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Poly(ethylene terephthalate) (PET) is the most abundant polyester plastic and a major contributor to plastic pollution. IsPETase, from the PET-assimilating bacterium Ideonella sakaiensis, is a unique PET-hydrolytic enzyme that shares high sequence identity to canonical cutinases, but shows substrate preference towards PET and exhibits higher PET-hydrolytic activity at ambient temperature. Structural analyses suggest that IsPETase harbours a substrate-binding residue, W185, with a wobbling conformation and a highly flexible W185-locating β6-β7 loop. Here, we show that these features result from the presence of S214 and I218 in IsPETase, whose equivalents are strictly His and Phe, respectively, in all other homologous enzymes. We found that mutating His/Phe residues to Ser/Ile could enhance the PET-hydrolytic activity of several IsPETase-like enzymes. In conclusion, the Ser/Ile mutations should provide an important strategy to improve the activity of potential PET-hydrolytic enzymes with properties that may be useful for various applications. In the face of global plastic pollution, enzymatic degradation of poly(ethylene terephthalate) (PET) has attracted much attention. Now, structural and biochemical studies reveal a minimal mutational strategy to increase the activity of PET-degrading enzymes, with potential evolutionary implications.

Activation of nucleotide-binding domain leucine-rich repeat containing family pyrin domain containing 3 (NLRP3) inflammasome in Kupffer cells (KCs) contributes significantly to hepatic ischemia/reperfusion (I/R) injury, while the mechanism of how NLRP3 inflammasome is regulated remains less well defined. Recent evidence has showed that mitophagy acts as a central player for maintaining mitochondrial homeostatis through elimination of damaged mitochondria, leading to the prevention of hyperinflammation triggered by NLRP3 activation. In this study, we aimed at investigating the potential role of PTEN-induced kinase 1 (PINK1)-mediated mitophagy in hepatic I/R injury. C57BL/6 mice subjected to partial warm hepatic I/R or primary KCs exposed to anoxia/reoxygenation (A/R) was used as in vivo or in vitro model, respectively. Mitophagy was measured by protein levels of PINK1, Parkin, LC3B-II, TOMM20 and p62. NLRP3, caspase-1 and IL-1β at mRNA and/or protein levels were used as indicators of inflammasome activation. Our results demonstrated remarkable hepatic inflammation and NLRP3 inflammasome activation during hepatic I/R, along with increased PINK1-mediated mitophagy. Notably, overexpression of PINK1 in vivo attenuated hepatic I/R injury, ROS production, NLRP3 activation and hepatic inflammation. In parallel, A/R challenge in vitro also triggered NLRP3 activation in KCs accompanied by increase in mitophagy. Enhanced mitophagy mediated by PINK1 overexpression further inhibited NLRP3 activation and reversed the KC-mediated inflammatory injury to hepatocytes. Kinase-dead mutation of PINK1 completely abolished the above protective effects by PINK1. Blocking of mitophagy/autophagy by silencing of PINK1/Parkin, ATG5, NDP52 or OPTN showed the totally opposite effects, respectively. Treatment with different autophagic inhibitors also consistently reversed the PINK1-mediated effects, suggesting that an intact PINK1-mediated mitophagy signaling was crucial for ablation of NLRP3 signaling in the presence of A/R. Together, these results support a critical role of PINK1-mediated mitophagy in mitochondrial quality control for KC activation and function in hepatic I/R.

The PI3K/AKT/mTOR pathway is one of the most highly activated cellular signaling pathways in advanced ovarian cancer. Although several PI3K/AKT/mTOR inhibitors have been developed to treat various types of cancer, the antitumor efficacy of many of these compounds against ovarian cancer has remained unclear. Here, we tested and compared a panel of 16 PI3K/AKT/mTOR inhibitors (XL765, Miltefosine, Rapamycin, CCI-779, RAD001, FK506, XL147, GSK2110183, IPI-145, GSK2141795, BYL719, GSK458, CAL-101, XL765 analogue SAR245409, Triciribine, and GDC0941) that have entered clinical trials for antitumor activity against ovarian cancer, as well as the front line drug, paclitaxel. Antitumor efficacy was measured in both ovarian cancer cell lines and patient-derived ovarian primary tumor cell lines in vitro and in vivo. We identified the PI3K/mTOR dual inhibitor GSK458 as a potent inhibitor of proliferation in all cell lines tested at half maximal inhibitory concentrations (IC50) of approximately 0.01-1 µM, a range tens to hundreds fold lower than that of the other PI3K/AKT/mTOR inhibitors tested. Additionally, GSK458 showed the highest inhibitory efficacy against ovarian cancer cell migration. GSK458 also inhibited tumor growth and metastasis in nude mice intraperitoneally engrafted with SKOV3 cells or a patient-derived tumor cell xenograft (PDCX). Importantly, the inhibitory efficiency of GSK458 on cell proliferation and migration both in vitro and in vivo was comparable to that of paclitaxel. Mechanistically, the anti-tumor activity of GSK458 was found to be associated with inactivation of AKT and mTOR, and induction of cell cycle arrest at the G0/G1 phase. Based on our results, we conclude that GSK458 may serve as an attractive candidate to treat ovarian cancer.

The Exocrine Differentiation and Proliferation Factor (EXDPF) gene could promote exocrine while inhibit endocrine functions. Although it is well known that ovary is an endocrine organ, the functions of EXDPF in ovarian cancer development is still unknown. This study demonstrated that EXDPF gene is significantly higher expressed in ovarian tumors compared to normal ovarian tissue controls. EXDPF DNA amplification was exhibited in lots of human tumors including 7.19% of ovarian tumors. Also, high expression of EXDPF positively correlated with poor overall survival (OS) of ovarian cancer patients. EXDPF expression could be universally detected in most epithelial ovarian cancer cells (SKOV3, IGROV1, MACS, HO8910PM, ES2, COV362 and A2780) tested in this study. Knock-down of EXDPF by siRNA delivered by plasmid or lentivirus largely inhibited ovarian cancer cells, IGROV1 and SKOV3 proliferation, migration and tumorigenesis in vitro and/or in vivo. Knock-down of EXDPF sensitized SKOV3 cells to the treatment of the front-line drug, paclitaxel. Mechanism study showed that EXDPF enhanced DNA replication pathway to promote ovarian cancer tumorigenesis. In conclusion, this study demonstrated that EXDPF could be a potential therapeutic target as a pro-oncogene of ovarian cancer.

Emerging evidence has classified the aberrant expression of long non‐coding RNAs (lncRNAs) as a basic signature of various malignancies including gastric cancer (GC). LINC01225 has been shown to act as a hepatocellular carcinoma‐related gene, with its expression pattern and biological function not clarified in GC. Here, we verified that LINC01225 was up‐regulated in tumour tissues and plasma of GC. Analysis with clinicopathological information suggested that up‐regulation of LINC01225 was associated with advanced disease and poorer overall survival. Receiver operating characteristic (ROC) analysis showed that plasma LINC01225 had a moderate accuracy for diagnosis of GC. In addition, knockdown of LINC01225 led to retardation of cell proliferation, invasion and migration, and overexpression of LINC01225 showed the opposite effects. Mechanistic investigations showed that LINC01225 silencing inhibited epithelial‐mesenchymal transition (EMT) process and attenuated Wnt/β‐catenin signalling of GC. Furthermore, ectopic expression of Wnt1 or suppression of GSK‐3β abolished the si‐LINC01225‐mediated suppression against EMT, thereby promoting cell proliferation, invasion and migration of GC. In conclusion, LINC01225 promotes the progression of GC through Wnt/β‐catenin signalling pathway, and it may serve as a potential target or strategy for diagnosis or treatment of GC.

Two A−π–D−π–A-type non-fullerene acceptors (IDT-ToFIC and IDT-TiFIC) with 5-hexylthienyl chains substituted at the inner and outer β-positions of the thiophene π-bridge have been designed, respecti...

Side-chain engineering could tune the crystallinity, solubility and aggregation styles of fused-ring electron acceptors (FREAs), and thus could influence the morphology and charge carrier mobility of blend films as well as the final device performances. Herein, we developed a novel FREA called spiro-IDT-O-IC, which is composed of a spiro-bridged IDT core and two 1,1-dicyanomethylene-3-indanone (IC) terminal units. Similar acceptor molecule IDT-O-IC with four 4-octyloxyphenyl side chains is also prepared for the control experiment. The absorptions, energy levels, molecular configurations, and electronic wave functions of these two acceptor molecules have been comparatively studied. Polymer solar cells (PSCs) fabricated with PBDB-T:spiro-IDT-O-IC as the active layer demonstrated a PCE of 6.23% with a Jsc of 11.76 mA/cm2, a Voc of 0.84 V and an FF of 0.63. To the best of our knowledge, this is the first report that a spiro-bridged ladder type core was used for the fabrication of fused ring acceptors.

Two novel fused ring electron acceptors PDT and PDT-T have been designed, synthesized and used in organic solar cells. PDT comprises a central 4,10-bis(hexyloxy)-6,6,12,12-tetrakis(4-hexylphenyl)-6,12-dihydropyreno[1,2-b:6,7-b′]dithiophene (DDT) donor unit and two flanked 2-(5,6-difluoro-3-oxo-2,3-dihydro-1H-inden-1-ylidene)malononitrile acceptor units, while PDT-T has an extra thiophene bridge unit between the central donor unit and the acceptor unit. The introduction of a thiophene bridge unit can markedly broaden the absorption of acceptors and enhance the film absorption coefficient. The optical bandgaps of PDT and PDT-T are 1.59 and 1.44 eV, respectively. The photovoltaic performance of these two acceptors was investigated using PBDB-T as the electron donor. Wide photo-current responses extending to 800 nm for PDT based devices and to 900 nm for PDT-T based ones were observed. A power conversion efficiency (PCE) of 7.07% for PBDB-T:PDT based cells was obtained with a Voc of 0.96 V, Jsc of 13.48 mA cm−2 and FF of 54.0%, while the as-cast devices based on PBDB-T:PDT-T gave rise to a PCE of 11.02% with a Voc of 0.88 V, Jsc of 18.88 mA cm−2 and FF of 66.3%. These results highlight that DDT is a promising building block for constructing highly efficient fused ring acceptors and π-bridging can further boost the photovoltaic performance of the devices.

A fused-ring electron acceptor (FREA) NDIC is designed and synthesized. Inspired by IDIC, NDIC was constructed by replacing the benzene with a naphthalene ring in its core unit. IDIC exhibits an optical bandgap of 1.60 eV and a lower lowest unoccupied molecular orbital (LUMO) energy level of −3.92 eV. In comparison, NDIC displays an optical band gap of 1.72 eV and a higher lying LUMO energy level of −3.88 eV. Due to the higher energy level, inverted devices based on NDIC exhibit a higher open circuit voltage (Voc) of 0.90 V, which is much higher than that of IDIC (0.77 V). After a series of optimizations, a power conversion efficiency (PCE) of 9.43% was obtained with a PBDB-T:NDIC blend active layer, in comparison, a PCE of 9.19% was achieved based on IDIC. Our results demonstrate that a tiny variation in the molecular structure could dramatically affect the optical and electrochemical properties, and thus the photovoltaic performance.

In this work, a ternary blend strategy based on PBDB-T and two small molecular acceptors (IDTT-OB and IDT-PDOT-C6) is demonstrated to simultaneously improve the photocurrent and reduce the voltage ...

We have designed and synthesized two fused-ring small molecular acceptors IDT-PDOT and IDT-EDOT, comprising 3,4-propylenedioxythiophene (PDOT) and 3,4-ethylenedioxythiophene (EDOT) bridging units, respectively. The only structural difference between these two acceptors is one methylene group at the π-bridging unit. However, such a tiny structural difference exerts a great influence on the optical, electrical and photovoltaic properties of the acceptors. The molar absorption coefficient of IDT-EDOT is more than four times higher than that of IDT-PDOT. The electron mobility of the IDT-EDOT based blend film is one order of magnitude higher than that of the IDT-PDOT based one. Consequently, a high power conversion efficiency (PCE) of 11.32% for IDT-EDOT based devices was obtained, whereas a PCE of only 2.18% was achieved for IDT-PDOT based ones. Our results have demonstrated that changing the π-bridging unit in fused ring acceptors is an effective strategy to adjust their photovoltaic performance.

Background: CircRNAs play important roles in cancer development and progression and have the potential to serve as cancer biomarkers. The aim of this study was to investigate the role of circular RNA CCDC66 (circCCDC66) in gastric cancer and to reveal the underlying mechanisms. Methods: The expression of circCCDC66 in GC tissues and cell lines was examined by qRT-PCR. The correlation between circCCDC66 expression level and clinicopathological characteristics was analyzed. The biological roles of circCCDC66 in GC cell apoptosis, proliferation, migration and invasion were determined by flow cytometry, cell counting, cell colony formation, wound healing, transwell migration and matrigel invasion assays. The role of circCCDC66 in GC growth was further confirmed by mouse xenograft tumor model. Western blot and qRT-PCR were used to explore the effects of circCCDC66 on epithelial-mesenchymal transition (EMT)-related gene and protein expression. Results: CircCCDC66 expression was elevated in both GC tissues and cell lines compared to adjacent normal tissues and normal gastric epithelial cell line. The upregulation of circCCDC66 in GC tissues was related to tumor stage and lymphatic metastasis. CircCCDC66 knockdown significantly inhibited GC cell proliferation, migration and invasion and induced cell apoptosis in GC cells. On the contrary, circCCDC66 overexpression had the opposite effects. In addition, circCCDC66 knockdown suppressed the tumorigenesis of GC cells in nude mice. Furthermore, circCCDC66 knockdown inhibited the activation of c-Myc and TGF-β signaling pathways and reversed EMT in GC cells. c-Myc and TGF-β interference blocked circCCDC66-mediated promotion of gastric cancer cell proliferation, migration and invasion. Conclusion: CircCCDC66 promotes GC growth and metastasis by activating c-Myc and TGF-β signaling pathways, suggesting that it may serve as a potential biomarker for GC.

Epithelial ovarian cancer (EOC) is a gynecological malignancy with high morbidity. Treating EOC remains a challenge, as the pathogenesis of this disease remains unclear and chemoresistance is a common occurrence. A number of previous studies have revealed that obesity is closely associated with cancer and leptin, as a link between cancer and obesity, has become a focus of research in recent years. In the present study, survival database analysis demonstrated that leptin expression was associated with poor prognoses in patients treated with platinum and paclitaxel/docetaxel. A cell activity assay demonstrated that leptin reduced the chemosensitivity of ovarian cancer cells to paclitaxel/docetaxel. Furthermore, flow cytometry results revealed that treatment with exogenous leptin reduced the proportion of ovarian cancer cells in G2/M phase, which was significantly elevated following paclitaxel/docetaxel chemotherapy. It was also verified that transcription factor CCAAT/Enhancer Binding Protein α can bind to the upstream promoter region of leptin and activate its transcription in ovarian cancer cells. Together, these results suggest that leptin serves an important role in chemoresistance and may serve as a novel therapeutic target for ovarian cancer in patients treated with platinum and paclitaxel chemotherapy.

Novel inhibitors are urgently needed for use as targeted therapies to improve the overall survival (OS) of patients with ovarian cancer. Here, we show that cell division cycle 25B (CDC25B) is over-expressed in ovarian tumors and associated with poor patient prognosis. All previously reported CDC25B inhibitors have been identified by their ability to reversibly inhibit the catalytic dephosphorylation activity of CDC25B in vitro; however, none of these compounds have entered clinical trials for ovarian cancer therapy. In this study, we synthesized a novel small molecule compound, WG-391D, that potently down-regulates CDC25B expression without affecting its catalytic dephosphorylation activity. The inhibition of CDC25B by WG-391D is irreversible, and WG-391D should therefore exhibit potent antitumor activity against ovarian cancer. WG-391D induces cell cycle progression arrest at the G2/M phase. Half maximal inhibitory concentration (IC50) values of WG-391D for inhibition of the proliferation and migration of eight representative ovarian cancer cell lines (SKOV3, ES2, OVCAR8, OVTOKO, A2780, IGROV1, HO8910PM, and MCAS) and five primary ovarian tumor cell lines (GFY004, GFY005, CZ001, CZ006, and CZ008) were lower than 10 and 1 μM, respectively. WG-391D inhibited tumor growth in nude mice inoculated with SKOV3 cells or a patient-derived xenograft (PDX). The underlying mechanisms were associated with the down-regulation of CDC25B and subsequent inactivation of cell division cycle 2 (CDC2) and the serine/threonine kinase, AKT. In conclusion, this study demonstrates that WG-391D exhibits strong antitumor activity against ovarian cancer and indicates that the down-regulation of CDC25B by inhibitors could provide a rationale for ovarian cancer therapy.

A nonfullerene acceptor, IDTT-OB, employing indacenodithieno[3,2-b]thiophene (IDTT) decorated with asymmetric substituents as the core, is designedly prepared. In comparison with the analogue IDT-OB, extending the five-heterocyclic indacenodithiophene (IDT) core to seven-heterocyclic fused ring endows IDTT-OB with more broad absorption and elevated highest occupied molecular orbital energy level. In addition, IDTT-OB shows a more intense molecular packing and a higher crystalline behavior with a strong face-on orientation in the neat film and the PBDB-T:IDTT-OB blend film. Furthermore, an ideal nanomorphology with a domain size of 19 nm can be obtained, which is in favor of exciton diffusion and charge separation. Accordingly, PBDB-T:IDTT-OB-based polymer solar cells demonstrate a maximum power conversion efficiency (PCEmax) of 11.19% with an impressive fill factor of 0.74, comparable to the state-of-the-art acceptors with similar molecular backbones. More importantly, IDTT-OB-based devices show good tole...

A base-mediated 2-aryl substituted benzothiophene formation from 2-bromobenzene aldehydes, benzylic esters and elemental sulfur under transition-metal-free conditions is described. Various 2-aryl substituted benzothiophene were efficiently obtained under mild conditions.

Hypothesis The role of non-cardiomyocytes in cardiac remodeling and fibrosis has not been totally understood until now. This study investigated if endothelial cell (EC)-specific calpain participates in myocardial endothelial injury via the endothelial- mesenchymal transition (EndMT) and in cardiac fibroblasts during cell proliferation, thereby contributing to cardiac fibrosis eventually. Methods in vitro cultured mouse cardiac ECs were induced with transforming growth factor (TGF)-β1 (10 ng/ml) and calpain inhibitor III (20 μM) or Akt inhibitor (LY294002, 20 μM). Isolated cardiac fibroblasts were induced by TGF-β1 and an HSP90 inhibitor (17AAG, 20 μM), and EndMT were analysed. Capn4-knockout (KO) specific to ECs of mice was generated. We induced the pathological process mimicking cardiac hypertrophy and fibrosis in both Capn4-KO mice and their wild-type littermates. The histological analysis was used to measure cardiomyocyte size and collagen contained in the heart. The immunofluorescence analysis was performed to demonstrate that the ECs went through the EndMT, transforming mesenchymal cells into fibroblasts and myofibroblasts. Results Capn4 deletion specific to ECs abrogated activity of both calpain 1 and calpain 2 in ECs, lowered the volume of cardiac collagen and cardiomyocytes size, and ameliorated myocardial dysfunction in the isoproterenol-treated cardiac fibrosis model. An ex vivo analysis of cardiomyocytes by Evans Blue staining revealed that isoproterenol increased cell death compared with the control, and Capn4-KO alleviated this result. Inhibiting calpain in cultured cardiac microvascular endothelial cells (MCECs) reversed the EndMT process, which was induced by TGF-β1. Overexpression of calpastatin decreased the pathological EndMT process, showing that the cultured MCECs have more mesenchymal markers, such as α-smooth muscle actin (SMA), and fewer endothelial markers, such as VE-cadherin. Activating calpain elevated phosphorylated Akt in mice cultured ECs, and inhibiting calpain decreased phosphorylated Akt. Upregulation of phosphorylated Akt by calpain promoted the EndMT, whereas inhibiting calpain switched on the protective mechanism during the EndMT via the heat shock protein (HSP)90/Akt signaling way in cultured ECs. Conclusions This study demonstrated a vital role of calpain in ECs for inducing myocardiocyte hypertrophy, cell death and the EndMT via the HSP90/Akt signaling pathway, thereby promoting cardiac fibrosis. The results indicate that inhibiting ECs calpain is a novel therapeutic target to retard cardiac fibrosis and has positive effects on heart failure.

Long noncoding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) has been reported to correlate with a variety of cancers, with its expression pattern and potential mechanism not clarified in gastric cancer (GC). In this study, we demonstrated that DGCR5 was downregulated in cancerous tissues and plasma samples from patients with GC, and its downregulation was associated with advanced TNM stage and positive lymphatic metastasis. Plasma DGCR5 had an area under the receiver operating characteristic curve (AUC) of 0.722 for diagnosis of GC. Gain- and loss-of-function of DGCR5 revealed that DGCR5 functioned as a competing endogenous RNA for miR-23b to suppress GC cell proliferation, invasion and migration, and facilitate apoptosis by regulating PTEN and BTG1 in vitro. Furthermore, the overexpression of DGCR5 suppressed tumor growth, and inhibited the expression of miR-23b and proliferation antigen Ki-67, but increased the expression of PTEN and BTG1 in vivo. In conclusion, our results show that DGCR5 is a tumor-suppressive lncRNA that regulates PTEN and BTG1 expression through directly binding to miR-23b. This mechanism may contribute to a better understanding of GC pathogenesis and provide a potential therapeutic strategy for GC.

Background The recurrence, metastasis and poor prognosis are important characteristics of ovarian carcinoma (OC), which are associated with exfoliation of cells from the primary tumor and colonization of the cells in pelvic cavity. On the other hand, the life quality of the patients undergoing surgical resection of OC was influenced by postoperative adhesions. Therefore, preventing postoperative implant tumor and adhesion may be effective methods to improve OC treatment. HyaRegen Gel, a cross-linked hyaluronan gel (CHAG), has been widely used as an anti-adhesive agent following pelvic operation in clinic. However, whether it can affect the implantation and growth of OC cells or not is still not clear. Methods Migration and invasion assays were applied to detect the effect of CHAG on migration and invasion of OC cells. Western blotting was performed to detect the phosphorylation/activation of EGFR and ERK, and the expression of PCNA and MMP7. Pull down assay was used to analyze the effect of CHAG on the activation of small G protein Rac1. Nude mice implantation tumor model was applied to observe the effect of CHAG on implantation tumor of OC cells. Results The results of in vitro experiments showed that CHAG suppressed both basic and EGF-induced migration and invasion of OC cells, blocked the activation of EGF-initiated EGFR activation, inhibited downstream signal transduction of EGFR, and decreased expression of proliferation and migration/invasion related proteins. Meanwhile, results of in vivo experiments showed that CHAG not only inhibited the formation of implantation tumor of OC cells but also delayed the of the growth of the tumors. Conclusions CHAG inhibited migration, invasion and proliferation of OC cells in vitro, and suppressed development of implantation tumor of OC in vivo. This made it as both anti-tumor and anti-adhesion agents. Electronic supplementary material The online version of this article (10.1186/s13048-018-0394-z) contains supplementary material, which is available to authorized users.

Vinyl sulfide formation with good yield and high regio- and stereoselectivities from thiols and acetylenes under transition-metal-free conditions is described. Potassium phosphate was used as an effective additive to enhance the reaction yield and selectivity. Z-Vinyl sulfides were predominately formed in the presence of potassium phosphate, whereas E-vinyl sulfides were formed under solvent- and base-free conditions.

A base-mediated 2-aryl substituted benzothiophene formation from 2-bromobenzene aldehydes, benzylic esters and elemental sulfur under transition-metal-free conditions is described. Various 2-aryl substituted benzothiophene were efficiently obtained under mild conditions.

A simple method is elaborated for the preparation of 2-arylsulfanylphenol derivatives by oxidative coupling of cyclohexanones with thiols.

Vinyl sulfide formation with good yield and high regio- and stereoselectivities from thiols and acetylenes under transition-metal-free conditions is described. Potassium phosphate was used as an effective additive to enhance the reaction yield and selectivity. Z-Vinyl sulfides were predominately formed in the presence of potassium phosphate, whereas E-vinyl sulfides were formed under solvent- and base-free conditions.

Various 2-aryl benzothiazoles are selectively obtained by the present new method using molecular oxygen as oxidant.

2-Aryl benzothiazole formation from aryl ketones and 2-aminobenzenethiols under metal- and I(2)-free conditions was described. Various 2-aryl benzothiazoles were selectively obtained in good yields using molecular oxygen as oxidant. DMSO played an important role in this transformation. Functional groups such as methyl, methoxy, fluoro, chloro, bromo and nitro groups were tolerated under the optimized reaction conditions.

A convenient method for the synthesis of various substituted phenothiazines from cyclohexanones and 2-aminobenzenethiols using molecular oxygen as hydrogen acceptor in the absence of transition-metals is described. For the first time cyclohexanones were used as coupling partners for the construction of phenothiazines.

A novel method for the formation of 2-arylsulfanylphenols from thiols and cyclohexanones is described. Iodine was used as an effective catalyst for this kind of transformation. Cyclohexanones were used as a phenol source via a dehydrogenation and tautomerization reaction.