21 research outputs found
Cobalt-Catalyzed TrifluoromethylationâPeroxidation of Unactivated Alkenes with Sodium TrifluoroÂmethaneÂsulfinate and Hydroperoxide
Disclosed
herein is an unprecedented cobalt-catalyzed trifluoromethylationâperoxidation
of unactivated alkenes. In this process the hydroperoxide acts as
a radical initiator as well as a coupling partner. The cheap and readily
available sodium trifluoroÂmethaneÂsulfinate serves as the
CF<sub>3</sub> source in the reaction. Various alkenes are transformed
into vicinal trifluoromethyl-peroxide compounds in moderate to good
yields
Polyurethane Foam-Based Ultramicroporous Carbons for CO<sub>2</sub> Capture
A series
of sustainable porous carbon materials were prepared from waste polyurethane
foam and investigated for capture of CO<sub>2</sub>. The effects of
preparation conditions, such as precarbonization, KOH to carbon precursor
weight ratio, and activation temperature, on the porous structure
and CO<sub>2</sub> adsorption properties were studied for the purpose
of controlling pore sizes and nitrogen content and developing high-performance
materials for capture of CO<sub>2</sub>. The sample prepared at optimum
conditions shows CO<sub>2</sub> adsorption capacities of 6.67 and
4.33 mmol·g<sup>â1</sup> at 0 and 25 °C under 1 bar,
respectively, which are comparable to those of the best reported porous
carbons prepared from waste materials. The HCl treatment experiment
reveals that about 80% of CO<sub>2</sub> adsorption capacity arises
from physical adsorption, while the other 20% is due to the chemical
adsorption originated from the interaction of basic N groups and CO<sub>2</sub> molecules. The relationship between CO<sub>2</sub> uptake
and pore size at different temperatures indicates that the micropores
with pore size smaller than 0.86 and 0.70 nm play a dominant role
in the CO<sub>2</sub> adsorption at 0 and 25 °C, respectively.
It was found that the obtained carbon materials exhibited high recyclability
and high selectivity to adsorption of CO<sub>2</sub> from the CO<sub>2</sub> and N<sub>2</sub> mixture
Novel 1,8-Naphthalimide Derivatives As Antitumor Agents and Potent Demethylase Inhibitors
Functional 1,8-naphthalimide derivatives are rapidly
developing
in the field of anticancer research. Herein, we designed and synthesized
a series of naphthalimide derivatives with different substituents.
Interestingly, 1,8-naphthalimide derivatives 1 and 7 inhibited a human demethylase FTO (the fat mass and obesity-associated
protein). Computer simulation studies further indicated that 1 and 7 entered the FTOâs structural domain
II binding pocket through hydrophobic and hydrogen bonding interactions.
Anticancer mechanism studies showed that 1 and 7 induced DNA damage and autophagic cell death in A549 cells.
The high antiproliferative activity of 1 and 7 was further confirmed by 3D multicellular A549 tumor spheroid assays.
This study focuses on the cytotoxicity and mode of action of naphthalimide
derivatives, which not only have potential anticancer activity but
also are potent demethylase inhibitors
Crystalline Mixed Halide Halobismuthates and Their Induced Second Harmonic Generation
Mixed
halide coordination has been widely used to finely tune the properties
of inorganic and inorganicâorganic hybrid compounds, especially
for emerging perovskites materials. Despite the increasing number
of reports on preparation methods and the affected functionalities,
the peculiar and precise role of the doping halogens in structural
regulation of the crystals and the resulting variations on the basic
properties remain to be addressed. Here, to shed light into the âblack
boxâ, a new series of [NH<sub>2</sub>(CH<sub>2</sub>CH<sub>3</sub>)<sub>2</sub>]<sub>3</sub>BiÂ(Cl<sub>1â<i>x</i></sub>Br<sub><i>x</i></sub>)<sub>6</sub> (<i>x</i> = 0, 0.135, 0.255, 0.385, 0.847, and 1) single crystals were grown
from the mixed halide solvents by the temperature lowering method.
The correlation between the inclusion amounts of Br in the final crystals
with the halide concentrations in the precursors is discussed from
different perspectives. The two kinds of halogens share the same position
in the mixed halide system, with every crystallographically independent
halide site possessing different halogen occupancies. The mixed halide
coordination exhibits a regulated effect on the distortion of the
anion octahedra. Optical absorption, thermogravimetric analysis (TGA),
differential scanning calorimetry (DSC), and the second harmonic generation
(SHG) measurements have confirmed that, with increased Br inclusion,
[NH<sub>2</sub>(CH<sub>2</sub>CH<sub>3</sub>)<sub>2</sub>]<sub>3</sub>BiÂ(Cl<sub>1â<i>x</i></sub>Br<sub><i>x</i></sub>)<sub>6</sub> crystals exhibit a regulated effect on their
bandgaps, thermal stabilities, and SHG capacities
The effect of DLF on HCC cell growth and cell cycle-related protein expression <i>in vitro</i>.
<p>(A, B) Growth inhibition resulting from the treatment of HCC cells with DLF extracts for 24 h and 48 h. (C) The cell cycle distribution of Huh7 and MHCC-97L cells that were treated with 3 mg/ml DLF for 24 h or 48 h. (D) The percentage of Huh7 cells in G2 phase following treatment with DLF extracts for various times. (E, F) Western blot analysis of the expression of G2/M phase transition-related proteins after treatment with DLF extracts at various concentrations and for various times.</p
The relative contributions of the Chk1, Chk2 and p53 pathways.
<p>(A) Western blot analysis of the activation of p53, MDM2, Chk1 and Chk2 in Huh7 and PLC/PFR/5 cells after ICD treatment for 48 h. (B) The cell cycle distribution of Huh7 cells after ICD treatment for 18 h following siRNA transfection. (C) Western blot analysis of the silencing effect of Chk1 or Chk2 expression levels after transfection with their corresponding siRNA. (D) Western blot analysis of p-CDK1 or CDK1 expression levels after ICD treatment for 18 h following transfection with their corresponding siRNA.</p
DLF extracts causes cell growth inhibition and apoptosis.
<p>(A) The growth inhibition rates of Huh7, SMMC-7721, PLC/PFR/5 and L-02 cells resulting from treatment with ICD for 48 h. (B) Following the treatment of Huh7 cells with 0, 100, 200 or 300 ”g/ml ICD for 48 h, apoptotic cells were detected by Annexin V and 7-AAD double staining. (C) Western blot analysis of cleaved PARP in Huh7, SMMC-7721 and PLC/PRF/5 cells following ICD treatment at their respective IC<sub>50</sub> values (250 ”g/ml, 200 ”g/ml, 250 ”g/ml). (D) An amount of 1Ă10<sup>6</sup> Huh7 or SMMC-7721 cells/mouse was subcutaneously injected into nude mice. After 2 weeks, 0.4 mg/ml of ICD or PBS was administered 5 times per week for 4 weeks. The resulting tumors were excised from the animals after treatment. (E) The tumor weights for the four groups of animals were compared, and statistical significance was determined using the Studentâs <i>t</i>-test. Each point represents the mean ± SD.</p
ICD treatment causes cells cycle arrest at the G2/M phase.
<p>(A) The cell cycle distribution of Huh7 cells that were treated with various doses of ICD for 18 h. (B) A statistical graph of the cell cycle distribution shown in (A). (C and D) Western blot analysis of G2/M transition-related proteins after ICD treatment of Huh7, SMMC-7721 and PLC/PRF/5 cells for 18 h.</p
Cell cycle distribution of SMMC-7721 HCC cells after ICD treatment with gradient concentrations.
<p>Data are mean ± SD of three independent experiments.</p>*<p>Significant differences (<i>p</i><0.05),</p>**<p>Significant differences (<i>p</i><0.001).</p
The effect of growth suppression on CD133<sup>+/â</sup> PLC/PRF/5.
<p>(A) PLC/PRF/5 cells were treated with various doses of ICD or 10 ng/ml vincristine for 48 h. The percentage of CD133<sup>+</sup> cells was then determined by flow cytometry. Statistically significant differences were determined using the Studentâs <i>t</i>-test (*â=â<i>p</i><0.05; each point represents the mean ± SD). (B) The hepatosphere formation of PLC/PFR/5 CD133<sup>+/â</sup> cells that were sorted by FACS and treated with PBS or 150 ”g/ml of ICD for 48 h. (C) The colony formation of PLC/PRF/5 CD133<sup>+/â</sup> cells that were sorted by FACS and then treated with PBS or 150 g/ml ICD for 48 h. (D) The growth inhibition rates of PLC/PFR/5 CD133<sup>+/â</sup> cells resulting from 48 and 72 h ICD treatments. (E and F) An amount of 5000 PLC/PFR/5 CD133<sup>+/â</sup> cells/mouse were subcutaneously injected into nude mice. After 2 weeks, 0.4 mg/ml of ICD or PBS was administered 5 times per week for 4 weeks. The resulting tumors were excised from the animals after treatment. Statistical significance was determined using the Studentâs <i>t</i>-test. Each point represents the mean ± SD.</p