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05). The objective of the present study was to determine the susceptibility of entomopathogenic nematodes to ivermectin and thiabendazole. Soil samples collected from the municipalities of Irapuato and León, Guanajuato, Mexico, were obtained, from which the entomopathogenic nematodes (EPNs) of the Steinernematidae and Heterorhabditidae families were isolated. The samples were classified from livestock and nonlivestock soils, and the susceptibility of EPNs to anthelmintics was determined with the larval motility assay (LMA, 24 h) and the larval migration inhibition assay (LMI assay, 48 h). Sterile distilled water (T1) and treatments with 1% ivermectin diluted in 5% DMSO (dimethyl sulfoxide) (T2) and 5% thiabendazole diluted in 5% DMSO (T3) were applied to infective juvenile larvae. Analysis of variance was performed with a factorial design and Tukey's test at 0.05 probability. In addition, different concentrations of ivermectin (0.1, 0.5, 1, 1.2, 1.5, and 2 μg) and thiabendazole (1, 5, 10, 12, 15, and 20 mg) were evaluated to perform a Probit analysis to determine their LC50. All strains of EPNs were susceptible to ivermectin in both the LMA and LMI assay. The results show that EPNs are susceptible to ivermectin and thiabendazole, and the degree depends on the type of test performed, the chemical product used, and the origin of the strain of EPN. Decreased chemosensitivity among tumor cells is often an obstacle in cisplatin (Cis) chemotherapy. Overexpression of multidrug resistance-associated protein 2 (MRP2) is a key mechanism underlying decreased Cis chemosensitivity and resistance. Astragaloside IV (AS IV) is an important component derived from the well-known traditional Chinese herb Astragalus membranaceus. The aim of this study was to explore the role of AS IV in enhancing the antitumor effect of Cis by suppressing MRP2 expression in HepG2 cells and H22 tumor-bearing mice. After co-treatment of HepG2 cells with Cis and AS IV, we assessed the effects on cell proliferation and apoptosis. Tumor growth and apoptosis assessment were performed to assess chemosensitivity in H22 tumor-bearing mice. We used western blotting, immunofluorescence assays, and immunohistochemistry assays to detect MRP2 expression in HepG2 cells, H22 tumor tissues and mouse kidney tissues. AS IV enhanced Cis chemosensitivity by increasing tumor cell apoptosis and slowing tumor growth in vitro and in vivo. MRP2 overexpression in tumor cells was induced by Cis, which contributes to decreased chemosensitivity and Cis resistance. Co-administration of AS IV suppressed MRP2 expression in tumor tissues, which might be an important mechanism for enhancing Cis chemosensitivity in hepatocellular carcinoma. Moreover, AS IV alleviated Cis-induced kidney injury in mice without changing MRP2 expression. In total, AS IV enhanced the antitumor effect of Cis against hepatocellular carcinoma by suppressing MRP2 expression in tumor cells. The results provide a new insight into the combined use of a chemotherapy drug and natural ingredients to treat cancer. To decide whether an active pharmaceutical ingredient can be used in its amorphous form in drug formulations, often the glass transition is studied in relation to the melting point of the pharmaceutical. If the glass transition temperature is high enough and found relatively close to the melting point, the pharmaceutical is considered to be a good glass former. However, it is obviously important that the observed melting point and glass transition involve exactly the same system, otherwise the two temperatures cannot be compared. Although this may seem trivial, in the case of hydrates, where water may leave the system on heating, the composition of the system may not be evident. Atorvastatin calcium is a case in point, where confusing terminology, absence of a proper anhydrate form, and loss of water on heating lead to several doubtful conclusions in the literature. However, considering that no anhydrate crystal has ever been observed and that the glass transition of the anhydrous system is found at 144 °C, it can be concluded that if the system is kept isolated from water, the chances that atorvastatin calcium crystallises at room temperature is negligible. The paper discusses the various thermal effects of atorvastatin calcium on heating and proposes a tentative binary phase diagram with water. Superficial mycoses are the fungal infections of skin, hair and nail which affect thousands of people worldwide. SKF96365 Emerging resistance to azole antifungals is a common problem in the treatment of superficial or systemic fungal infection. Ebselen (EB), an organoselenium compound, has demonstrated promising activity against pathogenic yeasts. EB showed negligible dynamic and kinetic solubility in water (~ 4.2 µg/mL) which severely limits the scope of conventional formulations. The objective of present study was to develop and characterize a novel topical nanoemulgel of EB for enhancing solubility and permeability. Based on saturation solubility study, EB loaded self-nanoemulsifying preconcentrate (EB-P) was prepared using Dimethylacetamide, Kolliphor® ELP and Medium chain triglyceride which spontaneously formed 54.82 ± 1.26 nm size nanoglobules with zeta potential of -1.69 mV. Nanoemulgel was prepared by homogenous dispersion of EB-P in various gel/ointment bases. Scanning electron microscopy images showed significant drug precipitation in nanoemulgels prepared without Soluplus®. Rheological study confirmed shear thinning behavior of Soluplus® based HPMC K4M (SBH) gel. EB-P loaded SBH showed 2.3 and 5-fold higher Strat-M® deposition of EB compared to HPMC gel and Aquaphor®, respectively. EB-P showed marked anti-fungal activity at 20 µM against Candida albicans and Candida tropicalis while terbinafine was ineffective even at 100 µM concentration. Thus, topical nanoemulgel of EB could be a promising alternative to existing therapy for treatment of candidiasis. BACKGROUND Limonin, a bioactive compound from citrus plants, exerts antioxidant activities, however its therapeutic potential in acetaminophen (APAP)-induced hepatotoxicity remains unclear. PURPOSE Our study aims to investigate the protective effect of limonin on APAP-induced hepatotoxicity and illuminate the underlying mechanisms. STUDY design In vitro, we chose L-02 cells to establish in vitro APAP-induced liver injury model. L-02 cells were treated with APAP (7.5 mM) for 24 h after pre-incubation with limonin (10, 25, 50 μM) or NAC (250 μM) for 2 h. In vivo, we used C57BL/6 mice as an in vivo APAP-induced liver injury model. C57BL/6 mice with pre-treatment of limonin (40, 80 mg/kg) or NAC (150 mg/kg) for 1 h, were given with a single dose of APAP (300 mg/kg). METHODS After pre-incubation with limonin (10, 25, 50 μM) for 2 h, L-02 cells were treated with APAP (7.5 mM) for 24 h.The experiments in vitro included MTT assay, Annexin V/PI staining, measurement of reactive oxygen species (ROS), quantitative real-time PCR analysis, Western blot analysis, immunofluorescence microscopy and analysis of LDH activity.
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