A convenient smartphone-assisted colorimetric for 6-Mercaptopurine detection using enhanced oxidase-like activity of ß-cyclodextrin modified MnO2 nanosheets.

6-mercaptopurine (6-MP) is widely used in the treatment of many diseases, but exhibits some serious side effects due to its toxicity. Therefore, it is important and imperative to effectively control and monitoring concentration of 6-MP. Herein, we designed a smartphone-assisted colorimetric sensing platform for 6-MP detection, based on an excellent ß-cyclodextrin modified MnO2 nanosheets (ß-CD@MnO2 NNS) mediated oxidase-like activity. ß-CD@MnO2 NNS can directly oxidizes 3,3',5,5'-tetramethylbenzidine (TMB) into oxidized TMB with color changes, yielding more than 3-fold higher oxidase-like catalytic activity compared with individual MnO2 NNS. After adding 6-MP, ß-CD@MnO2 NNS can be reduced to Mn2+ and lose their oxidase-like properties, resulting in a color and absorbance change for sensitive and selectivity detection of 6-MP. Meanwhile, the smartphone-based color recognition application can intuitively and simply measure the concentration of 6-MP. The limits of detection UV-vis instrument and smartphone were 0.35 µM and 0.86 µM, respectively. This method has also been successfully applied to the detection of real samples. Finally, this study provides a new promising platform for detection of 6-MP and is expected to be used in application of pharmaceutical analysis and biomedicine.

Identification and secondary structure analysis of a keratin-like fibrous protein discovered in ligament of the bivalve Siliqua radiata.

A novel keratin-like fibrous protein K58 with molecular weight of about 58 kDa was discovered in bivalve Siliqua radiata ligament and identified by amino acid composition and MALDI-TOF-TOF analysis. We found that the protein is composed of cylindrical fibers (~160 nm in diameter) and contains high glycine (27.4%) and phenylalanine (10.5%) contents. Furthermore, it is homologous to keratin type II cytoskeletal 1, with repeat motifs of SGGG and SYGSGG. FTIR and secondary structure analysis indicate that K58 is composed of 46.2% ß-sheet, 33.4% ß-turn, 13.1% α-helix, and 4.7% disordered structure. This structure feature is closely related to the superior tensile strength, elasticity, and solvent resistance property of K58. These discoveries provide some evidence for evolution of keratin and fibrous proteins and prompt further studies of ligament fibrous proteins.

Gan-Qing-Ning Formula Inhibits the Growth of Hepatocellular Carcinoma by Promoting Apoptosis and Inhibiting Angiogenesis in H22 Tumor-Bearing Mice.

OBJECTIVE: Gang-Qing-Ning (GQN) is a traditional Chinese medicine formula that has been used in the treatment of hepatocellular carcinoma (HCC) in the folk population for decades. However, scientific validation is still necessary to lend credibility to the traditional use of GQN against HCC. This study investigates the antitumor effect of GQN on H22 tumor-bearing mice and its possible mechanism. METHODS: Fifty H22 tumor-bearing mice were randomly assigned to five groups. Three groups were treated with high, medium, and low dosages of GQN (27.68, 13.84, and 6.92 g/kg, respectively); the positive control group was treated with cytoxan (CTX) (20 mg/kg) and the model group was treated with normal saline. After 10 days' treatment, the tumor inhibitory rates were calculated. Pathological changes in tumor tissue were observed, and the key proteins and genes of the mitochondrial apoptosis pathway were measured, as well as the mRNA expression levels of VEGF in tumor tissue. RESULTS: The tumor inhibitory rates of high, medium, and low dosages of GQN groups were 47.39%, 38.26%, and 22.17%, respectively. The high dosage of the GQN group significantly increased the protein and mRNA expression levels of Bax, Cyt-C, and cleaved Caspase 3 (or Caspase 3) (P < 0.01) but decreased the expression levels of Bcl-2, VEGF, and microvessel density (MVD) (P < 0.01). CONCLUSIONS: The high dosage of GQN can significantly inhibit the tumor growth in H22 tumor-bearing mice. It exerts the antitumor effect by enhancing proapoptotic factors and inhibiting the antiapoptotic factor of the mitochondrial apoptosis pathway and inhibiting tumor angiogenesis.