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An operationally simple and green protocol using a NiSO4·6H2O/cationic 2,2′-bipyridyl ligand system as a water-soluble catalyst for the coupling of arylboronic acids with (2-haloallyl)phosphonates and (2-haloallyl)sulfones in water under air was developed. The reaction was performed at 120 °C with arylboronic acids (2 mmol) and (2-haloallyl)phosphonates or sulfones (1 mmol) in the presence of 5 mol % of the Ni catalytic system in a basic aqueous solution for 1 h, giving the corresponding 2-aryl allyl phosphonates or sulfones in good to excellent yields. This reaction features the use of an abundant transition metal as a catalyst in water and exhibits high functional group tolerance, rendering it an eco-friendly procedure.

Therapeutic use of Chinese herbal medicines (CHMs) is a new approach to treat neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. The detection of soma volume and neurite outgrowth of living neurons is a highly relevant biomarker related to various application fields, including therapy efficacy and drug safety evaluation. Through the use of digital holographic microscopy (DHM), we may evaluate the therapeutic effect of CHMs in curing neurodegeneration. Panax ginseng has been used in traditional Chinese herbal medicine for centuries. In this study, DHM is applied to monitor the three-dimensional morphology change of retinoic acid-induced human neuroblastoma SH-SY5Y cells during Panax ginseng treatment. We demonstrate the capability of DHM to detect noninvasively SH-SY5Y cell apoptosis and rescue through the measurement of neuronal volume and neurite outgrowth regulation without any labeling reagent. Through DHM, we observed the phase images of the rapidly shrinking cells with decreasing soma volume and shortening neurite outgrowth during glutamate treatments. Then shrinkage in glutamate-induced cells is significantly alleviated during Panax ginseng treatment. The results through DHM are consistent with the result from MTT assay for assessing cell viability during Panax ginseng treatment. Thus, we suggest that application of DHM for measuring soma volume and neurite outgrowth of living neurons may be one appropriate therapeutic evaluation for CHMs.

Betel quid (BQ) chewing, a popular habit in numerous Asian countries including India and Taiwan, has a strong correlation with an increased risk of oral squamous cell carcinoma (OSCC). While substantial efforts have been made to test the cytotoxic, genotoxic and mutagenic effects of BQ extract and its components, the disease mechanisms underlying BQ-induced oral carcinogenesis remain obscure. Here, we show that a neuronal protein, microtubule-associated protein 2 (MAP2), was induced by BQ extract in cultured normal human oral keratinocytes (NHOKs). Subsequent analyses demonstrated that such induction was more eminent and consistent in the high-molecular-weight isoform of MAP2 (hmw-MAP2) than that in its low-molecular-weight counterpart (lmw-MAP2). Furthermore, we analyzed expression of hmw-MAP2 protein in 88 oral specimens consisting of clinicopathologically pre-malignant (leukoplakia) and malignant (OSCC) lesions, along with their adjacent normal mucosa. Immunohistochemistry revealed that, with the exposure to BQ, the hmw-MAP2 was over-expressed in 41.2% (7/17) of OSCC, 11.2% (1/9) of leukoplakia and none (0/19) of normal mucosa. In contrast, expression of the hmw-MAP2 was barely detected in BQ-free OSCC. These results suggest a significant correlation between expression of the hmw-MAP2 and BQ-associated progression of oral carcinogenesis (P = 0.0046). Interestingly, the hmw-MAP2 was found to preferentially express in histopathologically less differentiated OSCC (P = 0.014); the percentages of positive staining in poorly, moderately and well differentiated OSCC were 62.5, 21.4 and 7.1%, respectively. However, BQ chewing appeared to have marginal correlation with such propensity. Finally, we show that the majority of hmw-MAP2-positive poorly differentiated lesions were also histopathologically invasive. Taken together, these findings suggest the possibility that the hmw-MAP2 may be a diagnostic marker for BQ-chewing lesions and a potential therapeutic target. To our knowledge, this study has provided the first clinical implication that closely links a cytoskeletal protein to BQ-associated oral cancer.

Latent membrane protein 1 (LMP‐1) is the only Epstein‐Barr virus (EBV)‐encoded oncogenic protein that has been detected in nasopharyngeal carcinoma (NPC), a cancer that is closely associated with EBV. Previous in‐vitrostudies have demonstrated that LMP‐1 can upregulate epidermal growth factor receptor (EGFR) in epithelial cells. It was not established whether this cellular effect exists in NPC. To assess the association between LMP‐1 and EGFR in NPC tissues, 60 NPC specimens were examined by immunohistochemistry using anti‐LMP‐1 antibody (CS 1–4) and anti‐EGFR antibodies (EGFR 1, EGFR 1005). The results revealed that 41 (68.3%) specimens were immunopositive for LMP‐1 and 44 (73.3%) specimens over‐expressed EGFR. Morphologically, the expressions of LMP‐1 and EGFR were homogeneously distributed in the tumor nests. In addition, the correlation between LMP‐1 and EGFR was statistically significant (P<0.001, χ2test, d.f.=1). To elucidate further the correlation between LMP‐1 and EGFR in vivoand in situ, an indirect dual immunofluorescence assay was conducted, using secondary antibodies conjugated with fluorescein isothiocyanate (FITC) or indocarbocyanine (Cy3). The results disclosed an intimate co‐expression of LMP‐1 and EGFR. In summary, the data indicate that over‐expression of EGFR is a common phenomenon in NPC, and that EGFR is co‐expressed with LMP‐1 in NPC. Thus, EBV may play a role in the tumorigenesis of NPC through the effects of LMP‐1 and EGFR.