Ruozhu Dai, Huilin Zhuo, Yangchun Chen, Kelian Zhang, Yongda Dong, Chengbo Chen and Wei Wang. Mechanism of isosorbide dinitrate combined with exercise training rehabilitation to mobilize endothelial progenitor cells in patients with coronary heart disease. Bioengineered. 2021 Nov. doi: 10.1080/21655979.2021.2000258. Since publication, significant concerns have been raised about the compliance with ethical policies for human research and the integrity of the data reported in the article. When approached for an explanation, the authors provided some original data but were not able to provide all the necessary supporting information. As verifying the validity of published work is core to the scholarly record’s integrity, we are retracting the article. All authors listed in this publication have been informed. We have been informed in our decision-making by our editorial policies and the COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as ‘Retracted.’
Many studies have examined the association between paraoxonase 1 (PON1) -L55M polymorphisms and risk of coronary heart disease (CHD), but the results remained inconsistent. We therefore aimed to address this association by performing an updated meta-analysis in the Chinese population. The PubMed, EMBASE, Web of Science, and Chinese National Knowledge Infrastructure were searched up to May 2020. The strength of statistical association was assessed with odds ratio (OR) and 95% confidence interval (CI). A total of eight studies with 1826 CHD cases and 1817 controls were finally included in the analysis. In the overall and subgroup analyses by control sources and geographic areas, the results showed no significant associations with CHD among all analysis models. Furthermore, we performed the analysis by including or excluding the HWE-violating studies. The results suggested that the MM genetype were significantly associated with CHD in studies not consistent with HWE under recessive and dominant models. This meta-analysis demonstrates that the PON1 -L55M polymorphism may not be associated with CHD risk in the Chinese population. Further studies with strict selection of patients and controls in different ethnic populations will be required to clarify this finding.
Background: Low-density lipoprotein cholesterol (LDL-C) and small, dense LDL-C (sdLDL-C) are important risk indicator of coronary heart disease (CHD), but their application in therapy monitoring of CHD is still far from being elucidated. Following the concept of precision medicine, we investigated whether the scientific medication based on medication-sensitive genes can reverse the LDL-C and sdLDL-C status in human bloodstream, so as to reveal the possibility of them as a monitoring indicator of CHD efficacy.Methods: A prospective study of CHD cohort containing 208 Chinese CHD patients (158 males and 50 females) and 20 healthy people (14 males and 6 females) was recruited. LDL-C and its subfractions were detected before and after treatment. Polymorphism of medication-sensitive genes, including SLCO1B1 (rs4149056, 521T>C), CYP2C19*2 (rs4244285, c.681G>A), and CYP2C19*3 (rs4986893, c.636G>A) were detected for medication guidance.Results: Nearly half of Chinese CHD patients (47.60%, 99/208) had genetic polymorphisms with homozygous or heterozygous mutations within these three genes. LDL-1 and LDL-2, subfractions of LDL-C, had a 100% positive rate in CHD patients and healthy people. However, sdLDL-C components of LDL-5 to LDL-7 were only enrichment in CHD patients. Moreover, the mean amount of sdLDL-C subfractions in CHD patients was significantly higher than that in healthy people. Among 180 patients with treatment remission, 81.67% (n=147) of CHD patients had decreased LDL-C, while 61.67% (n=111) of patients had decreased sdLDL-C.Conclusion: sdLDL-C has better accuracy on CHD screening than LDL-C, while LDL-C was more suitable for CHD therapy monitoring. Combined medication-sensitive genes polymorphism, LDL-C and sdLDL-C detection would optimize the treatment strategy for CHD patients.
Purpose This study aimed to identify and validate the optimal 18F-FDG activity and acquisition time for cardiac viability imaging with intravenous insulin administration based on a fixed 18F-FDG activity. Methods Cardiac positron emission tomography (PET) images from 30 patients with coronary artery disease (CAD) were retrospectively reconstructed into 900, 360, 180, 90, and 45 s durations. An optimal product of the maximum standardized uptake value (SUV) of the myocardium and segmental uptake (SU) and acquisition time (MSAT) was determined through a receiver operating characteristic curve. The optimal acquisition time (OAT) was equal to MSAT divided by mean SUV of the myocardium (MyoSUV) and validated in another 26 patients with CAD. Results The MyoSUV, mean SUV of the blood, SU, and their biases on reconstructed image durations of 90, 180, and 360 s were equivalent to those on an image duration of 900 s. The optimal MSAT was 848.2. In the validation group, the OAT was 129 ± 76 s (95% confidence interval, 99–160), approximately one-third of the usual acquisition time. The MyoSUV and SU were equivalent for the difference (0.15 ± 0.21, P < 0.001; −0.01 ± 0.03, P < 0.001) between PET image duration of OAT and 600 s (7.71 ± 3.01 vs. 7.56 ± 2.94, 67.1 ± 15.4% vs. 67.7 ± 15.6%). Conclusion Intravenous insulin administration preparation has the potential to reduce radiation exposure and acquisition time of cardiac 18F-FDG viability imaging without losing the accurate measurement of MyoSUV and SU when reaching an OAT.
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