Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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Clinical Trial
Evaluation of thiol-disulfide homeostasis and oxidative stress parameters in newborns receiving phototherapy.
The aim of our study was to evaluate oxidative stress and thiol-disulfide homeostasis in term newborns receiving phototherapy. The study was planned as a single-blind, intervention study in a single center with level 3 neonatal intensive care unit to investigate the effect of phototherapy on the oxidative system in term newborns with hyperbilirubinemia. Neonates with hyperbilirubinemia were treated with total body exposure phototherapy technique for 18 h using a Novos® device. ⋯ We also determined significantly the lower bilirubin levels after phototherapy (p < 0.001). In conclusion, we found that phototherapy treatment induced decreased oxidative stress associated with hyperbilirubinemia in neonates. Thiol-disulfide homeostasis can be used as a marker of oxidative stress due to hyperbilirubinemia in the early period.
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Meta Analysis
Comparison of outcome among type 2 vs type 1 myocardial infarction: a systematic review and meta-analysis.
To date, there were limited studies available on myocardial infarction (MI), and consequently, the outcomes of patients with type 1 myocardial infarction (T1MI) compared to type 2 myocardial infarction (T2MI) remained inconclusive. We aimed to compare the outcomes of T1MI and T2MI patients in terms of mortality and adverse cardiovascular outcomes. We performed a systematic literature search on PubMed, Embase, and Scopus for relevant articles from inception until March 20, 2022. 341,049 patients had T1MI, while the remaining 67,537 patients had T2MI. ⋯ There was no significant difference in terms of 30-day mortality (OR 0.58, 95% CI 0.25-1.36, p = 0.21), cardiovascular mortality (OR 0.95, 95% CI 0.68-1.32, p = 0.74), all-cause readmission (OR 0.84, 95% CI 0.62-1.14, p = 0.26), and readmission due to MI (OR 1.22, 95% CI 0.66-2.27, p = 0.53) between both groups. Patients with T1MI had favorable outcomes in terms of mortality and MACE compared to that of T2MI patients. Further studies should aim at determining the optimal management strategy for these high-risk patients for better patient outcomes.
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Glycated hemoglobin A1c (HbA1c) has been recognized as a predictor of cardiovascular events. However, the relationship between HbA1c and coronary artery disease (CAD) in the Chinese population has yet to be systematically explored. In addition, factors associated with HbA1c were generally analyzed linearly, thereby failing to appreciate more complex nonlinear associations. ⋯ Both HbA1c > 7.2% and HbA1c < 5.7% were associated with the presence of MI. In conclusion, HbA1c value was highly associated with the severity of coronary artery stenosis in the whole study population, and in CAD patients without diagnosed diabetes. Compared with patients with HbA1c levels between 6.0% and 7.0%, HbA1c < 5.7% and HbA1c > 7.2% were associated with higher presence of MI.
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The molecular mechanisms of opium action with regard to coronary artery disease (CAD) have not yet been determined. The aim of this study was to evaluate the effect of opium on the expression of scavenger receptors including CD36, CD68, and CD9 tetraspanin in monocytes and the plasma levels of tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), malondialdehyde (MDA), and nitric oxide metabolites (NOx) in CAD patients with and without opium addiction. This case-control study was conducted on three groups: (1) opium-addicted CAD patients (CAD + OA, n = 30); (2) CAD patients with no opium addiction (CAD, n = 30); and (3) individuals without CAD and opium addiction as the control group (Ctrl, n = 17). ⋯ MDA levels significantly increased in CAD and CAD + OA patients in comparison with the Ctrl group (p = 0.010 and p = 0.002, respectively). No significant differences were found in CD9, CD36, CD68, IFN-γ, and NOx between the three groups. The findings demonstrated that opium did not have a significant effect on the expression of CD36, CD68, and CD9 at gene and protein levels, but it might be involved in the development of CAD by inducing inflammation through other mechanisms.