Lewis Acid-Catalyzed Asymmetric Selenocyanation of ß-Ketoesters with N-Selenocyanatosaccharin.

The first electrophilic asymmetric selenocyanation has been achieved in the presence of Ni(OTf)2 and (R,R)-DBFOX/Ph using N-selenocyanatosaccharin as the new selenocyanation reagent. Thus, a series of α-selenocyanato-ß-keto esters were synthesized with high yields (up to 99%) and good ee values (up to 92% ee). The readily preparation of the reagent and high enantioselectivity make this methodology much practical for the synthesis of chiral selenocyanates.

N-Thiocyanato-dibenzenesulfonimide: a new electrophilic thiocyanating reagent with enhanced reactivity.

A novel electrophilic thiocyanating reagent, N-thiocyanato-dibenzenesulfonimide, was prepared and exhibited enhanced electrophilicity with a wide scope of substrates. Thus, it reacted with activated aromatics such as phenols, indoles, anilines and anisoles without a catalyst giving the corresponding thicyanate derivatives in high yields, while TfOH for unactivated arenes and hetero aromatics and Zn(OTf)2 for ketones was used as the catalyst, respectively. It is noteworthy that internal alkenes and styrenes were bifunctionalized giving 1,2-amino thiocyanates in high yields.

Quercetin exerts cardiovascular protective effects in LPS-induced dysfunction in vivo by regulating inflammatory cytokine expression, NF-κB phosphorylation, and caspase activity.

Impaired myocardial contractile function, one of the well-documented features of sepsis, contributes greatly to the high rate of mortality. Quercetin is widely accepted as a potential antioxidant and free radical scavenger. Epidemiologic studies have suggested that an increase in the intake of dietary Quercetin can reduce the risk of cardiac disease. However, presently there is no report yet on the influence of Quercetin on LPS-induced myocardial dysfunction in vivo. Cardiovascular protective effects of Quercetin on LPS-induced sepsis in mice were measured after intragastric administration, using normal saline as a positive control. Quercetin pretreatment significantly alleviated LPS-induced cardiac abnormalities in mice. The histopathologic findings in the present study justify the findings reported from the biochemical analyses. Our observation from the present research work reveals that Quercetin suppressed the production of proinflammatory cytokines at different levels, such as TNF-α and IL-1ß, and inhibits the activation of I-κB phosphorylation, whereas the total content was not affected. Apoptotic pathways are related to Quercetin protection in the development of myocardial dysfunction. In conclusion, our findings demonstrate the adjuvant potentials of Quercetin for clinical sepsis treatment.

Design and Synthesis of Viologen-based Copolymers for High Performance Li-Dual-Ion Batteries.

Dual-ion batteries based on organic electrodes show great potential to break through the bottlenecks existed in conventional LIBs due to their high specific capacity, lifted working voltage, and environmental benignity. Herein, two innovative viologen-based bipolar copolymers poly(viologen-pyrene-4,5,9,10-tetrone dichloride) (PVPTOCl2 ) and poly(viologen-anthraquinone dichloride) (PVAQCl2 ) were synthesized and applied as high performance cathodes for lithium-dual-ion battery. Bearing the dual-ion storage capability of viologen and carbonyls, as well as the conjugated structure of pyrene-4,5,9,10-tetrone, the synthesized copolymers show remarkable electrochemical performances for LIBs. Compared to PVAQCl2 , PVPTOCl2 shows superior electrochemical performance with high initial specific capacity (235.0 mAh g-1 at 200 mA g-1 ), high reversibility (coulombic efficiency up to 99.96 % at 1 A g-1 ), excellent rate performance (150.3 mAh g-1 at 5 A g-1 ) and outstanding cycling stability (a reversible capacity of 197.5 mAh g-1 at a current density of 1 A g-1 and a low capacity loss per cycle of 0.11‰ during 3000 cycles). Moreover, the charge storage mechanism was systematically investigated by ex-situ FT-IR, ex-situ XPS and DFT calculations. The results clearly reveal the structure-property relationship of the bipolar-molecules, providing a new platform to develop efficient bipolar materials for dual-ion batteries.

Heme oxygenase-1 ameliorates hypoxia/reoxygenation via suppressing apoptosis and enhancing autophagy and cell proliferation though Sirt3 signaling pathway in H9c2 cells.

Cardiomyocyte infarction could lead to high morbidity and mortality worldwide. Recent studies demonstrated that Heme oxygenase-1 (HO-1) could exert cardiac protective effect and arouse attention. However, the detailed mechanism is still unclear. Our study provided evidences of the protective effect of HO-1 overexpression on cardiomyocytes against hypoxia/reoxygenation (H/R). We divided the treatment into four groups: the control group, H/R group, H/R+HO-1 group, and H/R+Null group. Immunofluorescent study was utilized to label the BrdU-positive and LC3-positive cells. Flow cytometry and TUNEL assay were used to examine the cell apoptosis. Protein levels of Bax, Bcl-2, Sirt3, beclin-1, LC3-I, and LC3-II were both measured using western blotting. The results indicated that HO-1 overexpression decreased the cell apoptosis and enhanced the cell proliferation. The level of Sirt3 and autophagy were also increased in H/R+HO-1 group compared with H/R group. However, ZnPP, a HO-1 inhibitor, and SiRNA of Sirt3 are both reversed the decrease of cell apoptosis of HO-1 overexpression. Moreover, ZnPP also decreased the expression of Sirt3 in HO-1 overexpression treatment group. In summary, HO-1 overexpression protects cardiomyocytes against H/R injury via ameliorating cell apoptosis and enhancing cell proliferation and autophagy through Sirt3 signaling pathway.

The Chemistry and Properties of Energetic Materials Bearing [1,2,4]Triazolo[4,3-b][1,2,4,5]tetrazine Fused Rings.

Treatment of heterocyclic amines featuring fused rings of [1,2,4]triazolo[4,3-b][1,2,4,5]tetrazine with fuming HNO3 /P2 O5 leads to six fully characterized explosives through multiple nitration and reduction or oxidation mechanism. Thus, 4-nitro-N-(3-nitro[1,2,4]triazolo[4,3-b][1,2,4,5]tetrazin-6-yl)-1,2,5-oxadiazol-3-amine (3 b, TTDNF) showed high performance (D=9180 m s-1 , P=36.7 GPa) and low impact sensitivity (IS>40 J) while N-([1,2,4]triazolo[4,3-b][1,2,4,5]tetrazin-6-yl)-3-nitro-1,2,4-oxadiazol-5-amine (4 a, TTNOA) exhibited a potential cast explosive component with low melting point at 88.2 °C and high onset decomposition temperature at 226.2 °C.

Quercetin attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways.

Quercetin (Que), a plant-derived flavonoid, possesses various biological functions. Moreover, Que exerts multiple beneficial actions in treatment of cardiovascular diseases and there are an inverse association between Que intakes and occurrence and development of various cardiovascular diseases. Some researchers have inferred that the mechanisms of Que to protect cardiomyocytes from ischemia/reperfusion (I/R) injury may be involved in modulation of intracellular signal pathways and regulation of proteins expression in vivo. The current study investigated whether Que has any protective effects on cardiomyocytes from hypoxia/reoxygenation (H/R) in vitro and its potential cardioprotective mechanisms. The cell viability of Que on H9c2 cardiomyoblast cells was assessed by MTT. Apoptosis was evaluated by both Hoechst33342 staining and Flow cytometric analysis (FACS). Furthermore, the effect of Que, SP600125 (JNK inhibitor) and SB203580 (p38 inhibitor) on mitogen-activated protein kinases (MAPKs) and the expression of apoptosis related proteins (Bcl-2, Bax and caspase-3) was determined by Western blotting. MTT assays showed that pretreatment with Que could increase the viability of H9c2 cardiomyocytes that suffered H/R. Both Hoechst33342 staining and FACS confirmed that Que could remarkably suppress the H/R-induced apoptotic cardiomyocytes. In addition, Que significantly alleviated H/R-induced the phosphorylation of JNK and p38, which further increased Bcl-2 expression and inhibited the activation of Bax and caspase-3 directly or indirectly. In summary, our results imply that Que can induce cardioprotection by inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways and modulate the expression of Bcl-2 and Bax proteins that provides a new experimental foundation for myocardial ischemia disease therapy.