Comparison of His-Purkinje Conduction System Pacing with Atrial-Ventricular Node Ablation and Pharmacotherapy in HFpEF Patients with Recurrent Persistent Atrial Fibrillation (HPP-AF study).

BACKGROUND: There is currently no particularly effective strategy for patients with persistent atrial fibrillation accompanying heart failure with preserved ejection fraction (HFpEF), especially with recurrent atrial fibrillation after ablation. In this study, we will evaluate a new treatment strategy for patients with persistent atrial fibrillation who had at least two attempts (≧2 times) of radio-frequency catheter ablation but experienced recurrence, and physiologic conduction was reconstructed after atrioventricular node ablation or drug therapy, to control the patient's ventricular rate to maintain a regular heart rhythm, which is called His-Purkinje conduction system pacing (HPCSP) with atrioventricular node ablation. METHODS AND RESULTS: This investigator-initiated, multicenter prospective randomized controlled trial aimed to recruit 296 randomized HFpEF patients with recurrent atrial fibrillation. All the enrolled patients were randomly assigned to the pacing group or the drug treatment group. The primary endpoint is differences in cardiovascular events and clinical composite endpoints (all-cause mortality) between patients in the HPCSP and drug-treated groups. Secondary endpoints included heart failure hospitalization, exercise capacity assessed by cardiopulmonary exercise tests, quality of life, echocardiogram parameters, 6-minute walk distance, NT-ProBNP, daily patient activity levels, and heart failure management report recorded by the CIED. It is planned to compete recruitment by the end of 2023 and report in 2025. CONCLUSIONS: The study aims to determine whether His-Purkinje conduction system pacing with atrioventricular node ablation can better improve patients' symptoms and quality of life, postpone the progression of heart failure, and reduce the rate of rehospitalization and mortality of patients with heart failure. CLINICAL TRIAL REGISTRATION NUMBER: ChiCTR1900027723, URL: http://www.chictr.org.cn/edit.aspx?pid=46128&htm=4.

Long non-coding RNA PCAT-1 promotes cardiac fibroblast proliferation via upregulating TGF-ß1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA PCAT-1 promotes cardiac fibroblast proliferation via upregulating TGF-ß1, by Q. Chen, C. Feng, Y. Liu, Q.-F. Li, F.-Y. Qiu, M.-H. Wang, Z.-D. Shen, G.-S. Fu, published in Eur Rev Med Pharmacol Sci 2019; 23(23): 10517-10522-DOI: 10.26355/eurrev_201912_19692-PMID: 31841207" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19692.

Silencing of linc00337 inhibits proliferation, cell cycle progression, migration, and invasion of colorectal cancer cells through the MEK/ERK pathway.

OBJECTIVE: To explore the expression and biological functions of linc00337 in colorectal cancer (CRC), as well as its underlying mechanism. PATIENTS AND METHODS: The relative expression of linc00337 in 47 cases of CRC tissues and cells was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The si-linc00337 interference sequences were designed and transiently transfected into CRC cells. The interference efficiency was detected via qRT-PCR. Regulatory effect of linc00337 on proliferation of CRC cells was detected via colony formation assay. Cell cycle distribution and apoptosis rate after interference in linc00337 expression were determined using flow cytometry. Moreover, the effects of linc00337 knockdown on cell migration and invasion were detected using transwell assay. At last, the effect of si-linc00337 on the MEK/ERK signaling pathway was detected using Western blotting. RESULTS: The results of qRT-PCR showed that among the 47 cases of CRC tissues, the expression of linc00337 was up-regulated in 40 cases. Similarly, it was highly expressed in CRC cell lines. The results of colony formation assay manifested that cell proliferation declined after interference in linc00337 expression. The results of flow cytometry and transwell assay showed that interference in linc00337 expression arrested the cell cycle in G1/G0 phase, increased the apoptosis rate, and inhibited the invasion and migration of CRC cells. According to the results of Western blotting, expressions of molecular markers in the MEK/ERK pathway after interference in linc00337 expression were significantly changed. CONCLUSIONS: Linc00337 is up-regulated in CRC tissues and cells. Interference in linc00337 expression can inhibit cell proliferation, migration, and invasion and promote apoptosis through the MEK/ERK pathway.

Long non-coding RNA PCAT-1 promotes cardiac fibroblast proliferation via upregulating TGF-ß1.

OBJECTIVE: Recently, the vital functions of long non-coding RNAs (lncRNAs) in many diseases have been explored. This study aims to identify the function of lncRNA PCAT-1 in the development of atrial fibrillation (AF). PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to detect PCAT-1 expression in right atrial appendage (RAA) tissues of 51 AF patients and 35 patients with sinus rhythm (SR). Besides, cell proliferation assay was conducted in AC16 cells with PCAT-1 knockdown. Molecular mechanism of PCAT-1 in influencing the progression of AF was finally investigated. RESULTS: PCAT-1 expression was higher in RAA tissues of AF patients than those of SR patients. Moreover, knockdown of PCAT-1 inhibited proliferation in AC16 cells. Transforming growth factor-ß1 (TGF-ß1) was a target of PCAT-1 and its expression in AF tissues positively correlated to PCAT-1 expression. CONCLUSIONS: PCAT-1 could promote cell proliferation of AF via promoting TGF-ß1, which may provide a new theory for AF development.

Significant enhancement of energy storage density and polarization in self-assembled PbZrO3 : NiO nano-columnar composite films.

Self-assembled nanostructures are important for determining the physical properties of epitaxial oxide films. We successfully fabricated perfectly ordered NiO nano-columns embedded in an antiferroelectric (AFE) PbZrO3 (PZO) matrix over large areas. In this system, a giant recoverable energy storage density of Wr = 24.6 J cm-3 and polarization of PS = 91 µC cm-2 were achieved in the structure of PZO : NiO nano-composites. These values are 333% and 253% larger than those of a pure PZO film, respectively. Additionally, the properties could be tuned by gradually changing the volume ratio of the constituents. Hence, we demonstrate a new approach for enhancing the energy storage of AFE materials and exercising control over nano-column-embedded nanocomposites.

MicroRNA-100 inhibits bone morphogenetic protein-induced osteoblast differentiation by targeting Smad1.

OBJECTIVE: MicroRNAs (miRNAs) act as key regulators of diverse cellular activities by regulating the expression of protein-coding genes. Osteoblast differentiation, a fundamental step in skeletal development, involves the activation of several signaling pathways, including transforming growth factor ß (TGF-ß), bone morphogenetic protein (BMP), and Wnt signaling pathways. MATERIALS AND METHODS: miRNA expression was measured using TaqManRT-PCR. Western blot was used to detect the protein expression of Smad1. Luciferase reporter assay was used to measure the luciferase activity. RESULTS: In this study, we found that miR-100 was expressed in mesenchymal progenitor cell lines; furthermore, its expression was reduced during osteoblast differentiation. Retroviral overexpression of miR-100 decreased Smad1 protein levels, whereas miR-100 inhibition had the opposite effect, suggesting that miR-100 acts as an endogenous attenuator of Smad1 in osteoblast differentiation. CONCLUSIONS: Together, our data demonstrate that miR-100 acts as an important endogenous negative regulator of BMP-induced osteoblast differentiation.

Propagation characteristics of a focused laser beam in a strontium barium niobate photorefractive crystal under reverse external electric field.

The propagation characteristics of a focused laser beam in a SBN:75 photorefractive crystal strongly depend on the signal-to-background intensity ratio (R=Is/Ib) under reverse external electric field. In the range 20>R>0.05, the laser beam shows enhanced self-defocusing behavior with increasing external electric field, while it shows self-focusing in the range 0.03>R>0.01. Spatial solitons are observed under a suitable reverse external electric field for R=0.025. A theoretical model is proposed to explain the experimental observations, which suggest a new type of soliton formation due to "enhancement" not "screening" of the external electrical field.

[High glucose promotes gap junctional communication in cultured neonatal cardiac fibroblasts via AMPK activation].

Cardiac fibroblasts are known to be essential for adaptiveresponses in the patho- genesis of cardiovascular diseases, and increased intercellular communication of myocardial cells and cardiac fibroblasts acts as a crucial factor in maintaining the functional integrity of the heart. AMP-activated kinase (AMPK) is a key stress signaling kinase, which plays an important role in promoting cell survival and improving cell function. However, the underlying link between AMPK and gap junctional communication (GJIC) is still poorly understood. In this study, a connection between AMPK and GJIC in high glucose-mediated neonatal cardiac fibroblasts was assessed using fibroblast migration, measurement of dye transfer and connexin43 (Cx43) expression. 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and Compound C (CC) were used to regulate AMPK activity. The levels of cell migration and Cx43 protein expression in neonatal cardiac fibroblasts increased during high glucose treatment, accompanied by developed dye transfer. In addition, high glucose induced abundant phosphorylation of AMPK. Suppression of AMPK phosphorylation using CC reduced dye transfer, cell migration and Cx43 protein expression in neonatal cardiac fibroblasts, whereas the activation of AMPK using AICAR mimicked the high glucose-mediated cell migration, Cx43 protein expression and dye transfer enhancement. AMPK appears to participate in regulating GJIC in high-glucose-treated neonatal cardiac fibroblasts, including cell migration, dye transfer, Cx43 expression and distribution.

[Pullback atherectomy. An alternative procedure in the treatment of coronary stenosis and in-stent restenosis]. / Pullback-Atherektomie: Ein alternatives Verfahren zur Behandlung von Koronarstenosen und in-Stent-Restenosen.

Optimized directional coronary atherectomy (DCA) has shown significantly superior acute and long-term results compared to conventional balloon angioplasty (BA). Nevertheless DCA has remained a niche application due to specific procedural aspects. The pullback atherectomy catheter (PAC), developed to retrieve atheromatous plaque material, is an alternative debulking device. We report on clinical and angiographic experience in 55 consecutive patients, in whom de novo lesions (35 pts) as well as instent restenoses (17 pts) were treated. The minimal luminal diameter (MLD, mm) rose after PAC and additional BA from 1.06 +/- 0.53 to 2.68 +/- 0.48 and from 1.10 +/- 0.48 to 2.55 +/- 0.49 mm, respectively. A stenosis reduction from 69 +/- 13 to 19 +/- 16 and from 64 +/- 15 to 16 +/- 10%, resp., could be documented. After 3-6 months a complete angiographic follow-up showed MLD values of 2.01 +/- 0.69 and 1.88 +/- 0.61 mm. Nine of 35 (26%) vs. 5 of 17 (29%) pts developed significant restenosis at the treated site (diameter stenoses > 50%). Stent implantation was necessary to achieve an optimal acute angiographic result or due to dissection in 17 vs. 5 pts. Major cardiac events did not occur; however, two restenosed coilstents were removed by PAC. With the pullback atherectomy catheter, a safe and effective alternative device is available for the treatment of coronary lesions and also of in-stent restenosis. Promising short and acceptable long-term results are comparable to those of other debulking procedures.

Repolarization dispersion and sudden cardiac death in patients with impaired left ventricular function.

AIMS: Prolongation of repolarization dispersion measured from the 12-lead surface ECG has been associated with sudden cardiac death and ventricular tachyarrhythmia in a variety of heart disorders. This study tested the hypothesis that increased repolarization dispersion is of prognostic value in identifying chronic heart failure patients at high risk of sudden cardiac death and ventricular tachyarrhythmia. RESULTS: In 163 patients, ischaemic (n = 126) and idiopathic dilated (n = 37) cardiomyopathy with a left ventricular ejection fraction < or = 40% were diagnosed by left ventricular angiography. During follow-up (26 +/- 15 months) 24 patients died suddenly, 10 experienced ventricular tachyarrhythmia, 19 died from pump failure, six died from acute myocardial infarction, and 97 survived. Bazett's formula rate-corrected JT-interval dispersion (JTc-d) was found to be 109 +/- 23 ms in sudden cardiac death/ventricular tachyarrhythmia patients, 57 +/- 20 ms in survivors, and 55 +/- 20 ms in patients who died from pump failure or acute myocardial infarction. Both univariate and multivariate analyses showed JTc-d to be the most important independent predictor of sudden cardiac death/ventricular tachyarrhythmia. A cut-off value of 85 ms for JTc-d had a 74% positive and a 98% negative predictive accuracy in identifying patients at risk for sudden cardiac death/ventricular tachyarrhythmia. CONCLUSION: Analysis of repolarization dispersion from the 12-lead surface ECG seems to be a useful screening method for identifying chronic heart failure patients at high risk for sudden cardiac death/ventricular tachyarrhythmia.