β‐In2S3 is a natural defective III–VI semiconductor attracting considerable interests but lack of efficient method for its 2D form fabrication. Here, for the first time, this paper reports controlled synthesis of ultrathin 2D β‐In2S3 flakes via a facile space‐confined chemical vapor deposition method. The natural defects in β‐In2S3 crystals, clearly revealed by optical spectra and optoelectronic measurement, strongly modulate the (opto)‐electronic of as‐fabricated β‐In2S3 and render it a broad detection range from visible to near‐infrared. Particularly, the as‐fabricated β‐In2S3 photodetector shows a high photoresponsivity of 137 A W−1, a high external quantum efficiency of 3.78 × 104%, and a detectivity of 4.74 × 1010 Jones, accompanied with a fast rise and decay time of 6 and 8 ms, respectively. In addition, an interesting linear response to the testing power intensities range is observed, which can also be understood by the presence of natural defects. The unique defective structure and intrinsic optical properties of β‐In2S3, together with its controllable growth, endow it with great potential for future applications in electronics and optoelectronics.

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A Pd/norbornene-catalyzed direct meta-alkylation of nosyl-protected phenylalanine derivatives with alkyl iodides is reported in moderate to good yields. The use of diisopropyl bicyclo[2.2.1]hept-5-ene-2,3-dicarboxylate is identified as a more suitable transient mediator. A simple pyridine ligand is also essential for this reaction to proceed. No racemization was observed in this meta-methylation reaction.

Quinazolinone scaffolds are common structures found in natural alkaloids and synthetic drugs.In recent years,some quinazolinonederivatives was found to exhibit good luminescence properties. Benefit fromthe excellent biocompatibility,low toxicity and high efficiency,...

The mitochondrial unfolded protein response (UPRmt) is a molecular mechanism that maintains mitochondrial proteostasis under stress and is closely related to various metabolic diseases, such as type 2 diabetes (T2D). Similarly, the unfolded protein response of the endoplasmic reticulum (UPRER) is responsible for maintaining proteomic stability in the endoplasmic reticulum (ER). Since the mitochondria and endoplasmic reticulum are the primary centers of energy metabolism and protein synthesis in cells, respectively, a synergistic mechanism must exist between UPRmt and UPRER to cooperatively resist stresses such as hyperglycemia in T2D. Increasing evidence suggests that the protein kinase RNA (PKR)-like endoplasmic reticulum kinase (PERK) signaling pathway is likely an important node for coordinating UPRmt and UPRER. The PERK pathway is activated in both UPRmt and UPRER, and its downstream molecules perform important functions. In this review, we discuss the mechanisms of UPRmt, UPRER and their crosstalk in T2D.