110 research outputs found
Evaluation of Surfactant-Enhanced Cleaning Solutions for Humic Acid and BSA Fouling on Ceramic Membranes
Get PDFChemically enhanced backwash (CEB) has achieved extensive application, offering substantial improvements in fouling mitigation and enhancing membrane performance and longevity. Two commercially available non-ionic surfactants, Tween 80 and Triton X100, were employed at their CMC and combined with conventional cleaning solutions to evaluate NOM fouling and cleaning at different concentrations, utilizing membrane permeability, resistance in series (RIS), carbon mass balance, and contact angle. The use of surfactants in CEB dropped the contact angle by 20%. The transmembrane pressure (TMP) with Tween 80 and Triton X-100 based CEB solutions were in the range of 83-100 kPa and 88-95 kPa with the medium concentrations (CEBMTw & CEBMTx) compared to DI which was 128 kPa for HA and BSA. Tween-based CEBs exhibited a 50% reduction in fouling resistance on HA and 90% on BSA when medium and high concentrations (CEBMTw and CEBHTw) were employed, in comparison to hydraulic (DI) backwash
Anaerobic digestion enhancement with microbial electrolysis cells: is biomethane production the direction to go for commercialization?
Get PDFThe engineering of replacements for crude oil is a priority within industrial biotechnology. Biogas, produced by anaerobic digestion (AD) during organic waste degradation, has been used for electricity generation and heating. Microbial electrolysis cells (MECs) are an emerging technology which when combined with AD can produce higher yields of such energy whilst simultaneously treating waste water and sludge. MECs are bioelectrochemical systems which utilize the metabolism of microbes to oxidize organics. The majority of the research has been focused on biohydrogen production, despite associated issues, which has resulted in poor commercialization prospects. Consequently, scientists are now suggesting that methane production should be the focus of MEC technology. This chapter presents lab research on the bioprocessing of biomethane using AD and MECs and addresses important issues, namely the lack of pilot-scale studies. Downstream processing techniques are discussed, as well as a novel suggestion of further utilising MECs in the purification process
Effectiveness of Constructivist Approach to the Teaching of Animal Classification in Science and Technology of Standard Ninth
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Asymmetric Conflict and Symmetric Crises:Exploring Womens\u27 Liberation movement in the Middle East
No full textTITLE:ASYMMETRIC ONFLICT AND SYMMETRIC CRISES: EXPLORING WOMEN’S LIBERATION MOVEMENT IN THE MIDDLE EAST.
Navneet Samuel (Ph.D),Author, Department of West Asian Studies, Aligarh Muslim University, Aligarh. India E-mail- [email protected] Rida Afreen (Ph. D) (Co-author) Center for Women’s Studies, AMU, Aligarh, India. E-mail- [email protected]
ABSTRACT-
During the past many decades, the Middle East has witnessed enormous small and large scale conflicts, where women and children were the most effected participants in every sphere of social, economic and political life. Due to these conflicts, the indigenous societal constructions of this area changed drastically, generating and reflecting multiple ideas of gender development narratives such as Islamic feminism,Arab women’s Liberation and work rights, protection of educational rights, and debates of socio-political inclusion of women. As an empirical qualitative study, this paper aims to explore Lila -Abu Logodh’s “Do Muslim women need saving”, as a premise in dealing with the changing dynamics of women’s role and status during the Arab-Israeli conflicts, and will try to see violence and war from gendered perspectives. It will also question on how women and children deal with post war regressions, coalitions with men, and in the state policy and decision making. As an anthropological descriptive study ,this paper will put to test Logodh’s theorization of Arab women’s development without any external intervention. In the process, it will study the rise of womens’ movement in the Middle East and how modalities of power and empowerment became a necessity in the region. Further, this study also examines the inter and intra conflicts and the resulting crises of this region which led women to continue with their struggle to bear the burden of being as producers and protectors of their families and societies. Furthermore, this study will analyze how national and international organizations have been significant in providing assistance to women in conflict zones in the Middle East, and how far bodies of crises relief are working to bring peace and harmony.Hence, this study will bring to the fore Arab womens’ movement as a catalyst in bringing women to the mainstream, and a model for womens’ empowerment around the world.
KEYWORDS- Women’s Movement, conflict, violence, empowerment, crises, Middle East
Race through the finish line with your customers: Customer Segmentation and Profiling of CredRev
Get PDFDuring a semester long research project, our research team analyzed the CRM of CredRev, an auto financing company based in Kelowna, BC with customers all over BC. Our research objectives were to perform customer segmentation and profiling for the chosen organization, promote greater CRM strategies with the use of customer databases, and increase the amount of customers for CredRev by further understanding their customer segments and profiles.This poster won the Vice-President, Students award (2020). Supervisor: Dr. David Dobson, School of Business
Synthesis of 4-aminophenyl substituted indole derivatives for the instrumental analysis and molecular docking evaluation studies
No full textCALCIUM SENSING RECEPTOR FUNCTION IN COLON: A ROBUST PROMOTER OF DIFFERENTIATION AND TUMOR SUPPRESSOR
No full textThe expression of calcium sensing receptor (CaSR) in the human colonic crypt epithelium is linked to cellular differentiation while its lack of expression is associated with undifferentiated and invasive colon carcinoma. Recent studies show that CaSR suppresses the malignant phenotype through a variety of pathways that inhibits growth and promotes differentiation. CaSR also promotes cytotoxic response to fluorouracil. These studies, taken together, have led me to formulate the following working hypotheses: (i), CaSR is a robust inducer of differentiation by virtue of its ability to activate and integrate diverse growth and differentiation control signals; (ii), loss of CaSR expression enable cellular escape from CaSR control and (iii), loss of CaSR expression is an underlying mechanism of malignant transformation, progression and drug resistance in colon cancer. Previous studies showed that there are endogenous small subpopulations that do not express CaSR in colon carcinoma cell lines. These cells are highly drug resistant. Indeed, immunocytochemical analyses of CaSR showed that the expression of CaSR in both the CBS and HCT116 colon carcinoma cell lines are heterogeneous. Human colon carcinoma cell lines contain small subpopulations (10-20%) that do not express CaSR (termed CaSR null cells). In order to further test my hypotheses, the isolation and characterization of CaSR null cells are required. Here, I report on the isolation, propagation, maintenance and characterization of CaSR null cells from the CBS and HCT116 human colon carcinoma cell lines. CaSR null cells grew as three-dimensional non-adherent spherical clusters with increased propensity for anchorage independent growth, cellular proliferation and invasion of matrigels. CaSR null cells were highly resistant to fluorouracil and expressed abundant amount of thymidylate synthase and survivin. Molecular profiling showed a high level of expression of the previously reported cancer stem cell markers CD133, CD44 and Nanog in CaSR null cells. A significant increase in the expression of epithelial-mesenchymal transitional (EMT) molecules and transcription factors was also observed. These include N-cadherin, β-catenin, vimentin, fibronectin, Snail1, Snail2, Twist and FOXC2. The expression of the tumor suppressive E-cadherin and miR145, on the other hand, was greatly reduced while the expression of oncogenic micro RNAs: miR21, miR135a and miR135b was significantly up-regulated. CaSR null cells possess a myriad of cellular and molecular features that drive and sustain the malignant phenotype. I conclude that CaSR null constitutes a highly malignant and drug resistant phenotype of colon cancer. I discovered that CaSR null cells, cultured in defined human embryonic stem cell culture medium, can be induced to differentiate and acquire CaSR expression when the medium of the null cells was changed to conventional cell culture medium containing fetal bovine serum. I hypothesize that expression of CaSR can alter the phenotype of the CaSR null cells. The objectives of this study were then three folds: (i), determine if induction of CaSR expression could circumvent the molecular phenotype of the CaSR null cells; (ii), determine if CaSR was required in altering the null phenotype and (iii), determine the underlying mechanism of CaSR induction. I hypothesize that if CaSR is a strong promoter of differentiation, then without CaSR, the constraint exerted by CaSR will not be functional and pathways normally inhibited by CaSR will be activated. I found that induction of CaSR expression led to a more indolent phenotype which includes the acquisition of epithelial morphology, down-regulated expression of cancer stem cell markers, down-regulated expression of thymidylate synthase and survivin and increased sensitivity to fluorouracil. Molecular profiling also revealed that the induction of CaSR expression was linked to a down-regulated expression of EMT molecules, EMT associated transcription factors and oncogenic miRNAs with a concurrent up-regulated expression of tumor-suppressive molecules. With the exception of the cancer stem cell markers, the reversal of molecular features, upon the induction of CaSR expression, was directly linked to the expression and function of CaSR because blocking CaSR induction by shRNA circumvented such reversal. I further report that demethylation of the CaSR gene promoter underlie CaSR induction. I conclude that induction of CaSR expression in CaSR null cells resulted in a more indolent phenotype concurrent with a variety of molecular changes and that these changes (with the exception of stem cell markers) are dependent on the expression and function of CaSR. I further conclude that methylation of the CaSR gene promoter is an underlying mechanism of maintaining the CaSR null phenotype while promoter demethylation is an underlying mechanism responsible for CaSR induction. CaSR null is a phenotype of the rapidly proliferating, undifferentiated crypt stem cells at the base of colonic crypts. Differentiation of crypt stem cells toward the apex of a crypt (in the direction of the lumen), on the other hand, is tightly linked to CaSR expression. What induces CaSR expression as the crypt stem cells migrate up the crypts is unknown. I hypothesize that as the colonic crypt stem cells migrate up the crypt, they become increasingly exposed to the colonic fluid in the lumen and components in the colonic fluid can trigger the induction of CaSR expression. Both Ca2+ and vitamin D are good candidates because either Ca2+ or vitamin D can stimulate CaSR expression in the parental CBS and HCT116 human colon carcinoma cells. Certainly, Ca2+ and vitamin D are not the only components involved in regulating CaSR expression. A variety of minerals in the colonic fluid may also serve as good candidates in the induction of CaSR. Of interest is Aquamin, a calcium-rich mineralized extract from the red marine algae, Lithothamnion calcareum, which has been shown to induce differentiation in colon carcinoma cells and possess chemopreventive properties against colon polyp formation in mice fed a high fat diet. CaSR null cells cultured in defined human embryonic stem cell culture medium were used to test this hypothesis because they offer an in vitro model in determining the triggers and the underlying mechanisms of CaSR induction that may resemble that of the colonic crypt stem cells in vivo. I found that all three agonists (Ca2+, vitamin D and Aquamin) induced CaSR mRNA and protein expression and inhibited cellular proliferation in the parental cells which express a heterogeneous mixture of cells with different level of CaSR expression. These agonists also induced CaSR mRNA and protein expression and inhibited cellular proliferation in the homogeneous isolated CaSR null cells. In both cases, Aquamin was found to be most potent in this regard. Induction of CaSR expression by these agonists in the CaSR null cells resulted in demethylation of the CaSR gene promoter with a concurrent increase in CaSR promoter reporter activity. Induction of CaSR expression resulted in a down-regulated expression of tumor inducers and up-regulated expression of tumor suppressors in the CaSR null cells. Again, Aquamin was found to be most potent in this regard. Taken together, I conclude that nutrients are good candidate in the induction of CaSR and differentiation in colonic epithelia cells. Similar to CaSR, transforming growth factor β (TGFβ) is also a robust promoter of differentiation in the colonic epithelium. The expression profile of both CaSR and TGFβ in the colonic epithelium is tightly linked to differentiation. Both CaSR and TGFβ expression progressively increases as the undifferentiated crypt stem cells migrate and differentiate toward the apex of a crypt in the direction of the lumen. Similar to the loss of CaSR in cancer cells, loss of TGFβ responsiveness has long been considered an underlying mechanism of early colon carcinogenesis. I hypothesize that there is functional linkage between CaSR and TGFβ function. Human colonic epithelial CBS cells originally developed from a differentiated human colon tumor, retain CaSR expression and function, TGFβ responsiveness and TGFβ receptor expression. Thus, these cells offer an opportunity to determine the functional linkage (if any) between CaSR and TGFβ. I found that knocking down CaSR expression in the CBS cells abrogated TGFβ-mediated cellular responses and attenuated the expression of TGFβ receptors. Ca2+ or vitamin D treatment induced CaSR expression with a concurrent up-regulation of TGFβ receptor expression. Ca2+ or vitamin D, however, did not induce CaSR in CaSR knocked down cells and without CaSR, there was no up-regulation of TGFβ receptor. I conclude that TGFβ receptor expression and TGFβ mediated responses requires CaSR expression and function. In summary, my research has revealed the important role of CaSR in controlling differentiation. CaSR also function as a robust tumor suppressor. My study clearly discerns the multifarious molecular signaling cascades involved in CaSR function and that methylation and demethylation regulates CaSR expression. My work has also established the importance of CaSR in the chemoprevention of colon cancer. My thoughts in regard to future studies and the potential role that CaSR could play in the management of colon cancer are given in the perspective section of this dissertation
A LITERATURE REVIEW: EFFICIENT VM MIGRATION TECHNIQUES FOR ENERGY REDUCTION IN CLOUD COMPUTING
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