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Objective To investigate the expression profile of circular RNAs (circRNAs) and proposed circRNA-microRNA (miRNA) regulatory network in atrial fibrillation (AF). Methods Atrial tissues from patients with persistent AF with rheumatic heart disease and non-AF myocardium with normal hearts were collected for circRNA differential expression analyses by high-throughput sequencing. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to predict the potential functions of the differentially expressed genes and AF-related pathways. Co-expression networks of circRNA-miRNA were constructed based on the correlation analyses between the differentially expressed RNAs. Quantitative reverse transcription polymerase chain reaction (PCR) was performed to validate the results. Results A total of 108 circRNAs were found to be differentially expressed in AF. Among them, 51 were up-regulated, and 57 were down-regulated. Dysregulated circRNAs were validated by quantitative real-time PCR. The GO and KEGG pathway enrichment analyses were executed to determine the principal functions of the significantly deregulated genes. Furthermore, we constructed correlated expression networks between circRNAs and miRNAs. circRNA19591, circRNA19596, and circRNA16175 interacted with 36, 28, and 18 miRNAs, respectively; miR-29b-1-5p and miR-29b-2-5p were related to 12 down-regulated circRNAs, respectively. Conclusion Our findings provide a novel perspective on circRNAs involved in AF due to rheumatic heart disease and establish the foundation for future research of the potential roles of circRNAs in AF.

Lighting can influence people's performance of eyes and their perception of depth cues. Both two factors are very important for depth perception. Hence, lighting is expected to have effects on depth perception. The current study conducted a within-subjects experiment to investigate the influence of three different indoor LED lighting environments on depth perception in the real world. 23 participants were involved, and they were required to play a shooting computer game under the designed lighting environment. Depth perception data were collected with a Depth Perception Tester both before and after the experiment. The experiment showed that depth perception of the operators was always influenced by their physical and mental state in the beginning, which was not changed by lighting environment. It was also found that the three lighting environments used in the current experiment did not change depth perception. Hence, we could conclude that luminance between 350Lux and 750Lux is a safe range that does not influence depth perception.

Objective: To identify the association between rs2910164 polymorphism and development of pulmonary hypertension, as well as underlying molecular mechanism. Methods and Results: 281 patients diagnosed with pulmonary hypertension and 325 normal controls were recruited, and rs2910164 genotype was determined in each participant: As a result, the rs2910164 polymorphism was significantly associated with the development of pulmonary hypertension after adjusting some potential confounding factors. Additionally, lung tissue samples were obtained from 39 patients who received surgical intervention for lung cancer, and mRNA and protein expression levels of miR-146a, COX-2 and PGI2 production were examined. Furthermore, we confirmed COX-2 is a target of miR-146a in pulmonary smooth muscle cells, and identified a differentially expressed miR-146a and COX-2 in each rs2910164 genotype group. We observed a significant association between rs2910164 polymorphism and the levels of either COX-2 or PGI2 using real-time PCR and western blot. In conclusion, the results of this study demonstrate that the rs2910164 CC and GC genotype is associated with a decreased risk of pulmonary hypertension, which could be attributed to defective miRNA processing and compromised ability to inhibit production of COX-2 and PGI2.

Objective Although imaging modalities, such as transesophageal and intracardiac echocardiography, have helped to improve the safety of atrial transseptal puncture (TSP), fluoroscopy is still traditionally and widely used in TSP. The aim of the present study was to evaluate an individual knack for TSP during cryoballoon ablation of atrial fibrillation (AF) under fluoroscopy. Methods Through the prospective study of 72 cases of patients with paroxysmal or persistent AF admitted for cryoablation in our center, 46 cases using a puncture site toward the bifurcation of the left main bronchus (LMB group) and 26 cases using an anterior-inferior puncture site (AI group) were included in the study. The acute pulmonary vein (PV) isolation success rate, single-procedure success rate, and time-to-effect (TTE) between the two groups were analyzed. Results All PVs were identified and successfully isolated, and there are no differences in the two groups. However, the mean TTE was shorter in the LMB group than in the AI group. Moreover, a higher single-procedure success rate was observed in the LMB group. Conclusion The bifurcation of the LMB can be clearly evaluated in each patient under fluoroscopy and is an anatomical landmark for the location of the left PV. TSP guided by the LMB is a new practical method for choosing individualized transseptal sites for catheter ablation of AF, which can help to shorten TTE and procedure time.

The branched-chain amino acids (BCAA) accumulated in type 2 diabetes are independent contributors to insulin resistance. The activity of branched-chain α-keto acid dehydrogenase (BCKD) complex, rate-limiting enzyme in BCAA catabolism, is reduced in diabetic states, which contributes to elevated BCAA concentrations. However, the mechanisms underlying decreased BCKD activity remain poorly understood. Here, we demonstrate that mitochondrial phosphatase 2C (PP2Cm), a newly identified BCKD phosphatase that increases BCKD activity, was significantly downregulated in ob/ob and type 2 diabetic mice. Interestingly, in adiponectin (APN) knockout (APN−/−) mice fed with a high-fat diet (HD), PP2Cm expression and BCKD activity were significantly decreased, whereas BCKD kinase (BDK), which inhibits BCKD activity, was markedly increased. Concurrently, plasma BCAA and branched-chain α-keto acids (BCKA) were significantly elevated. APN treatment markedly reverted PP2Cm, BDK, BCKD activity, and BCAA and BCKA levels in HD-fed APN−/− and diabetic animals. Additionally, increased BCKD activity caused by APN administration was partially but significantly inhibited in PP2Cm knockout mice. Finally, APN-mediated upregulation of PP2Cm expression and BCKD activity were abolished when AMPK was inhibited. Collectively, we have provided the first direct evidence that APN is a novel regulator of PP2Cm and systematic BCAA levels, suggesting that targeting APN may be a pharmacological approach to ameliorating BCAA catabolism in the diabetic state.

Cardiac metabolic remodeling is a central event during heart failure (HF) development following myocardial infarction (MI). It is well known that myocardial glucose and fatty acid dysmetabolism contribute to post-MI cardiac dysfunction and remodeling. However, the role of amino acid metabolism in post-MI HF remains elusive. Branched chain amino acids (BCAAs) are an important group of essential amino acids and function as crucial nutrient signaling in mammalian animals. The present study aimed to determine the role of cardiac BCAA metabolism in post-MI HF progression. Utilizing coronary artery ligation-induced murine MI models, we found that myocardial BCAA catabolism was significantly impaired in response to permanent MI, therefore leading to an obvious elevation of myocardial BCAA abundance. In MI-operated mice, oral BCAA administration further increased cardiac BCAA levels, activated the mammalian target of rapamycin (mTOR) signaling, and exacerbated cardiac dysfunction and remodeling. These data demonstrate that BCAAs act as a direct contributor to post-MI cardiac pathologies. Furthermore, these BCAA-mediated deleterious effects were improved by rapamycin cotreatment, revealing an indispensable role of mTOR in BCAA-mediated adverse effects on cardiac function/structure post-MI. Of note, pharmacological inhibition of branched chain ketoacid dehydrogenase kinase (BDK), a negative regulator of myocardial BCAA catabolism, significantly improved cardiac BCAA catabolic disorders, reduced myocardial BCAA levels, and ameliorated post-MI cardiac dysfunction and remodeling. In conclusion, our data provide the evidence that impaired cardiac BCAA catabolism directly contributes to post-MI cardiac dysfunction and remodeling. Moreover, improving cardiac BCAA catabolic defects may be a promising therapeutic strategy against post-MI HF.

Follicular dendritic cell sarcoma is a rare low-grade malignant tumor. At present, only twenty ca ses was discovered all over the world. This paper reports a case treated in our hospital, explores the clinical manifestations, pathological diagnosis and treatment to provide certain help to clinical doctor in diagnosis and treatment to reduce the misdiagnosis of the disease.