Decrypting the critical point of internal rotation of formaldehyde: A rotational study of the acrolein-formaldehyde complex.

The rotational spectrum of an acrolein-formaldehyde complex has been characterized using pulsed jet Fourier transform microwave spectroscopy complemented with quantum chemical calculations. One isomer has been observed in pulsed jets, which is stabilized by a dominant O=C⋯O tetrel bond (n → π* interaction) and a secondary C-H⋯O hydrogen bond. Splittings arising from the internal rotation of formaldehyde around its C2v axis were also observed, from which its V2 barrier was evaluated. It seems that when V2 equals or exceeds 4.61 kJ mol-1, no splitting of the spectral lines of the rotational spectrum was observed. The nature of the non-covalent interactions of the target complex is elucidated through natural bond orbital analysis. These findings contribute to a deeper understanding on the non-covalent interactions within the dimeric complex formed by two aldehydes.

CTRP5 Attenuates Doxorubicin-Induced Cardiotoxicity Via Inhibiting TLR4/NLRP3 Signaling.

BACKGROUND: C1q/tumor necrosis factor-related protein 5 (CTRP5) has been reported to be a crucial regulator in cardiac ischemia/reperfusion (I/R) injury. Nevertheless, the potential role of CTRP5 in doxorubicin (DOX)-induced cardiotoxicity and the potential mechanisms remain largely unclear. METHODS: We overexpressed CTRP5 in the hearts using an adeno-associated virus 9 (AAV9) system through tail vein injection. C57BL/6 mice were subjected to DOX (15 mg/kg/day, i.p.) to generate DOX-induced cardiotoxicity for 4 weeks. Subsequently, cardiac staining and molecular biological analysis were performed to analyze the morphological and biochemical effects of CTRP5 on the cardiac injury. H9c2 cells were used for validation in vitro. RESULTS: CTRP5 expression was down-regulated after DOX treatment both in vivo and in vitro. CTRP5 overexpression significantly attenuated DOX-induced cardiac injury, cardiac dysfunction, inhibited oxidative stress and inflammatory response. Mechanistically, CTRP5 overexpression markedly decreased the protein expression of toll-like receptor 4 (TLR4), NLRP3, cleaved caspase-1 and caspase-1, indicating TLR/NLRP3 signaling contributes to the cardioprotective role of CTRP5 in DOX-induced cardiotoxicity. CONCLUSIONS: Together, our findings demonstrated that CTRP5 overexpression could protect the heart from oxidative stress and inflammatory injury induced by DOX through inhibiting TLR4/NLRP3 signaling, suggesting that CTRP5 might be a potential therapeutic target in the prevention of DOX-induced cardiotoxicity.

Rotational spectra and semi-experimental structures of furonitrile and its water cluster.

Rotational spectroscopy represents an invaluable tool for several applications: from the identification of new molecules in interstellar objects to the characterization of van der Waals complexes, but also for the determination of very accurate molecular structures and for conformational analyses. In this work, we used high-resolution rotational spectroscopic techniques in combination with high-level quantum-chemical calculations to address all these aspects for two isomers of cyanofuran, namely 2-furonitrile and 3-furonitrile. In particular, we have recorded and analyzed the rotational spectra of both of them from 6 to 320 GHz; rotational transitions belonging to several singly-substituted isotopologues have been identified as well. The rotational constants derived in this way have been used in conjunction with computed rotation-vibration interaction constants in order to derive a semi-experimental equilibrium structure for both isomers. Moreover, we observed the rotational spectra of four different intermolecular adducts formed by furonitrile and water, whose identification has been supported by a conformational analysis and a theoretical spectroscopic characterization. A semi-experimental determination of the intermolecular parameters has been achieved for all of them and the results have been compared with those obtained for the analogous system formed by benzonitrile and water.

DNA methylation profile in the whole blood of acute coronary syndrome patients with aspirin resistance.

BACKGROUND: Aspirin resistance (AR) results in major adverse cardiovascular events, and DNA methylation might participate in the regulation of this pathological process. METHODS: In present study, a sum of 35 patients with AR and 35 non-AR (NAR) controls were enrolled. Samples from 5 AR and 5 NAR were evaluated in an 850 BeadChip DNA methylation assay, and another 30 AR versus 30 NAR were evaluated to validate the differentially methylated CpG loci (DML). Then, qRT-PCR was used to investigate the target mRNA expression of genes at CpG loci. Finally, Gene Ontology (GO) as well as Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to reveal the enriched pathways. RESULTS: The AR and NAR groups displayed significant differences in DNA methylation at 7707 positions, with 270 hypermethylated sites (e.g., cg09555818 located in APOC2) and 7437 sites hypomethylated sites (e.g., cg26828689 located in SLC12A5). Six DML were validated by pyrosequencing, and it was confirmed that DNA methylation (cg16391727, cg21008208, cg21293749, and cg13945576) was related to the increasing risk of AR. The relative mRNA expression of the ROR1 gene was also associated with AR (p = 0.007), suggesting that the change of cg21293749 in DNA methylation might lead to differential ROR1 mRNA expression, ultimately resulting in AR. Furthermore, the identified differentially methylated sites were associated with the molecular pathways such as circadian rhythms and insulin secretion. CONCLUSION: Hence, the distinct DNA methylation might play a vital role in the biological regulation of AR through the pathways such as circadian rhythms.

Gab1 Overexpression Alleviates Doxorubicin-Induced Cardiac Oxidative Stress, Inflammation, and Apoptosis Through PI3K/Akt Signaling Pathway.

ABSTRACT: Grb2-associated binding protein 1 (Gab1), an intracellular scaffolding adaptor, was involved in several cardiovascular diseases. However, the role of Gab1 in doxorubicin (DOX)-induced cardiotoxicity remains largely unknown. The present study investigated whether Gab1 protected against DOX-induced cardiotoxicity and the underlying mechanism. We overexpressed Gab1 in the hearts using an adeno-associated virus 9 system through tail vein injection. C57BL/6 mice were subjected to DOX (15 mg/kg/d, i.p.) to generate DOX-induced cardiotoxicity. Echocardiography, histological analysis, immunofluorescence and enzyme-linked immunosorbent assay (ELISA) kits, Western blotting, and quantitative real-time polymerase chain reaction (PCR) evaluated DOX-induced cardiotoxicity and the underlying mechanisms. Myocardial Gab1 protein and messenger RNA (mRNA) levels were markedly decreased in DOX-administered mice. Overexpression of Gab1 in myocardium significantly improved cardiac function and attenuated cardiac oxidative stress, inflammatory response, and apoptosis induced by DOX. Mechanistically, we found that PI3K/Akt signaling pathway was downregulated after DOX treatment, and Gab1 overexpression activated PI3K/Akt signaling pathway, whereas PI3K/Akt signaling pathway inhibition abolished the beneficial effect of Gab1 overexpression in the heart. Collectively, our results indicated that Gab1 is essential for cardioprotection against DOX-induced oxidative stress, inflammatory response, and apoptosis by mediating PI3K/Akt signaling pathway. And cardiac gene therapy with Gab1 provides a novel therapeutic strategy against DOX-induced cardiotoxicity.

Rotational Spectra of 2-Ethynylpyridine and Its Monohydrate: Influence of the Ortho-Substitution on Ring Geometry and Intermolecular Hydrogen Bonds.

Rotational spectra of the 2-ethynylpyridine monomer and its monohydrate have been characterized by pulsed jet Fourier transform microwave spectroscopy complemented with quantum chemical calculations. The measurements of rotational transitions of the 2-ethynylpyridine monomer and its eight monosubstituted isotopologues (15N and 13C) in natural abundances allow an accurate structural description of the skeleton of 2-ethynylpyridine. For the monohydrate, only the most stable isomer, stabilized by an O-H···N and a secondary C-H···O hydrogen bonds, has been observed in the supersonic jet. Johnson's noncovalent interaction and quantum theory of atoms in molecules analyses have been performed and compared with results for several ortho-substituted pyridine derivatives to elucidate the general trend in their binding energies.

Visfatin Amplifies Cardiac Inflammation and Aggravates Cardiac Injury via the NF-κB p65 Signaling Pathway in LPS-Treated Mice.

Background: Visfatin is an adipocytokine that has been demonstrated to be involved in cardiovascular diseases. This study aims at determining the role of visfatin in sepsis-induced cardiac injury and identify its possible mechanisms. Methods: Dynamic changes in visfatin expression in mice with lipopolysaccharide- (LPS-) induced septicemia were measured. Additionally, mice were pretreated with visfatin and further administered LPS to observe the effects of visfatin on cardiac injury. Finally, septic mice were also pretreated with JSH-23 to investigate whether visfatin regulates cardiac injury via the NF-κB p65 pathway. Results: Visfatin expression levels in both the heart and serum were increased in LPS-treated mice and peaked at 6 hours, and visfatin was derived from cardiac macrophages. In septic mice, pretreatment with visfatin reduced the survival rate, worsened cardiac dysfunction, and increased the expression of cardiac injury markers, including creatine kinase myocardial bound (CK-MB) and lactate dehydrogenase (LDH). Treatment with visfatin also increased the infiltration of CD3+ cells and F4/80+ cells, amplified the cardiac inflammatory response, and elevated myocardial cell apoptosis. Treatment with JSH-23 reversed the effects of visfatin in septic mice. Conclusions: This study showed that visfatin amplifies the cardiac inflammatory response and aggravates cardiac injury through the p65 signaling pathway. Visfatin may be a clinical target for preventing cardiac injury in sepsis.

Increased levels of inflammatory biomarker CX3CL1 in patients with chronic obstructive pulmonary disease.

OBJECTIVE: To investigate the concentration of CX3CL1 in serum of patients with chronic obstructive pulmonary disease (COPD), and to evaluate the associations between the CX3CL1 level and systemic inflammation, small airway obstruction, and COPD assessment test (CAT) scores in COPD patients. METHODS: Enzyme-linked immunosorbent assay were utilized to detect the CX3CL1 protein in serum separately from 64 patients with COPD and 53 healthy controls. RESULTS: Compared with healthy non-smokers, healthy smokers and COPD non-smokers, serum CX3CL1 protein levels were significantly elevated in COPD smokers (258.33 ±â€¯56.27 pg/mL versus 177.32 ±â€¯43.21 pg/mL, 185.64 ±â€¯47.03 pg/mL, and 226.55 ±â€¯51.79 pg/mL, P < 0.05). Correlation analysis indicated that serum CX3CL1 in COPD smokers was negatively correlated with FEV1/FVC (justified r = -0.319, P < 0.001), FEV1/Pre (justified r = -0.476, P < 0.001), FEV3/FVC (justified r = -0.354, P < 0.001), MMEF25-75/Pre (justified r = -0.428, P < 0.001), but positively correlated with CRP (justified r = 0.331, P < 0.001) and MMP-12 (justified r = 0.352, P < 0.001). However, our results showed no significant correlation between serum CX3CL1 of COPD smokers and the diffusing capacity of the lung for carbon monoxide (DLCO) (justified r = 0.0397, P = 0.6025), but a positive correlation with COPD assessment test (CAT) scores (justified r = 0.367, P < 0.001). Finally, through multivariate linear analysis, statistical results demonstrated age (ß = -0.2694, P = 0.005), FEV1/Pred (ß = -0.2653, P = 0.003), CRP (ß = 0.1427, P = 0.0478) and MMP-12 (ß = 0.430, P < 0.001) are independent parameters associated with CX3CL1. CONCLUSION: The results demonstrated that elevated circulating CX3CL1 level is associated with the systemic inflammation, small airway obstruction, and CAT scores in COPD patients, suggesting that CX3CL1 may play crucial roles in the pathogenesis of COPD. Blocking CX3CL1 might prevent the progression of chronic obstructive pulmonary disease.

Commonalities and Differences in Psychological Adjustment to Chronic Illnesses Among Older Adults: a Comparative Study Based on the Stress and Coping Paradigm.

BACKGROUND: This study aimed to validate the role of the stress and coping paradigm in the context of psychological adjustment to chronic illnesses among older adults by using the structural equation modeling technique, as well as investigating the differences in structural weights between older adults with arthritis and older adults with hypertension. METHOD: A cross-sectional study was conducted with 325 older adults with chronic illnesses (149 hypertension, 176 arthritis), aged 60-88 years, who completed questions on perceived social support, psychological resources, threat appraisal, self-efficacy, coping strategy, depressive symptoms, and anxiety. RESULTS: The results revealed that older adults with arthritis experienced significantly higher anxiety (t = 2.91, p < 0.01) than those with hypertension, whereas no significant difference in their depressive symptoms was observed (t = 1.61, p > 0.05). Social support, psychological resources, threat appraisal, and self-efficacy had a significant direct relationship with psychological distress (ß = - 0.15, ß = - 0.38, ß = 0.19, ß = - 0.23, respectively). Multi-group analyses showed significant differences in structural weights between older adults with hypertension and those with arthritis (Δχ2 = 41.336, Δdf = 18, p < 0.01). CONCLUSION: The stress and coping paradigm appears to be applicable for adjustment to chronic illnesses by allowing direct paths from social support, psychological resources, threat appraisal, and self-efficacy to psychological distress. The differences in structural weights may offer an intervening angle for clinical practitioners to design targeted interventions for older adults with different types of chronic illnesses.

Credulity rather than general trust may increase vulnerability to fraud in older adults: a moderated mediation model.

The present study aimed to clarify whether it is credulity or general trust that specifically affects vulnerability to fraud, as well as investigating the mediating role of susceptibility to persuasion and the moderating role of greed in this relationship. 254 Chinese older adults completed measures of credulity, general trust, susceptibility to persuasion, greed, and vulnerability to fraud. The results showed that credulity, but not general trust, was positively correlated with vulnerability to fraud, after controlling for demographic covariates. Susceptibility to persuasion partially mediated the effect of credulity on vulnerability to fraud. In addition, this mediating effect of susceptibility to persuasion was only significant in older adults with higher levels of greed. Our findings suggest that credulity, rather than general trust, is a risk factor in vulnerability to fraud among older adults, and may inform the development of supportive interventions to reduce this population's risk of falling victim to fraud.

[Epidemiological Analysis of Imported Malaria in Tai'an City] of Shandong Province During 2011-2015].

One hundred and sixty-three imported malaria cases were reported in Tai'an City of Shandong Province during 2011-2015, consisting of 120 cases of falciparum malaria（73.6%）, 20 vivax malaria（12.3%）, 14 ovale malaria（8.6%）, 7 quartan malaria（4.3%）, and 2 unclassified cases（1.2%）. The disease onset showed no significant seasonal variation. The reported cases were more at the age of 40～49 years（70/163, 42.9%）, and were imported mainly from Africa（156/163, 95.7%）. The median interval from symptom onset to diagnosis was 4 days, and only 15 patients（9.2%） received definite diagnosis within 24 h. After medication, 161 cases recovered and 2 cases died.

Correlation Between SNPs in Candidate Genes and VerifyNow-Detected Platelet Responsiveness to Aspirin and Clopidogrel Treatment.

PURPOSE: Patients with high on-treatment platelet reactivity (HPR) against aspirin or clopidogrel are at increased risk for adverse cardiovascular events. In this study, we explored the predictive value of common SNPs for the on-treatment platelet reactivity (OPR) against aspirin and clopidogrel assessed by VerifyNow assays. METHODS: This study recruited 286 Han Chinese individuals undergoing antiplatelet treatment, including 159 cases with aspirin only (100 mg/day) and 127 cases with dual therapy (aspirin 100 mg/day plus clopidogrel 75 mg/day) for at least 2 weeks. The OPR against aspirin and clopidogrel were assessed by VerifyNow Aspirin (ARU) and P2Y12 assays (PRU), respectively. Genotyping for the selected 25 SNPs within 11 genes and 2 GWAS loci was carried out by ABI multiplex SNaPshot method. RESULTS: The results indicated that rs4244285 (CYP2C19) and rs342293 (7q22.3) were significantly associated with PRU value (both P < 0.01). As for the OPR to aspirin, a weak statistical significance was observed in rs5445 (GNB3) (P = 0.049) and rs5758 (TBXA2R) (P = 0.045). After adjusting for the covariates including gender, age and smoking, carriers of allele A of rs4244285 remained as a strong predictor for HPR against clopidogrel. CONCLUSION: The current study suggests that common SNPs may predict OPR against clopidogrel as assessed by VerifyNow P2Y12, but are less likely to respond against aspirin as assessed by VerifyNow Aspirin.

Overexpression of MD1 ameliorates pathological myocardial remodeling in diabetic cardiomyopathy by TLR4/STAT3 signaling pathway.

Diabetic cardiomyopathy (DCM) is characterized by oxidative damage and inflammatory responses. Myeloid differentiation protein 1 (MD1) exhibits antioxidant and anti-inflammatory properties. However, the specific role of MD1 in DCM has yet to be elucidated. This study aims to investigate the role of MD1 in DCM and to elucidate the underlying mechanisms. We utilized a gain-of-function approach to explore the involvement of MD1 in DCM. Diabetes was induced in MD1-transgenic (MD1-TG) mice and their wild-type (WT) counterparts via streptozotocin (STZ) injection. Additionally, a diabetes cell model was established using H9c2 cells exposed to high glucose levels. We conducted comprehensive evaluations, including pathological analyses, echocardiography, electrocardiography, and molecular assessments, to elucidate the underlying mechanisms of MD1 in DCM. Notably, MD1 expression was reduced in the hearts of STZ-induced diabetic mice. Overexpression of MD1 significantly improved cardiac function and markedly inhibited ventricular pathological hypertrophy and fibrosis in these mice. Furthermore, MD1 overexpression resulted in a substantial decrease in myocardial reactive oxygen species (ROS) accumulation, mitigating myocardial oxidative stress and reducing the levels of inflammation-related markers such as IL-1ß, IL-6, and TNF-α. Mechanistically, MD1 overexpression inhibited the activation of the TLR4/STAT3 signaling pathway, as demonstrated in both in vivo and in vitro experiments. The overexpression of MD1 significantly impeded pathological cardiac remodeling and improved cardiac function in STZ-induced diabetic mice. This effect was primarily attributed to a reduction in ROS accumulation and mitigation of myocardial oxidative stress and inflammation, facilitated by the inhibition of the TLR4/STAT3 signaling pathway.

[Association research between polymorphism of IFN-gamma and IL-10, environmental risk factors, and susceptibility to esophageal cancer].

OBJECTIVE: To explore the polymorphism of interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) with susceptibility to esophageal cancer (EC), as well as the interaction between the environmental risk factors and the polymorphism of IFN-gamma or IL- 10. To explore the interaction between the polymorphism of IFN-gamma and IL-10. METHODS: According to the case-control design, 120 EC cases and 122 controls were examined. PCR technology was used to determine the genotypes of IFN-gamma + A874T and IL-10 -A1082G. Indicators of quantitative analysis for interaction between IFN-gamma and IL-10, and parts of environmental factors were calculated by crossover analysis multiplicative mode. RESULTS: Allele frequencies of T of IFN-gamma + A874T was 37.92% in case group higher than 28.7% in control group (chi2 = 4.6414, P = 0.0312). Compared with IFN-gamma + 874AA genotype, OR of IFN-gamma + 874AT genotype was 1.729 (95% CI 1.015-2.947), OR of IFN-gamma + 874TT genotype was 2.923 (95% CI 1.227-5.214) and OR of IFN-gamma + 874AT + TT genotype was 1.821 (95% CI 1.081-3.069). There was synergistic action between IFN-gamma + 874AT + TT and drink index, moldy food and regular diet habit, their S respectively were 1.909, 4.154 and 5.026. The interaction between IFN-gamma + 874AT + TT and IL-10 -1082AG + GG was not increased the risk of EC OR = 2.342 (95% CI 0.975-5.626). CONCLUSION: The IFN-gamma + 874AT genotype might be a risk factor to EC. T allele gene may be heredity predisposing gene of EC. IFN-gamma + 874 AT + TT genotype as the corresponding reduction of the environmental risk factors can reduce the incidence of esophageal cancer.

Research hotspots and trends of Kinesio Taping from 2011 to 2020: a bibliometric analysis.

The purpose of this study was to explore the research hotspots and trends of Kinesio Taping in the last decade and provide new sights in future studies. Publications in the area of Kinesio Taping were searched from the Web of Science Core Collection database between 2011 and 2020. Citespace software was used to analyze data on countries/regions, institutions, authors, co-cited references, and keywords. A total of 677 publications were obtained in the last decade. We identified the most prolific countries, institutions, and authors in the field of Kinesio Taping from 2011 to 2020. The annual number of publications showed an upward trend. The most prolific country and institution were Turkey and Hacettepe University, respectively. The author with the biggest number of publications was Gul Baltaci from Turkey. The top 5 most frequent keywords were "pain", "tape", "strength", "exercise", and "reliability". The keywords with the highest centrality were "proprioception", followed by "reliability", "clinical trial", "ankle", and "pain". Ten clusters were found and the biggest one was "quadricep". The top 9 keywords with the strongest bursts were detected and "trial" had the highest burst strength. The results from the bibliometric analysis provide hotspots and trends in the field of Kinesio Taping. It is still in the development stage of the past decade. Pain relief, sports injury prevention and treatment, and proprioception enhancement to improve postural control were the hotspots from 2011 to 2020. High-quality trials and standardized criteria for applications are needed in the future.

Comprehensive analysis of the RNA transcriptome expression profiles and construction of the ceRNA network in heart failure patients with sacubitril/valsartan therapeutic heterogeneity after acute myocardial infarction.

Sacubitril/valsartan has a noteworthy advantage in improving ventricular remodelling, as well as reducing cardiovascular mortality and the rate of heart failure (HF) readmission. However, clinically, some patients with HF still have low sensitivity to sacubitril/valsartan, indicating sacubitril/valsartan resistance (SVR). A total of 46 patients with HF after AMI (23 SVR and 23 non-sacubitril/valsartan resistance (NSVR)) were selected. Five SVR and 5 matched NSVR samples were screened for differentially expressed ncRNAs along with mRNAs. A total of 124 differentially expressed miRNAs, 137 circRNAs, 237 lncRNAs and 50 mRNAs were screened by RNA sequencing technology. After quantitative real-time PCR (qRT‒PCR) verification of selected biomarkers in 18 pairs of samples, we found that for patients with SVR, hsa-miR-543, hsa-miR-642b-5p, hsa-miR-760, hsa_circ_0137499, ENST00000474394, ENST00000528337, E2F1, NEAT1, and YTHDF2 were upregulated, and hsa-miR-424-5p, hsa-miR-21-3p, hsa_circRNA_0003275, hsa_circRNA_0004494, hsa_circ_0093522, ENST00000467951, ENST00000558177, ACTA2, ANPEP, and CAMP were downregulated. Then, with the help of our constructed ceRNA network and functional annotation enrichment, we speculated that inflammatory pathways (such as the apelin signalling pathway) and lipid metabolism pathways (such as fatty acid metabolism) may be involved in the regulation of SVR. These discoveries lay a foundation for further mechanistic research and provide a direction for individualized drug administration.

Transcriptome-wide map of N6-methyladenosine (m6A) profiling in coronary artery disease (CAD) with clopidogrel resistance.

BACKGROUND: Clopidogrel resistance profoundly increases the risk of major cardiovascular events in coronary artery disease (CAD) patients. Here, we comprehensively analyse global m6A modification alterations in clopidogrel-resistant (CR) and non-CR patients. METHODS: After RNA isolation, the RNA transcriptome expression (lncRNA, circRNA, and mRNA) was analysed via RNA-seq, and m6A peaks were identified by MeRIP-seq. The altered m6A methylation sites on mRNAs, lncRNAs, and circRNAs were identified, and then, GO and KEGG pathway analyses were performed. Through joint analysis with RNA-seq and MeRIP-seq data, differentially expressed mRNAs harbouring differentially methylated sites were identified. The changes in m6A regulator levels and the abundance of differentially methylated sites were measured by RT-PCR. The identification of m6A-modified RNAs was verified by m6A-IP-qPCR. RESULTS: The expression of 2919 hypermethylated and 2519 hypomethylated mRNAs, 192 hypermethylated and 391 hypomethylated lncRNAs, and 375 hypermethylated and 546 hypomethylated circRNAs was shown to be altered in CR patients. The m6A peaks related to CR indicated lower mark density at the CDS region. Functional enrichment analysis revealed that inflammatory pathways and insulin signalling pathways might be involved in the pathological processes underlying CR. The expression of mRNAs (ST5, KDM6B, GLB1L2, and LSM14B), lncRNAs (MSTRG.13776.1 and ENST00000627981.1), and circRNAs (hsa_circ_0070675_CBC1, hsa-circRNA13011-5_CBC1, and hsa-circRNA6406-3_CBC1) was upregulated in CR patients, while the expression of mRNAs (RPS16 and CREG1), lncRNAs (MSTRG.9215.1), and circRNAs (hsa_circ_0082972_CBC1) was downregulated in CR patients. Moreover, m6A regulators (FTO, YTHDF3, and WTAP) were also differentially expressed. An additional combined analysis of gene expression and m6A peaks revealed that the expression of mRNAs (such as ST5, LYPD2, and RPS16 mRNAs) was significantly altered in the CR patients. CONCLUSION: The expression of m6A regulators, the RNA transcriptome, and the m6A landscape was altered in CR patients. These findings reveal epitranscriptomic regulation in CR patients, which might be novel therapeutic targets in future.

[Diagnostic value of 320-slice computed tomography coronary angiography to assess in-stent restenosis].

OBJECTIVE: To evaluate the diagnostic accuracy of 320-slice CT coronary angiography (CTA) in the evaluation of in-stent restenosis (ISR, ≥50% luminal narrowing) in comparison with quantitative coronary angiography (CAG). METHODS: A total of 69 patients with previous stent implantation who underwent both CTA and CAG were prospectively included. We assessed diagnostic valve for ISR with CTA in comparison with CAG. RESULTS: A total of 110 stents were implanted in these patients.CAG identified 14 ISR. CTA correctly identified 13 ISR and misdiagnosed 5 ISR in stents without ISR. Besides, 6 stents could not be evaluated by CTA due to unsatisfied image quality. Accordingly, sensitivity, specificity, positive and negative predictive value of CTA for diagnosing ISR were 93%, 89%, 54% and 99%, respectively. The image quality of CTA was significantly better in larger stents (percentages of good and moderate stent image of ≥3.0 mm and <3.0 mm: 56% vs. 27%, 25% vs. 49%) and which was linked with better diagnostic coincidence rate (95% vs. 78%) for larger stents. The image quality of CTA was significantly better in stents with thinner stent strut thickness (percentages of poor CTA stent image quality of stent strut thickness<140 µm and ≥140 µm: 12% vs. 45%, P<0.01) and which was associated with better diagnostic coincidence rate for stents with thinner stent strut thickness (94% vs. 76%, P<0.05). The image quality of CTA was also significantly better in single stent (percentages of poor CTA stent image quality of single stent vs. overlap and dedicated stent: 17% vs. 36%, P<0.05). However, heart rate (≥65 beats/min vs. <65 beats/min) during CTA acquisition was not associated with image quality and the diagnostic coincidence rate (all P>0.05). CONCLUSIONS: Our results indicate that 320-slice CTA allows accurate noninvasive assessment of significant in-stent restenosis in selected patients. Stents with a large diameter and thin struts are associated with better image quality and higher diagnostic accuracy.

[Clinical application of VerifyNow-P2Y12 assay in evaluation of platelet inhibition efficacy of clopidogrel].

OBJECTIVE: To evaluate the platelet inhibition efficacy in patients under regular maintenance dose of clopidogrel by VerifyNow-P2Y12 assay and explore the clinical characteristics of clopidogrel non-responders and related predicting factors. METHODS: A total of 99 patients underwent percutaneous coronary intervention procedure and receiving clopidogrel in regular maintenance dose for at least 1 week were enrolled. Platelet reactivity, including baseline, P2Y12 reaction unit (PRU), and platelet inhibition rate were measured with VeifyNow-P2Y12 assay. The dosage of anti-platelet drugs, combination with any other drugs, clinical characters in baseline of all enrolled patients were analyzed. PRU ≤ 240 was used as cut-off to identify clopidogrel responder and clopidogrel non-responder. In the non-responder group, patients were further separated into 3 sub-groups (types) according to the baseline and platelet inhibition rate: type I with high baseline, high inhibition rate, representing false non-responder; type II with low inhibition rate, representing true non-responder and type III mixed type. RESULTS: In this study, 48 of 99 patients were found to be clopidogrel non-responder (48.5%). The ratio of type I, type II and type III in the non-responder group was 9.1% (n = 9), 27.3% (n = 27), and 12.1% (n = 12), respectively. Baseline platelet value in female patients was significantly higher than in males (P < 0.01), number of females with high PRU also is higher than males (P < 0.01), female gender was a predict factor for type I non-responder (OR = 6.5, 95%CI 2.295 - 18.407, P < 0.01). BMI > 24 kg/m(2) was a risk factor for clopidogrel non-responder (P < 0.05), and may be regarded as a predict factor for type II non-responder (OR = 3.207, 95%CI 1.375 - 7.485, P < 0.01). Age, hypertension, diabetics, smoking, hyperlipidemia, CRP and pantoprazole use do not show significant correlation with baseline and platelet inhibition rate. CONCLUSIONS: Clopidogrel responses could be reliably detected by VerifyNow-P2Y12 assay. Female gender and high body weight are independent risk factors for clopidogrel non-responses.

Rotational spectrum of anisole-CO2: Cooperative C···O tetrel bond and CH···O hydrogen bond.

Rotational spectrum of the 1:1 anisole-CO2 complex has been investigated using a pulsed jet Fourier transform microwave spectrometer supplemented with quantum chemical calculations. In the pulsed jet, only one isomer has been observed which is characterized by a dominant C···O tetrel bond and two CH···OCO2 weak hydrogen bonds. Different theoretical methods predict different orders of relative energies of plausible conformations. The experimental observation is most consistent with the theoretical estimation at the B3LYP-D3(BJ)/6-311++G(d,p) level of theory. Johnson's non-covalent interaction, quantum theory of atoms in molecules and natural bond orbital analyses have been applied to better understand the nature of non-covalent interactions at play in the anisole-CO2 complex.