Moderate dose alcohol protects against serum amyloid protein A1‐induced endothelial dysfunction via both notch‐dependent and notch‐independent pathways

Author(s):  
Naresh K. Rajendran ◽  
Weimin Liu ◽  
Charles C. Chu ◽  
Paul A. Cahill ◽  
Eileen M. Redmond
2013 ◽  
Vol 11 (S2) ◽  
Author(s):  
S Pastore ◽  
◽  
G Paloni ◽  
M Gattorno ◽  
A Taddio ◽  
...  

1993 ◽  
Vol 39 (2) ◽  
pp. 293-297 ◽  
Author(s):  
T Nakayama ◽  
S Sonoda ◽  
T Urano ◽  
T Yamada ◽  
M Okada

Abstract We examined serum amyloid protein A (SAA) and C-reactive protein (CRP) as inflammatory markers of viral and bacterial infections. Both acute-phase reactants increased in the acute stage and thereafter decreased in the convalescent stage. In viral infections, the mean serum concentrations of SAA during the acute stage were 141 mg/L in infections with adenovirus, 77 mg/L with measles virus, 63 mg/L with influenza virus, 55 mg/L with parainfluenza virus, 31 mg/L with respiratory syncytial virus, and 31 mg/L in aseptic meningitis. The mean serum concentration of CRP was 19 mg/L for adenovirus infection and < 7 mg/L in all other viral infections. The SAA concentrations were 5- to 11-fold greater than the CRP concentrations. Both the SAA and the CRP concentrations were higher in bacterial infections than in viral infections. Changes in the concentrations of serum SAA paralleled those in serum CRP in bacterial infection; during the course of viral infection, however, serum SAA tended to disappear more quickly than CRP did. SAA appears to be a clinically useful marker of inflammation in acute viral infections, with or without significant changes in the CRP concentration.


2008 ◽  
Vol 295 (6) ◽  
pp. H2399-H2408 ◽  
Author(s):  
Xinwen Wang ◽  
Hong Chai ◽  
Zehao Wang ◽  
Peter H. Lin ◽  
Qizhi Yao ◽  
...  

The objective of this study was to determine the effects and mechanisms of serum amyloid A (SAA) on coronary endothelial function. Porcine coronary arteries and human coronary arterial endothelial cells (HCAECs) were treated with SAA (0, 1, 10, or 25 μg/ml). Vasomotor reactivity was studied using a myograph tension system. SAA significantly reduced endothelium-dependent vasorelaxation of porcine coronary arteries in response to bradykinin in a concentration-dependent manner. SAA significantly decreased endothelial nitric oxide (NO) synthase (eNOS) mRNA and protein levels as well as NO bioavailability, whereas it increased ROS in both artery rings and HCAECs. In addition, the activities of internal antioxidant enzymes catalase and SOD were decreased in SAA-treated HCAECs. Bio-plex immunoassay analysis showed the activation of JNK, ERK2, and IκB-α after SAA treatment. Consequently, the antioxidants seleno-l-methionine and Mn(III) tetrakis-(4-benzoic acid)porphyrin and specific inhibitors for JNK and ERK1/2 effectively blocked the SAA-induced eNOS mRNA decrease and SAA-induced decrease in endothelium-dependent vasorelaxation in porcine coronary arteries. Thus, SAA at clinically relevant concentrations causes endothelial dysfunction in both porcine coronary arteries and HCAECs through molecular mechanisms involving eNOS downregulation, oxidative stress, and activation of JNK and ERK1/2 as well as NF-κB. These findings suggest that SAA may contribute to the progress of coronary artery disease.


1983 ◽  
Vol 2 (4) ◽  
pp. 431-433
Author(s):  
M. A. Scheinberg

Heart ◽  
2013 ◽  
Vol 99 (Suppl 1) ◽  
pp. A52.3-A53
Author(s):  
Xie Xiang ◽  
Ma Yitong ◽  
Yang Yining ◽  
Liu Fen ◽  
Li Xiaomei ◽  
...  

2020 ◽  
Author(s):  
Weiping Ji ◽  
Gautam Bishnu ◽  
Zhenzhai Cai ◽  
Xian Shen

AbstractObjectiveBased on the clinical characteristics of infected patients with novel coronavirus in secondary epidemic areas, we aimed to identify potential biomarkers for the evaluation of novel coronavirus-infected patients, guide the diagnosis and treatment of this disease in secondary epidemic areas and provide a reference for the clinical prevention and control of this epidemic situation.MethodsThe clinical data of 33 patients with respiratory symptoms caused by the novel coronavirus in Wenzhou city from January 15 to February 12, 2020, were thoroughly reviewed. At the onset of the disease, we found that the primary symptoms were fever, cough, fatigue, chest tightness, chest pain and specific blood test results. According to the patients’ histories, the patients were divided into two groups: those who spent time in the main epidemic area and those who did not spend time in the main epidemic area. The differences in the clinical manifestations between these two groups were analyzed.ResultsThe main clinical symptoms of patients infected with novel coronavirus in the secondary epidemic area were respiratory tract ailments and systemic symptoms. After grouping patients based on the presence or absence of residency in or travel history to the main epidemic area, there was no significant difference between the baseline data of these two groups, and there were no significant differences in symptoms and signs between the two groups (P>0.05). Some patients had abnormally increased serum amyloid protein A (SAA). There were statistically significant differences in the leukocyte count/C-reactive protein, monocyte ratio/C-reactive protein, neutrophil count/C-reactive protein, monocyte count/C-reactive protein and hemoglobin/C-reactive protein values between the two groups (P < 0.05).ConclusionRespiratory tract ailments and systemic symptoms were the primary symptoms of novel coronavirus infection in the secondary epidemic area; these symptoms are not typical. The abnormal increase in serum amyloid protein (SAA) may be used as an auxiliary index for diagnosis and treatment. CRP changes before other blood parameters and thus may be an effective evaluation index for patients with COVID-19 infection.


QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
K H Swidan ◽  
M S Sweed ◽  
A M Abbas ◽  
M K Jewi

Abstract Background Preeclampsia is a common complication of pregnancy and remains a common cause of maternal and fetal mortality. The clinical symptoms of preeclampsia are caused by widespread endothelial dysfunction suggested to be a part of an exaggerated maternal inflammatory response to pregnancy. Since preeclampsia is associated with widespread endothelial dysfunction, proposed to be provoked by an increased maternal systemic inflammatory response, the maternal plasma level of SAA might be expected to be increased when compared to normal pregnancy levels. The maternal plasma level of SAA in normal pregnancy could differ from non-pregnant level due to increased hormone levels, increased adipose tissue and\or secondary to modifications of inflammatory response in normal pregnancy. Aims The aim of our study is to estimate the relation between serum amyloid A in pregnant women and preeclampsia. Methodology the study conducted this case control study in the emergency room of Ain Shams University Maternity Hospital starting from April 2018 on women with preeclampsia to estimate serum amyloid A in pregnant women with preeclampsia. Members of the control group are healthy, non-smoker pregnant women who had an uncomplicated antenatal course and all arterial blood pressure measurements were normal. Results The current study was conducted in Ain Shams University Maternity Hospital in the period between January 2017 and August 2018. A total of 75 women were included in the study. The process of recruitment and handling the study population during the course of the study is shown in the flow diagram (figure 1). In order to avoid any confounding effect for a possible subclinical ongoing pathophysiological process, four women with preeclampsia lacking severe features were excluded following the development of severe features shortly after measurement of serum amyloid A level. Conclusion Our data sustain the limited number of studies investigating the SAA levels in both preeclamptic and healthy pregnant women, in which it was hard to reach a consensus regarding the association between SAA levels and preeclampsia. Taken in consideration that an elevated plasma level of SAA in preeclamptic women should be considered pathologic, we believe that the response of relationship between the preeclampsia and SAA levels could be caused by an inflammatory condition associated with preeclampsia. Also, serum amyloid A can be used to discriminate between mild preeclampsia cases and controls and as discriminate between severe preeclampsia cases and controls. Recommendation We recommended further investigation on large sample size for the elucidation of the role of SAA in pre-eclampsia neonatal outcome and the possibility of these biochemical factors to be novel markers of such disorders in pregnant women.


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