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Here, the ZnO/polyacrylamide (ZnO/PAM) macroporous composite monolith was first prepared through the radical polymerization of acrylamide in ZnO‐costabilized CO2‐in‐water Pickering high internal phase emulsions (HIPEs). An efficient and green synthesis method was used to prepare the ZnO/PAM porous precursor materials, and ZnO nanoparticles (NPs) were used as a metal ion source to grow the metal organic frameworks (MOF) phase through secondary recrystallization, thereby synthesizing the target MOF/PAM porous monolith. The effects of the contents of ZnO NPs on the formation of HIPEs and properties of the target MOF/PAM composites for the photocatalytic degradation of cationic dye were studied. As the content of ZnO NPs increased to 3.75 wt%, the composite monolith had high mechanical stress (0.24 MPa) at 80% strain and recovered their shape. The as‐synthesized ZIF‐8/PAM composites were characterized using X‐ray diffraction, scanning electron microscope (SEM), Brunauer Emmett Teller (BET), energy dispersive X‐ray spectrometer (EDS) mapping, and TG methods. SEM images showed that the hybrid materials were interconnected, and the sizes of the open macropore and interconnected pore throats were 30–125 and about 2–20 μm, respectively. In addition, the ZIF‐8/PAM material could be used as a high‐efficiency photocatalyst to remove the cationic dye at a fast rate (88.6%). [ABSTRACT FROM AUTHOR]

Background: A low appropriate therapy rate indicates that a minority of patients will benefit from their implantable cardioverter defibrillator (ICD). Quantitative measurements from 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) may predict ventricular arrhythmia (VA) occurrence after ICD placement.Methods: We performed a prospective observational study and recruited patients who required ICD placement. Pre-procedure image scans were performed. Patients were followed up for VA occurrence. Associations between image results and VA were analyzed.Results: In 51 patients (33 males, 53.9 ± 17.2 years) analyzed, 17 (33.3%) developed VA. Compared with patients without VA, patients with VA had significantly larger values in scar area (17.7 ± 12.4% vs. 7.0 ± 7.9%), phase standard deviation (51.4° ± 14.0° vs. 34.0° ± 15.0°), bandwidth (172.9° ± 39.8° vs. 128.7° ± 49.9°), sum thickening score (STS, 29.5 ± 11.1 vs. 17.8 ± 13.2), and sum motion score (42.9 ± 11.5 vs. 33.0 ± 19.0). Cox regression analysis and receiver operating characteristic curve analysis showed that scar size, dyssynchrony, and STS were associated with VA occurrence (HR, 4.956, 95% CI 1.70-14.46).Conclusion: Larger left ventricular scar burden, increased dyssynchrony, and higher STS quantified by 18F-FDG PET may indicate a higher VA incidence after ICD placement. [ABSTRACT FROM AUTHOR]

The maternally heritable endosymbiont provides many ecosystem functions. Antibiotic elimination of a specific symbiont and establishment of experimental host lines lacking certain symbionts enable the roles of a given symbiont to be explored. The whitefly Bemisia tabaci (Gennadius) in China harbors obligate symbiont Portiera infecting each individual, as well as facultative symbionts, such as Hamiltonella, Rickettsia and Cardinium, with co‐infections occurring relatively frequently. So far no studies have evaluated the selectivity and efficacy of a specific symbiont elimination using antibiotics in whiteflies co‐infected with different symbionts. Furthermore, no success has been achieved in establishing certain symbiont‐free B. tabaci lines. In this study, we treated Hamiltonella‐infected B. tabaci line, Hamiltonella‐Rickettsia‐co‐infected line and Hamiltonella‐Cardinium co‐infected line by feeding B. tabaci adults with cotton plants cultured in water containing rifampicin, ampicillin or a mixture of them, aiming to selectively curing symbiont infections and establishing stable symbiont‐free lines. We found ampicillin selectively eliminated Cardinium without affecting Portiera, Hamiltonella and Rickettsia, although they coexisted in the same host body. Meanwhile, all of the symbionts considered in our study can be removed by rifampicin. The reduction of facultative symbionts occurred at a much quicker pace than obligate symbiont Portiera during rifampicin treatment. Also, we measured the stability of symbiont elimination in whitefly successive generations and established Rickettsia‐infected and Cardinium‐infected lines which are absent in natural populations. Our results provide new protocols for selective elimination of symbionts co‐existing in a host and establishment of different symbiont‐infected host lines. [ABSTRACT FROM AUTHOR]

Background: The enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase and induces the trimethylation of histone H3 lysine 27 (H3K27me3) in the promoter of many key genes; EZH2 acts as a transcriptional repressor and is an epigenetic regulator for several cancers. However, the role of EZH2 in nonneoplastic diseases, such as kidney diseases, is unknown and has been investigated. Materials and method: NRK-52E cells were treated with DZNep, a potent inhibitor of EZH2, with different concentrations and for different times to evaluate the apoptosis level of NRK-52E cells by Western blot and Flow cytometry analysis. The binding of EZH2 to the Deptor promoter was determined by ChIP assay. Results: The inhibition of EZH2 with 3-deazaneplanocin A (DZNep), a specific inhibitor of EZH2, led to the apoptosis of NRK-52E cells and the inhibition of mTORC1 and mTORC2 activity. A ChIP assay demonstrated that EZH2 bound the promoter region of Deptor, an endogenous inhibitor of mTORC1 and mTORC2, and regulated the transcription of Deptor by modulating H3K27me3 in its promoter region. Further experiments were performed to examine the effects of EZH2 inhibition on cisplatin-induced injured cells. Cisplatin induced the activation of mTORC1 and mTORC2 and apoptosis in NRK-52E cells, and DZNep inhibited mTORC1 and mTORC2 activity and aggravated cell apoptosis. Conclusions: These data suggested that EZH2 inhibition increased the transcription of Deptor by modifying H3K27me3 in its promoter region, subsequently inhibited mTORC1 and mTORC2 activities, downregulated the expression of apoptosis suppressor genes, and finally led to apoptosis in renal tubular cells. The inhibition of EZH2 aggravated the cisplatin-induced injury in renal tubular cells by inactivating the mTOR complexes. The present study provides new insight into renal protection and suggests that EZH2 might be a target. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the clinical and echocardiographic effects of prolonged cessation and resumption of left ventricular pacing among patients with chronic cardiac resynchronization therapy (CRT).Methods: This was a retrospective analysis of patients with long-term CRT who had loss of left ventricular pacing because of battery depletion. Clinical assessment and echocardiographic data were analyzed with comparisons between implant, chronic CRT, loss of CRT, and after resumption of CRT.Results: There were 7 CRT responders who underwent 8 successful pulse generator replacements due to loss of CRT 6.3 ± 2.3 months after reaching elective replacement interval. With initial CRT implantation, QRS duration decreased from 171 ± 25 to 145 ± 28 ms (P < 0.001) and left ventricular ejection fraction increased from 27.6 ± 8.1 to 53.9 ± 9.6% (P < 0.001). At pulse generator replacement, worsening heart failure was present 6 of 7 patients with significant deterioration of left ventricular function and the left ventricular ejection fraction decreased to 43.4 ± 8.4%(P = 0.001). After resumption of CRT, clinical status and cardiac function recovered with left ventricular ejection fraction increasing to 53.7 ± 8.7% (P = 0.001).Conclusions: Prolonged loss of CRT is associated with significant deterioration of left ventricular function and functional status that is fully reversible with resumption of left ventricular pacing. [ABSTRACT FROM AUTHOR]