Inhibitory Effect of Phthalic Acid on Tyrosinase: The Mixed-Type Inhibition and Docking Simulations

Tyrosinase inhibition studies are needed due to the medicinal applications such as hyperpigmentation. For probing effective inhibitors of tyrosinase, a combination of computational prediction and enzymatic assay via kinetics was important. We predicted the 3D structure of tyrosinase, used a docking algorithm to simulate binding between tyrosinase and phthalic acid (PA), and studied the reversible inhibition of tyrosinase by PA. PA inhibited tyrosinase in a mixed-type manner with a Ki = 65.84 ± 1.10 mM. Measurements of intrinsic and ANS-binding fluorescences showed that PA induced changes in the active site structure via indirect binding. Simulation was successful (binding energies for Dock6.3 = −27.22 and AutoDock4.2 = −0.97 kcal/mol), suggesting that PA interacts with LEU73 residue that is predicted commonly by both programs. The present study suggested that the strategy of predicting tyrosinase inhibition based on hydroxyl groups and orientation may prove useful for screening of potential tyrosinase inhibitors

Spatial and Modal Optimal Transport for Fast Cross-Modal MRI Reconstruction

Multi-modal magnetic resonance imaging (MRI) plays a crucial role in comprehensive disease diagnosis in clinical medicine. However, acquiring certain modalities, such as T2-weighted images (T2WIs), is time-consuming and prone to be with motion artifacts. It negatively impacts subsequent multi-modal image analysis. To address this issue, we propose an end-to-end deep learning framework that utilizes T1-weighted images (T1WIs) as auxiliary modalities to expedite T2WIs' acquisitions. While image pre-processing is capable of mitigating misalignment, improper parameter selection leads to adverse pre-processing effects, requiring iterative experimentation and adjustment. To overcome this shortage, we employ Optimal Transport (OT) to synthesize T2WIs by aligning T1WIs and performing cross-modal synthesis, effectively mitigating spatial misalignment effects. Furthermore, we adopt an alternating iteration framework between the reconstruction task and the cross-modal synthesis task to optimize the final results. Then, we prove that the reconstructed T2WIs and the synthetic T2WIs become closer on the T2 image manifold with iterations increasing, and further illustrate that the improved reconstruction result enhances the synthesis process, whereas the enhanced synthesis result improves the reconstruction process. Finally, experimental results from FastMRI and internal datasets confirm the effectiveness of our method, demonstrating significant improvements in image reconstruction quality even at low sampling rates

Identity-Obscured Neural Radiance Fields: Privacy-Preserving 3D Facial Reconstruction

Neural radiance fields (NeRF) typically require a complete set of images taken from multiple camera perspectives to accurately reconstruct geometric details. However, this approach raise significant privacy concerns in the context of facial reconstruction. The critical need for privacy protection often leads invidividuals to be reluctant in sharing their facial images, due to fears of potential misuse or security risks. Addressing these concerns, we propose a method that leverages privacy-preserving images for reconstructing 3D head geometry within the NeRF framework. Our method stands apart from traditional facial reconstruction techniques as it does not depend on RGB information from images containing sensitive facial data. Instead, it effectively generates plausible facial geometry using a series of identity-obscured inputs, thereby protecting facial privacy

Research Progress in Understanding the Relationship Between Heme Oxygenase-1 and Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) is a fatal acute cerebrovascular disease, with a high morbidity and mortality. Following ICH, erythrocytes release heme and several of its metabolites, thereby contributing to brain edema and secondary brain damage. Heme oxygenase is the initial and rate-limiting enzyme of heme catabolism, and the expression of heme oxygenase-1 (HO-1) is rapidly induced following acute brain injury. As HO-1 exerts it effects via various metabolites, its role during ICH remains complex. Therefore, in-depth studies regarding the role of HO-1 in secondary brain damage following ICH may provide a theoretical basis for neuroprotective function after ICH. The present review aims to summarize recent key studies regarding the effects of HO-1 following ICH, as well as its influence on ICH prognosis

3-[4-(Dimethyl­amino)benzyl­ideneamino]benzonitrile

The mol­ecule of the title Schiff base, C16H15N3, is non-planar and displays a trans configuration with respect to the C=N double bond. The two benzene rings make a dihedral angle of 49.24 (3)°

Lipoxin A4 Regulates Lipopolysaccharide-Induced BV2 Microglial Activation and Differentiation via the Notch Signaling Pathway

Inflammatory responses contribute to the pathogenesis of various neurological diseases, and microglia plays an important role in the process. Activated microglia can differentiate into the pro-inflammatory, tissue-damaging M1 phenotype or the anti-inflammatory, tissue-repairing M2 phenotype. Regulating microglia differentiation, hence limiting a harmful response, might help improve the prognosis of inflammation-related nervous system diseases. The present study aimed 1. to observe the anti-inflammatory effect of lipoxin A4 (LXA4) on the inflammatory response associated to lipopolysaccharide (LPS)-induced microglia activation, 2. to clarify that LXA4 modulates the activation and differentiation of microglia induced by LPS stimulation, 3. to determine whether LXA4 regulates the activation and differentiation of microglia through the Notch signaling pathway, 4. to provide a foundation for the use of LXA4 for the treatment of inflammatory related neurological diseases. To construct a model of cellular inflammation, immortalized murine BV2 microglia cells were provided 200 ng/ml LPS. To measure the mRNA and protein levels of inflammatory factors (interleukin [IL]-1β, IL-10, and tumor necrosis factor [TNF]-α) and M1 and M2 microglia markers (inducible nitric oxide synthase [iNOS], cluster of differentiation [CD]32, arginase [Arg]1, and CD206), we performed quantitative reverse transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), immunofluorescence, or flow cytometry. To determine the mRNA and protein levels of Notch signaling components (Notch1, Hes1, and Hes5), we performed qRT-PCR and western blot. LXA4 inhibits the expression of Notch1 and Hes1 associated with M1 type microglial differentiation and decreases the M1 type microglia marker iNOS and related inflammatory factors IL-1β and TNF-α. Moreover, LXA4 upregulates the expression of the M2-associated Hes5, as well as the expression of the M2 microglia marker Arg1 and the associated inflammatory factor IL-10. These effects are blocked by the administration of the γ-secretase inhibitor DAPT, a specific blocker of the Notch signaling pathway. LXA4 inhibits the microglia activation induced by LPS and the differentiation into M1 type with pro-inflammatory effect, while promoting the differentiation to M2 type with anti-inflammatory effect. LXA4 downregulates the inflammatory mediators IL-1β, TNF-α, and iNOS, while upregulating the anti-inflammatory mediator IL-10, which acts through the Notch signaling pathway