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Acid anhydrides have been used to carry out the regioselective acylation of primary hydroxyl group in benzyl 3-hydroxy-2-(hydroxymethyl)-2-methylpropanoate and 4-fluorobenzyl 3-hydroxy-2-(hydroxymethyl)-2-methylpropanoate and deacylation of their diesters in the presence of Lipozyme ® TL IM in diisopropyl ether. Amongst different acid anhydrides used, butanoic anhydride was found to be the best acylating agent as compared to others. Both acylation and deacylation reactions were highly selective and efficient yielding exclusively the monoacylated products in 70–88 % yields. Graphical Abstract

The C–C chemokines, macrophage inflammatory protein (MIP)1α and MIP1β are potent chemoattractants for the monocytes, which form an important component of the stroma of tumor tissue and may regulate tumor growth and associated inflammation. We examined the role of MIP1α and MIP1β in inducing the release of inflammatory cytokines and the generation of tumoricidal monocytes from the peripheral blood monocytes (PBM) of healthy women and patients with carcinoma of breast (CaBr). Interleukin-1 (IL-1) and tumor necrosis factor (TNF) α release by the PBM was markedly stimulated by MIP1α in CaBr patients, but only marginally so in healthy women. In contrast, MIP1β stimulated the release of these cytokines by the PBM of healthy women, but failed to do so in CaBr patients. MIP1α, but not MIP1β, synergized with LPS in inducing the release of IL-1 from the PBM of both healthy women and CaBr patients. Both MIP1α and MIP1β augmented respiratory bursts in PBM and generated tumoricidal PBM that killed T24 cells, MIP1α being more effective in CaBr patients and MIP1β in healthy women. IFN-γ co-stimulated and IL-4 suppressed MIP1α and β-induced cytotoxicity in PBM. The synergy of IFN-γ was more marked with MIP1α than with MIP1β. The differential effects of MIP1α and MIP1β on the PBM of healthy women and CaBr patients co-related with the levels of expression of CCR1 and CCR5 in these monocytes. The expression of CCR5 was higher than that of CCR1 in the PBM of healthy women and the PBM of the CaBr patients showed overexpression of CCR1 and downregulation of CCR5.

Novel 3-hydrazino-3-oxo-N-(4-sulfamoylphenyl)propanamide has been efficiently synthesized from DEM and hydrazine hydrate. The synthesized hydrazide was screened for anti-tubercular activity.

3-Hydrazino-3-oxo-N-(4-sulfamoylphenyl)propanamide has been used as a synthon for the preparation of 3-[2-(4-chlorobenzylidene)hydrazino]-3-oxo-N-(4-sulfamoylphenyl)propanamide

Acid anhydrides have been used to carry out the regioselective acylation of primary hydroxyl group in benzyl 3-hydroxy-2-(hydroxymethyl)-2-methylpropanoate and 4-fluorobenzyl 3-hydroxy-2-(hydroxymethyl)-2-methylpropanoate and deacylation of their diesters in the presence of Lipozyme.sup.® TL IM in diisopropyl ether. Amongst different acid anhydrides used, butanoic anhydride was found to be the best acylating agent as compared to others. Both acylation and deacylation reactions were highly selective and efficient yielding exclusively the monoacylated products in 70-88 % yields.

The C-C chemokines, macrophage inflammatory protein (MIP)1α and MIP1β are potent chemoattractants for the monocytes, which form an important component of the stroma of tumor tissue and may regulate tumor growth and associated inflammation. We examined the role of MIP1α and MIP1β in inducing the release of inflammatory cytokines and the generation of tumoricidal monocytes from the peripheral blood monocytes (PBM) of healthy women and patients with carcinoma of breast (CaBr). Interleukin-1 (IL-1) and tumor necrosis factor (TNF) α release by the PBM was markedly stimulated by MIP1α in CaBr patients, but only marginally so in healthy women. In contrast, MIP1β stimulated the release of these cytokines by the PBM of healthy women, but failed to do so in CaBr patients. MIP1α, but not MIP1β, synergized with LPS in inducing the release of IL-1 from the PBM of both healthy women and CaBr patients. Both MIP1α and MIP1β augmented respiratory bursts in PBM and generated tumoricidal PBM that killed T24 cells, MIP1α being more effective in CaBr patients and MIP1β in healthy women. IFN-γ co-stimulated and IL-4 suppressed MIP1α and β-induced cytotoxicity in PBM. The synergy of IFN-γ was more marked with MIP1α than with MIP1β. The differential effects of MIP1α and MIP1β on the PBM of healthy women and CaBr patients co-related with the levels of expression of CCR1 and CCR5 in these monocytes. The expression of CCR5 was higher than that of CCR1 in the PBM of healthy women and the PBM of the CaBr patients showed overexpression of CCR1 and downregulation of CCR5.

The C-C chemokines, macrophage inflammatory protein (MIP)1alpha and MIP1beta are potent chemoattractants for the monocytes, which form an important component of the stroma of tumor tissue and may regulate tumor growth and associated inflammation. We examined the role of MIP1alpha and MIP1beta in inducing the release of inflammatory cytokines and the generation of tumoricidal monocytes from the peripheral blood monocytes (PBM) of healthy women and patients with carcinoma of breast (CaBr). Interleukin-1 (IL-1) and tumor necrosis factor (TNF) alpha release by the PBM was markedly stimulated by MIP1alpha in CaBr patients, but only marginally so in healthy women. In contrast, MIP1beta stimulated the release of these cytokines by the PBM of healthy women, but failed to do so in CaBr patients. MIP1alpha, but not MIP1beta, synergized with LPS in inducing the release of IL-1 from the PBM of both healthy women and CaBr patients. Both MIP1alpha and MIP1beta augmented respiratory bursts in PBM and generated tumoricidal PBM that killed T24 cells, MIP1alpha being more effective in CaBr patients and MIP1beta in healthy women. IFN-gamma co-stimulated and IL-4 suppressed MIP1alpha and beta-induced cytotoxicity in PBM. The synergy of IFN-gamma was more marked with MIP1alpha than with MIP1beta. The differential effects of MIP1alpha and MIP1beta on the PBM of healthy women and CaBr patients co-related with the levels of expression of CCR1 and CCR5 in these monocytes. The expression of CCR5 was higher than that of CCR1 in the PBM of healthy women and the PBM of the CaBr patients showed overexpression of CCR1 and downregulation of CCR5.

Iron (Fe),a micronutrient,plays an important role in agriculture world wideand its smaller amount because a small amount is required for plant growth and development.All major functions in thea plant’s life from chlorophyllbiosynthesisto energy transfer are performed by Fe.Iron also acts as a major constituent of many plant proteins and enzymes. The Acacquisition of Fein plants occurs throughby two strategies i.e. stragegystrategy I and strategy II. Under various stress conditions, Nramp and the YSL gene families help in translocation of Fe,which further actsas amineral regulatory element and defends plants against stresses.Iron plays an irreplaceable role in alleviating stress imposed by salinity,drought, and heavy metal stress. This is because,as it activates plant enzymatic antioxidants like catalase (CAT),peroxidase, andone anisoform of superoxide dismutase (SOD) whichthat act as a scavengers of reactive oxygen species (ROS).In contrast, both its deficiency and excess amount can disturb the homeostasis of the a plant’s cell as a result of via decliningits declining the photosynthetic rate, respiration, and increased accumulation of Na+ and ClCal- ions which ultimately resulted intoculminate in an excessive formation of ROS. The short-range-order hydrated Fe oxides and organic functional groups show affinities for metal ions. Iron plaque biofilm matricesx could sequester a large amount of metals at the soil-root interface.Hence, it has attracted the attentions of plant physiologists and agricultural scientists for who are discovering more exciting and hidden applications of Fe and its potential in the development of bio-factories.This review looks into recent progress made in putting forward the role of Fe in plant growth, development, and acclimation under major abiotic stresses i.e.salinity, drought, and heavy metals.

The present study investigates ameliorative effects of nitric oxide (NO) against zinc oxide nanoparticles (ZnONPs) phytotoxicity in wheat seedlings. ZnONPs exposure hampered growth of wheat seedlings, which coincided with reduced photosynthetic efficiency (F /F and qP), due to increased accumulation of zinc (Zn) in xylem and phloem saps. However, SNP supplementation partially mitigated the ZnONPs-mediated toxicity through the modulation of photosynthetic activity and Zn accumulation in xylem and phloem saps. Further, the results reveal that ZnONPs treatments enhanced levels of hydrogen peroxide and lipid peroxidation (as malondialdehyde; MDA) due to severely inhibited activities of the following ascorbate-glutatione cycle (AsA-GSH) enzymes: ascorbate peroxidase, glutathione reductase, monodehydroascorbate reductase and dehydroascorbate reductase, and its associated metabolites ascorbate and glutathione. In contrast to this, the addition of SNP together with ZnONPs maintained the cellular functioning of the AsA-GSH cycle properly, hence lesser damage was noticed in comparison to ZnONPs treatments alone. The protective effect of SNP against ZnONPs toxicity on fresh weight (growth) can be reversed by 2-(4carboxy-2-phenyl)-4,4,5,5-tetramethyl- imidazoline-1-oxyl-3-oxide, a NO scavenger, and thus suggesting that NO released from SNP ameliorates ZnONPs toxicity. Overall, the results of the present study have shown the role of NO in the reducing of ZnONPs toxicity through the regulation of accumulation of Zn as well as the functioning of the AsA-GSH cycle.

Heavy metal (HMs) pollution is regarded as one of the major concerns for soil and water, causing varieties of toxic and stress effects on plants and ecosystems. It has become one of the important limiting factors to crop productivity and quality. Due to an ever-increasing population growth and food demands, this situation has further worsened. Rice, a leading staple food crop that feeds more than 50% populations of the world, is constantly affected by abiotic stressors including HMs. In most of the countries, a major source of HM intake by humans is the rice grain produced through the paddy soils contaminated with HMs such as As, Al, Cu, Cr, Cd, Pb, Hg, Mn, Se, and Zn. Thus, gradual agglomeration of HMs in rice grains and their subsequent transfer to the food chain is a major menace to agriculture and human health. In recent years, several studies examined the impact of HMs toxicity on rice at multiple levels: molecular, biochemical, physiological, cellular and tissue, and demonstrated a correlation between HMs toxicity and the decreasing trend in rice productivity. Therefore, it is necessary to understand the interaction of HMs with rice crop spanning from the cell to whole plant level and devise appropriate effective means to alleviate these stress responses. This review focuses on tracing the pathways involved in stress responses and stress tolerance mechanisms displayed by different varieties of rice. However, it is essential to uncover the mechanisms related to stress responses in rice for designing improved investigations to develop novel varieties with high attributes. Therefore, this communication summarizes various defense strategies induced against HM stress and includes the function of metabolites (metabolomics), trace elements (ionomics), transcription factors (transcriptomics), and various stress-inducible proteins (proteomics) including the role of plant hormones.