Six daughter complexes based on two-dimensional (2-D) luminescent Cu4I4-Cu3Pz3(Pz = pyrazolate) coordination networks, which exhibit an uncommon Cu4I4L3L' (L = pyridine; L' = acetonitrile, pyridine, pyrazine, 1,4-diazabicyclo[2.2.2]octane, triphenylphosphine, none) local configuration, were prepared through a postsynthetic modification method starting from a parent complex (L' = NH3). This work has successfully implemented the single-site substitution of Cu4I4-based coordination frameworks, which have rarely been reported for isolated Cu4I4-type compounds, by taking advantage of the solvent-assisted ligand substitution strategy recently developed in metal-organic framework (MOF) chemistry. Such a procedure not only resulted in the variation of local geometry in the Cu4I4units but also led to interlayer network displacement and entanglement. Particularly, an interesting topological transformation (from 2-D to 2-D → 3-D interpenetration) occurred when linear bidentate linkers (e.g., pyrazine and 1,4-diazabicyclo[2.2.2]octane) are inserted between the 2-D layers. Moreover, the variation in the L' sites can effectively tune the emission colors, ranging from green to orange (λemmax540-605 nm at room temperature). The photoluminescence origins are tentatively assigned to be a mixture of3MLCT and3XLCT, different from that of the well-studied isolated Cu4I4-type complexes.
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.