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Razia Khan P. Bhawana M. H. Fulekar 《Reviews in Environmental Science and Biotechnology》2013,12(1):75-97
The synthesis of dyes and pigments used in textiles and other industries generate the hazardous wastes. A dye is used to impart color to materials of which it becomes an integral part. The waste generated during the process and operation of the dyes commonly found to contain the inorganic and organic contaminant leading to the hazard to ecosystem and biodiversity causing impact on the environment. The amount of azo dyes concentration present in wastewater varied from lower to higher concentration that lead to color dye effluent causing toxicity to biological ecosystem. The physico-chemical treatment does not remove the color and dye compound concentration. The decolorization of the dye takes place either by adsorption on the microbial biomass or biodegradation by the cells. Bioremediation takes place by anaerobic and/or aerobic process. The anaerobic process converts dye in toxic amino compounds which on further treatment with aerobic reaction convert the intermediate into CO2 biomass and inorganics. In the present review the decolorization and degradation of azo dyes by fungi, algae, yeast and bacteria have been cited along with the anaerobic to aerobic treatment processes. The factors affecting decolorization and biodegradation of azo dye compounds such as pH, temperature, dye concentration, effects of CO2 and Nitrogen, agitation, effect of dye structure, electron donor and enzymes involved in microbial decolorization of azo dyes have been discussed. This paper will have the application for the decolorization and degradation of azo dye compound into environmental friendly compounds. 相似文献
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Ramona Moles Sarkis Sarkis Veronica Galli Maria Omsland Maria Artesi Massimiliano Bissa Katherine McKinnon Sophia Brown Vincent Hahaut Robyn Washington-Parks Joshua Welsh David J. Venzon Anna Gutowska Melvin N. Doster Matthew W. Breed Kristin E. Killoran Joshua Kramer Jennifer Jones Marcin Moniuszko Anne Van den Broeke Cynthia A. Pise-Masison Genoveffa Franchini 《PLoS pathogens》2022,18(4)
We investigated the impact of monocytes, NK cells, and CD8+ T-cells in primary HTLV-1 infection by depleting cell subsets and exposing macaques to either HTLV-1 wild type (HTLV-1WT) or to the HTLV-1p12KO mutant unable to infect replete animals due to a single point mutation in orf-I that inhibits its expression. The orf-I encoded p8/p12 proteins counteract cytotoxic NK and CD8+ T-cells and favor viral DNA persistence in monocytes. Double NK and CD8+ T-cells or CD8 depletion alone accelerated seroconversion in all animals exposed to HTLV-1WT. In contrast, HTLV-1p12KO infectivity was fully restored only when NK cells were also depleted, demonstrating a critical role of NK cells in primary infection. Monocyte/macrophage depletion resulted in accelerated seroconversion in all animals exposed to HTLV-1WT, but antibody titers to the virus were low and not sustained. Seroconversion did not occur in most animals exposed to HTLV-1p12KO. In vitro experiments in human primary monocytes or THP-1 cells comparing HTLV-1WT and HTLV-1p12KO demonstrated that orf-I expression is associated with inhibition of inflammasome activation in primary cells, with increased CD47 “don’t-eat-me” signal surface expression in virus infected cells and decreased monocyte engulfment of infected cells. Collectively, our data demonstrate a critical role for innate NK cells in primary infection and suggest a dual role of monocytes in primary infection. On one hand, orf-I expression increases the chances of viral transmission by sparing infected cells from efferocytosis, and on the other may protect the engulfed infected cells by modulating inflammasome activation. These data also suggest that, once infection is established, the stoichiometry of orf-I expression may contribute to the chronic inflammation observed in HTLV-1 infection by modulating monocyte efferocytosis. 相似文献
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BACKGROUND: There are only rare case reports of preoperative fine needle aspiration cytologic (FNAC) diagnosis of myoepithelioma of the salivary gland. Myoepitheliomas with pure spindle cell morphology may simulate a variety of benign or malignant spindle cell soft tissue tumors. CASE: A 54-year-old woman presented with a history of progressively increasing swelling in the right parotid region. The clinical diagnosis was parotid malignancy. Routine FNAC yielded highly particulate material. The smears were cellular, with tissue fragments, clusters of spindle cells and numerous small globules and strands of bright magenta material. High cellular yield and pure spindle cell population with an accentuated chromatin pattern in Papanicolaou-stained smears simulated a low-grade spindle cell soft tissue sarcoma. A vague resemblance to a schwannoma was also noted. However, based on the characteristic findings of the May-Grünwald-Giemsa (MGG)-stained smears, a preoperative diagnosis of myoepithelioma was made and confirmed by subsequent histopathologic examination and immunohistochemistry. CONCLUSION: Cytologically, spindle cell myoepithelioma of the salivary gland may simulate low-grade spindle cell soft tissue sarcoma or schwannoma. However, optimal sampling of the lesion and logical interpretation of the MGG-stained smears, in the appropriate clinical situation, allow a confident preoperative diagnosis of these tumors. 相似文献
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Poudel B Bilbao D Sarathchandra P Germack R Rosenthal N Santini MP 《Biochemical and biophysical research communications》2011,416(3-4):293-299
The mechanism implicated in differentiation of endogenous cardiac stem cells into cardiomyocytes to regenerate the heart tissue upon an insult remains elusive, limiting the therapeutical goals to exogenous cell injection and/or gene therapy. We have shown previously that cardiac specific overexpression of the insulin-like growth factor 1 propeptide IGF-1Ea induces beneficial myocardial repair after infarct. Although the mechanism is still under investigation, the possibility that this propeptide may be involved in promoting stem cell differentiation into the cardiac lineage has yet to be explored. To investigate whether IGF-1Ea promote cardiogenesis, we initially modified P19 embryonal carcinoma cells to express IGF-1Ea. Taking advantage of their cardiomyogenic nature, we analyzed whether overexpression of this propeptide affected cardiac differentiation program. The data herein presented showed for the first time that constitutively overexpressed IGF-1Ea increased cardiogenic differentiation program in both undifferentiated and DMSO-differentiated cells. In details, IGF-1Ea overexpression promoted localization of alpha-actinin in finely organized sarcomeric structure compared to control cells and upregulated the cardiac mesodermal marker NKX-2.5 and the ventricular structural protein MLC2v. Furthermore, activated IGF-1 signaling promoted cardiac mesodermal induction in undifferentiated cells independently of cell proliferation. This analysis suggests that IGF-1Ea may be a good candidate to improve both in vitro production of cardiomyocytes from pluripotent stem cells and in vivo activation of the differentiation program of cardiac progenitor cells. 相似文献
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Neeraj Jain Jun Hou Tan Shijin Feng Bhawana George Thirumaran Thanabalu 《Journal of biomedical science》2014,21(1)
Background
Mutation in the Wiskott-Aldrich syndrome Protein (WASP) causes Wiskott-Aldrich syndrome (WAS), X-linked thrombocytopenia (XLT) and X-linked congenital neutropenia (XLN). The majority of missense mutations causing WAS and XLT are found in the WH1 (WASP Homology) domain of WASP, known to mediate interaction with WIP (WASP Interacting Protein) and CIB1 (Calcium and Integrin Binding).Results
We analyzed two WASP missense mutants (L46P and A47D) causing XLT for their effects on T cell chemotaxis. Both mutants, WASPRL46P and WASPRA47D (S1-WASP shRNA resistant) expressed well in JurkatWASP-KD T cells (WASP knockdown), however expression of these two mutants did not rescue the chemotaxis defect of JurkatWASP-KD T cells towards SDF-1α. In addition JurkatWASP-KD T cells expressing these two WASP mutants were found to be defective in T cell polarization when stimulated with SDF-1α. WASP exists in a closed conformation in the presence of WIP, however both the mutants (WASPRL46P and WASPRA47D) were found to be in an open conformation as determined in the bi-molecular complementation assay. WASP protein undergoes proteolysis upon phosphorylation and this turnover of WASP is critical for T cell migration. Both the WASP mutants were found to be stable and have reduced tyrosine phosphorylation after stimulation with SDF-1α.Conclusion
Thus our data suggest that missense mutations WASPRL46P or WASPRA47D affect the activity of WASP in T cell chemotaxis probably by affecting the turnover of the protein.Electronic supplementary material
The online version of this article (doi:10.1186/s12929-014-0091-1) contains supplementary material, which is available to authorized users. 相似文献8.
Bhawana George Neeraj Jain Pei Fen Chong Jun Hou Tan Thirumaran Thanabalu 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》2014
Skeletal muscle formation is a multistep process involving proliferation, differentiation, alignment and fusion of myoblasts to form myotubes which fuse with additional myoblast to form myofibers. Toca-1 (Transducer of Cdc42-dependent actin assembly), is an adaptor protein which activates N-WASP in conjunction with Cdc42 to facilitate membrane invagination, endocytosis and actin cytoskeleton remodeling. Expression of Toca-1 in mouse primary myoblasts and C2C12 myoblasts was up-regulated on day 1 of differentiation and subsequently down-regulated during differentiation. Knocking down Toca-1 expression in C2C12 cells (Toca-1KD cells) resulted in a significant decrease in myotube formation and expression of shRNA-resistant Toca-1 in Toca-1KD cells rescued the myogenic defect, suggesting that the knockdown was specific and Toca-1 is essential for myotube formation. Toca-1KD cells exhibited elongated spindle-like morphology, expressed myogenic markers (MyoD and MyHC) and localized N-Cadherin at cell periphery similar to control cells suggesting that Toca-1 is not essential for morphological changes or expression of proteins critical for differentiation. Toca-1KD cells displayed prominent actin fibers suggesting a defect in actin cytoskeleton turnover necessary for cell–cell fusion. Toca-1KD cells migrated faster than control cells and had a reduced number of vinculin patches similar to N-WASPKO MEF cells. Transfection of N-WASP-expressing plasmid into Toca-1KD cells restored myotube formation of Toca-1KD cells. Thus, our results suggest that Toca-1KD cells have defects in formation of myotubes probably due to reduced activity of actin cytoskeleton regulators such as N-WASP. This is the first study to identify and characterize the role of Toca-1 in myogenesis. 相似文献
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