Relevant bibliographies by topics / Β2m

Academic literature on the topic 'Β2m'

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Published: 11 March 2023

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Journal articles on the topic "Β2m"

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Chen, Zhaosan, Nianzhi Zhang, Shuangshuang Lu, Mansoor Tariq, Junya Wang, and Chun Xia. "Crystallization and preliminary X-ray diffraction analysis of the two distinct types of zebrafish β2-microglobulin." Acta Crystallographica Section F Structural Biology Communications 71, no. 6 (May 22, 2015): 794–98. http://dx.doi.org/10.1107/s2053230x15005737.

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β2-Microglobulin (β2m) noncovalently associates with the heavy chain of major histocompatibility complex class I (MHC I) molecules, which bind foreign antigen peptides to control the cytotoxic T lymphocyte (CTL) immune response. In contrast to mammals, there are distinct types of β2ms derived from two loci in a number of teleost species. In order to clarify the structures of the β2ms, the zebrafish (Danio rerio) β2msDare-β2m-I andDare-β2m-II were expressed inEscherichia coli, purified and crystallized, and diffraction data were collected to 1.6 and 1.9 Å resolution, respectively. Both crystals belonged to space groupP212121. The unit-cell parameters were determined to bea= 38.2,b= 50.4,c= 50.9 Å forDare-β2m-I anda= 38.9,b= 52.7,c= 65.8 Å forDare-β2m-II. Each asymmetric unit was constituted of one molecule, with Matthews coefficients of 2.22 and 3.01 Å3 Da−1and solvent contents of 45 and 59% forDare-β2m-I andDare-β2m-II, respectively. These two β2m structures will provide relevant information for further studies of the structures of the MHC I complex.
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Lonnemann, Gerhard, and Karl M. Koch. "β2-Microglobulin Amyloidosis: Effects of Ultrapure Dialysate and Type of Dialyzer Membrane." Journal of the American Society of Nephrology 13, suppl 1 (January 2002): S72—S77. http://dx.doi.org/10.1681/asn.v13suppl_1s72.

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ABSTRACT. The available data on the pathophysiology of β2-microglobulin amyloidosis (β2mA) suggest that this progressive disease associated with end-stage renal failure develops in several consecutive phases. First, declining kidney function leads to retention of β2 microglobulin (β2m) and its deposition preferentially in the synovial tissue of bigger joints such as wrists, shoulders, and hips. Second, at the site of deposition, formation of unique amyloid fibrils, whose major component is β2m, takes place. Deposition and fibril formation occur in the absence of modification of β2mA by advanced glycoxidation end products and also in the absence of a local inflammatory response. It is later, in the third phase, that advanced glycoxidation end product modification of β2m induces a local inflammatory response by attracting macrophages chemotactically and by stimulating these cells to produce and release proinflammatory cytokines. In addition, unmodified β2m itself induces inflammatory activities such as upregulation of cyclooxygenase-2 and metalloproteinase-1. The severity of the local inflammation seems to determine the degree of the destructive processes in tissue and bone accompanying β2mA.
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Shields, Michael J., Nassim Assefi, Wesley Hodgson, Ellen J. Kim, and Randall K. Ribaudo. "Characterization of the Interactions Between MHC Class I Subunits: A Systematic Approach for the Engineering of Higher Affinity Variants of β2-Microglobulin." Journal of Immunology 160, no. 5 (March 1, 1998): 2297–307. http://dx.doi.org/10.4049/jimmunol.160.5.2297.

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Abstract Human β2m (hβ2m) binds to murine MHC I molecules with higher affinity than does murine β2m and therefore can be used as a model system to define and dissect the interactions between β2m and MHC I heavy chains that promote the stability of the complex. In the present study we compare three-dimensional crystal structures of human and murine MHC I molecules and use functional studies of chimeric human:murine β2m variants to define a region of β2m that is involved in the higher affinity of hβ2m for murine MHC I heavy chains. Further examination of the three-dimensional structure in this region revealed conformational differences between human and murine β2m that affect the ability of an aspartic acid residue at position 53 (D53) conserved in both β2ms to form an ionic bond with arginine residues at positions 35 and 48 of the heavy chain. Mutation of residue D53 to either asparagine (D53N) or valine (D53V) largely abrogated the stabilizing effects of hβ2m on murine MHC I expression in a predictable manner. Based on this observation a variant of hβ2m was engineered to create an ionic bond between the heavy chain and β2m. This variant stabilizes cell surface H-2Dd heavy chains to a greater extent than wild-type hβ2m. Studying these interactions in light of the growing database of MHC I crystal structures should allow the rational design of higher affinity hβ2m variants for use in novel peptide-based vaccines capable of inducing cell-mediated immune responses to viruses and tumors.
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Stefanovic', Vladisav, Svetislav Kostic', Vidojko Djordjevic', Marina Mitic', and Momcilo Bogicevic'. "β2-Microglobulin Elimination in End-Stage Renal Disease Patients on Renal Replacement Therapy." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 13, no. 2_suppl (January 1993): 520–22. http://dx.doi.org/10.1177/089686089301302s127.

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β2-microglobulin (β2M) is a small molecular mass protein associated with dialysis amyloidosis. We have studied β2M elimination in end-stage renal disease (EsRD) patients treated by peritoneal dialysis. In 12 patients on continuous ambulatory peritoneal dialysis (CAPD) and 7 patients on intermittent peritoneal dialysis (IPD) 30.4±4.2 mg/day and 21.3± 1.8 mg/12 hour of β2M, respectively, were removed by dialysis fluid. Approximately the same amount of β2M was removed by each of four 2-L exchanges in CAPD; however, the most efficient removal of β2M was in the first IPD exchange. Serum β2M levels in these patients were 25.7 ±4.4 and 31.4±5.2 mg/L, respectively. In 24 patients on hemodialysis using cuprophan membrane the serum level of β2M was 55.1±4.1 mg/L. After a 3-month dialysis on polyacrylonitrile (PAN) membrane, the serum β2M level decreased to 45.0±2.3 mg/L. A substantial amount of β2M was removed by urine, 14.6.:1:2.3 mg/L, and saliva, 2.3±0.4 mg/L. This study has shown markedly increased β2M levels in patients on conventional hemodialysis treatment, predisposing to β2M-related amyloidosis. A significant amount of β2M was removed during both CAPD and IPD treatment.
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Zhang, Fan, Yu-Ming Chu, and Wei-Mao Qian. "Bounds for the Arithmetic Mean in Terms of the Neuman-Sándor and Other Bivariate Means." Journal of Applied Mathematics 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/582504.

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We present the largest valuesα1,α2, andα3and the smallest valuesβ1,β2, andβ3such that the double inequalitiesα1M(a,b)+(1-α1)H(a,b)<A(a,b)<β1M(a,b)+ (1-β1)H(a,b),α2M(a,b)+(1-α2) H-(a,b) < A(a,b)<β2M(a,b)+(1-β2)H-(a,b), andα3M(a,b)+(1-α3)He(a,b)< A(a,b)<β3M (a,b)+(1-β3)He(a,b)hold for alla,b>0witha≠b, whereM(a,b),A(a,b),He(a,b),H(a,b)andH-(a,b)denote the Neuman-Sándor, arithmetic, Heronian, harmonic, and harmonic root-square means ofaandb, respectively.
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Corlin, Dorthe B., Jette W. Sen, Søren Ladefoged, Grethe Bjerregaard Lund, Mogens H. Nissen, and Niels HH Heegaard. "Quantification of Cleaved β2-Microglobulin in Serum from Patients Undergoing Chronic Hemodialysis." Clinical Chemistry 51, no. 7 (July 1, 2005): 1177–84. http://dx.doi.org/10.1373/clinchem.2005.049544.

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Abstract Background: Patients on chronic hemodialysis are prone to develop amyloid deposits of misfolded β2-microglobulin (β2M) in osteoarticular tissues. β2M with various deletions/truncations and chemical modifications has been found together with structurally intact β2M in extracts of β2M amyloid fibrils. The state of the circulating population of β2M molecules has not been characterized previously with high-resolution methods. Methods: We used immunoaffinity–liquid chromatography–mass spectrometry analysis of serum samples to examine whether structurally modified β2M is generated in the circulation. In addition, we developed an immunoassay for the quantification of a cleaved β2M variant in biological fluids based on novel monoclonal antibodies and applied this assay to patient and control sera. Results: A specific alteration compatible with the generation of lysine-58–cleaved and truncated β2M (ΔK58-β2M) was found in the sera of many (20%–40%) dialysis patients but not in control sera or sera from patients with cerebral amyloidosis (Alzheimer disease). Applied to patient sera, specific immunoassays revealed that dialysis, as expected, significantly lowered the total β2M concentration, but the concentrations of ΔK58-β2M remained unchanged after dialysis. The results also show that patients dialyzed with less biocompatible membranes have higher serum concentrations of cleaved β2M (mean, 8.5, 1.8, and 0.7 mg/L in cuprophane membrane-dialyzed, polysulfone membrane-dialyzed, and control sera, respectively). Conclusions: This study for the first time demonstrates and assigns the structure of a specific β2M variant in sera from dialysis patients. Because this variant is conformationally unstable in vitro, it may be involved in in vivo amyloidogenesis.
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ZHU, Xiaoping, Junmin PENG, Raktima RAYCHOWDHURY, Atsushi NAKAJIMA, Wayne I. LENCER, and Richard S. BLUMBERG. "The heavy chain of neonatal Fc receptor for IgG is sequestered in endoplasmic reticulum by forming oligomers in the absence of β2-microglobulin association." Biochemical Journal 367, no. 3 (November 1, 2002): 703–14. http://dx.doi.org/10.1042/bj20020200.

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The heavy chain (HC) of the neonatal Fc receptor (FcRn) for IgG is non-convalently associated with β2-microglobulin (β2m). In β2m-/- mice, FcRn functions are greatly impaired. We sought to determine how FcRn HC, particularly its structure and biogenesis, is affected by the absence of β2m. Human FcRn HC, expressed from the β2m-null cell line FO-1FcRn, was present as a monomeric 45-kDa protein under reducing conditions but primarily as a 92-kDa oligomeric protein under non-reducing conditions. Two-dimensional electrophoresis and MS analysis showed that the 92-kDa protein was a dimer of the 45-kDa HC. Immunostaining showed that FcRn HC in FO-1FcRn was co-localized with the endoplasmic reticulum (ER) protein Bip/GRP78 but not with an endosome protein, EEA1. In contrast, FcRn HC in FO-1FcRn+β2m was detected in both the ER and endosome. The dimeric HC in FcRn oligomers was free of β2m association in FO-1FcRn+β2m. Mutation of non-paired cysteine residues at positions 48 and 251 within the human FcRn cDNA failed to eliminate the oligomers. The FcRn HC oligomers could be reduced by reconstitution of FO-1FcRn with β2m or by balanced expression of FcRn HC with β2m, or β2m fused with a KDEL retention sequence. Similarly, the majority of FcRn HC isolated from neonatal β2m-/- mice was in a dimeric form under non-reducing conditions. The amount of FcRn HC was significantly decreased in β2m-/- mice and FO-1FcRn. Furthermore, β2m-free FcRn HC was sensitive to endoglycosidase digestion. These results indicate that FcRn HC alone can form disulphide-bonded oligomers in the ER, which may represent a misfolded protein. The β2m association with FcRn HC is critical for correct folding of FcRn and exiting the ER for routing to endosomes and the cell surface.
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Good, Sarah C., Katherine M. Dewison, Sheena E. Radford, and Patricija van Oosten-Hawle. "Global Proteotoxicity Caused by Human β2 Microglobulin Variants Impairs the Unfolded Protein Response in C. elegans." International Journal of Molecular Sciences 22, no. 19 (October 4, 2021): 10752. http://dx.doi.org/10.3390/ijms221910752.

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Aggregation of β2 microglobulin (β2m) into amyloid fibrils is associated with systemic amyloidosis, caused by the deposition of amyloid fibrils containing the wild-type protein and its truncated variant, ΔN6 β2m, in haemo-dialysed patients. A second form of familial systemic amyloidosis caused by the β2m variant, D76N, results in amyloid deposits in the viscera, without renal dysfunction. Although the folding and misfolding mechanisms of β2 microglobulin have been widely studied in vitro and in vivo, we lack a comparable understanding of the molecular mechanisms underlying toxicity in a cellular and organismal environment. Here, we established transgenic C. elegans lines expressing wild-type (WT) human β2m, or the two highly amyloidogenic naturally occurring variants, D76N β2m and ΔN6 β2m, in the C. elegans bodywall muscle. Nematodes expressing the D76N β2m and ΔN6 β2m variants exhibit increased age-dependent and cell nonautonomous proteotoxicity associated with reduced motility, delayed development and shortened lifespan. Both β2m variants cause widespread endogenous protein aggregation contributing to the increased toxicity in aged animals. We show that expression of β2m reduces the capacity of C. elegans to cope with heat and endoplasmic reticulum (ER) stress, correlating with a deficiency to upregulate BiP/hsp-4 transcripts in response to ER stress in young adult animals. Interestingly, protein secretion in all β2m variants is reduced, despite the presence of the natural signal sequence, suggesting a possible link between organismal β2m toxicity and a disrupted ER secretory metabolism.
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Yuichiro Higashimoto and Yoshihiro Motomiya. "Heparin and β2-microglobulin amyloidogenesis." GSC Biological and Pharmaceutical Sciences 22, no. 2 (February 28, 2023): 070–78. http://dx.doi.org/10.30574/gscbps.2023.22.2.0061.

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β2-Microglobulin (β2M) occurs as a precursor protein in dialysis-related amyloidosis (DRA), which is a major complication in lives of patients undergoing dialysis. However, the underlying mechanism by which a native β2M transform into an amyloid β2M remain unclear. This disease has developed exclusively in interstitial tissues, which suggest possible implication of extracellular matrix substances in amyloidogenesis of this precursor protein. By using our monoclonal antibody specific for amyloid β2M, we investigated the function of heparin, that is, one of the glycosaminoglycans, as associated with amyloidogenic conversion of the β2M molecule. We confirmed that heparin induced a dose-dependent and time-dependent unfolding at the C-terminal region of the β2M molecule, which led to amyloidogenic transformation of the β2M molecule and brought about intermolecular interactions between β2M and substances in the interstitial matrix such as GAGs and collagen.
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Morales, Pedro J., Judith L. Pace, Jeralyn S. Platt, and Joan S. Hunt. "Placental cytotrophoblast HLA-G5 is synthesized as a β2m-free heavy chain homodimer (42.13)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S35—S36. http://dx.doi.org/10.4049/jimmunol.178.supp.42.13.

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Abstract Placental villous cytotrophoblast cells (vCTB) contain an unusual member of the HLA class I gene family, HLA-G5. Recently we showed that HEK293-derived recombinant HLA-G5 protein is predominantly composed of H:H homodimers. Here, we examined the HLA-G5 produced in primary vCTB. Determining the structure is critical because recombinant ectodomains of the inhibitory leukocyte Ig-like LILRB1 (ILT2) and LILRB2 (ILT4) receptors bind HLA-G dimers with higher affinity than monomers. Analysis of vCTB cell extracts by immunoblotting demonstrated that vCTB cell HLA-G5 H chain proteins are primarily disulfide bonded dimers. The H chains were not associated with β2m L chains; although β2m mRNA was identified by RT-PCR, immunoblots failed to detect β2m protein even when additional β2m mRNA was introduced. Furthermore, sequencing failed to reveal any abnormalities in the translational start codon of either endogenous β2m mRNA or introduced β2m mRNA, and EGF-induced syncytialization did not promote β2m in vCTB cells. The inability of vCTB cells to translate β2m messages in vitro was reflected in failure to detect β2m in vCTB cells in situ. Thus, vCTB cells may synthesize a disulfide-bonded, β2m-free homodimeric form of HLA-G5 due to an inability to synthesize β2m protein. This molecule could comprise a particularly effective tolerogenic molecule at the maternal-fetal interface.
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Dissertations / Theses on the topic "Β2m"

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Alhawsawi, Sana Mahmoud. "β2m antibody is a suitable antibody to detect major histocompatibility complex class Ι as well as α chain antibody in healthy tissues and tissues infected with mouse parvovirus 1." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1432738096.

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Carbone, Anna Lisa. "Engineering and functional characterisation of pentameric concatenated (α4)₂(β2)₃ and (α4)₃(β2)₂ nicotinic acetylcholine receptors." Thesis, Oxford Brookes University, 2009. https://radar.brookes.ac.uk/radar/items/6b5c0ace-ecf1-488d-95e6-b112bd79e252/1/.

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Neuronal nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that influence neurotransmitter release, hence constituting a key component of the physiological mechanisms of neuronal signalling. This thesis is concerned with the properties of the a4P2 nAChR, the most abundant nAChR in the brain, and the major contributor to the central effects of nicotine. The a4P2 nAChR is made up of five subunits, which in heterologous systems can assemble into at least two different stoichiometries: the high sensitivity (HS) (a4h(P2)3 stoichiometry and the low sensitivity (LS) (a4)3(p2)2 stoichiometry, which might both exist in native tissues. Despite the attractiveness of the a.4P2 nAChR as a target for therapeutic intervention, progress in the development of a4P2 nAChR-selective drugs has been slowed, partly because of the lack of stoichiometric-specific receptor models. This study presents a strategy to express homogenous populations of a4P2 nAChRs with fixed stoichiometry. By using standard molecular biological techniques, pentameric concatenated (a4)2(P2)3 and (a4)3(P2)2 nAChRs were engineered. These receptors were expressed in Xenopus laevis oocytes and functional studies showed that their functional properties resembled those of their non-linked counterparts. Subsequent site-directed mutagenesis in combination with functional analysis allowed the identification of the agonist-binding subunits in both concatamers. Concatenated receptors proved to be suitable for comparative studies of the effects of receptor mutation linked to autosomal dominant nocturnal frontal lobe epilepsy. Studies carried out on non-linked receptors, showed that the properties of the (a4)3(p2)2 stoichiometry were affected more markedly than those of the (a4)2(p2)3 stoichiometry. Insertion of the mutation in concatenated receptors revealed that the mutation not only affected the functional properties of a.4P2 nAChRs but also altered the subunit composition of the receptor. These studies show that pentameric concatenated constructs are a powerful tool to study the function and structure of receptors that assemble in multimeric types in expression systems.
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Bohlin, Maria E. "Capillary electrophoresis of β2-glycoprotein I." Licentiate thesis, Karlstads universitet, Fakulteten för teknik- och naturvetenskap, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-3826.

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Jones, J. M. "β2 adrenergic receptor gene therapy during cardiopulmonary bypass." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.605686.

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Cross, Deborah Jane. "β2-adrenoceptor gene polymorphisms and hypertension in African Trinidadians." Thesis, University of Nottingham, 2004. http://eprints.nottingham.ac.uk/13194/.

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Background Essential hypertension remains a major risk factor for coronary heart disease (CHO) and stroke, and its prevalence is greater, more severe, occurs earlier, and is less well controlled among black individuals than among white individuals, at all ages after young adult hood (Comoni-Huntley et al, 1989). In Caucasians, studies have shown that β2-adrenoceptor polymorphism accounts for the variability in the vascular responsiveness to the agonist isoprenaline (Cockcroft et al, 1994 and Lang et al, 1995). Individuals homozygous for Gln 27 β2-adrenoceptor showed reduced responses due to chronic down regulation of β2-adrenoceptor in the vasculature. Therefore, variability in response to isoprenaline was determined by β2-adrenoceptor gene polymorphism. Aim and Objectives This study investigated whether there is a relationship between the ArglGly16 and Gln/Glu 27 β2-adrenoceptor polymorphisms by examining whether the incidence of occurrence is prevalent in African Trinidadians. In addition, comparison data of vascular responses with arterial compliance using pulse wave analysis (PWA) was correlated. The study aimed to give evidence if these polymorphisms contributed fully or in part, to determine the disease severity, or response to therapy in hypertensive individuals. It also aimed to prove that PWA is a reliable and therapeutic tool, in diagnosing and treating blood pressure, as reliance on brachial artery recording of blood pressure, alone, is becoming a poor indicator and predictor of risk. Methods The study genotyped 408 African Trinidadian subjects for the β2-adrenoceptor polymorphism and used the technique of applanation tonometry to analyse the central pulse wave, generating information on arterial compliance, left ventricular function and coronary perfusion. Blood pressure was measured in triplicate using a semiautomatic blood pressure meter after 15 minutes of supine rest and bloods lipids assessed using a validated portable lipid cartridge. This was achieved by subjects attending a nurse-led cardiovascular risk clinic. Results There is no significant association between the Arg-Glyl6 polymorphism and the Gln-Glu27 polymorphism and hypertension in African Trinidadians. Interestingly, the appearance of the Glu27 polymorphism was very uncommon in African Trinidadians and this is constant with findings by Candy et al, 2000. Conclusion There is no difference in the frequency of β2-polymorphisms between normotensive and hypertensive African Trinidadians, and are unlikely to be a contributing factor for essential hypertension. Therefore, hypertension would indicate that it is polygenic with complex gene to gene and gene environmental interactions, through multiple, indirect and intermediate phenotypes and interactions.
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Dropmann, Anne [Verfasser], and Steven [Akademischer Betreuer] Dooley. "TGF-β2 abundance in mice and men: A successful anti-TGF-β2 strategy in biliary-derived liver disease / Anne Dropmann ; Betreuer: Steven Dooley." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177150050/34.

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Sweetman, Chlöe A. "TGF-β2 in human milk research: Exploration of a new field methodology and new findings of biosimilar TGF-β2 in non-human milk." Scholar Commons, 2018. http://scholarcommons.usf.edu/etd/7233.

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Objectives: There are three aims for this thesis: the first is to develop a field and laboratory protocol for the storage and analysis of transforming growth factor–beta 2 (TGF-β2) in human breastmilk; second, to validate this protocol and the immunoassay used to assess this new method; and lastly, to explore the ramifications of biosimilar TGF-β2 across multiple milks on human health, growth, and immunity through the review of laboratory findings and previous literature. Rational: Little anthropological research has been done on TGF-β2 in human milk. Anthropology as a discipline is well positioned to provide insight into TGF-β2, combining biocultural, evolutionary, and ecological approaches to holistically illustrate the effects this cytokine has on human immunity. This thesis provides an applied anthropological perspective and methodology on TGF-β2 in human milk. Methods: A protocol was developed for a new method of drying breastmilk on polystyrene microplates. Samples were then reconstituted using reagent diluent with 1% BSA and assayed using a Human TGF-beta 2 DuoSet enzyme-linked immunosorbent assay (ELIZA) assay kit from R&D Systems. Other mammalian milks and infant formula samples were also dried and tested for TGF-β2 concentrations. Validity of the assay and TGF-β2 concentrations were then statistically measured using linear regression analysis and Bland-Altman plots. Results: The results of the first objective in the development of a laboratory and field protocol for drying breastmilk on polystyrene plates for the extraction of TGF-β2 showed this method to hold promise for future application, but lacked statistical power in this study to confirm if this method is viable. The second objective of assay validation was unsuccessful, with the percent coefficient of variation for the intra-assay variation and inter-assay validation 38.28% and 17.70%, respectively indicating that this assay struggled to produce consistent and reliable results from the reconstituted samples. Results from the third objective suggest that biosimilar TGF-β2 in non-human milk can influence human growth and development, the extent of which, however, needs further study. Conclusions: Given these findings, more work with TGF-β2 in milk is required. TGF-β2 is a cytokine which could reveal a great deal about the developmental origins of human immunity and how it is maintained and altered across our life course and therefore an area of biology worth further research.
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Wagner, Ylva. "Conformational Change of β2-glycoprotein I : Evaluation of Difference in Binding Capacity of Autoantibodies to Open and Closed Forms of β2-glycoprotein I." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-24838.

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Antiphospolipidsyndrome (APS) is one of the most common autoimmune diseases characterized bythrombosis, fetal loss and presence of antiphospholipid antibodies. In APS research the antibodies of biggestinterest are anti-β2-glycoprotein I antibodies (Aβ2GPIA). β2-glycoprotein I (β2GPI)is a plasma protein which becomes activated and obtains a open structure incontact with negative charged surface molecules such as phospholipids. Inactiveβ2GPI has a closed, circular shape which can’t bind autoantibodies. Thereis no golden standard for APS diagnosing and the methods used often giveinconsistent results. The purpose of this examination project work was toconvert β2GPI into the open and closed forms, respectively, by dialyzing againsthigh ionic strength, low and high pH and determine if there is any differencein binding capacity between the two forms and Aβ2GPIAon a microtiter plate.                                                The binding capacity was tested inan ELISA (enzyme-linkedimmunosorbent assay) using purified IgG from patient sera and thedifferent conformational forms of β2GPI. An ELISA for measuring of Aβ2GPIAon several patient samples was also performed.               No difference in binding capacitycould be detected which might be explained by that the conversion of β2GPI was unsuccessful.Perhaps no difference can be measured between the structures because the closedform is expected to open on microtiter plates. An unexpected result was thepresence of immune complexes of β2GPI-Aβ2GPIA found in the serum of one of the patients. In theory an ELISA based on theopen form of β2GPI would provide more reliable diagnoses and furtherresearch is needed in this area.
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COATTI, AURORA. "Heteromeric nicotinic receptors regulate developing and mature prefrontal circuits: interaction with other neuromodulators, and implications for sleep-related hypermotor epilepsy." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/199023.

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Il sistema colinergico proietta in modo diffuso alla corteccia prefrontale (PFC) matura e sostiene l’attivazione corticale durante la veglia e il sonno REM. Il ruolo dei recettori nicotinici (nAChRs) nel mediare questi processi è sempre più riconosciuto. Inoltre, i nAChRs regolano anche lo sviluppo dei circuiti corticali durante le prime settimane di vita. Innanzitutto abbiamo studiato topi esprimenti β2-V287L, una subunità mutata del nAChR associata all’epilessia notturna autosomica dominante del lobo frontale (ADNFLE). β2-V287L svolge la sua azione epilettogenica alterando la stabilizzazione sinaptica durante le fasi critiche della maturazione circuitale, infatti, la sua espressione durante le prime due settimane di vita è necessaria per lo sviluppo del fenotipo epilettico nel topo adulto. Questa fase critica, inoltre, coincide con lo switch del GABA da eccitatorio a inibitorio, determinato dalla diminuzione progressiva del rapporto tra l’espressione del cotrasportatore-1 Na+/K+/Cl- (NKCC1) e del cotrasportatore-2 (KCC2) K+/Cl-. La regolazione di questi trasportatori nella PFC e nel talamo è ancora largamente sconosciuta. Abbiamo indagato la distribuzione di NKCC1 e KCC2 in topi wild-type (WT) durante lo sviluppo. I livelli di entrambi i trasportatori aumentano progressivamente durante le prime due settimane di vita sia nella PFC che nella corteccia somato-sensoriale. Alla nascita, KCC2 è localizzato principalmente nei corpi cellulari neuronali e in seguito migra verso le membrane somato-dendritiche. In topi esprimenti β2-V287L, i livelli di KCC2 nel V strato della PFC a 8 giorni (P8) sono inferiori rispetto ai topi controllo, ma raggiungono livelli di espressione maggiori a P60. Anche la tempistica dello switch del GABA, misurato tramite patch perforato, risulta ritardato nel V strato della PFC nei topi mutati. Al momento della nascita NKCC1 e KCC2 sono molto espressi nel neuropilo dei nuclei talamici, indipendentemente dal genotipo. Il loro livello d’espressione rimane alto nei nuclei sensoriali nell’adulto, mentre KCC2 diminuisce significativamente nel nucleo reticolare a P40. Tale riduzione è più pronunciata nei topi esprimenti β2-V287L. Questi risultati indicano che i nAChRs contenenti la subunità β2 interagiscono con KCC2 durante la sinaptogenesi e questo può contribuire alla patogenesi dell’ADNFLE. In secondo luogo, abbiamo esplorato alcuni aspetti della complessa interazione tra i principali neurotrasmettitori che partecipano all’attivazione corticale, ovvero acetilcolina (ACh), noradrenalina (NE) e oressina A (OrxA), allo scopo di caratterizzare il loro effetto sull’eccitabilità del V strato della PFC. In particolare, tramite patch-clamp in topi WT adulti, abbiamo indagato il loro ruolo nel modulare il rilascio di glutammato sui neuroni piramidali del V strato. La somministrazione tonica di ACh stimola il rilascio di glutammato, principalmente attraverso i nAChRs contenenti la subunità α4. Inoltre, l’OrxA è in grado di stimolare il rilascio di glutammato sui neuroni piramidali attivando i recettori 1 dell’Orx (OrxR1). Anche basse concentrazioni di NE (10 nM) sono efficaci nell’aumentare il rilascio di glutammato. Possiamo concludere che questi neuromodulatori cooperano nel regolare la trasmissione glutammatergica nella PFC. Tale interazione potrebbe essere cruciale nella regolazione dei meccanismi cellulari alla base delle funzioni cognitive ed esecutive svolte da questa regione. Questo avviene sia in condizioni normali che patologiche, le quali sono spesso accompagnate da alterazioni dei ritmi theta, generati da dinamiche proprie dei neuroni piramidali. Questi risultati possono aiutare a comprendere la complessa regolazione dei microcircuiti della PFC, e pongono le basi per ulteriori indagini sui meccanismi patogenetici responsabili di anomalie corticali, tipiche di alcuni disordini legati al sonno, come l’epilessia frontale e la narcolessia con cataplessia.
The cholinergic system extensively innervates mature prefrontal cortex (PFC) and is critical to sustain cortical activation during wakefulness and REM sleep. The implication of nicotinic receptors (nAChRs) in these processes is increasingly recognized. Moreover, nAChRs regulate developing cortical circuits during the first postnatal weeks. First, we studied mice expressing β2-V287L, a mutant subunit of the nAChR linked to Autosomal Dominant Nocturnal Frontal Lobe Epilepsy (ADNFLE). β2-V287L exerts the epileptogenic action by altering the synaptic stabilization during sensitive phases of network maturation, since its expression during the first two postnatal weeks is necessary to develop the epileptic phenotype. The peak of postnatal expression of nAChRs coincides with the excitatory to inhibitory GABAergic switch, which is determined by the progressive decrease in the ratio between the expression of the Na+/K+/Cl- cotransporter-1 (NKCC1) and the K+/Cl- cotransporter-2 (KCC2). How these transporters are regulated in PFC and thalamus is largely unknown. We first studied the distribution of NKCC1 and KCC2 in developing wild-type (WT) mice. The amount of NKCC1 and KCC2 in PFC and somatosensory cortex progressively increased during the first two postnatal weeks. NKCC1 was found in neurons as well as astrocytes. KCC2 was mainly localized in neuronal somata at birth, and subsequently migrated to the somatodendritic membranes. Next, in mice expressing β2-V287L, the KCC2 amount in PFC layer V was lower than in the control littermates at postnatal day 8 (P8), but reached higher amounts by P60. Consistently, the time course of the GABAergic switch was delayed in PFC layer V of mice carrying β2-V287L, as measured by perforated patch method. Irrespective of genotype, NKCC1 and KCC2 were highly expressed in the neuropil of thalamic nuclei at birth. Their amount remained high in the adult sensory nuclei, whereas a significant decrease of KCC2 was observed in the reticular nucleus by P40. Such a decrease was more pronounced in mice expressing β2-V287L. Our results indicate that β2-containing nAChRs interact with KCC2 during synaptogenesis as well as in mature circuits, which may contribute to the pathogenesis of ADNFLE. Second, we explored some aspects of the complex interplay between the main neurotransmitters involved in cortical arousal, i. e. acetylcholine (ACh), norepinephrine (NE) and orexin A (OrxA), in order to characterize their combined effect on the PFC layer V circuit. In particular, by patch-clamp methods, we investigated how these neurotransmitters regulate glutamate release onto pyramidal neurons in PFC layer V of adult wild-type mice. Tonic administration of ACh stimulated glutamate release, mainly through α4-containing nAChRs. Moreover, OrxA increased the glutamate release onto pyramidal neurons, through Orx Receptor 1 (OrxR1). Low concentrations of NE (10 nM) were also effective in increasing glutamatergic release. We conclude that these neuromodulators cooperate in regulating glutamatergic transmission in PFC. Such interaction may be crucial in the cellular mechanisms underlying the cognitive and executive functions in this area, in normal and pathological conditions, which are often accompanied by alterations in the theta rhythms, largely determined by pyramidal neurons dynamics. These results may yield new insights into the complex regulation of the PFC microcircuit and lay the basis for further investigations on the pathogenic mechanisms responsible of altered cortical activity in sleep-related disorders such as frontal epilepsy and narcolepsy with cataplexy.
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Haidar, Malak. "Rôle du facteur de croissance transformant (TGF-β2) dans la virulence des macrophages infectés par Theileria annulata." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T044.

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Les parasites Theileria (Theileria. annulata and T. parva) sont des protozoaires intracellulaires qui font partie du phylum des Apicomplexa. Theileria infecte les leucocytes bovins et les transforment en cellules cancéreuses, induisant un genre de leucémie chez le bovin et conduisant à la mort de l’animal. Les cellules infectées par Theileria démontrent certaines caractéristiques de cellules cancéreuses telles qu’une importante capacité d’invasion et de migration cellulaire. Cependant, le traitement de cellules infectées avec une drogue Theiléricide spécifique (buparvaquone) permet l'élimination du parasite et la réversion du phénotype transformé. De plus, la virulence peut être atténuée par passages répétés sur culture cellulaire. La similitude entre les cellules transformées par Theileria et la leucémie humaine fait de Theileria un modèle très important permettant l’étude des mécanismes cellulaires induits par le parasite au cours de la transformation de la cellule hôte. Mon laboratoire d’accueil a publié une augmentation significative de TGF-β2 dans les cellules virulentes et a constaté que parmi les 1158 cibles de TGF-β, 68 gènes ont été reconnus d'avoir modifié leurs niveaux de transcription concomitante avec l'atténuation. Dans ce travail de thèse, nous avons étudié les voies de signalisations impliquées dans la régulation de l’adhésion et l’invasion des cellules infectées par Theileria. Nous nous sommes particulièrement intéressés à l’étude de la voie de signalisation TGF-β2 et ses effecteurs. Nos résultats montrent que l’activation de la voie de signalisation de TGF-β2 par Theileria entraîne une augmentation de l’invasion et de l’adhérence des cellules transformées par deux mécanismes différents, soit en activant la voie de signalisation PGE2/EP4/cAMP/PKA/EPAC/CREB, soit en stimulant la voie GRB2/PI3-K/AP-1. Les macrophages atténués infectés par Theileria sont plus stressés oxydativement ce qui diminue leur adhérence et leur invasion cellulaire. Ceci nous a amené à étudier en collaboration avec un autre doctorant (Mehdi Metheni) le rôle de TGF-β2 dans la régulation du stress oxydatif dans les macrophages infectés par Theileria. Nos données montrent que les niveaux élevés de TGF-β2 stimule l’expression de la catalase, une enzyme anti-oxydante qui convertit le H2O2 en H2O et la baisse de H2O2 favorise la virulence en augmentant l’invasion et l’adhésion des cellules infectées par Theileria (résultats supplémentaires). De plus, nous avons examiné le statut de stress oxydatif et le type de glycolyse utilisé par les cellules infectées par Theileria. Les cellules transformées par Theileria agissent comme des cellules cancéreuses, elles consomment énormément de glucose. La protéine BAD joue un rôle important dans l’apoptose ainsi que dans la voie de glycolyse. Son activité est régulée par phosphorylation en réponse à des facteurs de croissance et de survie. BAD peut être phosphorylée par la PKA sur le résidu sérine 155. Durant ma thèse, nous avons examiné le rôle de la phosphorylation de BAD par la PKA dans la régulation du métabolisme cellulaire des macrophages infectés par Theileria. Nos résultats montrent que l’abolition de la phosphorylation de BAD par la PKA dissocie le complexe mitochondrial formé entre BAD et HK2, ce qui induit l’ubiquitynation et la dégradation de HK2 par le protéasome. La baisse de HK2 stimule la voie de phosphorylation oxydative en faveur de l’effet Warburg dans les cellules infectées par Theileria
Theileria parasites (Theileria. annulata and T. parva) are intracellular protozoa and members of the phylum Apicomplexa. Theileria parasites are the only eukaryotes that possess the property of being able to transform another eukaryote, their leukocyte host cells. Transformed leukocytes show many characteristics of tumour cells such as heightened invasive capacity; however the tumour-like phenotype can be totally reversed upon drug induced parasite death and attenuated by multiple in vitro passages. Such multiple-passaged attenuated lines are used as live vaccines against tropical theileriosis. The similarities in tumour hyper-invasiveness between Theileria-transformed leukcocytes and human lymphomas imply that observations on Theileria-induced leukocyte transformation have the potential to give generally applicable insights into the mechanisms underpinning tumour virulence. My host laboratory described higher TGF-β2 levels in virulent infected macrophages and following microarray analysis of virulent compared to attenuated macrophages found that among the 1158 TGF-β-targets, 68 genes had altered transcript levels concomitant with attenuation. In this study, we investigate the signalling pathways involved in the regulation of cellular adhesion and invasiveness of Theileria-infected cells. We were especially interested in the study of TGF-β2 signalling in Theileria-transformed virulent versus attenuated macrophages. My results indicate that following Theileria infection of macrophages, the TGF-β2 signalling pathway is activated and induces an increase in adhesion of virulent transformed macrophages through two different mechanisms: either by activating a PGE2 / EP4 / cAMP / PKA / EPAC / CREB signaling pathway, or by stimulating a GRB2 / PI3-K / AP-1 pathway. As attenuated macrophages display heightened oxidative stress, which underpins their loss of adhesion and invasiveness, in collaboration with another PhD student (Mehdi Metheni) we investigated the role of TGF-β2 in the regulation of the oxidative stress status of Theileria-infected macrophages. Our data show that high levels of TGF-β2 increase the expression of catalase, an anti-oxidant enzyme that converts H2O2 into H2O and the drop in H2O2 output results in regain of the virulence trait heightened adhesion of Theileria-transformed macrophages to fibronectin. Theileria-transformed macrophages display many features of cancer cells such as their consumption of larger quantities of glucose. The BCL-2 family protein BAD has an alternative function in glucose metabolism separate from its role in apoptosis. The activity of BAD is regulated by phosphorylation in response to growth/survival factors. BAD can be phosphorylated on Ser155 by PKA. So during my thesis studies I examined the role of PKA mediated phosphorylation of BAD in the regulation of the cellular metabolism of Theileria-transformed macrophages. My results showed that ablation of BAD S155 phosphorylation dissociates the mitochondrial complex of BAD and HK2 and cytosolic HK2 becomes ubiquitinated and degraded by the proteasome. Loss of HK2 switches the metabolism of Theileria-transformed leukocytes from Warburg-like to OXPHOS-like glycolysis
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Book chapters on the topic "Β2m"

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Coon, Joanna S. Thompson, and Anne E. Tattersfield. "β2-Agonists." In Anti-Inflammatory Drugs in Asthma, 137–51. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8751-9_4.

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Kikkawa, Yamato, and Hiroshi Nishimune. "Laminin β2." In Encyclopedia of Signaling Molecules, 2816–26. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101519.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, and I. Savysyuk. "Na2ThF6 β2." In Structure Types. Part 8: Space Groups (156) P3m1 – (148) R-3, 516. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-70892-6_300.

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Yamamoto, Suguru, Junichiro James Kazama, Hiroki Maruyama, Ichiei Narita, and Fumitake Gejyo. "β2-Microglobulin." In Uremic Toxins, 249–58. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118424032.ch16.

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Holdenrieder, S., and P. Stieber. "β2-Mikroglobulin." In Springer Reference Medizin, 1653–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3400.

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Holdenrieder, S., and P. Stieber. "β2-Mikroglobulin." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_3400-1.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, I. Savysyuk, and R. Zaremba. "Ta2H β2." In Structure Types. Part 10: Space Groups (140) I4/mcm – (136) P42/mnm, 209. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19662-1_153.

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Ward, Tony Milford. "β2-Microglobulin." In Proteins and Tumour Markers May 1995, 1259–75. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0681-8_50.

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Kikkawa, Yamato, and Hiroshi Nishimune. "Laminin β2." In Encyclopedia of Signaling Molecules, 1–11. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101519-1.

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Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "IFN-β2." In Encyclopedia of Signaling Molecules, 892. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100639.

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Conference papers on the topic "Β2m"

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Lei, Wei-Yi, Chin-Hsuan Hsieh, Chien-Chung Chang, Shao-Hsuan Wen, Chi-Tan Hu, and Shuen-Kuei Liao. "Abstract 3622: Total loss of HLA class I expression by two sarcomatoid hepatocellular carcinoma cell lines sHCC29 and sHCC63 was caused by a ∼49-kbp deletion at chromosome 15q15 across the β2m gene locus." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3622.

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Franson, J. D. "Nonlocal cancellation of dispersion." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/oam.1991.thr1.

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Two classical, coincident light pulses propagating through two different dispersive media will become broadened and their degree of coincidence will be reduced. The width of the coincidence curve can be shown to be proportional to ( β 1 2 + β 2 2 ) x 2 , where β1, and β2 are the dispersion coefficients in the two media and x is the distance traveled. When entangled photon pairs from parametric down conversion are considered instead, it is found that the width of the coincidence curve is then proportional to (β1 + β2)2x2, which gives an interference term of 2β1β1. If β1 = β2, the dispersion experienced by one photon can exactly cancel the dispersion experienced by the other in such a way that their coincidence is maintained.
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Gamo, Hideya. "Quasi-evanescent waves of the total internal reflection at the lossy or gain medium." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1986. http://dx.doi.org/10.1364/oam.1986.fx3.

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The propagation constant β = ω μ 0 ε in the lossy or gain medium is a complex quantity, of which the imaginary part represents damping or growing amplitude. The propagation constant in the free space β 0 = ω μ 0 ε 0 is real, but the component of propagation constant parallel to the boundary surface is a complex quantity, because of the continuity of tangential components of the propagation vectors: β1 t = β2 t (generalized Snell’s law). Consequently, the normal component of propagation vector β 2 n = ( β 0 2 − β 2 t 2 ) 1 / 2 becomes complex. By using the wave impedances ηTM= β n /ωϵand ηTE= ω μ /β n for TM and TE waves, we obtain the complex reflection and transmission coefficients (generalized Fresnel formulas). In the case of total internal reflection at lossless media, β2 t is real and greater than β0, and hence β2 n is imaginary. This is the well-known evanescent damping. In the case of lossy or gain medium, however, β2 n becomes a complex quantity. The waves outside lossy or gain media are not perfectly evanescent but contain some radiating components. This phenomena which corresponds to the leaky surface waves will be compared with observation using an absorbing 90° prism.
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Alom, Nur, and Bikash Kumar Sarkar. "Effect of Exit Blade Angle on the Performance of Cross Flow Hydro Turbine: A Numerical Study." In ASME 2021 Gas Turbine India Conference. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/gtindia2021-76037.

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Abstract Cross-flow hydro turbines (CFHTs) are generally used in micro hydraulic power plants due to their simplicity in design and fabrication, moderate efficiency, ease of maintenance. The CFHT can be used in low flow and low head conditions with an efficiency of around 90% at rated conditions. However, the efficiency of the CFHT can further be improved by changing its geometric parameters Hence, in the present investigation, 3D unsteady simulations are performed in order to locate the exit blade angle (β2) with the intention is to improve the efficiency of the turbine. In the proposed investigation, the multi-physics FVM solver ANSYS Fluent has been used with the help of the SST k-ω turbulence model to carry out the unsteady simulations. The 3D unsteady simulations are performed by varying the exit blade angle (β2) from 60° to 90° to improve its efficiency when the rotational speed is fixed with the number of blades being 20. From the unsteady simulations, the maximum efficiency of the CFHT is at the exit blade angle (β2) = 80°.
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Yang, C. C., A. Villeneuve, G. I. Stegeman, Cheng-Hui Lin, and Hao-Hsiung Lin. "Anisotropic Two-Photon Transition in GaAs/AlGaAs Multiple Quantum Well Waveguides." In Nonlinear Optics. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/nlo.1992.pd2.

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Two-photon transitions near the absorption edge in a multiple quantum well (MQW) structure are important because, on one hand, they provide information about the energy states involved in the forbidden direct transitions1 and, on the other hand, the induced Kerr-like optical nonlinearity has potential for ultrafast nonlinear switching applications2. In this paper, we report the first direct measurements of the two-photon absorption coefficient β2 and nonlinear refractive-index n2 in GaAs/AlGaAs MQW channel waveguides from 1490 to 1660 nm. We observed significant differences between TE and TM modes for both β2 and n2.
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Yulin, Chen, Chen Kangmin, and Zhang Dangfang. "A Variational Finite Element Method for Solving the Blade-to-Blade Flow in Centrifugal Compressor’s Cascades With Splitter Blades on an Arbitrary Streamsheet of Revolution and a Mathematical Treatment to the Region Behind Cascades." In ASME 1985 Beijing International Gas Turbine Symposium and Exposition. American Society of Mechanical Engineers, 1985. http://dx.doi.org/10.1115/85-igt-148.

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A variational finite element method for solving the blade-to-blade flow in centrifugal compressor’s cascades with splitter blades on an arbitrary streamsheet of revolution is suggested in this paper. At first, the variational principles Ref.(1) is modified, then the variational principle after modification is discretized by eight node isoparametric finite elements to carry out the system of nonlinear algebraic equations for solving the velocity potential function. Finally, the flow field which agrees with Kutta condition and has an region behind the cascade of enough length has been worked out. In this paper, it has been discovered that when the region behind cascade L3 spreads too long the system of equations might become unsolvable as a suitable exit angle β2 can't be found. The linear relation between the velocity defference of the two side of the trailing edge and the exit angle β2 has been found, it shows the range of linear variation of β2 decreases with the increasing of the length of the region behind cascades, in addition, the linear variational relation between tan⁡β2 and L3 has also been obtained. The iterative computational method for the flow field with different length L3 is used to get the solution of flow field satisfying Kutta condition and with enough length L3.
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Carroll, CL, P. Stoltz, AR Zucker, and CM Schramm. "Determining β2-Agonist Response in Children with Bronchiolitis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5816.

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Archała, Aneta, and Anita Płazińska. "β2-adrenergic receptor polymorphism in intracellular signalling pathways." In 1st International Electronic Conference on Biomedicine. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecb2021-10265.

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Elshaarawey, Ahmed, Aida Abdel Hafiz, Hesham Abdou, and Osama Khorais. "Applying Machine Learning to Optimize Electrical Submersible Pumps Design for Handling Viscous Oil." In International Petroleum Technology Conference. IPTC, 2022. http://dx.doi.org/10.2523/iptc-22657-ms.

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Abstract Most of the electrical submersible pumps available at the market currently are designed using water as a fluid base during the design phase, however, while they are used to handle viscous fluids they are suffered from significant reduction at the head per stage and overall pump efficiency. Using viscous fluid as base fluid during the design phase will lead to adapting the geometrical parameters to get the best efficiency while handling viscous fluid like heavy oil. This well resulted in a significant reduction in the production cost of heavy oil and will open new potentials and bring more reserves to the economic limit and add more oil production. This study aims to select the optimum pump geometrical parameters: Impeller ratio r1/ r2, horizontal blade Impeller angles β1 and β2, horizontal blade Diffuser angles β1‘ and β2‘ and vertical blade Diffuser ɣ1‘ and ɣ2‘ to enhance ESP performance while pumping viscous fluid especially like heavy crude oil. Increasing ESP efficiency will reduce operating cost.
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Vaghasiya, J. M., A. Sikarwar, A. Dalvand, S. Basu, and A. J. Halayko. "Oxidized Phosphatidylcholine Impairs β2-Adrenoceptor Mediated Relaxation of Murine Airways." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3275.

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