This study details
the synthesis of high-activity g-C3N4 catalysts
for H2 generation from a triethanolamine
aqueous solution under visible light. We anneal a mixture of urea
and NH4Cl to obtain g-C3N4 nanosheets,
which are subsequently solvated with ethanol molecules and annealed
to form aromatic carbon-doped g-C3N4. The results
of analyses conducted using X-ray photoelectron, Fourier-transform
infrared, and carbon-13 nuclear magnetic resonance spectroscopies
demonstrated that annealing the ethanol molecules leads to the grafting
of aromatic heterocycles on the g-C3N4 nanosheets
and substitution of nitrogen with carbon. The grafted aromatic heterocycles
and doped carbon atoms extend the π-conjugation system in g-C3N4 to reduce the band gap and facilitate the separation
of photogenerated charges. The carbon-incorporating also preserve
the crystallinity of g-C3N4 during high-temperature
annealing, which facilitates the suppression of the recombination
of photogenerated charges at defect sites. The developed aromatic
carbon-doped g-C3N4 effectively catalyzes H2 generation from the aqueous solution, achieving apparent
quantum yields of 14% and 2.2% under 420 and 550 nm monochromatic
irradiation, respectively, whereas urea-derived g-C3N4 reached only 3.4% and 0.1%. The proposed strategy of extending
the π-conjugation system is promising for promoting the activity
of carbon-nitride photocatalysts.
The discovery of cancer stem cells (CSCs), which are responsible for self-renewal and tumor growth in heterogeneous cancer tissues, has stimulated interests in developing new cancer therapies and early diagnosis. However, the markers currently used for isolation of CSCs are often not selective enough to enrich CSCs for the study of this special cell population. Here we show that the breast CSCs isolated with CD44+CD24-/loSSEA-3+ or ESAhiPROCRhiSSEA-3+ markers had higher tumorigenicity than those with conventional markers in vitro and in vivo. As few as 10 cells with CD44+CD24-/loSSEA-3+ formed tumor in mice, compared with more than 100 cells with CD44+CD24-/lo. Suppression of SSEA-3 expression by knockdown of the gene encoding β-1,3-galactosyltransferase 5 (β3GalT5) in the globo-series pathway, led to apoptosis in cancer cells specifically but had no effect on normal cells. This finding is further supported by the analysis of SSEA-3 and the two related globo-series epitopes SSEA4 and globo-H in stem cells (embryonic stem cells and induced pluripotent stem cells) and various normal and cancer cells, and by the antibody approach to target the globo-series glycans and the late-stage clinical trials of a breast cancer vaccine.
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