number of accompanied anomalies described as the typical characteristics of status thymico-lymphaticus, but no macroscopic and microscopic findings related to SUDA in patients with thymic hypertrophy. Cytokeratins (CKs) showed distinctly different immunohistochemical expression patterns in individuals who had different death causes and disease background. Instead of a disease entity “status thymico-lymphaticus” is a systematic abnormality with thymic hypertrophy as a feature involving mainly immune and/or cardiovascular system, probably caused by gene mutations.


2008 ◽  
Vol 93 (12) ◽  
pp. 1048-1053 ◽  
Author(s):  
M A Weber ◽  
M T Ashworth ◽  
R A Risdon ◽  
J C Hartley ◽  
M Malone ◽  
...  

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