CHITNet: A Complementary to Harmonious Information Transfer Network for Infrared and Visible Image Fusion

Current infrared and visible image fusion (IVIF) methods go to great lengths to excavate complementary features and design complex fusion strategies, which is extremely challenging. To this end, we rethink the IVIF outside the box, proposing a complementary to harmonious information transfer network (CHITNet). It reasonably transfers complementary information into harmonious one, which integrates both the shared and complementary features from two modalities. Specifically, to skillfully sidestep aggregating complementary information in IVIF, we design a mutual information transfer (MIT) module to mutually represent features from two modalities, roughly transferring complementary information into harmonious one. Then, a harmonious information acquisition supervised by source image (HIASSI) module is devised to further ensure the complementary to harmonious information transfer after MIT. Meanwhile, we also propose a structure information preservation (SIP) module to guarantee that the edge structure information of the source images can be transferred to the fusion results. Moreover, a mutual promotion training paradigm (MPTP) with interaction loss is adopted to facilitate better collaboration among MIT, HIASSI and SIP. In this way, the proposed method is able to generate fused images with higher qualities. Extensive experimental results demonstrate the superiority of our CHITNet over state-of-the-art algorithms in terms of visual quality and quantitative evaluations

Pt Nanoparticles Anchored on NH2-MIL-101 with Efficient Peroxidase-Like Activity for Colorimetric Detection of Dopamine

Dopamine (DA) is an important catecholamine neurotransmitter that plays a highly relevant role in regulating the central nervous system, and abnormal DA content can cause many immune-related diseases. Hence, it is of significance to sensitively and specifically identify DA for clinical medicine. In this work, Pt/NH2-MIL-101 hybrid nanozymes with bimetallic catalytic centers were fabricated by forming coordinate bonds between Pt nanoparticles (Pt NPs) and –NH2 on metal–organic frameworks (MOF). The catalytic activity of Pt/NH2-MIL-101 was increased by 1.5 times via enlarging the exposure of more active sites and improving the activity of the active sites through the strategy of forming bimetallic catalytic centers. In the presence of DA, competing with 3, 3′, 5, 5′-tetramethylbenzidine (TMB) for the generated hydroxyl radicals (•OH), the blue oxidation state TMB (Ox-TMB) is reduced to colorless TMB, showing dramatic color changes. The Pt/NH2-MIL-101-based colorimetric assay enables the sensitive and robust detection of DA molecules with a detection limit of only 0.42 μM and has an observable potential in clinical applications

Bayesian reference prior analysis for polynomial calibration models

Clearance circle bioassay, inverse prediction, Noninformative prior, polynomial regression, 62F15, 62F25, 62J05, 62P10,

KAT2A/E2F1 Promotes Cell Proliferation and Migration via Upregulating the Expression of UBE2C in Pan-Cancer

Various studies have shown that lysine acetyltransferase 2A (KAT2A), E2F transcription factor 1 (E2F1), and ubiquitin conjugating enzyme E2 C (UBE2C) genes regulated the proliferation and migration of tumor cells through regulating the cell cycle. However, there is a lack of in-depth and systematic research on their mechanisms of action. This study analyzed The Cancer Genome Atlas (TCGA) to screen potential candidate genes and the regulation network of KAT2A and E2F1 complex in pan-cancer. Quantitative real-time PCR (qRT-PCR) and Western blotting (WB), cell phenotype detection, immunofluorescence co-localization, chromatin immunoprecipitation assay (ChIP), and RNA-Seq techniques were used to explore the functional of a candidate gene, UBE2C. We found that the expression of these three genes was significantly higher in more than 10 tumor types compared to normal tissue. Moreover, UBE2C was mainly expressed in tumor cells, which highlighted the impacts of UBE2C as a specific therapeutic strategy. Moreover, KAT2A and E2F1 could promote cell proliferation and the migration of cancer cells by enhancing the expression of UBE2C. Mechanically, KAT2A was found to cooperate with E2F1 and be recruited by E2F1 to the UBE2C promoter for elevating the expression of UBE2C by increasing the acetylation level of H3K9