Electron donor–acceptor (EDA) complexes provide a means to initiate radical reactions under visible light irradiation using substrates that do not absorb visible light individually. Catalytic approaches to complex formation are vital for advancing this synthetic strategy as it decouples the complexation and photogeneration of radicals from substrate functionalization, a limitation inherent to stoichiometric approaches that restricts structural diversity. This Synopsis highlights recent developments in EDA complex photochemistry in which either the donor or acceptor are employed catalytically.

Exploiting charge-transfer complexes in visible light-promoted single-electron redox reactions is a promising route for opening novel synthetic pathways, and catalytic approaches to complex formation are critical for facilitating this chemistry. This report describes the use of a substituted hydroquinone catalyst to promote radical perfluoroalkylation reactions. Mechanistic studies indicate that the reaction is initiated through formation of a visible light-absorbing halogen bonding complex between the hydroquinone catalyst and the perfluoroalkyl halide radical precursor.

In appearance related society that we live in , the younger adolescent patient caneasily become self conscious if their teeth are different to others. A common from of microdontia which affect the maxillary lateral incisor is known as "peg lateral". Treatment approach has to be case specific and depends on the condition of primary predecessor, number of missing teeth, status of occlusion and patient preference.This clinical report describes the treatment of both sided peg-shaped lateral incisors that were restored with resin composite laminate veneers. The aim of the treatment is to close the diastema and restore the contours of the tooth. These simple procedures may be a cost -effective treatment alternative to restore the esthetics of these teeth and may prove particularly growing patients before more definitive restorations can be considered.

Despite the many recent advances in exploiting stoichiometric charge-transfer complexes in visible light promoted single-electron redox reactions, catalytic approaches to charge-transfer complex formation remain limited. This report describes the radical perfluoroalkylation of electron-rich (hetero)arenes and iodoperfluoroalkylation of alkenes and alkynes promoted by a substituted hydroquinone catalyst. Mechanistic and computational studies indicate that the reaction is initiated by the formation of a visible light absorbing halogen bonding complex between the hydroquinone catalyst and the perfluoroalkyl iodide radical precursor.

Efferocytosis – the phagocytic removal of apoptotic cells – is a central component of tissue homeostasis and contributes to inflammatory and autoimmune conditions including atherosclerosis and multiple sclerosis. MER tyrosine kinase (MERTK) is the predominant or sole efferocytic receptor in multiple tissues, and is the predominant efferocytic receptor on macrophages. MERTK is an opsonin-dependent receptor tyrosine kinase that triggers a poorly understood signaling pathway to mediate apoptotic cell engulfment. Using immunoprecipitation, mass spectrometry, and super-resolution microscopy, we have identified a pre-formed receptor complex on the macrophage plasma membrane comprised of ~100 nm clusters of MERTK, β2 integrins, and multiple signaling molecules including Src-family kinases, PI3-kinases, and the integrin regulatory proteins ILK and FAK. MERTK is unable to mediate efferocytosis in the absence of β2 integrins or their opsonins, while β2 integrins require activation via MERTK signaling to induce the engulfment of apoptotic cells. Using FRET microscopy, we determined that MERTK directly induces the conformational change of β2 integrins from the low to high-affinity form via a PI3-kinase, FAK and ILK-dependent signaling pathway. Activation of this pathway then drives the coalescence of the MERTK/β2 integrin clusters into a larger synapse through which efferocytosis occurs. The identification of the MERTK signaling pathway and the role of β2 integrins in this pathway provides new insights into the function of this critical homeostatic receptor and provides new insights into how MERTK mutations and signaling defects may contribute to inflammatory and autoimmune diseases.