Room Temperature Phosphorescence in Crystalline Iodinated Eumelanin Monomer.

We report the room temperature phosphorescence upon iodination on a crystalline eumelanin monomer with shielded hydroxyl moieties, ethyl 5,6-dimethoxyindole-2-carboxylate (DMICE). Ultrafast intersystem crossing (ISC) is observed in the iodinated (IDMICE) as well as brominated (BDMICE) analogues of the eumelanin monomer derivative in solution. The triplet quantum yields (φT) and intersystem crossing rates (kISC) of the halogenated eumelanin derivatives are φ T B D M I C E ${{\phi{} }_{T}^{BDMICE}}$ =25.4±1.1 %; k I S C B D M I C E ${{k}_{ISC}^{BDMICE}}$ =1.95×109 s-1 and φ T I D M I C E ${{\phi{} }_{T}^{IDMICE}}$ =59.1±1.6 %; k I S C I D M I C E = ${{k}_{ISC}^{IDMICE}=}$ 1.36×1010 s-1, as monitored using transient absorption spectroscopy. Theoretical calculations based on nuclear ensemble method reveal that computed kISC and spin-orbit coupling matrix elements for eumelanin derivatives are larger for IDMICE relative to BDMICE. The halogen and π-π interactions, with distinct excitonic coupling and higher ISC rate promote phosphorescence in IDMICE molecular crystals. Accessing triplet excited states and resultant photoluminescence through structural modification of eumelanin scaffolds paves way for exploring the versatility of eumelanin-inspired molecules as bio-functional materials.

Canagliflozin shares common mTOR and MAPK signaling mechanisms with other lifespan extension treatments.

Long-lived mouse models and treatments that extend lifespan, such as Rapamycin, acarbose and 17α- -estradiol, lead to reduction in mTORC1 activity, declines in cap-dependent translation and increases in cap-independent translation. In addition, these treatments reduce the MEK-ERK-MNK (ERK1-2) signaling cascade, leading to reduction in eIF4E phosphorylation, which also regulates mRNA translation. Here, we report that Canagliflozin, a drug that extends lifespan only in male mice reduces mTORC1 and ERK1-2 signaling in male mice only. The data suggest reduction in mTORC1 and ERK pathways are common mechanisms shared by both genetic and pharmacological models of slowed aging in mice. Our data also reveal a significant sexual dimorphism in the ERK1-2 signaling pathway which might help to explain why some drugs can extend lifespan in males but have no effects in female mice.

Modulating singlet fission through interchromophoric rotation.

Singlet fission (SF) is a spin-allowed, exciton-multiplying phenomenon that can be utilized to improve the efficiency of organic solar cells. It is well-understood that SF is sensitive to the local crystal morphology and an appropriately balanced coupling is essential to facilitate efficient SF. In this study, we show how the interchromophoric rotation selectively modulates the interaction between the monomer frontier molecular orbitals, promoting both fast and exothermal SF. We evaluate the effective electronic coupling for SF (VSF), the square of which is proportional to the SF rate, and the effective energies of the Frenkel exciton (FE/S1S0) and triplet pair exciton (TT) in a terrylene dimer model. Optimal interplanar rotation of the chromophoric moieties in slip-stacked arrangements pulls the effective energy of the TT state below that of the FE state. Consequently, SF is favored over competing pathways such as excimer formation, thereby enhancing the overall triplet yield. This work represents a step towards improvising the molecular design guidelines for SF and understanding the importance of interchromophoric rotation over the conventional slip-stacked arrangements for achieving favorable intermolecular electronic coupling towards efficient SF.