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A critical issue in photodynamic therapy (PDT) is inadequate reactive oxygen species (ROS) generation in tumors, causing inevitable survival of tumor cells that usually results in tumor recurrence and metastasis. Existing photosensitizers frequently suffer from relatively low light‐to‐ROS conversion efficiency with far‐red/near‐infrared (NIR) light excitation due to low‐lying excited states that lead to rapid non‐radiative decays. Here, a neutral Ir(III) complex bearing distyryl boron dipyrromethene (BODIPY‐Ir) is reported to efficiently produce both ROS and hyperthermia upon far‐red light activation for potentiating in vivo tumor suppression through micellization of BODIPY‐Ir to form “Micelle‐Ir”. BODIPY‐Ir absorbs strongly at 550–750 nm with a band maximum at 685 nm, and possesses a long‐lived triplet excited state with sufficient non‐radiative decays. Upon micellization, BODIPY‐Ir forms J‐type aggregates within Micelle‐Ir, which boosts both singlet oxygen generation and the photothermal effect through the high molar extinction coefficient and amplification of light‐to‐ROS/heat conversion, causing severe cell apoptosis. Bifunctional Micelle‐Ir that accumulates in tumors completely destroys orthotopic 4T1 breast tumors via synergistic PDT/photothermal therapy (PTT) damage under light irradiation, and enables remarkable suppression of metastatic nodules in the lungs, together without significant dark cytotoxicity. The present study offers an emerging approach to develop far‐red/NIR photosensitizers toward potent cancer therapy.

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Patients on the protocol of enhanced recovery after surgery used significantly less opioid analgesics, possibly contributing to decreased postoperative ileus and shorter length of hospital stay.

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An efficient and practical method for the one-step synthesis of benzothiazole-2-thiols, benzoxazole-2-thiols and benzimidazoline-2-thiones in water was described.

On the basis of three new building blocks, dithieno[3,2- b:2',3'- d]selenophene ( tt-DTS), diseleno[3,2- b:2',3'- d]thiophene ( tt-DST), and diseleno[3,2- b:2',3'- d]selenophene ( tt-DSS), four thiophene- and selenophene-based heteroacenes (3a-d) with up to seven fused rings were designed and synthesized. Another two selenophene-based heteroacenes (1 and 2) with three and five fused rings were prepared. The molecular structures of 1, 2, 3a, and 3c were confirmed by single-crystal analysis. The results showed that molecular structures, spectroscopy features, and cyclic voltammetry behaviors could be modulated by changing the heteroatoms from sulfur to selenium for 3a-d or changing the numbers of selenophene rings for 1, 2, and 3d.

Voltage-gated sodium channels (VGSCs), especially the tetrodotoxin-sensitive Nav1.3 and Nav1.7, and the tetrodotoxin-resistant Nav1.8 and Nav1.9, have been implicated in acute and chronic neuropathic pain. The aim of this study was to investigate the expression of VGSC Nav1.3, Nav1.7, Nav1.8, and Nav1.9 after nerve injury and their roles in the development of trigeminal neuralgia (TN). We used the infraorbital nerve-chronic constriction injury model of TN in the rat. The time course of changes in the mechanical pain threshold was examined. In addition, real-time PCR and double immunofluorescence staining of VGSC α subunits were used to evaluate messenger RNA and protein expression, respectively, in the trigeminal ganglion. Behavioral tests showed that the mechanical pain threshold decreased significantly 4-42 days after surgery and reached the lowest observed value by day 12. Compared with sham-operated controls, we found that trigeminal ganglion in rats subjected to an infraorbital nerve-chronic constriction injury showed upregulation of Nav1.3 and downregulation of Nav1.7, Nav1.8, and Nav1.9 messenger RNA and protein levels. Our findings suggest that VGSC may participate in the regulation of TN.