This study applies parallel reaction monitoring (PRM) proteomics and CRISPR-Cas9 mutagenesis to identify relationships between cell metabolism, cell death, and disease resistance. In oscul3a (oscullin3a) mutants, OsCUL3a-associated molecular switches are responsible for disrupted cell metabolism that leads to increased total lipid content in rice grain, a late accumulation of H2O2 in leaves, enhanced Xanthomonas oryzae pv. PCO371 molecular weight oryzae disease resistance, and suppressed panicle and first internode growth. In oscul3a mutants, PRM-confirmed upregulated molecular switch proteins include lipoxygenases (CM-LOX1 and CM-LOX2), suggesting a novel connection between ferroptosis and rice lesion mimic formation. Rice immunity-associated proteins OsNPR1 and OsNPR3 were shown to interact with each other and have opposing regulatory effects based on the cell death phenotype of osnpr1/oscul3a and osnpr3/oscul3a double mutants. Together, these results describe a network that regulates plant growth, disease resistance, and grain quality that includes the E3 ligase OsCUL3a, cell metabolism-associated molecular switches, and immunity switches OsNPR1 and OsNPR3.Pt is the best catalyst for the oxygen reduction reactions (ORRs), but it is far too slow. Huang and co-workers showed that dealloying 5 nm Ni7Pt3 nanowires (NW) led to 2 nm pure Pt jagged NW (J-PtNW) with ORRs 50 times faster than Pt/C. They suggested that the undercoordinated surface Pt atoms, mechanical strain, and high electrochemically active surface area (ECSA) are the main contributors. We report here multiscale atomic simulations that further explain this remarkably accelerated ORR activity from an atomistic perspective. We used the ReaxFF reactive force field to convert the 5 nm Ni7Pt3 NW to the jagged 2 nm NW. We applied quantum mechanics to find that 14.4% of the surface sites are barrierless for Oads + H2Oads → 2OHads, the rate-determining step (RDS). The reason is that the concave nature of many surface sites pushes the OH bond of the H2Oads close to the Oads, leading to a dramatically reduced barrier. We used this observation to predict the performance improvement of the J-PtNW relative to Pt (111). Assuming every surface site reacts independently with this predicted rate leads to a 212-fold enhancement at 298.15 K, compared to 50 times experimentally. The atomic structures of the active sites provide insights for designing high-performance electrocatalysts for ORR.The synthesis of water-soluble thioglycosylated A2B2 type porphyrins and their zinc(II) complexes is reported. The water-soluble trans-A2B2 porphyrins were synthesized in two steps, via [2+2] condensation between thioglycosylated dipyrromethanes and aromatic aldehydes in 15-21% yields. The thioglycosylated trans-A2B2 porphyrins showed decent in vitro singlet oxygen generation, which was supported by the intracellular DCFDA study. The in vitro cellular investigations of thioglycosylated A2B2 porphyrins were carried out in lung cancer cells (A549) to test their photodynamic therapeutic (PDT) activity. The PDT study revealed significant cytotoxicities of porphyrins with IC50 values between 23.3 and 44.2 μM in the dark, whereas, after visible light exposure, the photosensitizers exhibited IC50 values around 11.1-23.8 μM. The water-soluble thioglycosylated zinc(II) porphyrins having two meso-N-butylcarbazole groups exhibited an excellent degree of photocytotoxicity (IC50 = 4.6-8.8 μM). The flow cytometry analysis revealed that cellular uptake and ROS (reactive oxygen species) generation efficiency of water-soluble thioglycosylated zinc(II) porphyrins were considerably higher than nonmetalated porphyrins. Confocal microscopy images displayed substantial distribution in the endoplasmic reticulum with partial colocalization in mitochondria and lysosomes of water-soluble thioglycosylated zinc(II) porphyrins in A549 cells.To seek the novel application of organophosphorus compounds, the designed tri(4-formylphenyl) phosphonate (TFP) derivatives were successfully synthesized herein, which were used as C-terminal protecting groups of amino acid or greener triple-equivalent supports in liquid-phase peptide synthesis (LPPS). Through the support-aided precipitation effect of TFP derivatives, the peptide intermediates during peptide synthesis were separated and collected via rapid precipitation and facile filtration without chromatographic purification. Furthermore, the TFP derivative support can be directly recycled for reuse without further regeneration after being sheared from the target peptide.Benzoazetinone was photochemically generated by UV irradiation of isatin isolated in low-temperature Ar matrixes. Upon UV (λ = 278 nm) excitation of isatin, monomers of the compound underwent decarbonylation and the remaining part of the molecule adopted the benzoazetinone structure or the structure of its open-ring isomer α-iminoketene. The same products (benzoazetinone and α-iminoketene) were generated by UV (λ = 278 nm) induced decarboxylation of matrix-isolated monomers of isatoic anhydride. Photoproduced α-iminoketene appeared in the low-temperature matrixes as a mixture of syn and anti isomers. Photoproducts generated upon λ = 278 nm irradiation of matrix-isolated isatin were subsequently exposed to λ = 532 nm light. That irradiation resulted in the shift of the α-iminoketene-benzoazetinone population ratio in favor of the latter closed-ring structure. The next irradiation at 305 nm caused the shift of the α-iminoketene-benzoazetinone population ratio in the opposite direction, that is, in favor of the open-ring isomer. Neither benzoazetinone nor its α-iminoketene open-ring isomer was generated upon UV (λ = 278 nm) irradiation of phthalimide isolated in Ar matrixes. Instead, the UV-excited monomers of this compound underwent such phototransformations as oxo → hydroxy phototautomerism or degradation of the five-membered ring with release of HNCO and CO. The efficiency of these photoconversions was low.Histone deacetylases (HDACs) play an important role in regulating target gene expression. They have been highlighted as a novel category of anticancer targets, and their inhibition can induce apoptosis, differentiation, and growth arrest in cancer cells. In view of the fact that HDAC inhibitors and other antitumor agents, such as BET inhibitors, topoisomerase inhibitors, and RTK pathway inhibitors, exert a synergistic effect on cellular processes in cancer cells, the combined inhibition of two targets is regarded as a rational strategy to improve the effectiveness of these single-target drugs for cancer treatment. In this review, we discuss the theoretical basis for designing HDAC-involved dual-target drugs and provide insight into the structure-activity relationships of these dual-target agents.