A [(C(18)H(37))(2)N(+)(CH(3))(2)](3)[PW(12)O(40)] catalyst, assembled in an emulsion in diesel, can selectively oxidize the sulfur-containing molecules present in diesel into their corresponding sulfones by using H(2)O(2) as the oxidant under mild conditions. The sulfones can be readily separated from the diesel using an extractant, and the sulfur level of the desulfurized diesel can be lowered from about 500 ppm to 0.1 ppm without changing the properties of the diesel. The catalyst demonstrates high performance (>/=96 % efficiency of H(2)O(2), is easily recycled, and approximately 100 % selectivity to sulfones). Metastable emulsion droplets (water in oil) act like a homogeneous catalyst and are formed when the catalyst (as the surfactant) and H(2)O(2) (30 %) are mixed in the diesel. However, the catalyst can be separated from the diesel after demulsification.

Gastric cancer is the fourth most common cancer and the second leading cause of cancer deaths worldwide. Chemotherapy is one of the major treatments for gastric cancer, but drug resistance limits the effectiveness of chemotherapy, which results in treatment failure. Resistance to chemotherapy can be present intrinsically before the administration of chemotherapy or it can develop during chemotherapy. The mechanisms of chemotherapy resistance in gastric cancer are complex and multifactorial. A variety of factors have been demonstrated to be involved in chemoresistance, including the reduced intracellular concentrations of drugs, alterations in drug targets, the dysregulation of cell survival and death signaling pathways, and interactions between cancer cells and the tumor microenvironment. This review focuses on the molecular mechanisms of chemoresistance in gastric cancer and on recent studies that have sought to overcome the underlying mechanisms of chemoresistance.

Abstract. Drug resistance is a primary cause of chemotherapeutic failure; however, how this resistance develops is complex. A comprehensive understanding of chemotherapeutic resistance mechanisms may aid in identifying more effective drugs and improve the survival rates of patients with cancer. Insulin-like growth factor 1 receptor (IGF1R), a member of the insulin receptor family, has been extensively assessed for biological activity, and its putative contribution to tumor cell development and progression. Furthermore, researchers have attended to drugs that target IGF1R since IGF1R functions as a membrane receptor. However, how IGF1R participates in chemotherapeutic resistance remains unclear. Therefore, the present study described the IGF1R gene and its associated signaling pathways, and offered details of IGF1R-induced tumor chemoresistance associated with promoting cell proliferation, inhibition of apoptosis, regulation of ATP-binding cassette transporter proteins and interactions with the extracellular matrix. The present study offered additional explanations for tumor chemotherapy resistance and provided a theoretical basis of IGF1R and its downstream pathways for future possible chemotherapy treatment options.