Enantioselective Copper-Catalyzed sp2/sp3 Diborylation of 1-Chloro-1-Trifluoromethylalkenes.

Fluorine-containing organoboron compounds have emerged as novel building blocks in chemical synthesis; among them, fluorinated sp2/sp3 diborylated compounds are particularly appealing, since they might undergo chemoselective and diversified transformations of different C-B bonds with fluorinated functionality, thus bringing versatility and complexity to the eventual products. However, expedient, synthetic strategies for the construction of such fluorinated diborylative compounds are very sparse. Herein, we disclose enantioselective Cu-catalyzed sp2/sp3 diborylations of 1-chloro-1-trifluoromethylalkenes, leading to diborylated compounds bearing a gem-difluoroalkenyl moiety; most intriguingly, the new formed C-B bonds include one stereoselective and optically pure Csp3-B bond. Further transformations on the eventual products demonstrated the values of our presented strategy.

Copper-Catalyzed Aerobic Cyclization of ß,γ-Unsaturated Hydrazones with Concomitant C═C Bond Cleavage.

A Cu-catalyzed aerobic oxidative cyclization of ß,γ-unsaturated hydrazones for the preparation of pyrazole derivatives has been developed. The hydrazonyl radical promoted the cyclization, along with a concomitant C═C bond cleavage of ß,γ-unsaturated hydrazones. This process has been verified via several control experiments, including a radical-trapping study, an 18O-labeling method, and the identification of the possible byproducts. The advantages of this reaction include operational simplicity, a broad reaction scope, and a mild selective reaction process.

Systematic Identification of lncRNA-Associated ceRNA Networks in Immune Thrombocytopenia.

Primary immune thrombocytopenia (ITP) is an autoimmune disease. However, the molecular mechanisms underlying ITP remained to be further investigated. In the present study, we analyzed a series of public datasets (including GSE43177 and GSE43178) and identified 468 upregulated mRNAs, 272 downregulated mRNAs, 134 upregulated lncRNAs, 23 downregulated lncRNAs, 29 upregulated miRNAs, and 39 downregulated miRNAs in ITP patients. Then, we constructed protein-protein interaction networks, miRNA-mRNA and lncRNA coexpression networks in ITP. Bioinformatics analysis showed these genes regulated multiple biological processes in ITP, such as mRNA nonsense-mediated decay, translation, cell-cell adhesion, proteasome-mediated ubiquitin, and mRNA splicing. We thought the present study could broaden our insights into the mechanism underlying the progression of ITP and provide a potential biomarker for the prognosis of ITP.

Overexpression of lncRNA GATA6-AS inhibits cancer cell proliferation in mantle cell lymphoma by downregulating GLUT1.

Long non-coding RNA GATA6 antisense RNA 1 (lncRNA GATA6-AS) is a recently identified lncRNA that is involved in endothelial-mesenchymal transition. The present study aimed to investigate the involvement of GATA6-AS in the progression of mantle cell lymphoma (MCL). It was found that plasma lncRNA GATA6-AS expression level was downregulated in patients with MCL, compared with that in healthy controls. Downregulation of lncRNA GATA6-AS has potential diagnostic value in early stage MCL. Overexpression of lncRNA GATA6-AS resulted in inhibited glucose uptake in the human cell lines JVM-2 and Z-138 MCL. Inhibited expression of glucose transporter 1 (GLUT1) was observed in MCL cells following lncRNA GATA6-AS overexpression, whilst GLUT1 overexpression did not alter the expression of lncRNA GATA6-AS. Additionally, lncRNA GATA6-AS overexpression inhibited, whilst GLUT1 overexpression promoted the proliferation of JVM-2 and Z-138 MCL cells; GLUT1 overexpression partially reversed the inhibitory effects of lncRNA GATA6-AS overexpression. It was therefore concluded that lncRNA GATA6-AS may inhibit cancer cell proliferation in MCL by downregulating GLUT1.

MAPK Pathway Inhibitors Attenuated Hydrogen Peroxide Induced Damage in Neural Cells.

BACKGROUND: Oxidative stress due to reactive oxygen species plays a central role in pathophysiology of neurodegenerative diseases. Inhibition of mitogen-activated protein kinase (MAPK) cascades attenuates the oxidative induced cell stress and behaves as potential neuroprotection agent. MATERIALS AND METHODS: In this study, we evaluate hydrogen peroxide induced neural cell stress and determine how different MAPK inhibitors restore the cell damage. RESULTS: The results indicated that oxidative stress induced by neural cell damage commonly exists, and MAPK inhibitors partially and selectively attenuated the cell damage by reducing ROS production and cell apoptosis. The cultured neurons are more susceptible to hydrogen peroxide than subculture cells. CONCLUSION: We conclude that the essential role of different MAPK inhibitors is to attenuate the hydrogen peroxide induced neuronal cell damage. Those data broaden the implication between individual neural cells and different MAPK inhibitors and give clues for oxidative stress induced neural diseases.

Copper-Catalyzed Aerobic 6-Endo-Trig Cyclization of ß,γ-Unsaturated Hydrazones for the Divergent Synthesis of Dihydropyridazines and Pyridazines.

A divergent synthetic strategy to 1,6-dihydropyridazines and pyridazines through Cu(II)-catalyzed controllable aerobic 6-endo-trig cyclization was developed. The selectivity can be rationally tuned via the judicious choice of reaction solvent. It was found that the 1,6-dihydropyridazines were obtained in moderate to high yields with CH3CN as the reaction solvent, whereas employment of AcOH directly afforded pyridazines in up to 92% yields, probably arising from the oxidation of the in situ generated 1,6-dihydropyridazines.

Palladium-catalyzed C-H olefination of uracils and caffeines using molecular oxygen as the sole oxidant.

The palladium-catalyzed oxidative C-H olefination of uracils or caffeines with alkenes using an atmospheric pressure of molecular oxygen as the sole oxidant has been disclosed. This novel strategy offers an efficient and environmentally friendly method to biologically important C5-alkene uracil derivatives or C8-alkene caffeine derivatives.

The effects of Smad6 via small RNA pathways on the ischemic injury in PC12 cells.

BACKGROUND: Though we have reported the neuroprotective effect of exogenous ActA on oxygen-glucose deprivation (OGD) injury, the endogenous role of Smad6 remains not well understood. Smad6 is an important regulator of the ActA/smads signaling via a negative feedback circuit. METHODS: In this study, nerve growth factor (NGF) and OGD were used to stimulate (rat adrenal pheochromocytoma) PC12 cells converting them into neurons to establish an ischemia in vitro model. Combined with the small interfering technology of Smad6 and FCM, Hoechst and Western blot were used to identify the apoptosis rate. The effect of silencing of Smad6 with siRNA was observed. RESULTS: These results showed that the apoptosis rate was 21.54% by 16-h OGD. For the combined Smad6-siRNA, the apoptosis rate was 10.55%. CONCLUSIONS: The expression of procaspase-3 protein was increased by Smad6-siRNA.The expression of ActA and p300 was also increased. The apoptosis rate was decreased in the ischemic injury with Smad6-siRNA. At the same time, it provided a reference to study the mechanism of Smad6 and its signaling in response to the acute ischemic damage.