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Striking the right nutrient balance is essential for sustainable farming and ecosystem health. In this regard, field experiments were conducted in three phases viz., fertility gradient experiment, main experiment and validation experiment through a soil test crop response approach to develop and validate fertilizer prescription equations for sweet corn in comparison with general recommended dose and soil fertility rating approach. The soil data, fresh cob yield, and NPK uptake were used for establishing four important basic parameters, viz., nutrient requirement (kg t-1), contribution of nutrients from fertilizers, soil, and organic manure. The results revealed that nutrients required to produce one tonne of fresh cob yield (NR) were 5.85 kg, 0.87 kg and 4.31kg for N, P and K, respectively under the STCR NPK alone approach and 6.07 kg, 0.92 kg and 4.33 kg for N, P and K, respectively under STCR NPK+FYM approach. In the validation experiment, STCR NPK+FYM approach for the targeted yield of 25 t ha−1 recorded higher fresh cob yield (23.38 t ha−1) and dry stover yield (35.07 t ha−1) which were significantly higher compared to general recommended dose and soil fertility rating approach. The developed STCR equations for the aforesaid crop are valid as the percent deviation of cob yield from the targeted yield was within ±10%. Similarly, highest nutrient use efficiency was achieved with the STCR approach, specifically when targeting a lower yield through an NPK+FYM mode. Thus, implementation of the STCR approach of fertilizer prescription, with or without FYM, at targeted yields of 25 and 22 t ha−1, not only surpassed the effects of the other fertilizer recommendation approach in terms of cob yields, but also increased NPK uptake, improved nutrient use efficiency and greater economic returns. [ABSTRACT FROM AUTHOR]

Breast tumor metastasis is a leading cause of cancer-related deaths worldwide. Breast tumor cells frequently metastasize to brain and initiate severe therapeutic complications. The chances of brain metastasis are further elevated in patients with HER2 overexpression. In the current study, we evaluated the anti-metastatic effects of phenethyl isothiocyanate (PEITC) in a novel murine model of breast tumor metastasis. The MDA-MB-231-BR (BR-brain seeking) breast tumor cells stably transfected with luciferase were injected into the left ventricle of mouse heart and the migration of cells to brain was monitored using a non-invasive IVIS bio-luminescent imaging system. In order to study the efficacy of PEITC in preventing the number of tumor cells migrating to brain, mice were given 10 µmol PEITC by oral gavage for ten days prior to intra-cardiac injection of tumor cells labeled with quantum dots. To evaluate the tumor growth suppressive effects, 10 µmol PEITC was given to mice every day starting 14th day after intra-cardiac cell injection. Based on the presence of quantum dots in the brain section of control and treated mice, our results reveal that PEITC significantly prevented the metastasis of breast cancer cells to brain. Our results demonstrate that the growth of metastatic brain tumors in PEITC treated mice was about 50% less than that of control. According to Kaplan Meir’s curve, median survival of tumor bearing mice treated with PEITC was prolonged by 20.5%. Furthermore as compared to controls, we observed reduced HER2, EGFR and VEGF expression in the brain sections of PEITC treated mice. To the best of our knowledge, our study for the first time demonstrates the anti-metastatic effects of PEITC in vivo in a novel breast tumor metastasis model and provides the rationale for further clinical investigation. [ABSTRACT FROM AUTHOR]

Our previous studies have shown that benzyl isothiocyanate (BITC) suppresses pancreatic tumor growth by inhibiting STAT- 3; however, the exact mechanism of tumor growth suppression was not clear. Here we evaluated the effects and mechanism of BITC on pancreatic tumor angiogenesis. Our results reveal that BITC significantly inhibits neovasularization on rat aorta and Chicken-Chorioallantoic membrane. Furthermore, BITC blocks the migration and invasion of BxPC-3 and PanC- 1 pancreatic cancer cells in a dose dependant manner. Moreover, secretion of VEGF and MMP-2 in normoxic and hypoxic BxPC-3 and PanC-1 cells was significantly suppressed by BITC. Both VEGF and MMP-2 play a critical role in angiogenesis and metastasis. Our results reveal that BITC significantly suppresses the phosphorylation of VEGFR-2 (Tyr-1175), and expression of HIF-α. Rho-GTPases, which are regulated by VEGF play a crucial role in pancreatic cancer progression. BITC treatment reduced the expression of RhoC whereas up-regulated the expression of tumor suppressor RhoB. STAT-3 over-expression or IL-6 treatment significantly induced HIF-1α and VEGF expression; however, BITC substantially suppressed STAT-3 as well as STAT-3-induced HIF-1α and VEGF expression. Finally, in vivo tumor growth and matrigel-plug assay show reduced tumor growth and substantial reduction of hemoglobin content in the matrigel plugs and tumors of mice treated orally with 12 mmol BITC, indicating reduced tumor angiogenesis. Immunoblotting of BITC treated tumors show reduced expression of STAT-3 phosphorylation (Tyr-705), HIF-α, VEGFR-2, VEGF, MMP-2, CD31 and RhoC. Taken together, our results suggest that BITC suppresses pancreatic tumor growth by inhibiting tumor angiogenesis through STAT-3-dependant pathway. [ABSTRACT FROM AUTHOR]