It is found that Prussian Blue nanoparticles (PBNPs) possess a catalase‐like activity to catalyse the breakdown of H2O2 into oxygen (O2) molecules under the neutral conditions (pH = 7.4). Based on this finding, we have developed a new strategy in which PBNPs can be excellent ultrasound (US) and magnetic‐resonance (MR) dual modality imaging contrast agents for H2O2 diagnostics in vitro and in vivo.

In inverted perovskite solar cells (PSCs), the fullerene derivative [6,6]-phenyl-C61-butyric acid methyl ester (PCBM) is a widely used electron transport material. However, a high degree of energy disorder and inadequate passivation of PCBM limit the efficiency of devices, and severe self-aggregation and unstable morphology limit the lifespan of devices. Here, we design a series of fullerene dyads FP-Cn (n = 4, 8, 12) to replace PCBM as an electron transport layer, where [60]­fullerene is linked with a terpyridine chelating group via a flexible alkyl chain of different lengths as a spacer. Among three fullerene dyads, FP-C8 shows the most enhanced molecule ordering and adhesion with the perovskite surface due to the balanced decoupling between the chelation effect from terpyridine and the self-assembly of fullerene, leading to lower energy disorder and higher morphological stability relative to PCBM. The FP-C8/C60-based devices using Cs0.05FA0.90MA0.05PbI2.85Br0.15 as a light absorber show a power conversion efficiency of 21.69%, higher than that of PCBM/C60 (20.09%), benefiting from improved electron extraction and transport as well as reduced charge recombination loss. When employing FAPbI3 as a light absorber, the FP-C8/C60-based devices exhibit an efficiency of 23.08%, which is the champion value of inverted PSCs with solution-processed fullerene derivatives. Moreover, the FP-C8/C60-based devices show better moisture and thermal stability than PCBM/C60-based devices and maintain 96% of their original efficiency after 1200 h of operation, while their counterpart PCBM/C60 maintains 60% after 670 h.

Activation of NF-E2-related factor 2 (Nrf2) signaling could protect cells from ultra violet (UV) radiation. We aim to provoke Nrf2 activation via downregulating its inhibitor Keap1 by microRNA-141 (“miR-141”). In both human retinal pigment epithelium cells (RPEs) and retinal ganglion cells (RGCs), forced-expression of miR-141 downregulated Keap1, causing Nrf2 stabilization, accumulation and nuclear translocation, which led to transcription of multiple antioxidant-responsive element (ARE) genes (HO1, NOQ1 and GCLC). Further, UV-induced reactive oxygen species (ROS) production and cell death were significantly attenuated in miR-141-expressing RPEs and RGCs. On the other hand, depletion of miR-141 via expressing its inhibitor antagomiR-141 led to Keap1 upregulation and Nrf2 degradation, which aggravated UV-induced death of RPEs and RGCs. Significantly, Nrf2 shRNA knockdown almost abolished miR-141-mediated cytoprotection against UV in RPEs. These results demonstrate that miR-141 targets Keap1 to activate Nrf2 signaling, which protects RPEs and RGCs from UV radiation.

Transcription regulation by histone modifications is a major contributing factor to the structural and functional diversity in biology. These modifications are encrypted as histone codes or histone languages and function to establish and maintain heritable epigenetic codes that define the identity and the fate of the cell. Despite recent advances revealing numerous histone modifications associated with transcription regulation, how such modifications dictate the process of transcription is not fully understood. Here we describe spatial and temporal analyses of the histone modifications that are introduced during estrogen receptor ␣ (ER␣)-activated transcription. We demonstrated that aborting RNA polymerase II caused a disruption of the histone modifications that are associated with transcription elongation but had a minimal effect on modifications deposited during transcription initiation. We also found that the histone H3S10 phosphorylation mark is catalyzed by mitogen-and stress-activated protein kinase 1 (MSK1) and is recognized by a 14-3-3/14-3-3⑀ heterodimer through its interaction with H3K4 trimethyltransferase SMYD3 and the p52 subunit of TFIIH. We showed that H3S10 phosphorylation is a prerequisite for H3K4 trimethylation. In addition, we demonstrated that SET8/PRSet7/KMT5A is required for ER␣-regulated transcription and its catalyzed H4K20 monomethylation is implicated in both transcription initiation and elongation. Our experiments provide a relatively comprehensive analysis of histone modifications associated with ER␣-regulated transcription and define the biological meaning of several key components of the histone code that governs ER␣-regulated transcription.Histones are basic proteins that organize genomic DNA into a hierarchical chromatin structure (1). Histones undergo a plethora of post-translational modifications, including phosphorylation, acetylation, methylation, ubiquitination, sumoylation, and ADP-ribosylation, which occur in their flexible N-and C-terminal tails or within their globular folds in the nucleosome core (2). Acting individually or in combination, these modifications, in conjunction with DNA methylation, are believed to encipher inheritable epigenetic programs that encode distinct nucleosome functions such as gene transcription, X-chromosome inactivation, heterochromatin formation, mitosis, and DNA repair and replication (2-4). Mechanistically, these functions are mediated either directly by altering nucleosome interactions within chromatin or indirectly by recruiting effector proteins that possess characteristic modules that recognize specific histone modifications in a sequence-dependent manner (5, 6). The underlying basis of these epigenetic codes resides in the substrate specificity of the enzymes that catalyze the numerous covalent modifications, as well as the enzymes that remove these marks to alter the modifications.Given that chromatin is the physiological template for all DNA-mediated processes, it is not surprising that histone modifications represent an essential co...

Purpose 68 Ga-prostate-specific membrane antigen (PSMA) positron emission tomography/computed tomography (PET/CT) is valuable for detecting primary and recurrent prostatic lesions. This study aimed to evaluate the efficacy of 68 Ga-PSMA-11 PET/CT as a triage tool for prostate biopsy (PSMA-TB) and compare with transrectal ultrasound-guided biopsy (TRUS-GB) for the diagnosis of clinically significant prostate cancer (csPCa). Methods This single-centre study randomly allocated 120 patients with elevated serum prostate-specific antigen (PSA) levels (> 4 ng/ml) to PSMA-PET or TRUS group. Patients with PSMA-avid lesions (SUVmax ≥ 8.0) underwent PSMA-TB via a single-puncture percutaneous transgluteal approach ( n = 25), whilst patients with negative PSMA-PET underwent systematic TRUS-GB ( n = 35). All patients in the TRUS group underwent TRUS-GB directly ( n = 60). Results PCa and csPCa were detected in 26/60 (43.3%) and 24/60 (40.0%) patients in the PSMA-PET group and 19/60 (31.6%) and 15/60 (25.0%) in the TRUS group, respectively. In the PSMA-PET group, the detection rate of PCa and csPCa were significantly higher in PSMA-PET-positive than negative patients (PCa, 23/25 (92.0%) vs 3/35 (8.6%), P < 0.01; csPCa, 22/25 (88.0%) vs 2/35 (5.7%), P < 0.01). PSMA-TB detected significantly more PCa and csPCa than TRUS-GB in the TRUS controls (PCa, 21/25 (84.0%) vs 19/60 (31.6%), P < 0.01 ; csPCa, 20/25 (80.0%) vs 15/60 (25.0%), P < 0.01). PSMA-PET detected significantly more cases of csPCa amongst patients with PSA 4.0–20.0 ng/ml than TRUS (27.02% vs 8.82%, P < 0.05). No haematuria, urinary retention or pelvic infection was observed after PSMA-TB compare with TRUS-GB. Conclusions 68 Ga-PSMA-11 PET/CT is a feasible imaging technique that may serve as a triage tool for prostate biopsy, and may improve the detection rate of csPCa compared with TRUS-GB, especially in patients with serum PSA 4.0–20.0 ng/ml.