Connectedness of Kronecker sum and partial Kronecker row sum of designs

In this paper we discuss connectedness of a design which is a Kronecker sum or a partial Kronecker row sum of any two equi-replicate and equi-block size designs.Kronecker sum partial Kronecker sum connectedness balanced designs

Stability studies of cuticle degrading and mycolytic enzymes of <em>Myrothecium verrucaria</em> for control of insect pests and fungal phytopathogens

404-412Myrothecium verrucaria produced extracellularly hydrolytic enzymes which can hydrolyse the insect cuticle as well as fungal cell wall. The addition of polyols, such as glycerol, sorbitol, xylitol (1 M) during ultra-filtration or freeze- drying of enzyme mixture increased the recovery of the enzymes in a concentrated form. Polyols (5 M) increased the temperature and pH stability of the enzymes, in the presence of glycerol chitinase , β-1,3-glucanase, lipase and protease retained 50-60% of initial activities at 40°C after 3 h. While xylitol (5 M) was effective in stabilizing activities at pH 5.0 and 7.5 at 25°C for 7 d. In the freeze-dried powder form, > 90% at 4°C for 1 year and 80-85% at 25°C for 2 months enzyme activities were retained. The addition of glycerol (1 M) to the enzyme mixture protected enzyme activities under sunlight (60-65% activity at RT) for 5 d. Because of glycerol (1 M), the efficacy of M. verrucaria enzyme preparation to control Helicoverpa armigera infestation in chick pea was increased to 70 ± 19%. While without glycerol the efficacy was 55 ± 23%. The germination of peanut seeds infected with Sclerotium rolfsii was observed to be increased (70 ± 5%) in a pot irrigated with enzyme mixture

Quinomycin A targets Notch signaling pathway in pancreatic cancer stem cells

Cancer stem cells (CSCs) appear to explain many aspects of the neoplastic evolution of tumors and likely account for enhanced therapeutic resistance following treatment. Dysregulated Notch signaling, which affects CSCs plays an important role in pancreatic cancer progression. We have determined the ability of Quinomycin to inhibit CSCs and the Notch signaling pathway. Quinomycin treatment resulted in significant inhibition of proliferation and colony formation in pancreatic cancer cell lines, but not in normal pancreatic epithelial cells. Moreover, Quinomycin affected pancreatosphere formation. The compound also decreased the expression of CSC marker proteins DCLK1, CD44, CD24 and EPCAM. In addition, flow cytometry studies demonstrated that Quinomycin reduced the number of DCLK1+ cells. Furthermore, levels of Notch 1-4 receptors, their ligands Jagged1, Jagged2, DLL1, DLL3, DLL4 and the downstream target protein Hes-1 were reduced. The γ-secretase complex proteins, Presenilin 1, Nicastrin, Pen2, and APH-1, required for Notch activation also exhibited decreased expression. Ectopic expression of the Notch Intracellular Domain (NICD) partially rescued the cells from Quinomycin mediated growth suppression. To determine the effect of Quinomycin on tumor growth in vivo, nude mice carrying tumor xenografts were administered Quinomycin intraperitoneally every day for 21 days. Treatment with the compound significantly inhibited tumor xenograft growth, coupled with significant reduction in the expression of CSC markers and Notch signaling proteins. Together, these data suggest that Quinomycin is a potent inhibitor of pancreatic cancer that targets the stem cells by inhibiting Notch signaling proteins