The left adrenal vein: An important direction for right adrenal venous sampling.

This study aimed to evaluate the guiding role of left adrenal vein (LAV) for right adrenal venous sampling (AVS). A total of 347 patients who were diagnosed with primary aldosteronism (PA) and underwent successful AVS procedures from January 2020 to July 2021 were retrospectively analyzed. According to the different quadrant position of the orifice of right adrenal vein (RAV), the area where the orifice of RAV is located is divided into three areas: A, B, and C and the area A is further subdivided into A1, A2, and A3 areas. By counting the area where the orifice of RAV is located, the guiding role of the LAV on the RAV is determined. Most of the orifice of RAV are located in area A, and the proportions of areas A, B, and C was 96.8%, 1.4%, and 1.7%, respectively. In area A, areas A1, A2, and A3 account for 80.9%, 17.0%, and 2.1%, respectively. High body mass index, female and smaller the angle between the LAV and horizontal line was associated with the closer positional relationship between the LAV on the RAV. These findings suggest that most of the horizontal position of the RAV orifice is close to the horizontal position of the most distal end of the LAV, which indicate that the LAV location can play an important role on the guiding for right AVS. Additionally, body mass index, sex, and the angle of the LAV was largely related to location of the orifice of the RAV.

Superselective adrenal arterial embolization for primary aldosteronism without lateralized aldosterone secretion: an efficacy and safety, proof-of-principle study.

Superselective adrenal arterial embolization (SAAE) appears to be beneficial in primary aldosteronism (PA) patients with lateralized aldosterone secretion (unilateral PA). As confirmed by adrenal vein sampling (AVS), nearly 40% of PA patients would be PA without lateralized aldosterone secretion (bilateral PA). We aimed to investigate the efficacy and safety of SAAE on bilateral PA. We identified 171 bilateral PA patients from 503 PA patients who completed AVS. Thirty-eight bilateral PA patients received SAAE, and 31 completed a median 12-month clinical follow-up. The blood pressure and biochemical improvements of these patients were carefully analyzed. 34% of patients were identified as bilateral PA. Plasma aldosterone concentration, plasma renin activity, and aldosterone/renin ratio (ARR) were significantly improved 24-h after SAAE. SAAE was associated with 38.7% and 58.6% of complete/partial clinical and biochemical success within a median 12-month follow-up. A significant reduction in left ventricular hypertrophy was shown in patients who obtained complete biochemical success compared with partial/absent biochemical success. SAAE was associated with a more apparent nighttime blood pressure reduction than daytime blood pressure reduction in patients with complete biochemical success. No major adverse safety events related to SAAE were reported during the intraoperative, postoperative, and follow-up periods. SAAE was associated with blood pressure and biochemical improvements in part of bilateral PA and appeared safe. The biochemistry success was accompanied by improved cardiac remodeling and a more prominent decrease in nocturnal blood pressure. This study was part of a trial registered with the Chinese Clinical Trial Registry, number ChiCTR2100047689.

Single-channel EEG signal extraction based on DWT, CEEMDAN, and ICA method.

In special application scenarios, such as portable anesthesia depth monitoring, portable emotional state recognition and portable sleep monitoring, electroencephalogram (EEG) signal acquisition equipment is required to be convenient and easy to use. It is difficult to remove electrooculogram (EOG) artifacts when the number of EEG acquisition channels is small, especially when the number of observed signals is less than that of the source signals, and the overcomplete problem will arise. The independent component analysis (ICA) algorithm commonly used for artifact removal requires the number of basis vectors to be smaller than the dimension of the input data due to a set of standard orthonormal bases learned during the convergence process, so it cannot be used to solve the overcomplete problem. The empirical mode decomposition method decomposes the signal into several independent intrinsic mode functions so that the number of observed signals is more than that of the source signals, solving the overcomplete problem. However, when using this method to solve overcompleteness, the modal aliasing problem will arise, which is caused by abnormal events such as sharp signals, impulse interference, and noise. Aiming at the above problems, we propose a novel EEG artifact removal method based on discrete wavelet transform, complete empirical mode decomposition for adaptive noise (CEEMDAN) and ICA in this paper. First, the input signals are transformed by discrete wavelet (DWT), and then CEEMDAN is used to solve the overcomplete and mode aliasing problems, meeting the a priori conditions of the ICA algorithm. Finally, the components belonging to EOG artifacts are removed according to the sample entropy value of each independent component. Experiments show that this method can effectively remove EOG artifacts while solving the overcomplete and modal aliasing problems.

Classification of motor imagery electroencephalogram signals by using adaptive cross-subject transfer learning.

Introduction: Electroencephalogram (EEG)-based motor imagery (MI) classification is an important aspect in brain-computer interfaces (BCIs), which bridges between neural system and computer devices decoding brain signals into recognizable machine commands. However, due to the small number of training samples of MI electroencephalogram (MI-EEG) for a single subject and the great individual differences of MI-EEG among different subjects, the generalization and accuracy of the model on the specific MI task may be poor. Methods: To solve these problems, an adaptive cross-subject transfer learning algorithm is proposed, which is based on kernel mean matching (KMM) and transfer learning adaptive boosting (TrAdaBoost) method. First, the common spatial pattern (CSP) is used to extract the spatial features. Then, in order to make the feature distribution more similar among different subjects, the KMM algorithm is used to compute a sample weight matrix for aligning the mean between source and target domains and reducing distribution differences among different subjects. Finally, the sample weight matrix from KMM is used as the initialization weight of TrAdaBoost, and then TrAdaBoost is used to adaptively select source domain samples that are closer to the target task distribution to assist in building a classification model. Results: In order to verify the effectiveness and feasibility of the proposed method, the algorithm is applied to BCI Competition IV datasets and in-house datasets. The results show that the average classification accuracy of the proposed method on the public datasets is 89.1%, and the average classification accuracy on the in-house datasets is 80.4%. Discussion: Compared with the existing methods, the proposed method effectively improves the classification accuracy of MI-EEG signals. At the same time, this paper also applies the proposed algorithm to the in-house dataset, the results verify the effectiveness of the algorithm again, and the results of this study have certain clinical guiding significance for brain rehabilitation.

Functional damage of endothelial progenitor cells is attenuated by 14-3-3-n through inhibition of mitochondrial injury and oxidative stress.

Endothelial progenitor cells (EPCs) are precursor cells of vascular endothelial cells, which are widely involved in the pathological process of cardiovascular diseases. EPCs apoptosis could accelerate the process of cardiovascular diseases. 14-3-3-η protein has been proved to be a potent antiapoptosis molecule. However, inhibition of EPCs apoptosis by 14-3-3-η and further specific mechanism have not been investigated. EPCs were isolated from human cord blood, and identified using VEGFR2 and CD34. 14-3-3-η overexpression model in vitro was established. Cell invasion, apoptosis, and proliferation were measured by transwell, flow cytometry, and Cell Counting Kit-8, respectively. Expression of 14-3-3-η, Bcl-2, and voltage-dependent anion channel 1 (VDAC1) were measured using quantitative real-time polymerase chain reaction and western blot analysis. Reactive oxygen species (ROS) intensity was measured using 2'-7' dichlorofluorescin diacetate probe. Mitochondrial membrane potential was detected using JC-1 dye. Overexpression of 14-3-3-η significantly promoted invasion and proliferation, but suppressed apoptosis of EPCs. Overexpression of 14-3-3-η remarkably inhibited ROS and promoted antioxidant enzyme levels in EPCs. 14-3-3-η might inhibit apoptosis of EPCs through attenuating mitochondrial injury. This study might provide a new target, 14-3-3-η, for the prevention and treatment of cardiovascular diseases through targeting EPCs.

High-Choline Diet Exacerbates Cardiac Dysfunction, Fibrosis, and Inflammation in a Mouse Model of Heart Failure With Preserved Ejection Fraction.

BACKGROUND: Trimethylamine N-oxide, a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients, has been associated with a poor prognosis for patients with cardiovascular disease. However, the role and underlying mechanisms of trimethylamine N-oxide in the cardiac function of patients with heart failure with preserved ejection fraction (HFpEF) have not been elucidated. METHODS AND RESULTS: C57BL/6 mice were fed a normal diet, high-choline (1.2%) diet, and/or 3-dimethyl-1-butanol diet 3 weeks before the operation (uninephrectomy followed by a continuous saline or aldosterone infusion). Mice were assessed for 4 weeks after the operation. Echocardiographic and hemodynamic measurements were performed. Blood samples were evaluated for choline, trimethylamine N-oxide, and inflammatory factor levels. Left ventricular tissues were collected to assess myocardial fibrosis and inflammation. Left ventricular hypertrophy, pulmonary congestion, and diastolic dysfunction were markedly exacerbated in HFpEF mice fed high-choline diets compared with mice fed the control diet. Myocardial fibrosis and inflammation were markedly increased in HFpEF mice fed high-choline diets compared with animals fed the control diet. Additionally, 3,3-dimethyl-1-butanol DMB markedly ameliorated cardiac diastolic dysfunction, myocardial fibrosis and inflammation in the choline-fed HFpEF mice. CONCLUSIONS: A high-choline diet exacerbates cardiac dysfunction, myocardial fibrosis, and inflammation in HFpEF mice, and 3,3-dimethyl-1-butanol ameliorates the high-choline diet-induced cardiac remodeling.

Knockdown of Long Non-Coding RNA-ZFAS1 Protects Cardiomyocytes Against Acute Myocardial Infarction Via Anti-Apoptosis by Regulating miR-150/CRP.

ZFAS1 is one of cardiac-specific or cardiac-related lncRNAs. This study was to explore the functional involvement of ZFAS1 and its regulatory role in AMI. In this study, the models of AMI rat and myocardial cell cultured under hypoxia were made. The expression of ZFAS1 and miR-150 of myocardial infarction tissue or cardiac myocytes was determined by quantitative real time PCR. The regulatory role of ZFAS1 on miR-150 was examined by RNA pull down assay. The effect of miR-150 or ZFAS1 expression on cell viability was analyzed by MTT assay. The relative expression of ZFAS1 in the myocardium infracted zone and border zone was significantly upregulated at 1-48 h of AMI rats, but it downregulated at 1 week and 2 weeks; miR-150 was significantly downregulated at AMI-1-48 h and upregulated at 1 and 2 weeks after model establishment. The result of RNA pull down assay indicated that ZFAS1 could interact directly with miR-150. C-reactive protein (CRP) was regulated by ZFAS1/miR-150 axis and negatively targeted by miR-150. Hypoxia caused the decrease of cell viability and the upregulation of CRP at mRNA and protein levels; whereas this upregulation could be attenuated by miR-150 mimic or si-ZFAS1 in H9C2 cells and cardiomyocytes. Knockdown of ZFAS1 or miR-150 overexpression effectively relieved AMI-induced myocardial infarction in AMI-1 week rats. The ZFAS1/miR-150 axis was involved in the molecular mechanism of AMI induced cardiomyocytes apoptosis via regulating CRP. J. Cell. Biochem. 118: 3281-3289, 2017. © 2017 Wiley Periodicals, Inc.