This study was conducted to determine the optimum extraction conditions for the effective separation and removal of Cu(2+), Fe(2+), and Fe(3+) using N-benzoyl-n-phenylhydroxylamine (BPA) as an analytical reagent. An efficient liquid-liquid extraction method was developed for the separation and removal of Cu(2+), Fe(2+), and Fe(3+) from environmental waste samples. In this method, BPA was used as a chelating agent and the effect of different parameters- including solvents, pH, stripping agents, extraction time, and the interference of other ions- on the quantitative removal of these metals was investigated. This study demonstrates that chloroform is the most effective solvent for BPA. The maximum extraction of the selected metallic species was found between pH 3 and 5. It was demonstrated that the maximum percentage recovery of the metals can be attained using 1?M HCl as a stripping agent. Optimized conditions of different parameters could be beneficial for industry and environmental laboratories.
Hydrous bismuth oxides (HBOs) have been investigated as a possible adsorbent for fluoride removal from water. Apart from bismuth trioxide (Bi2O3) compound, three additional HBOs, named as HBO1, HBO2, and HBO3 were synthesized in the laboratory and examined for their relative potentials for fluoride removal from aqueous solutions. HBO1 was observed to have highest fluoride removal at 10mg/L initial concentration in aqueous environment. Among competitive anions, sulfate and chloride affect the fluoride removal by HBO1 more adversely than bicarbonate. Characterization of HBOs using X-ray diffraction (XRD) pattern analyses indicated crystalline structures, and the broad chemical composition of materials showed successive increase of Bi(OH)3 from HBO1 to HBO3, with decrease of BiOCl in the same order. Fourier Transform Infrared (FTIR) spectroscopy analyses indicated presence of Bi-O bond and successively increasing number of peaks corresponding to OH ion from HBO1 to HBO3. Scanning Electron Microscopic (SEM) images of HBOs show rough and porous structure of the materials. Presence of higher proportion of chloride compound in HBO1 with respect to others appears to be the factor responsible for its better performance in fluoride removal from aqueous solutions.
We have recently isolated novel IFN-inducible gene, Gene associated with Retinoid-Interferon-induced Mortality-1 (GRIM-1), using a genetic technique. Moderate ectopic expression of GRIM-1 caused growth inhibition and sensitized cells to retinoic acid (RA)/IFN-induced cell death while high expression caused apoptosis. GRIM-1 depletion, using RNAi, conferred a growth advantage. Three protein isoforms (1?, 1? and 1?) with identical C-termini are produced from GRIM-1 mRNA. We show that GRIM-1 isoforms interact with NAF1 and DKC1, two essential proteins required for box H/ACA sno/sca RNP biogenesis and suppresses box H/ACA RNA levels in mammalian cells by delocalizing NAF1. Suppression of these small RNAs manifests as inefficient rRNA maturation and growth suppression. Interestingly, yeast Shq1p also caused growth suppression in mammalian cells. Consistent with its growth-suppressive property, GRIM-1 expression is lost in a number of human primary prostate tumors. Our observations support a recent study that GRIM-1 might act as a co-tumor suppressor in the prostate.
Protective immune responses during Mycobacterium tuberculosis (M. tuberculosis) infection are regulated at multiple levels and critically dependent on the balance in the secretion of pro-inflammatory and regulatory cytokines. A key factor that governs this balance at the cellular level is suppressors of cytokine signaling (SOCS). We recently demonstrated that toll-like receptor 2 and dendritic cell (DC)-SIGNR1 differentially regulate SOCS1 expression in DCs during M. tuberculosis infection. This consecutively regulated IL-12 production and determined M. tuberculosis survival. In this study, we characterized the role of SOCS1 in regulating effector responses from CD4(+) and CD8(+) T cells during M. tuberculosis infection. Our data indicate that T cells from M. tuberculosis-infected mice show increased and differential association of SOCS1 with CD3 and CD28, when compared with uninfected mice. While SOCS1 displays increased association with CD3 than CD28 in CD4(+) T cells; SOCS1 is associated more with CD28 than CD3 in CD8(+) T cells. Further, SOCS1 shows increased association with IL-12 and IL-2 receptors in both CD4(+) and CD8(+) T cells from infected mice when compared with naive mice. Silencing SOCS1 in T cells increased signal transduction from T cell receptor (TCR) and CD28 with enhanced activation of key signaling molecules and proliferation. Significantly, SOCS1-silenced T cells mediated enhanced clearance of M. tuberculosis inside macrophages. Finally, adoptive transfer of SOCS1-silenced T cells in M. tuberculosis-infected mice mediated significant reduction in M. tuberculosis loads in spleen. These results exemplify the negative role played by SOCS1 during T cell priming and effector functions during M. tuberculosis infection.
A hallmark of protective immunity during Mycobacterium tuberculosis (M. tb) infection is the regulated secretion of pro-inflammatory and regulatory cytokines. Suppressors of Cytokine Signaling (SOCS) are key regulators of cytokine secretion and function. In this study we investigated regulation of Toll-like receptor 2 (TLR2) and dendritic cell-specific ICAM-3 grabbing non-integrin receptor 1 (DC-SIGNR1)-mediated SOCS1 expression in DCs during M. tb infection. We show that, compared with TLR2, stimulating DC-SIGNR1 on DCs induces higher SOCS1 expression and lower interleukin-12 production. Co-stimulating DC-SIGNR1 and TLR2 differentially regulates SOCS1 expression depending on the relative concentration of their ligands. Stimulating DC-SIGNR1 with M. tb infection increases SOCS1 expression, while stimulating TLR2 with M. tb infection reduces SOCS1 expression. Knockdown of SOCS1 in DCs by siRNA enhances interleukin-12 transcription and protein expression upon DC-SIGNR1 stimulation. Raf-1 and Syk differentially regulate TLR2- and DC-SIGNR1-mediated SOCS1 expression. In addition, DC-SIGNR1 shows greater association with SOCS1 when compared with TLR2. Interestingly, compared with healthy asymptomatic individuals, peripheral blood mononuclear cells of patients with active tuberculosis disease showed higher expression of SOCS1, which was reduced following chemotherapy. Similarly, stimulating DC-SIGNR1 on DCs from M. tb-infected TLR2(-/-) mice enhanced SOCS1 expression that was reduced following chemotherapy. Further, knockdown of SOCS1 in mouse DCs or human peripheral blood mononuclear cells resulted in increased killing of virulent M. tb. These results indicate that TLR2 and DC-SIGNR1 differentially regulate SOCS1 expression during M. tb infection. This in turn regulates M. tb survival by governing key cytokine expression.
Mycobacterium tuberculosis modulates levels and activity of key intracellular second messengers to evade protective immune responses. Calcium release from voltage gated calcium channels (VGCC) regulates immune responses to pathogens. In this study, we investigated the roles of VGCC in regulating protective immunity to mycobacteria in vitro and in vivo. Inhibiting L-type or R-type VGCC in dendritic cells (DCs) either using antibodies or by siRNA increased calcium influx in an inositol 1,4,5-phosphate and calcium release calcium activated channel dependent mechanism that resulted in increased expression of genes favoring pro-inflammatory responses. Further, VGCC-blocked DCs activated T cells that in turn mediated killing of M. tuberculosis inside macrophages. Likewise, inhibiting VGCC in infected macrophages and PBMCs induced calcium influx, upregulated the expression of pro-inflammatory genes and resulted in enhanced killing of intracellular M. tuberculosis. Importantly, compared to healthy controls, PBMCs of tuberculosis patients expressed higher levels of both VGCC, which were significantly reduced following chemotherapy. Finally, blocking VGCC in vivo in M. tuberculosis infected mice using specific antibodies increased intracellular calcium and significantly reduced bacterial loads. These results indicate that L-type and R-type VGCC play a negative role in M. tuberculosis infection by regulating calcium mobilization in cells that determine protective immunity.
This paper highlights the utility of riverbed sand (RS) for the treatment of Ni(II) from aqueous solutions. For enhancement of removal efficiency, RS was modified by simple methods. Raw and modified sands were characterized by scanning electron microscope (SEM), Energy Dispersive Spectroscopy (EDS), and Fourier Transform Infrared Spectroscopy (FTIR) to investigate the effect of modifying the surface of RS. For optimization of various important process parameters, batch mode experiments were conducted by choosing specific parameters such as pH (4.0-8.0), adsorbent dose (1.0-2.0 g), and metal ion concentrations (5-15 mg/L). Removal efficiency decreased from 68.76 to 54.09 % by increasing the concentration of Ni(II) in solution from 5 to 15 mg/L. Removal was found to be highly dependent on pH of aqueous solutions and maximum removal was achieved at pH 8.0. The process of removal follows first-order kinetics, and the value of rate constant was found to be 0.048 min(-1) at 5 mg/L and 25 °C. Value of intraparticle diffusion rate constant (k(id)) was found to be 0.021 mg/g min(1/2) at 25 °C. Removal of Ni(II) decreased by increasing temperature which confirms exothermic nature of this system. For equilibrium studies, adsorption data was analyzed by Freundlich and Langmuir models. Thermodynamic studies for the present process were performed by determining the values of ?G°, ?H°, and ?S°. Negative value of ?H° further confirms the exothermic nature of the removal process. The results of the present investigation indicate that modified riverbed sand (MRS) has high potential for the removal of Ni(II) from aqueous solutions, and resultant data can serve as baseline data for designing treatment plants at industrial scale.
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