Response of tomato to fertilizer nutrients integration and herbicides spray: Evaluating growth, yield, fruit quality and herbicides residue

The interaction between fertilizer nutrients and pesticides and their impact on tomato production and quality has been insufficiently studied in tropical agricultural conditions. This research investigated four fertilizer nutrient management (FNM) approaches: major nutrients (NPK), micronutrients, farmyard manure (FYM) and traditional farmer practices (FP), alongside three herbicides—glyphosate, pendimethalin and metribuzin applied using seven methods. Results highlighted the substantial influence of FNM strategies and herbicide applications on tomato growth and yield parameters such as plant height, cluster count, fruits per plant, fruit number and yield per plant. Notably, the NPK+FYM strategy consistently yielded superior results across herbicides and application methods. Individually applied herbicides, particularly glyphosate, exhibited detrimental effects on growth and yield parameters, and the negative impact was conspicuously higher with glyphosate > metribuzin > pendimethalin than with their sequential or combined application. While herbicides decreased tomato yield across FNM practices, the reduction ranged from 1.90–10.95%, 1.79–6.75%, 1.62–6.49% and 1.40–9.10% in NPK, NPK+MN, NPK+FYM and FP treatments, respectively. Fruit quality remained unaffected by FNM practices and herbicides, except for elevated ascorbic acid content and shelf life under NPK+FYM. Herbicide residues in tomato fruits were within permissible limits (below 0.1 mg/kg for glyphosate and 0.05 mg/kg for pendimethalin and metribuzin) across treatments. This study showed that the NPK+FYM practice is the best strategy for increasing the tomato yield and quality parameters besides reducing the herbicide’s toxicity effect on tomato growth at an early stage

FYN is overexpressed in human prostate cancer

To test the hypothesis that FYN , a member of the SRC family of kinases (SFKs), is up-regulated in prostate cancer, as FYN is functionally distinct from other SFKs, and interacts with FAK and paxillin (PXN), regulators of cell morphology and motility. MATERIALS AND METHODS Through data-mining in Oncomine ( http://www.oncomine.org ), cell-line profiling with immunoblotting, quantitative reverse transcription and polymerase chain reaction (RT-PCR) and immunohistochemical analysis, we described FYN expression in prostate cancer. The analysis included 32 cases of prostate cancer, nine of prostatic intraepithelial neoplasia (PIN) and 19 normal prostates. Samples were scored for the percentage of stained glands and intensity of staining (from 0 to 3). Each sample was assigned a composite score generated by multiplying percentage and intensity. RESULTS Data-mining showed an eight times greater FYN expression in prostate cancer than in normal tissue; this was specific to FYN and not present for other SFKs. Expression of FYN in prostate cancer cell lines (LNCaP, 22Rv1, PC3, DuPro) was detected using quantitative RT-PCR and immunoblotting. Expression of FYN and its signalling partners FAK and PXN was detected in human tissue. Comparing normal with cancer samples, there was a 2.1-fold increase in median composite score for FYN ( P  < 0.001) 1.7-fold increase in FAK ( P  < 0.001), and a doubling in PXN ( P  < 0.05). There was a 1.7-fold increase in FYN ( P  < 0.05) and a 1.6-fold increase in FAK ( P  < 0.01) in cancer compared with PIN. CONCLUSIONS These studies support the hypothesis that FYN and its related signalling partners are up-regulated in prostate cancer, and support further investigation into the role of the FYN as a therapeutic target.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71987/1/j.1464-410X.2008.08009.x.pd

All-Trans Retinoic Acid Induces TGF-β2 in Intestinal Epithelial Cells via RhoA- and p38α MAPK-Mediated Activation of the Transcription Factor ATF2.

We have shown previously that preterm infants are at risk of necrotizing enterocolitis (NEC), an inflammatory bowel necrosis typically seen in infants born prior to 32 weeks' gestation, because of the developmental deficiency of transforming growth factor (TGF)-β2 in the intestine. The present study was designed to investigate all-trans retinoic acid (atRA) as an inducer of TGF-β2 in intestinal epithelial cells (IECs) and to elucidate the involved signaling mechanisms.AtRA effects on intestinal epithelium were investigated using IEC6 cells. TGF-β2 expression was measured using reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR) and Western blots. Signaling pathways were investigated using Western blots, transiently-transfected/transduced cells, kinase arrays, chromatin immunoprecipitation, and selective small molecule inhibitors.AtRA-treatment of IEC6 cells selectively increased TGF-β2 mRNA and protein expression in a time- and dose-dependent fashion, and increased the activity of the TGF-β2 promoter. AtRA effects were mediated via RhoA GTPase, Rho-associated, coiled-coil-containing protein kinase 1 (ROCK1), p38α MAPK, and activating transcription factor (ATF)-2. AtRA increased phospho-ATF2 binding to the TGF-β2 promoter and increased histone H2B acetylation in the TGF-β2 nucleosome, which is typically associated with transcriptional activation.AtRA induces TGF-β2 expression in IECs via RhoA- and p38α MAPK-mediated activation of the transcription factor ATF2. Further studies are needed to investigate the role of atRA as a protective/therapeutic agent in gut mucosal inflammation