circSSPO boosts growth of esophageal squamous cell carcinoma through upregulation of micrRNA-6820-5p-mediated KLK8 and PKD1 expression.

Investigation on a competitive endogenous RNA (ceRNA) network attracted lots of attention due its function in cancer regulation. Here, we probed into the possible molecular mechanism of circSSPO/microRNA-6820-5p (miR-6820-5p)/kallikrein-related peptidase 8 (KLK8)/PKD1 network in the esophageal squamous cell carcinoma (ESCC). Following whole-transcriptome sequencing and differential analysis in collected ESCC tissue samples, circRNA-miRNA-mRNA regulatory network affecting ESCC was investigated. After interaction measurement among circSSPO/miR-6820-5p/KLK8/PKD1, their regulatory roles in ESCC cell functions in vitro and xenograft tumor growth and lung metastasis in vivo were analyzed. The bioinformatics prediction and sequencing results screened that circSSPO, miR-6820-5p, KLK8, and PKD1 were associated with ESCC development. In ESCC, miR-6820-5p was expressed at very low levels, while circSSPO, KLK8, and PKD1 were highly expressed. In vitro cell experiments further proved that circSSPO competitively inhibited miR-6820-5p to induce ESCC cell malignant properties. Moreover, knockdown of KLK8 or PKD1 inhibited ESCC cell malignant properties. circSSPO also promoted the tumorigenic and metastasis of ESCC through the upregulation of KLK8 and PKD1 expression in vivo. We found that circSSPO was an oncogenic circRNA that was significantly abundant in ESCC tissues and circSSPO exhibited an oncogenic activity in ESCC by elevating expression of KLK8 and PKD1 through suppressing miR-6820-5p expression.

MIAT shuttled by tumor-secreted exosomes promotes paclitaxel resistance in esophageal cancer cells by activating the TAF1/SREBF1 axis.

Chemoresistance remains a major obstacle to the treatment of esophageal cancer (EC). Exosome-mediated transfer of long noncoding RNAs (lncRNAs) has recently been unveiled to correlate with the regulation of drug resistance in EC. This study aimed to investigate the physiological mechanisms by which exosome-encapsulated lncRNA myocardial infarction-associated transcript (MIAT) derived from tumor cells might mediate the paclitaxel (PTX) resistance of EC cells. First, MIAT was experimentally determined to be upregulated in PTX nonresponders and PTX-resistant EC cells. Silencing of MIAT in PTX-resistant EC cells decreased cell viability and enhanced apoptosis, corresponding to a reduced half-maximal inhibitory concentration (IC50 ) value. Next, exosomes were isolated from EC109 and EC109/T cells, and EC109 cells were cocultured with EC109/T-cell-derived exosomes. Accordingly, MIAT was revealed to be transmitted through exosomes from EC109/T cells to EC109 cells. Tumor-derived exosomes carrying MIAT increased the IC50 value of PTX and suppressed apoptosis in EC109 cells to promote PTX resistance. Furthermore, MIAT promoted the enrichment of TATA-box binding protein-associated Factor 1 (TAF1) in the promoter region of sterol regulatory element binding transcription factor 1 (SREBF1), as shown by a chromatin immunoprecipitation assay. This might be the mechanism by which MIAT could promote PTX resistance. Finally, in vivo experiments further confirmed that the knockdown of MIAT attenuated the resistance of EC cells to PTX. Collectively, these results indicate that tumor-derived exosome-loaded MIAT activates the TAF1/SREBF1 axis to induce PTX resistance in EC cells, providing a potential therapeutic target for overcoming PTX resistance in EC.

Thyrotoxic Periodic Paralysis: An Under-Recognized Cause of Paralysis in Young Hispanic Men.

BACKGROUND: Patients presenting to the emergency department with paralysis can have a wide differential diagnosis. Thyrotoxic periodic paralysis (TPP) is a rare disorder causing transient flaccid paralysis in the setting of thyrotoxicosis and hypokalemia. It has been reported in Asian male populations predominantly, and the diagnosis is rarely considered in non-Asian populations. Recent research has identified cases in patients with diverse ethnic backgrounds, although epidemiologic data from the United States are very limited. OBJECTIVE: Our aim was to report our experience with TPP at a tertiary care center in the United States. METHODS: A retrospective chart review was conducted between January 2006 and February 2022 to identify cases of TPP and determine their demographic and clinical characteristics. Prevalence of TPP was estimated using the institutional hyperthyroidism registry. RESULTS: Thirty-three patients with TPP were identified. All of the patients were male; median age was 28 years, and 85% were Hispanic. All patients had hypokalemia at presentation and 23% had rebound hyperkalemia after treatment. Prevalence of TPP in our population of patients with hyperthyroidism was approximately 0.5%. CONCLUSIONS: Young Hispanic men presenting with paralysis should be evaluated for TPP, as the prevalence in this population may be higher than estimated previously. Management of TPP involves treatment of underlying hyperthyroidism and cautious potassium repletion, with an initial dose of no more than 60 mEq/L of potassium chloride to avoid rebound hyperkalemia.

Micro-Three-Coil Sensor with Dual Excitation Signals Use Asymmetric Magnetic Fields to Distinguish between Non-Ferrous Metals.

Intelligent operation and maintenance technology for vessels can ensure the safety of the entire system, especially for the development of intelligent and unmanned marine technology. The material properties of metal abrasive particles in oil could demonstrate the wear areas of the marine mechanical system because different components consist of different materials. However, most sensors can only roughly separate metallic contaminants into ferromagnetic and non-ferromagnetic particles but cannot differentiate them in greater detail. A micro-three-coil sensor is designed in this paper; the device applies different excitation signals to two excitation coils to differentiate materials, based on the different effects of different material particles in the asymmetric magnetic field. Therefore, a particle's material can be judged by the shape of the induction electromotive force output signal from the induction coil, while the particle size can be judged by the amplitude of the signal. Experimental results show that the material differentiation of four different types of particles can be achieved, namely, of aluminum, iron, 304 stainless steel, and carbon steel. This newly designed sensor provides a new research prospect for the realization of an inductive detection method to distinguish non-ferrous metals and a reference for the subsequent detection of metal contaminants in oil and other liquids.

Investigation of the Effect of Debris Position on the Detection Stability of a Magnetic Plug Sensor Based on Alternating Current Bridge.

Magnetic plug-type abrasive particle sensors have a wide range of applications in oil detection, but there is little literature on the effect of abrasive particle position on detection accuracy. In this paper, an alternating current (AC) bridge-type abrasive particle detection sensor is designed, in which the sensing module utilizes permanent magnets to attract iron particles, and the induction coil is specially designed to detect the magnetic field fluctuation caused by iron particles. A corresponding model was also designed to evaluate the sensor's sensitivity at different locations. In this paper, the magnetic field distribution of the sensor was first analyzed using finite element analysis software to obtain the magnetic field strength at different positions. Then, the response sensitivity of the sensor to particles and the effect of different positions on the detection results are explored through experiments. The simulation and the experimental results show substantial signal difference signal at different sensor positions. The method outlined in this article can determine the optimal sensing range for subsequent magnetic plug-type abrasive particle detection sensors and subsequently improve their reliability.

Involvement of the TNF-α/SATB2 axis in the induced apoptosis and inhibited autophagy of osteoblasts by the antipsychotic Risperidone.

BACKGROUND: Risperidone, an atypical antipsychotic, impedes serotonin and dopamine receptor systems. Meanwhile, tumor necrosis factor-α (TNF-α) is known to participate in regulating osteoblast functions. Consequently, the current study aimed to investigate whether the influences of Risperidone on osteoblast functions are associated with TNF-α and special AT-rich sequence-binding protein (SATB2). METHODS: Firstly, we searched the DGIdb, MEM and GeneCards databases to identify the critical factors involved in the effects of Risperidone on osteoblasts, as well as their interactions. Afterwards, osteoblast cell line MC3T3-E1 was transduced with lentivirus carrying si-TNF-α, si-SATB2 or both and subsequently treated with Risperidone. Various abilities including differentiation, autophagy and apoptosis of osteoblasts were examined after different treatments. Finally, animal experiments were performed with Risperidone alone or together with lentivirus to verify the function of Risperidone in vivo and the mechanism. RESULTS: It was found that Risperidone might promote TNF-α expression, thereby inhibiting the expression of SATB2 to affect the autophagy and apoptosis in osteoblasts. Furthermore, as shown by our experimental findings, Risperidone treatment inhibited the differentiation and autophagy, and promoted the apoptosis of osteoblasts, as evidenced by elevated levels of OPG, p62, cleaved PARP1, cleaved caspase-3, cleaved caspase-8, and cleaved caspase-9, and reduced levels of LC3 II/I, Beclin1, collagen I, and RANKL. In addition, Risperidone was also found to elevate the expression of TNF-α to down-regulate SATB2, thereby inhibiting the differentiation and autophagy and enhancing the apoptosis of osteoblasts in vitro and in vivo. CONCLUSIONS: Collectively, our findings indicated that Risperidone affects the differentiation of osteoblasts by inhibiting autophagy and enhancing apoptosis via TNF-α-mediated down-regulation of SATB2.

Tumor-derived extracellular vesicles confer 5-fluorouracil resistance in esophageal cancer via long noncoding RNA AC116025.2 delivery.

5-Fluorouracil (5-FU) resistance is one of the main causes for treatment failure in esophageal cancer (EC). Here, we intended to elucidate the mechanism of tumor-derived extracellular vesicles (TEVs)-encapsulated long noncoding RNAs (lncRNAs) AC116025.2 in 5-FU resistance in EC. EVs were isolated from the serum samples of EC patients and HEEC, TE-1, and TE-1/5-FU cells, followed by RT-qPCR detection of AC116025.2 expression in EVs. The relationship among AC116025.2, microRNA (miR)-4496, and SEMA5A was evaluated. Next, EC cells were cocultured with EVs, followed by lentivirus transduction and plasmid transfection for studying the role of TEVs-AC116025.2 in EC cells in relation to miR-4496 and SEMA5A. Tumor formation in nude mice was applied for in vivo confirmation. Elevated AC116025.2 expression was seen in the EVs from the serum of 5-FU insensitive patients and from 5-FU-resistant EC cells. Mechanistically, AC116025.2 bound to miR-4496 that inversely targeted SEMA5A in EC cells. EVs-oe-AC116025.2 augmented EC cell viability, colony formation, and 5-FU resistance, but diminished their apoptosis through miR-4496-mediated SEMA5A. Furthermore, EVs-oe-AC116025.2 augmented tumor formation and 5-FU resistance of EC cells in vivo. Conclusively, our data offered evidence of the promoting mechanism of TEVs in the 5-FU resistance of EC by delivering AC116025.2.

Chiral Hemilabile P,N-Ligand-Assisted Gold Redox Catalysis for Enantioselective Alkene Aminoarylation.

Enantioselective, intermolecular alkene arylamination was achieved through gold redox catalysis. Screening of ligands revealed chiral P,N ligands as the optimal choice, giving alkene aminoarylation with good yields (up to 80 %) and excellent stereoselectivity (up to 99 : 1 er). As the first example of enantioselective gold redox catalysis, this work confirmed the feasibility of applying a chiral ligand at the gold(I) stage, with the stereodetermining step (SDS) at the gold(III) intermediate, thus opening up a new way to conduct gold redox catalysis with stereochemistry control.

LINC00152 upregulates ZEB1 expression and enhances epithelial-mesenchymal transition and oxaliplatin resistance in esophageal cancer by interacting with EZH2.

BACKGROUND: Expression of the long non-coding mRNA LINC00152 has been reported to correlate with cancer cell resistance to oxaliplatin (L-OHP). However, little is known regarding the molecular mechanism of LINC00152 in esophageal cancer (EC). Hence, we intended to characterize the role of LINC00152 in EC, with a special focus on epithelial-mesenchymal transition (EMT) and L-OHP resistance. METHODS: We collected EC tissues and identified EC cell lines with higher L-OHP resistance, and then characterized expression patterns of LINC00152, Zeste Homologue 2 (EZH2), Zinc finger e-box binding homeobox (ZEB1) and EMT-related genes using RT-qPCR and Western blot analysis. Furthermore, their functional significance was identified by gain and loss-of-function experiments. The relationship among LINC00152, EZH2 and ZEB1 was examined using RIP, RNA pull-down and ChIP assays. Additionally, resistance of EC cells to L-OHP was reflected by CCK-8 assay to detect cell viability. Animal experiments were also conducted to detect the effects of the LINC00152/EZH2/ZEB1 on EMT and L-OHP resistance. RESULTS: LINC00152, EZH2 and ZEB1 were highly expressed in EC tissues and Kyse-150/TE-1 cells. As revealed by assays in vitro and in vivo, LINC00152 positively regulated ZEB1 expression through interaction with EZH2 to enhance EMT and L-OHP resistance in EC cells. In contrast, silencing of LINC00152 contributed to attenuated EMT and drug resistance of EC cells to L-OHP. CONCLUSIONS: Our study demonstrates that LINC00152/EZH2/ZEB1 axis can regulate EMT and resistance of EC cells to L-OHP, thus presenting a potential therapeutic target for EC treatment.

Long noncoding RNA LINC00261 induces chemosensitization to 5-fluorouracil by mediating methylation-dependent repression of DPYD in human esophageal cancer.

Approximately 85% of a single administered dose of 5-fluorouracil (5-FU) will be degraded by dihydropyrimidine dehydrogenase (DYPD). Studies have highlighted a link between the complete or partial loss of DYPD function and clinical responses to 5-FU; however, the underlying molecular basis of DPD deficiency remains poorly understood. Hence, the aim of the present study was to evaluate the prevailing hypothesis which suggests that overexpression of LINC00261 possesses the ability to modulate the methylation-dependent repression of DPYD, ultimately resulting in an elevation of the sensitivity of human esophageal cancer cells to 5-FU. LINC00261 levels were initially quantified, followed by analysis of DYPD methylation within the cancerous tissues collected from 75 patients diagnosed with esophageal cancer undergoing 5-FU-based adjuvant chemotherapy. In an attempt to determine the levels of LINC00261 related to the esophageal cancer cell resistance to 5-FU and to identify the interaction between the levels of LINC00261 and methylation of the DYPD promoter, esophageal cancer cells TE-1 and -5 were prepared, in which LINC00261 and the 5-FU-resistant TE-1 and -5 cells were overexpressed. The levels of LINC00261 were reduced among the cancerous tissues obtained from patients exhibiting resistance to 5-FU. Overexpression of LINC00261 was determined to dramatically inhibit proliferation and resistance to apoptosis among 5-FU-resistant TE-1 and -5 cells, whereas silencing of LINC00261 was determined to enhance proliferation and resistance to apoptosis among the TE-1 and -5 cells. DPYD, a confirmed target of LINC00261, displayed a greater incidence of DNA methylation among patient's sensitive to 5-FU. A key finding revealed that overexpressed LINC00261 could increase the methylation of the DPYD promoter through the recruitment of DNA methyltransferase (DNMT), which, in turn, acts to decrease DPYD activity in 5-FU-resistant TE-1 cells, whereas a reversible change was recorded once the demethylation reagent 5-aza-2'-deoxyctidine was employed to treat the 5-FU-resistant TE-1 cells. Taken together, the results of the study provided evidence emphasizing the distinct antitumor ability of LINC00261 in cases of esophageal cancer, which was manifested by overexpression of LINC00261 detected to increase the sensitivity of human esophageal cancer cells to 5-FU by mediating methylation-dependent repression of DPYD. Our study highlighted the potential of LINC00261 as a novel target capable of improving the chemotherapeutic response and survival of patients with esophageal cancer.-Lin, K., Jiang, H., Zhuang, S.-S., Qin, Y.-S., Qiu, G.-D., She, Y.-Q., Zheng, J.-T., Chen, C., Fang, L., Zhang, S.-Y. Long noncoding RNA LINC00261 induces chemosensitization to 5-fluorouracil by mediating methylation-dependent repression of DPYD in human esophageal cancer.

Postautologous stem cell transplantation engraftment syndrome: Improved treatment and outcomes.

Postautologous stem cell transplantation (ASCT) engraftment syndrome (ES) is a well-known clinical complication; however, many aspects remain largely controversial. In this retrospective study, we reviewed records of 156 ASCTs done over 2 years in our institution. Our results show that 45 (34 multiple myeloma/amyloidosis and 11 lymphoma) of 156 adult patients (29%) were diagnosed with ES. Patients with ES were significantly more likely to have fever, rash, and diarrhea upon engraftment. Risk factors for ES included shorter time from diagnosis to ASCT (P = .029), and lower number of pretransplant treatment regimens (0.012). Post-ASCT, patients with ES had significantly lower absolute lymphocyte count on first engraftment day (P = .014). Most ES patients received treatment with steroids. Initial dose of prednisone/methylprednisolone was 2 mg/kg (n = 34), 1 mg/kg (n = 7), while four patients received 1000 mg IV with median length of therapy 7.5 days. One ES patient with inadequate steroid therapy died of ES complications, while another developed respiratory failure requiring intubation but had full recovery with steroids treatment. In conclusion, patients with shorter time from diagnosis to ASCT and with less prior therapy are more likely to develop ES. Overall survival of ES patients has improved with greater awareness of the diagnosis and earlier use of steroids.

Burkholderia Cepacia Complex in Personal Care Products: Molecular Epidemiology and Susceptibility to Preservatives.

Many outbreaks of Burkholderia cepacia complex (Bcc) infections are associated with contaminations in personal care products (PCPs). This study aimed to analyze a collection of Bcc isolates in PCPs and assess the susceptibility of preservatives, including dimethoxy dimethyl hydantoin (DMDMH), methylisothiazolinone-chloromethylisothiazolinone (MIT/cMIT), and methyl 4-hydroxybenzoate (MH). The Bcc isolates collected during the 3-year (2015-2017) study period were further examined by biochemical identification system, phylogenetic analysis based on recA nucleotide sequences, and multilocus sequence typing analysis. Preservatives susceptibility testing of Bcc bacteria were evaluated by minimum inhibitory concentration and minimum bactericidal concentration. A total of seven distinct sequence types (STs) were identified, which belonged to four different Bcc species: Burkholderia cenocepacia (ST621, ST258, and novel ST), Burkholderia lata (ST339 and ST336), Burkholderia contaminans (ST482), Burkholderia cepacia (ST922). For DMDMH and MH, the maximum permitted concentrations according to the safety specification of cosmetics (0.6% and 0.4%) were able to inhibit or kill all Bcc strains, but 40% of Bcc isolates could survive at higher than maximum permitted concentrations of MIT/cMIT (of a mixture in the ratio 3:1 of 5-chloro-2-methyl-4-isothiazolin-3-one and 2-methyl-4-isothiazolin-3-one). The PCPs contamination of Bcc strains should be given more attention by manufacturers because of its diversity in molecular epidemiology and its low susceptibility to preservatives such as MIT/cMIT.

Intermolecular Alkene Difunctionalization via Gold-Catalyzed Oxyarylation.

The gold-catalyzed intermolecular oxyarylation of alkenes is reported. This work employed the oxidative addition of aryl iodides to Me-DalphosAu+ for the formation of a AuIII -Ar intermediate. The better binding ability of alkenes over O nucleophiles ensured the success of intermolecular oxyarylation, giving desired products with a broad substrate scope and high efficiency (>50 examples with up to 95 % yield). One-pot converting of methoxy groups into other nucleophiles allowed achieving alkene difunctionalization with the construction of C-N, C-S, and C-C bonds under mild conditions.

The Type 1 Diabetes-Resistance Locus Idd22 Controls Trafficking of Autoreactive CTLs into the Pancreatic Islets of NOD Mice.

Type 1 diabetes (T1D) has a strong genetic component. The insulin dependent diabetes (Idd)22 locus was identified in crosses of T1D-susceptible NOD mice with the strongly T1D-resistant ALR strain. The NODcALR-(D8Mit293-D8Mit137)/Mx (NOD-Idd22) recombinant congenic mouse strain was generated in which NOD mice carry the full Idd22 confidence interval. NOD-Idd22 mice exhibit almost complete protection from spontaneous T1D and a significant reduction in insulitis. Our goal was to unravel the mode of Idd22-based protection using in vivo and in vitro models. We determined that Idd22 did not impact immune cell diabetogenicity or ß cell resistance to cytotoxicity in vitro. However, NOD-Idd22 mice were highly protected against adoptive transfer of T1D. Transferred CTLs trafficked to the pancreatic lymph node and proliferated to the same extent in NOD and NOD-Idd22 mice, yet the accumulation of pathogenic CTLs in the islets was significantly reduced in NOD-Idd22 mice, correlating with disease resistance. Pancreatic endothelial cells from NOD-Idd22 animals expressed lower levels of adhesion molecules, even in response to inflammatory stimuli. Lower adhesion molecule expression resulted in weaker adherence of T cells to NOD-Idd22 endothelium compared with NOD-derived endothelium. Taken together, these results provide evidence that Idd22 regulates the ability of ß cell-autoreactive T cells to traffic into the pancreatic islets and may represent a new target for pharmaceutical intervention to potentially prevent T1D.

A biomass-derived porous carbon-based nanocomposite for voltammetric determination of quercetin.

Porous carbon was prepared from wheat flour by alkali treatment and carbonization. The resulting biomass-derived porous carbon (BPC) was employed to prepare a Pt-Au-BPC nanocomposite by a hydrothermal method. The material was then placed on the surface of a carbon ionic liquid electrode (CILE). The Pt-Au-BPC was characterized by SEM, XPS, and the modified CILE by electrochemical methods. They revealed a porous structure, a large specific surface with high conductivity. Pt-Au-BPC/CILE was applied to the sensitive determination of quercetin. Electrochemical response was studied by cyclic voltammetry and differential pulse voltammetry (DPV). Under optimized experimental conditions, the oxidation peak current (measured at 0.48 V vs. Ag/AgCl by DPV) increases linearly in the 0.15 to 6.0 µM and in the 10.0 to 25.0 µM quercetin concentration range. The detection limit is 50.0 nM (at 3σ). The Pt-Au-BPC/CILE was applied to the direct determination of quercetin in ginkgo tablets sample and gave satisfactory results. Graphical abstract A Pt-Au-BPC nanocomposite modified carbon ionic liquid electrode was applied to differential pulse voltammetric determination of quercetin. BPC: biomass-derived porous carbon.

Facilitating Gold Redox Catalysis with Electrochemistry: An Efficient Chemical-Oxidant-Free Approach.

Due to the high oxidation potential between AuI and AuIII , gold redox catalysis requires at least stoichiometric amounts of a strong oxidant. We herein report the first example of an electrochemical approach in promoting gold-catalyzed oxidative coupling of terminal alkynes. Oxidation of AuI to AuIII was successfully achieved through anode oxidation, which enabled facile access to either symmetrical or unsymmetrical conjugated diynes through homo-coupling or cross-coupling. This report extends the reaction scope of this transformation to substrates that are not compatible with strong chemical oxidants and potentiates the versatility of gold redox chemistry through the utilization of electrochemical oxidative conditions.

Correction to: Metabolic Abnormalities in the Pathogenesis of Type 1 Diabetes.

The original version of this article unfortunately contained a mistake in the author group section. Shuyao Zhang's family name was misspelled as "Zheng".

Down-Regulated LncRNA-HOTAIR Suppressed Colorectal Cancer Cell Proliferation, Invasion, and Migration by Mediating p21.

BACKGROUND AND AIM: HOX transcript antisense intergenic RNA (HOTAIR) is a relatively well-understood RNA, which plays a central role in the pathogenesis of various tumors. The aim of the present study was to investigate the effect by which HOTAIR acts to influence the biological processes of colorectal cancer (CRC) through p21. METHODS: Reverse transcription quantitative polymerase chain reaction and Western blot methods were employed to provide verification regarding the changes in HOTAIR, PCNA, Ki67, p21, cyclin E, and CDK2 among the CRC tissues and cells. The correlation between the clinicopathological characteristics of patients and expression of HOTAIR and p21 was subsequently evaluated, followed by an analysis into the effects of HOTAIR on the biological processes of M5 cells. RESULTS: HOTAIR was found to be expressed at high levels, while p21 was determined to be at a low level among both the CRC tissues and the CRC cell lines. The expressions of HOTAIR and p21 were determined to be related to lymph node metastasis, tumor node metastasis, Dukes staging, distant metastases, histological types, and the degree of differentiation. Cells transfected with HOTAIR siRNA displayed inhibited rates of proliferation, invasion, and migration, as well as decreased cyclin E and CDK2, while apoptosis and p21 were increased. CONCLUSION: The principal findings demonstrated that down-regulation of HOTAIR elicits an inhibitory effect on proliferation, invasion, and migration, while promoting the apoptosis of CRC cells through the up-regulation of p21. We believe that HOTAIR could represent a novel target for the treatment of CRC.

Highly Efficient and Stereoselective Thioallylation of Alkynes: Possible Gold Redox Catalysis with No Need for a Strong Oxidant.

Stereoselective thioallylation of alkynes under possible gold redox catalysis was accomplished with high efficiency (as low as 0.1 % catalyst loading, up to 99 % yield) and broad substrate scope (various alkynes, inter- and intramolecular fashion). The gold(I) catalyst acts as both a π-acid for alkyne activation and a redox catalyst for AuI/III coupling, whereas the sulfonium cation generated in situ functions as a mild oxidant. This novel methodology provides an exciting system for gold redox catalysis without the need for a strong oxidant.

Selective removal of alkynes from diene mixtures using ether-functionalized Cu(i)-containing ionic liquids as extractants.

Cu(i)-Containing room temperature ionic liquids (Cu-EnA), prepared from CuCl and ether-functionalized ionic liquids (ILs) bearing a methanesulfonate anion (EnA, n = 1, 2 or 3), were thermally stable and highly effective for the removal of alkynes such as isopropenylacetylene (IPA) and 2-butyne (2-BT) contained in dienes like isoprene (2-methyl-1,3-butadiene). Cu-EnA were found to reversibly and selectively interact with IPA and 2-BT, thereby enabling the regeneration of Cu-EnA. Fast atom bombardment (FAB)-mass spectral and computational results imply that EnA consists of an ether-functionalized imidazolium cation and a methanesulfonate-coordinated Cu(i) anion such as [CuCl(CH3SO3)]- ([CuClA]-) or [Cu(CH3SO3)2]- ([CuA2]-). Computational studies demonstrate that the preferential extraction of IPA and 2-BT to isoprene by Cu-EnA originated from the difference in the strength of the hydrogen bonding and π-complexation.