Relevant bibliographies by topics / Half antibody

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Half antibody'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Half antibody"

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Herrington-Symes, Annabelle Patricia, Monika Farys, Hanieh Khalili, and Steve Brocchini. "Antibody fragments: Prolonging circulation half-life special issue-antibody research." Advances in Bioscience and Biotechnology 04, no. 05 (2013): 689–98. http://dx.doi.org/10.4236/abb.2013.45090.

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Wu, Shangquan, Hong Liu, Xin M. Liang, Xiaoping Wu, Baomin Wang, and Qingchuan Zhang. "Highly Sensitive Nanomechanical Immunosensor Using Half Antibody Fragments." Analytical Chemistry 86, no. 9 (2014): 4271–77. http://dx.doi.org/10.1021/ac404065m.

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Zalevsky, Jonathan, Aaron K. Chamberlain, Holly M. Horton, et al. "Enhanced antibody half-life improves in vivo activity." Nature Biotechnology 28, no. 2 (2010): 157–59. http://dx.doi.org/10.1038/nbt.1601.

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Makaraviciute, Asta, Carolyn D. Jackson, Paul A. Millner, and Almira Ramanaviciene. "Considerations in producing preferentially reduced half-antibody fragments." Journal of Immunological Methods 429 (February 2016): 50–56. http://dx.doi.org/10.1016/j.jim.2016.01.001.

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Chapman, Andrew P., Pari Antoniw, Mariangela Spitali, Shauna West, Sue Stephens, and David J. King. "Therapeutic antibody fragments with prolonged in vivo half-lives." Nature Biotechnology 17, no. 8 (1999): 780–83. http://dx.doi.org/10.1038/11717.

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Sievers, Stuart A., Louise Scharf, Anthony P. West, and Pamela J. Bjorkman. "Antibody engineering for increased potency, breadth and half-life." Current Opinion in HIV and AIDS 10, no. 3 (2015): 151–59. http://dx.doi.org/10.1097/coh.0000000000000148.

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Chen, Xiujuan, Ying Wang, and Yifeng Li. "Removing half antibody byproduct by Protein A chromatography during the purification of a bispecific antibody." Protein Expression and Purification 172 (August 2020): 105635. http://dx.doi.org/10.1016/j.pep.2020.105635.

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Yoshida, H., S. Maeda, K. Ogura, et al. "Short half-life of serum anti-CagA antibody: Comparison with conventional anti-Helicobacter pylori antibody." Gastroenterology 114 (April 1998): A342. http://dx.doi.org/10.1016/s0016-5085(98)81386-3.

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Herbener, Peter, Kurt Schönfeld, Martin König, et al. "Functional relevance of in vivo half antibody exchange of an IgG4 therapeutic antibody-drug conjugate." PLOS ONE 13, no. 4 (2018): e0195823. http://dx.doi.org/10.1371/journal.pone.0195823.

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Hinton, Paul R., Joanna M. Xiong, Mary G. Johlfs, Meina Tao Tang, Stephen Keller, and Naoya Tsurushita. "An Engineered Human IgG1 Antibody with Longer Serum Half-Life." Journal of Immunology 176, no. 1 (2005): 346–56. http://dx.doi.org/10.4049/jimmunol.176.1.346.

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Dissertations / Theses on the topic "Half antibody"

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Sabek, Jad. "Combination of nanophotonic biosensors and light-assisted immobilization procedures for the detection of cardiac biomarkers." Doctoral thesis, Universitat Politècnica de València, 2019. http://hdl.handle.net/10251/124821.

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[ES] El cuidado de la salud es un campo en el que la detección precoz de enfermedades está cobrando cada vez más importancia. Hoy en día, profesionales y ciudadanos demandan que las técnicas de diagnóstico sean de alta calidad, tanto para el sistema de sanidad privado como para el público. Cuando se utilizan técnicas de diagnóstico de manera inadecuada, eso puede acarrear bastantes consecuencias, tales como un serio peligro sobre la salud y la sobrecarga técnica y económica de los servicios de salud. Eso es debido a que las técnicas de diagnóstico disponibles hoy en día son demasiado costosas, centralizadas en laboratorios y necesitan profesionales altamente cualificados para poder llevar a cabo dichas tareas, lo que conllevaría una demora en el tiempo, siendo este muchas veces vital para los enfermos. Es muy necesario, por lo tanto, reflexionar sobre la necesidad y emergencia de tales prácticas preventivas, especialmente para enfermedades de alto riesgo como el cáncer, el Alzheimer o la primera causa de muerte en el mundo, las enfermedades cardiovasculares. En este contexto, el objetivo principal del trabajo realizado durante esta Tesis Doctoral es ayudar a superar estos problemas mediante la exploración de la posibilidad de utilizar tecnología fotónica para el desarrollo de sistemas de análisis que puedan ser utilizados para el diagnóstico y pronóstico de las enfermedades cardiovasculares. Este objetivo se ha abordado mediante la combinación de la tecnología nanofotónica, consistiendo en la nanofabricación de las estructuras PBG de sensado que ofrece varios beneficios, como una alta sensibilidad, una extrema reducción de tamaño y un proceso de fabricación compatible con el de la industria microelectrónica, con un método de biofuncionalización obteniendo una capa de bioreconocimiento estable y selectiva mediante el uso de la reacción TEC asistida por luz capaz de proporcionar unas capas de bio-reconocimiento extremadamente finas con una inmovilización espacialmente selectiva.<br>[CAT] L'atenció a la salut és un camp en què la detecció precoç de malalties està cobrant cada vegada més importància. Hui en dia, professionals i ciutadans demanen que les tècniques de diagnòstic siguin d'alta qualitat, tant per al sistema de sanitat privat com per al públic. Quan s'utilitzen tècniques de diagnòstic de manera inadequada, això pot comportar bastants conseqüències, com ara, un seriós perill sobre la salut i la sobrecàrrega tècnica i econòmica dels serveis de salut. Això és degut al fet que les tècniques de diagnòstic disponibles hui en dia són molt costoses, centralitzades en laboratoris i necessiten professionals altament qualificats per poder realitzar aquestes tasques, lo que comportaria a una demora en el temps que moltes vegades es vital pels malalts. És molt necessari, per tant, reflexionar sobre la necessitat i emergència de tals practiques preventives, especialment per a malalties d'alt risc com el càncer, l'Alzheimer o la primera causa de mort al món, les malalties cardiovasculars. En aquest context, l'objectiu principal del treball realitzat durant aquesta Tesi Doctoral és ajudar a superar aquests problemes mitjançant l'exploració de la possibilitat d'utilitzar tecnologia fotònica per al desenvolupament de sistemes d'anàlisis que puguin ser utilitzats per al diagnòstic i pronòstic de les malalties cardiovasculars. Aquest objectiu s'ha abordat mitjançant la combinació de la tecnologia nanofotònica, consistint en la nanofabricació de les estructures de detecció de PBG fotòniques que ofereix diversos beneficis, com una alta sensibilitat, una extrema reducció de mida i un procés de fabricació compatible amb el de la indústria microelectrònica, amb un mètode de biofuncionalització obtenint una capa de bio-reconeixement estable i selectiva mitjançant l'ús de la reacció TEC assistida per llum capaç de proporcionar unes capes de bioreconeixement extremadament fines amb una immobilització espacialment selectiva. preventives, especialment per a malalties d'alt risc com el càncer, l'Alzheimer o la primera causa de mort al món, les malalties cardiovasculars. En aquest context, l'objectiu principal del treball realitzat durant aquesta Tesi Doctoral és ajudar a superar aquests problemes mitjançant l'exploració de la possibilitat d'utilitzar tecnologia fotònica per al desenvolupament de sistemes d'anàlisis que puguin ser utilitzats per al diagnòstic i pronòstic de les malalties cardiovasculars. Aquest objectiu s'ha abordat mitjançant la combinació de la tecnologia nanofotònica, consistint en la nanofabricació de les estructures de detecció de PBG fotòniques que ofereix diversos beneficis, com una alta sensibilitat, una extrema reducció de mida i un procés de fabricació compatible amb el de la indústria microelectrònica, amb un mètode de biofuncionalització obtenint una capa de bio-reconeixement estable i selectiva mitjançant l'ús de la reacció TEC assistida per llum capaç de proporcionar unes capes de bioreconeixement extremadament fines amb una immobilització espacialment selectiva.<br>[EN] Healthcare is a field where the early detection of diseases is becoming more and more important. Nowadays, professionals and citizens demand high quality diagnosis techniques offered by both private and public health systems. When the application of diagnostic tests is not adequate, different consequences can be observed such as health hazard and technical and economic overload of health services. This is due to the fact that the diagnostic techniques available are expensive, centralized in laboratories and with the need for highly qualified professionals to carry out these tasks, what can fundamentally lead to delays in time, being critical for the patient's health. It is very necessary, therefore, to reflect on the need and emergency of such preventive practices, especially for high-risk diseases such as cancer, Alzheimer or the first cause of death in the world, the cardiovascular diseases. Within this context, the main objective of the work done during this PhD Thesis is to help on overcoming these problems by exploring the possibility of using photonic technology for the development of analysis devices which might be used for the early diagnosis and prognosis of cardiovascular diseases. This objective has been addressed by combining nanophotonic technology, by the nanofabrication of the photonic PBG sensing structures, which provides several benefits such as a high sensitivity, an extreme size reduction and a fabrication process being compatible with that from the microelectronics industry, with a light-assisted biofunctionalization method forming a stable and selective biorecognition layer using TEC reaction able to provide extremely thin biorecognition layers with a spatially-selective immobilization.<br>Sabek, J. (2019). Combination of nanophotonic biosensors and light-assisted immobilization procedures for the detection of cardiac biomarkers [Tesis doctoral no publicada]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/124821<br>TESIS
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Ettaki, Zacharia Nabil. "Developing Novel Methods to Identify RNA-Associated Mechanisms for Inheritance." Thesis, 2020. http://hdl.handle.net/1805/24500.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Animals depend on inheriting non-genetic information early in life to grow and develop naturally. This inherited, non-genetic information was previously thought to be limited to DNA modifications and DNA binding proteins. But recent studies have expanded our understanding of inheritance to include RNA and RNA binding proteins. We currently lack methods to identify and enrich for RNA binding proteins that might be involved in providing non-genetic information from mother to daughter cells. Others have developed a method using modified enzyme tags to pulse-label proteins with small molecule fluorescent ligands and follow these proteins as they are inherited by cells. Here I characterized and tested the application of a fluorescent small molecule targeting antibody to enrich for these labeled proteins. I first tested the ability of this antibody to bind to fluorescent ligand-labeled enzymes. I determined that the antibody can efficiently bind to at least one of the labeled enzymes. Second, I determined crystallization conditions for the ligand binding antibody fragment. This thesis sets the stage for structure determination and to test whether this antibody can work in vivo to enrich for RNA binding proteins involved in the delivery of non-genetic information to cells.
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Balakrishnan, Arjun. "Unravelling the Mechanism of Bactericidal/Permeability-Increasing Protein Expression during Bacterial Pathogenesis." Thesis, 2016. http://hdl.handle.net/2005/3155.

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Anti-microbial proteins (AMP) are the key effector arm of the innate immune system. The prevalence of AMP in single-celled eukaryotes to humans shows its importance during the course of evolution. The first report for the role of the anti-microbial peptide in clearing infection was given by Alexander Fleming in 1990’s through the discovery of Penicillin and Lysozyme. The search for antimicrobial agents in human granulocytes was begun by Ehrlich in 1870’s but the first successful isolation of an antimicrobial agent from rabbit neutrophils was done by Zeya and Spitznagel in 1969. Later work by Peter Elshbach and his group on AMPs in rabbit neutrophils brought to light an AMP that can increase the permeability of the bacterial membrane. This AMP named as Bactericidal/permeability-increasing protein (BPI) was further isolated from human neutrophils. Since then many studies have been carried out to understand the mode of action of BPI, which culminated in understanding the new functional activity of this protein viz opsonisation, LPS neutralization and anti-angiogenic function. Knowing to the role of BPI as an anti-inflammatory agent, multiple studies have tried to use BPI for treating endotoxic shock. Dysregulation of BPI expression is associated with various inflammatory diseases like Crohn’s Disease (CD), Ulcerative colitis (UC) and Infectious enteritis’s. Mutations in BPI are also linked to susceptibility to various infections. Even though there are several studies focusing on the functional aspects of BPI, the regulation of BPI expression is poorly understood. Knowing the clinical importance of dysregulation of BPI, it is vital to understand the regulation of BPI expression during the course of bacterial infection. The Thesis is divided into four chapters. As the main aim of this study is to understand the regulation of BPI expression, in Chapter 1 we introduce the known facts about the protein. A brief overview of the mode of action and regulation of BPI is discussed in this chapter. The subsequent sections describe the diseases associated with Dysregulation of BPI and the use of BPI as a therapeutic agent in various diseases. Towards the end, the objective of the present study is discussed. BPI is primarily known to be expressed in human neutrophils and epithelial cells. Previous studies have shown that among innate immune cells, murine BPI is expressed only in dendritic cells and neutrophils, but not in macrophages. Based on these results, it was presumed that BPI is not expressed in human macrophages. In Chapter 2, we report the presence of BPI in human macrophages. Our studies revealed increased expression of BPI in human macrophages stimulated with various PAMPs (Pathogen-associated molecular patterns) viz., LPS, flagellin as well as during bacterial infection. Further, during the course of an infection, BPI interacted with Gram-negative bacteria, resulting in enhanced phagocytosis and subsequent control of the bacterial replication. However, it was observed that bacteria which can maintain an active replicating niche (Salmonella Typhimurium) avoid the interaction with BPI during later stages of infection. On the other hand Salmonella mutants, which cannot maintain a replicating niche, as well as Shigella flexneri, which quit the endosomal vesicle, showed interaction with BPI. BPI was induced in both M1 and M2 differentiated macrophages suggesting its role in limiting Gram-negative bacteria and parasitic infection. These results propose an active role of BPI in Gram-negative bacterial clearance by human macrophages. This chapter concludes with a discussion on the importance of BPI expression in human but not murine macrophages. The importance of maintaining an active replicating niche by STM to evade interaction with BPI is also discussed. As the first line of defense against invading pathogens, intestinal epithelium produces various antimicrobial proteins (AMP) that help with clearance of pathogen. The precise mechanism of AMP regulation in intestinal epithelium is not clear. Intestinal epithelium being a primary entry point for various pathogens, we tried to understand the regulation of BPI expression in the intestine during the course of bacterial infection. In Chapter 3, we report a direct correlation between intestinal damage and BPI expression. In Caco-2 cells, we see a significant increase in BPI levels upon membrane damage mediated by S.aureus infection and pore-forming toxins (Streptolysin and Listeriolysin). Cells detect changes in potassium levels as a Danger-associated molecular pattern (DAMP) associated with cell damage and induce BPI expression in a p38 dependent manner. These results are further supported by in vivo findings that BPI expression in the murine intestinal epithelium is induced upon infection with bacteria which cause intestinal damage (Salmonella Typhimurium & Shigella flexneri) whereas mutants which don’t cause intestinal damage (STM fliC & STM invC), didn’t induce BPI expression. These findings have a huge impact on our current understanding of AMP response during inflammatory bowel diseases (IBD). Our results suggest that dysregulation of BPI expression might be an effect rather than a cause of IBD. This chapter concludes with a discussion on the importance of potassium efflux associated with membrane damage as an important signal that helps in discriminating the invading pathogen from the pool of gut microflora. Bactericidal/permeability-increasing protein had been shown to possess anti-inflammatory and endotoxin neutralizing activity by interacting with LPS of Gram-negative bacteria. Even though rBPI (recombinant BPI) has cleared phase III clinical trials for treating endotoxemia, the high cost of purified BPI provided by pharmaceutical companies makes it inaccessible or unavailable for the common man. In Chapter 4, we examined the feasibility of using murine BPI (mBPI) expressed on halophilic Archaeal gas vesicle nanoparticles (GVNPs) for the treatment of endotoxemia in high-risk patients, using a murine model of D-galactosamine-induced endotoxic shock. Halobacterium sp. NRC-1 was used to express the N-terminal 199 amino acid residues of mBPI fused to the GVNP GvpC protein, and bound to the surface of the haloarchaeal GVNPs. Our results indicate that delivery of mBPIN-GVNPs increase the survival rate of mice challenged with lethal concentrations of lipopolysaccharide (LPS) and D-galactosamine. Additionally, the mBPIN-GVNP-treated mice displayed reduced symptoms of inflammation including inflammatory anemia, recruitment of neutrophils, liver apoptosis and pro-inflammatory serum cytokine levels. This chapter concludes with a discussion of the advantages of using mBPIN-GVNPs over purified protein in treating endotoxic shock.
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Books on the topic "Half antibody"

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Laureno, Robert. Selected Concepts. Edited by Robert Laureno. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190607166.003.0016.

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This chapter on “Selected Concepts” examines the evolution of neurological concepts during the modern era. Examples presented include the concepts of transient ischemic attack, disconnection syndrome, thoracic outlet syndrome, and Wilbrand’s knee. Over the past half century, neurology has witnessed great technological advances. Newer scientific methods, such as MRI scanning, have led to new knowledge that has necessitated changes in neurologic concepts. During recent decades, new concepts have emerged. Infectious proteins, antibody-mediated brain disease, channelopathies, and the glymphatic system are relatively new ideas, and we cannot foresee how our understanding of these concepts will be advanced or modified in the coming decades.
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Book chapters on the topic "Half antibody"

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Morrow, K. John. "Antibody Half-Life." In Biosimilars of Monoclonal Antibodies. John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118940648.ch21.

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Olafsen, Tove. "Fc Engineering: Serum Half-Life Modulation Through FcRn Binding." In Antibody Engineering. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-974-7_31.

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Jevševar, Simona, Mateja Kusterle, and Maja Kenig. "PEGylation of Antibody Fragments for Half-Life Extension." In Methods in Molecular Biology. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-931-0_15.

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Becker, Richard C., and Frederick A. Spencer. "Platelet Glycoprotein IIb/IIIa Receptor Antagonists." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0014.

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The glycoprotein (GP) IIb/IIIa (αIIb/β3) receptor totalling 50,000 to 70,000 copies per platelet represents a common pathway for platelet aggregation in response to a wide variety of biochemical and mechanical stimuli. Accordingly, it represents an attractive target for pharmacologic inhibition that can be applied to patients with acute coronary syndromes. The evolution of GPIIb/IIIa receptor antagonists began with murine monoclonal antibodies and subsequently expanded to include small peptide or nonpeptide molecules with structural similarities to fibrinogen. There are three intravenous GPIIb/IIIa receptor antagonists that have been approved by the U.S. Food and Drug Administration: . . . • Abciximab (ReoPro) . . . . . . • Tirofiban (Aggrastat) . . . . . . • Eptifibatide (Integrilin) . . . Abciximab (ReoPro) is the Fab fragment of the chimeric human–murine monoclonal antibody c7E3. Following an intravenous bolus, free plasma concentrations of abciximab decrease rapidly with an initial half-life of less than 10 minutes and a second-phase half-life of 30 minutes, representing rapid binding to the platelet GPIIb/IIIa receptor. Abciximab remains in the circulation for 10 or more days in the platelet-bound state. Intravenous administration of abciximab in doses ranging from 0.15 mg/kg to 0.3 mg/kg produces a rapid dose-dependent inhibition of platelet aggregation in response to adenosine diphosphate (ADP). At the highest dose, 80% of platelet GPIIb/IIIa receptors are occupied within 2 hours and platelet aggregation, even with 20 μM ADP, is completely inhibited. Sustained inhibition is achieved with prolonged infusions (12 to 24 hours) and low-level receptor blockade is present for up to 10 days following cessation of the infusion; however, platelet inhibition during infusions beyond 24 hours has not been well characterized. Platelet aggregation in response to 5 μM ADP returns to greater than or equal to 50% of baseline within 24 hours of drug cessation. In nearly 2,100 patients undergoing either balloon coronary angioplasty or atherectomy at high risk for ischemic (thrombotic) complications, a bolus of abciximab (0.25 mg/kg) followed by a 12-hour continuous infusion (10 μg/min) reduced the occurrence of death, the occurrence myocardial infarction (MI), or the need for an urgent intervention (repeat angioplasty, stent placement, balloon pump insertion, or bypass grafting) by 35% (EPIC Investigators, 1994).
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Calderón-Garcidueñas, Lilian, Partha S. Mukherjee, Katharina Waniek, et al. "Non-Phosphorylated Tau in Cerebrospinal Fluid is a Marker of Alzheimer’s Disease Continuum in Young Urbanites Exposed to Air Pollution." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210040.

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Long-term exposure to fine particulate matter (PM2.5) and ozone (O3) above USEPA standards is associated with Alzheimer’s disease (AD) risk. Metropolitan Mexico City (MMC) children exhibit subcortical pretangles in infancy and cortical tau pre-tangles, NFTs, and amyloid phases 1–2 by the 2nd decade. Given their AD continuum, we measured in 507 normal cerebrospinal fluid (CSF) samples (MMC 354, controls 153, 12.82 ± 6.73 y), a high affinity monoclonal non- phosphorylated tau antibody (non-P-Tau), as a potential biomarker of AD and axonal damage. In 81 samples, we also measured total tau (T-Tau), tau phosphorylated at threonine 181 (P-Tau), amyloid-β1–42, BDNF, and vitamin D. We documented by electron microscopy myelinated axonal size and the pathology associated with combustion-derived nanoparticles (CDNPs) in anterior cingulate cortex white matter in 6 young residents (16.25 ± 3.34 y). Non-P-Tau showed a strong increase with age significantly faster among MMC versus controls (p = 0.0055). Aβ1–42 and BDNF concentrations were lower in MMC children (p = 0.002 and 0.03, respectively). Anterior cingulate cortex showed a significant decrease (p = &lt;0.0001) in the average axonal size and CDNPs were associated with organelle pathology. Significant age increases in non-P-Tau support tau changes early in a population with axonal pathology and evolving AD hallmarks in the first two decades of life. Non-P-Tau is an early biomarker of axonal damage and potentially valuable to monitor progressive longitudinal changes along with AD multianalyte classical CSF markers. Neuroprotection of young urbanites with PM2.5 and CDNPs exposures ought to be a public health priority to halt the development of AD in the first two decades of life.
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"cases, have been from Western Australia, with a further thirteen cases from the Northern Territory. It is also interesting to note that the first confirmed case of encephalitis due to Kunjin virus occurred in Western Australia in 1978, and three additional cases have been diagnosed since, two from Western Australia in 1991 and 1995, and one in Victoria in 1984 (Table 8.1). Most of the cases of Australian encephalitis in Western Australia have occurred in areas distant from the Ord River irrigation area. Of particular significance was the spread of MVE virus from the Kimberley area south to the Pilbara and Gascoyne regions causing one case of encephalitis in 1978 and three cases in 1981. It is hypothesized that movement of virus to the Pilbara region in 1978 was due to an increase in viral activity in the West Kimberley area following heavy rainfall and flooding, and that with subsequent extensive cyclonic rainfall in the Pilbara region, viraemic waterbirds moved south down the narrow coastal strip, introducing the virus into Pilbara (Stanley 1979). It is probable that a similar mechanism may have occurred in 1981. Although there has been evidence (see next section), of MVE virus activity in the Pilbara region in recent years, there have been no further cases. Analysis of the cases of Australian encephalitis has indicated that Aboriginal infants, particularly male infants, are most at risk of fatal or severe disease (Mackenzie et al. 1993a). However, tourists and visitors to the Kimberley region (and Northern Territory) have also been shown to have an increased risk of disease. Sentinel chicken surveillance Following the 1978 outbreak of Australian encephalitis, a number of sentinel chicken flocks were established in the Kimberley area. Six flocks had been established by 1981 and the number rose to twenty-four flocks in twenty-two regional centres in the Kimberley, Pilbara and Gascoyne regions by 1989 (Broom et al. 1989; Mackenzie et al. 1992; 1994c). Each flock contains twelve chickens which are bled at two weekly intervals between November and June, the period of increased risk of virus transmission, and monthly at other times. The sera are then assayed for antibody to MVE and Kunjin viruses in our laboratory in Perth to provide an early warning system of increased virus activity. Initially sera were tested by HI for the presence of antibody, and positive sera were then subjected to neutralization assay to determine the identity of the infecting virus. A more rapid enzyme-linked immunosorbent assay (ELISA) was introduced in 1986 (Broom et al. 1987), and more recently a competitive ELISA using specific monoclonal antibodies to identify the virus is being used (Hall et al. 1992; 1995). Sentinel chicken flocks were also established in 1992 in the Northern Territory to monitor MVE activity (Aldred et al. 1992). The sentinel chicken programme has clearly shown that MVE virus is enzootic in several areas of the Kimberley region, particularly in the Ord River area at Kununurra. Seroconversions in sentinel chickens occur every year during the latter half of the wet season." In Water Resources. CRC Press, 1998. http://dx.doi.org/10.4324/9780203027851-24.

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"roles of carrier proteins. The identification and usefulness of blood group antigens as markers will be described and possible explanations for their variation in expression will be discussed. Most red cell antigens have been investigated because they are clinically important [1]. The antibodies to some antigens have caused haemolytic disease of the newborn and/or transfusion reactions. Other antigens are involved in haemolytic anaemia and some are important in transplantation. Red cell antigens provided a tool for investigation of the red cell surface and for use as genetic, immunological and biochemical markers. More than 500 red cell antigens are serologically defined, about half of which have been officially recognised and have been numbered by the International Society of Blood Transfusion Working Party on Terminology for Red Cell Surface Antigens [2,3]. Antigens are divided into systems (antigens controlled by a locus or closely linked loci) and three holding files: collections (related antigens whose genetic relationship is unknown), antigens of high incidence or antigens of low incidence. THE MAIEA TECHNIQUE Sometimes if an antigen has a very high or a very low incidence it is hard to relate it to other antigens or to assign it to a system. Immunochemical studies and in the case of high incidence antigens, use of cells of rare phenotype can be informative and recently the MAIEA technique, monoclonal antibody specific immobilisation of erythrocyte antigens, has proved useful. MAIEA was an adaptation of a technique, MAIPA, frequently used for studying platelets. MAIEA can be used to assign red cells antigens, as recognised by human alloantisera, to particular components of the red cell membrane [4]. Location of antigens on specific red cell membrane components The Knops system consists of 4 high incidence antigens Kna, McCa, Sla and Yka with frequencies greater than 90% in populations tested. There is also a low incidence antigen Knb found in Whites [3]. The antibodies to these public antigens are difficult to identify serologically. The antigens show a wide variation of strength on different donor’s cells. There is a null phenotype, the Helgeson phenotype, which appears from serological tests to lack all 4 antigens [5]. Cells which lack one Knops antigen may have weakened expression of other Knops antigens. The mists about these serologically difficult antigens were cleared when Moulds et al [6] and Rao et al [7] independently showed that these antigens were carried on the CR1 (complement receptor 1, CD35) protein. The related antigen Csa was not located on CR1, so Csa and Csb were left in the Cost collection [3]." In Transfusion Immunology and Medicine. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-7.

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Conference papers on the topic "Half antibody"

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Brettler, D., A. A. Forsberg, P. Levine, J. Petillo, K. Lamon, and J. Sullivan. "FACTOR VIII:C PURIFIED FROM PLASMA VIA MONOCLONAL ANTIBODIES: HUMAN STUDIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643923.

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Factor VIII:C purified utilizing a mouse monoclonal antibody to FVIII:VWF was used exclusively for 6 months to treat hemorrhages on a demand basis in 7 patients with severe hemophilia A and no inhibitor. The mean age of the patients was 26.1 years with a range of 16-39 years. The dose administered was from 15-18 u/kg at the time of hemorrhage. The patients infused on the average of once every 5 days. One patient required 40-50 u/kg every day for 3 days secondary to an automobile accident. Laboratory assessments included: a fall-off study to determine the factor VIII half-life both when the study commenced and after 6 months on study; inhibitor levels, and ELISA assay to detect antibody to mouse protein. Additionally, immunological data including quantitative T cell subsets and skin testing on each patient was obtained on entrance to the study, at 1 month, 3 months and at conclusion in order to ascertain whether immune function in these patients would improve with the use of purer factor concentrate. The initial mean half-life of the infused concentrate was 15.4 hours ± 2.2 with a range of 12.6 to 18.4 hours. The mean half-life after the patients had been on the concentrate for 6 months was 17.5 ± 5.9 hours (range 11.0 to 29 hours). No inhibitor developed in any patient. Six of seven patients did not develop significant levels of anti-mouse IgG antibody. One patient had a rheumatoid factor which interfered with the ELISA assay for anti-mouse antibody and thus its presence could not be assessed. There were no adverse reactions to the material, and hemostatic efficacy was judged as excellent. There were no significant changes in quantitative T cell subsets. Three out of six patients lost their previous total skin test anergy and two other patients increased the number of antigens to which they reacted. This concentrate proved to be safe and efficacious, to have excellent half-life, and to be associated with apparent improvement in the immune response.
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2

Arvedson, Tara L., Mercedesz Balazs, Pamela Bogner, et al. "Abstract 55: Generation of half-life extended anti-CD33 BiTE® antibody constructs compatible with once-weekly dosing." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-55.

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3

Sternjak, Alexander, Fei Lee, Joachim Wahl, et al. "Abstract 3630: Preclinical evaluation of a BiTE® antibody construct with extended half-life that targets the tumor differentiation marker mesothelin." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3630.

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4

Nolan-Stevaux, Olivier. "Abstract DDT02-03: AMG 509: A novel, humanized, half-Life extended, bispecific STEAP1 × CD3 T cell recruiting XmAb®2+1 antibody." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-ddt02-03.

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5

Valencia, Xavier, Christen Glogowski, Azra Hussaini, Richard Mountfield, and Peter Ho. "24 Phase 1 study in healthy volunteers to assess PK, PD safety & tolerability of BOS161721, an extended half-life anti-IL21 monoclonal antibody." In 13th International Congress on Systemic Lupus Erythematosus (LUPUS 2019), San Francisco, California, USA, April 5–8, 2019, Abstract Presentations. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-lsm.24.

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6

Nilsson, I. M., E. Berntorp, and O. Zettervall. "TOLERANCE INDUCTION IN HIGH-RESPONDING HEMOPHILIACS WITH F VIII ANTIBODIES BY MEANS OF COMBINED TREATMENT WITH IgG, CYCLOPHOSPHAMIDE AND F VIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644717.

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Of 10 patients with hemophilia A and antibodies, 7 have been rendered tolerant by means of combined treatment with high-dose IgG i.v., cyclophosphamide and F VIII. When the initial antibody concentration exceeded 10 Bethesda inhibitor units per ml, the treatment was preceded by antibody adsorption to protein A. Six of the tolerant patients were originally classified as high-responders. After one week of the combined treatment, VI11:C dropped and the inhibitor reappeared in low titer. The F VIII infusions being continued alone, the inhibitor disappeared in the following week and VIII:C increased satisfactorily after infusion, while VIII:Ag (assayed immunoradiometrically) reached very high concentrations. In one patient the treatment had to be repeated once. Except for transient leukopenia, no side effects occurred. Earlier treatments with F VIII in combination with cyclophosphamide gave high anamnestic response. In two of the remaining three non-tolerant patients, anamnestic response decreased dramatically after two courses of the combined treatment. The tolerant state seems to be stable, as the tolerant patients have now been on regular prophylaxis with F VIII concentrate for periods varying from four months to four years. The half-life of infused F VIII is normal, while that of VIII:Ag is prolonged. On the basis of similar findings in hemophilia B patients, we believe the VIII:Ag to have become modi Tied and complexed to a 'new' antibody which lacks VIII:C inhibitory activity. It is known that modified antigen may act as a tolerogen. The tolerant state may thus be sustained by maintaining consistent concentrations of the modified antigen by means of the F VIII treatment. We conclude that the combined treatment described here is a safe and effective method of tolerance induction in hemophilia A patients.
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7

Matsuda, M., Y. Sakata, T. Sugo, S. Tanabe, J. Mimuro, and H. Murayama. "PROTEIN C TOCHIGI: AN ABNORMAL PROTEIN C CHARACTERIZED BY DEFECTIVE RELEASE OF ACTIVATION PEPTIDE BY THROMBIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643646.

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A molecular abnormality of protein C (PC) has been found in an 18-year-old female who has been thrombophilic since she was one-year old. Detailed coagulation studies revealed that PC antigen was only 25% of normal while PC activity was substantially undetectable in her plasma. Other related plasma proteins including vitamin K-dependent blood coagulation factors, antithrombinin and plasminogen were all within normal limits.Family study demonstrated that her father, one of her paternal uncles andher half-bred sister had half-normal levels of both activity and antigen of PC. They thus appear to be heterozygotes for PC deficiency. Her mother had anormal level of PC as antigen but only60% of normal as activity. We thus presumed that nearly a half population ofPC was not properly functioning in hermother's plasma. By utilizing insolubilized monoclonal* antibodies against PC, we isolated both single-chain and two-chain forms of PC from the propositus' plasma. They were found to have normal molecular weights by SDS-PAGE, but they failed to exhibit amidolytic activity and to incorporate 3H-labeled DFP after thrombin-treatment. By immunoblotting and ELISA utilizing a monoclonal antibody that recognizes the activation peptide part of the heavy chain of PC, we found that cleavage of the activation peptide by thrombin was impaired totally in the proposi and partly in her mother’s PC. It is thus most probable that the propositus inherited PC deficiency from her father and a molecular abnormality of non-activatable protein C from her mother, respectively. Accordingly, all the PC molecules in the propositus’ plasma are non-functional, which may have culminated in the occurrence of cerebral thrombosis at the age of 1 and severe deep venous thrombosis and bilateral pulmonary embolisms at the age of 10.
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8

KÖhlin, A., and J. Stenflo. "HIGH AFFINITY CALCIUM BINDING TO DOMAINES OF PROTEIN C THAT ARE HOMOLOGUS TO THE EPIDERMAL GROWTH FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643645.

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In addition to γ-carboxyglutamic acid (Gla)-dependent calcium binding all of the vitamin K-dependent plasma proteins, except prothrombin, have one or two high affinity calcium binding sites that do not require the Gla residues. A common denominator among these proteins (factors IX, X, protein C, protein Z and protein S) is that they have domaines that are homologus to the epidermal growth factor (EGF) precursor. In factors VII,IX,X, protein C and in protein Z the aminoterminal of two EGF homology regions contain one residue of β-hydroxyaspartic acid (Hya) whereas in protein S the aminoterminal EGF homology region contains Hya and the three following contain one β-hydroxyasparagine residue each.In an attempt to elucidate the role of the EGF homology regions in the Gla independent calcium binding we have isolated a tryptic fragment (residue 44-138) from the light chain of human protein C. The fragment was isolated using a monoclonal antibody that recognizes a calcium ion stabilized epitope that is expressed both in intact protein C and in protein C lacking the Gla domaine.The antibody bound the isolated EGF homology region in the presence of calcium ions but not in EDTA containing buffer. A calcium ion titration showed half maximal binding at approximately 200 μM Ca2+. The metal ion induced conformational change in the isolated fragment was also studied with affinity purified rabbit antibodies against Gla domainless protein C. Antibodies that bound in the presence of calcium ions and that could be eluted with EDTA recognized the metal ion induced conformational change in the isolated EGF homology domain. Our results suggest that one or both of the EGF homology regions are involved in the Gla-independent high affinity calcium binding in the vitamin K-dependent plasma proteins.
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9

Morrissey, J. H., D. S. Fair, and T. S. Edgington. "STRUCTURE AND PROPERTIES OF THE HUMAN TISSUE FACTOR APOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643738.

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Tissue factor (TF), an integral membrane glycoprotein, is an initiating molecule for the coagulation protease cascade. TF must reside in a phospholipid membrane for optimal activity where it functions as the receptor and essential allosteric activator for factor Vll/VIIa.TF apoprotein was purified from human brain and placenta using factor Vll-affinity chromatography or immunoaffinity chromatography with a mouse anti-TF monoclonal antibody. Both methods resulted in a homogeneous preparation consisting of a highly glycosylated 47 kDa heavy chain and a 12.5 kDa light chain.Removal of asparagine-linked carbohydrate chains with glycopeptidase F reduced the apparentmolecular weight of the heavy chain to 37 kDa but hadno effect on the mobility of the light chain in SDS gel electrophoresis. Electrophoretic analysis of theintact protein with and without reduction indicates that the light chain is disulfide-linked to the heavychain in about half of the TF molecules and is notessential for function.The majority of polyclonal andtwenty- nine monoclonal antibodies against purified TF strongly inhibit coagulation and in all cases aredirected against epitopes on the heavy chain alone. Functional regions of the TF heavy chain have been investigated using a library of twenty-nine monoclonalantibodies and a series of overlapping, synthetic oligopeptides based on sequence information obtained from cloning the cDNA for TF. Supported by NIH grantsHL-16411 and CA-41085.
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10

Picard, P., J. Y. Borg, M. Vasse, et al. "BIOLOGICAL PRETHROMBOTIC MARKERS AND COAGULATION INHIBITORS IN NEPHROTIC SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643051.

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Nephrotic syndrome (NS) has long been recognized as a clinical prethrombotic state, because of severe thrombo-embolic complications. But underlying mechanisms are still poorly defined. In 56 untreated nephrotic adult patients (most of them without renal failure), we investigate in vivo coagulation activation by measuring 0 plasmatic specific fibrin degradation products (FbDP) (immuno-enzymological assay using a monoclonal anti D-neo antibody) and (2) the ratio of factor VII coagulant activity (V11c) to factor VII:Anti gen (VII;Ag) tested by an ELISA method. We examined coagulation inhibitors in plasmas and urines (antithrombin III—AT III, heparin cofactor II-HC II by amidolytic and laurell methods; protein C-PC by an ELISA assay ;free and bound protein S—PS:Ag by laurell assays). In few patients we also determinecjfribronectin and t-PA inhibitor.Results in plasma are submitted and expressed as mean ± DS and compared (t test) with controls (C) without nephropathySignificantly elevated activated factor VII and FbDP levels show an “in vivo activation” of coagulation in NS. Plasmatic fibronectin, HC II, PC:frg, and tPA-I levels are alsp significantly elevated and roughly paralleled fibrinogen (6,25 ± 2,9 g/1) and other acute-phase proteins measurements. Significant amounts of AT 111:Ag were present in about half tested urines, but in a degraded form with low or absent heparin cofactor activity. Mean plasmatic AT III concentration was in normal range, but three of the 4 patients with a thrombotic disease had the lowest values of AT III and the highest fibrinogen levels.We could demonstrate a biological prethrombotic state in NS and suggest the way of identifying patients with high risk of thrombosis.
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