In the present study, urine samples were collected from healthy human volunteers to determine the metabolic fates of phenolic compounds and glucosinolates after a single meal of kale and daikon radish. The major glucosinolates and phenolic compounds in kale and daikon radish were measured. The urinary metabolome after feeding at different time periods was investigated. A targeted metabolite analysis method was developed based on the known metabolic pathways for glucosinolates and phenolic compounds. Using a targeted approach, a total of 18 metabolites were found in urine 4 from phenolic compounds and 14 from glucosinolates. Among these metabolites, 4-methylsulfinyl-3-butenyl isothiocyanate, 4-methylsulfinyl-3-butenyl isothiocyanate-cysteine, and 4-methylsulfinyl-3-butenylglucosinolate-N-acetyl cysteine were reported for the first time in human urine. The combination of non-targeted and targeted metabolomic approaches can gain a full metabolite profile for human dietary intervention studies.Chemoresistance and toxicity are the main obstacles that limit the efficacy of 5-fluorouracil (5-FU) in colorectal cancer (CRC) therapy. Hence, it is urgent to identify new adjuvants that can sensitize CRC cells to conventional chemotherapeutic approaches. Cucurbitacin E (CE) is a natural triterpenoid, widely distributed in dietary plants, and shows antitumor effects. Here, we report that CE enhances the sensitivity of CRC cells to chemotherapy via attenuating the expression of adenosine 5'-triphosphate (ATP)-binding cassette transporters ABCC1 and MDR1. Combined with CE-functionalized magnetite nanoparticles and gene ontology analysis, we found that CE-binding proteins may involve Wnt/β-catenin signaling. To validate the findings, β-catenin was upregulated in drug-resistant cell lines, and the synergistic effects of CE and chemotherapeutics were accompanied by the downregulation of β-catenin. Moreover, TFAP4 was identified as an intracellular target of CE. Remarkably, the combination of CE and 5-FU treatment attenuated β-catenin, MDR1, and ABCC1 expressions, while TFAP4 overexpression reversed their expressions by 2.68 ± 0.46-, 0.72 ± 0.44-, and 0.93 ± 0.21-fold, respectively. Thus, our results indicate that CE sensitizes CRC cells to chemotherapy by decreasing the TFAP4/Wnt/β-catenin signaling, suggesting that the dietary compound CE can be used as a chemosensitizing adjuvant for CRC treatment.Breast cancer is the most frequently diagnosed cancer among women, and the circulating tumor cell (CTC)-meditated distant metastasis is the leading cause of death. Thus, the detection of CTCs is of great importance for the early diagnosis of breast cancer and the prevention of metastasis. In this study, using human breast carcinoma BT474 cells as the model CTCs, a powerful assay platform is demonstrated by fluorescence spectrometry for the highly sensitive CTC detection by combining the dual-recognizing elements receptor-binding antibody and aptamer-mediated separation with double rolling circle amplification reactions (d-RCA, including RCA1 and RCA2). The aptamer-inserted RCA1 product (RCA1-p) exhibits the considerably improved affinity towards target cells originating from the multivalent binding effect. The immunomagnetic separation removes nontarget cells coexisting in complex biological milieu, while the centrifugal separation of cells/DNAs mixture eliminates the excess probes, thereby circumventing the unwanted interferences. The fluorescence spectrometric results show that a 34-fold enhanced fluorescence signal is achieved upon BT474 cells, and the target cells can be quantitatively detected down to 9 cells/200 μL with the linear range of five orders of magnitude, indicating a significantly enhanced detection performance. Even if BT474 cells are spiked in the fresh whole blood, no obvious fluctuation in the fluorescence signal is detected, demonstrating that the newly developed d-RCA assay system is suitable for screening CTCs in complex environments and is expected to be a promising tool for estimating distant metastasis and predicting the recurrence of tumors.In this study, iron selenide nanoparticles (FeSe2) were synthesized and applied in Fenton-like reactions for degradation of pollutants.  https://www.selleckchem.com/products/azd9291.html  It was found that FeSe2 exerts excellent catalytic reactivity toward different oxidants including peroxymonosulfate (PMS), peroxydisulfate, and H2O2, which can degrade a wide range of pollutants such as 2,4,4'-trichlorobiphenyl, bisphenol A, sulfamethoxazole, chlortetracycline, and perfluorooctanoic acid, with the degradation efficiency and TOC removal of pollutants reaching 55-95 and 20.3-50.9%, respectively. The mechanism of PMS activation by FeSe2 was elucidated, and the synergistic effect between Fe and Se for PMS activation was discovered to be the dominant catalytic mechanism, as evidenced by free-radical quenching, electron paramagnetic resonance, and density functional theory studies. Briefly, the Fe(II) site on the FeSe2 surface (111) accounted for PMS activation, while the reducing Se species on the surface not only acted as an electron donor contributing to Fe(II) regeneration but also produced Se vacancies further facilitating Fe(II) regeneration to improve the performance of PMS activation. In addition, FeSe2 exhibited high catalytic activity and stability for PMS activation with different pH, and can degrade PCBs efficiently in the presence of anions, natural organic matter water matrices or in complex soil eluents. This study presents the development and evaluation of FeSe2 as a novel and highly efficient activator that exhibits promise for practical applications for the degradation of pollutants in wastewater and soil wash eluent with Fenton-like reactions.Alcohol exposure has been postulated to adversely affect the physiology and function of the red blood cells (RBCs). The global pervasiveness of alcohol abuse, causing health issues and social problems, makes it imperative to resolve the physiological effects of alcohol on RBC physiology. Alcohol consumed recreationally or otherwise almost immediately alters cell physiology in ways that is subtle and still unresolved. In this paper, we introduce a high-resolution device for quantitative electrofluidic measurement of changes in RBC volume upon alcohol exposure. We present an exhaustive calibration of our device using model cells to measure and resolve volume changes down to 0.6 fL. We find an RBC shrinkage of 5.3% at 0.125% ethanol (the legal limit in the United States) and a shrinkage of 18.5% at 0.5% ethanol (the lethal limit) exposure. Further, we also measure the time dependence of cell volume shrinkage (upon alcohol exposure) and then recovery (upon alcohol removal) to quantify shrinkage and recovery of RBC volumes.