Utilization of Water Hyacinth and Banana Wastes Compost in Reclamation of Sandy Soils for Increasing Growth, Yield of Cowpea

Pot experiments were carried out in the greenhouse of the Faculty of Agriculture, Fayoum University, to study the effect of water hyacinth and banana wastes compost (0, 10, 15 and 20 ton/fed) combined with inorganic nitrogenous fertilizers namely ammonium sulphate, ammonium nitrate and urea (in the rate of 60 kg N/Fed and this rate was 50% of the recommended dose), on the growth, yield and nutrient content of cowpea plants. All pots received P and K as recommended. The addition of various rates of water hyacinth and banana wastes composts (H.B.C.) under study significantly increased all plant growth parameters under the study, i.e., plant height, plant fresh weight and dry weight of both shoots and roots, the number of root nodules as well as the nutrient content of the different plant organs compared with the control and the chemical fertilizer application of the recommended dose (100%). There was a marked increase in pod characters, yield and its components, i.e., number of pods per plant, length, diameter and weight of pods per plant. The highest values of growth characters of yield and its components and the contents of nutrient elements were noticed when applying compost at the higher rates (20 ton/fed.) followed by 15 and 10 ton/fed., in a descending order as compared with the control. The best combination of nitrogen forms and the compost is considered to be one of the primary factors for high yield production and quality as well as yield components of cowpea. The highest significant increase in growth characters, yield and yield components, as well as the total carbohydrates and crude protein content of the seeds, were obtained via the application of compost in combination with ammonium sulphate at the rate of 20 ton/fed

Fingolimod Alters Tissue Distribution and Cytokine Production of Human and Murine Innate Lymphoid Cells

Sphingosine-1 phosphate receptor 1 (S1PR1) is expressed by lymphocytes and regulates their egress from secondary lymphoid organs. Innate lymphoid cell (ILC) family has been expanded with the discovery of group 1, 2 and 3 ILCs, namely ILC1, ILC2 and ILC3. ILC3 and ILC1 have remarkable similarity to CD4+ helper T cell lineage members Th17 and Th1, respectively, which are important in the pathology of multiple sclerosis (MS). Whether human ILC subsets express S1PR1 or respond to its ligands have not been studied. In this study, we used peripheral blood/cord blood and tonsil lymphocytes as a source of human ILCs. We show that human ILCs express S1PR1 mRNA and protein and migrate toward S1P receptor ligands. Comparison of peripheral blood ILC numbers between fingolimod-receiving and treatment-free MS patients revealed that, in vivo, ILCs respond to fingolimod, an S1PR1 agonist, resulting in ILC-penia in circulation. Similarly, murine ILCs responded to fingolimod by exiting blood and accumulating in the secondary lymph nodes. Importantly, ex vivo exposure of ILC3 and ILC1 to fingolimod or SEW2871, another S1PR1 antagonist, reduced production of ILC3- and ILC1- associated cytokines GM-CSF, IL-22, IL-17, and IFN-γ, respectively. Surprisingly, despite reduced number of lamina propria-resident ILC3s in the long-term fingolimod-treated mice, ILC3-associated IL-22, IL-17A, GM-CSF and antimicrobial peptides were high in the gut compared to controls, suggesting that its long term use may not compromise mucosal barrier function. To our knowledge, this is the first study to investigate the impact of fingolimod on human ILC subsets in vivo and ex vivo, and provides insight into the impact of long term fingolimod use on ILC populations

Peripheral blood memory B cell frequency predicts conversion from clinically isolated syndrome to multiple sclerosis

Background: Starting from the first attack, activated B cells are found in multiple sclerosis (MS) patients and are associated with disease activity

Flavopiridol Suppresses Cell Proliferation and Migration and Induces Apoptotic Cell Death by Inhibiting Oncogenic FOXM1 Signaling in IDH Wild-Type and IDH-Mutant GBM Cells

Glioblastoma multiforme (GBM) remains one of the most challenging solid cancers to treat due to its highly aggressive and drug-resistant nature. Flavopiridol is synthetic flavone that was recently approved by the FDA for the treatment of acute myeloid leukemia. Flavopiridol exhibits antiproliferative activity in several solid cancer cells and currently evaluated in clinical trials in several solid and hematological cancers. In this study, we investigated the molecular mechanisms underlying antiproliferative effects of flavopiridol in GBM cell lines with wild-type and mutant encoding isocitrate dehydrogenase 1 (IDH1). We found that flavopiridol inhibits proliferation, colony formation, and migration and induces apoptosis in IDH1 wild-type and IDH-mutant cells through inhibition of FOXM1 oncogenic signaling. Furthermore, flavopiridol treatment also inhibits of NF-KB, mediators unfolded protein response (UPR), including, GRP78, PERK and IRE1α, and DNA repair enzyme PARP, which have been shown to be potential therapeutic targets by downregulating FOXM1 in GBM cells. Our findings suggest for the first time that flavopiridol suppresses proliferation, survival, and migration and induces apoptosis in IDH1 wild-type and IDH1-mutant GBM cells by targeting FOXM1 oncogenic signaling which also regulates NF-KB, PARP, and UPR response in GBM cells. Flavopiridol may be a potential novel therapeutic strategy in the treatment of patients IDH1 wild-type and IDH1-mutant GBM