Stereospecific monoclonal antibodies to nicotine and cotinine and their use in enzyme-linked immunosorbent assays

Bjercke, Robert J.; Cook, Gary; Rychlik, Norman; Gjika, Hilda B.; Vunakis, Helen Van; Langone, John J.

doi:10.1016/0022-1759(86)90077-3

Cited by 89 publications

(59 citation statements)

References 13 publications

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“…The mouse with the highest serum titer to sRAGE as measured by enzymelinked immunosorbent assay was injected intravenously with an additional 30 g immunogen in PBS, 21 days after the last immunization. Three days later, spleen cells were harvested for production of hybridomas to sRAGE using previously described techniques (19). The hybridoma cell line with highest antibody titer and neutralizing antibody activity was selected after cloning three to four times by limiting dilution in 96-well microtiter plates, grown in a Cellmax Bioreactor (Spectrum, Rancho Dominguez, CA) using Dulbecco's modified Eagle's medium.…”

Section: Methodsmentioning

confidence: 99%

Long-Term Renal Effects of a Neutralizing RAGE Antibody in Obese Type 2 Diabetic Mice

et al. 2004

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Advanced glycation end products (AGEs) have been implicated in the pathogenesis of diabetic kidney disease. The actions of AGEs are mediated both through a non-receptor-mediated pathway and through specific receptors for AGE (RAGEs). To explore a specific role for RAGE in renal changes in type 2 diabetes, we examined the renal effects of a neutralizing murine RAGE antibody in db/db mice, a model of obese type 2 diabetes. One group of db/db mice was treated for 2 months with the RAGE antibody, and another db/db group was treated for the same period with an irrelevant IgG. Two groups of nondiabetic db/؉ mice were treated with either RAGE antibody or isotype-matched IgG for 2 months. Placebo-treated db/db mice showed a pronounced increase in kidney weight, glomerular volume, basement membrane thickness (BMT), total mesangial volume, urinary albumin excretion (UAE), and creatinine clearance compared with nondiabetic controls. In RAGE antibody-treated db/db mice, the increase in kidney weight, glomerular volume, mesangial volume, and UAE was reduced, whereas the increase in creatinine clearance and BMT was fully normalized. Notably, these effects in db/db mice were seen without impact on body weight, blood glucose, insulin levels, or food consumption. In conclusion, RAGE is an important pathogenetic factor in the renal changes in an animal model of type 2 diabetes. Diabetes 53: 166 -172, 2004 T he prevalence of type 2 diabetes is increasing worldwide. The development of diabetic nephropathy is seen in up to 30 -40% of all type 2 diabetic subjects followed by an increased morbidity and mortality. Furthermore, diabetic nephropathy is the most common cause of end-stage renal failure in the western world. Among the many potential pathogenic mechanisms responsible for the development of diabetic kidney disease (1,2), advanced glycation end products (AGEs) have been suggested to have measurable effects on the development of diabetic kidney changes as they appear in animal models of type 1 and type 2 diabetes (3-12). Recently, the receptor for AGEs (RAGE) has been proposed to play a key role in the development of diabetic renal changes in experimental type 1 diabetes (11). Accordingly, streptozotocin (STZ)-induced diabetic mice overexpressing RAGE showed a pronounced increase in renal damage compared with changes seen in nontransgenic diabetic animals (11). Furthermore, in a recent study, administration of soluble RAGE (sRAGE), a truncated form of RAGE, was shown to blunt the renal changes seen in a mouse model of type 2 diabetes (12).The aim of the present study was to explore the role of RAGE in the development of renal changes in type 2 diabetes. Accordingly, a specific neutralizing murine RAGE antibody (RAGE antibody) was administered for 2 months in db/db mice, a genetic model of type 2 diabetes characterized by obesity, sustained hyperglycemia, hyperinsulinemia, lack of ketonuria, and progressive renal kidney disease (11-17). RESEARCH DESIGN AND METHODSAdult female db/db mice (C57BLKS/J-lepr db /lepr db ) and their...

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Section: Methodsmentioning

confidence: 99%

Long-Term Renal Effects of a Neutralizing RAGE Antibody in Obese Type 2 Diabetic Mice

et al. 2004

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“…Cotinine can be measured in plasma, urine and saliva, and the choice of the optimal body fluid is still a controversial question [5,58]. Cotinine can be quantified with a double antibody radioimmunoassay [56], with an enzyme-linked immunosorbent assay [59] or with gas chromatography [58,[60][61][62].…”

Section: Biomarkersmentioning

confidence: 99%

Assessment of exposure to environmental tobacco smoke

Jaakkola¹,

Jaakkola²

1997

Eur Respir J

237

221

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Since the early 1980s, there has been growing concern about potential adverse health effects related to exposure to environmental tobacco smoke (ETS). Evidence has accumulated on ill-health associated with ETS, and such exposure has now been documented among children and adults in many countries [1][2][3][4][5][6][7][8]. A major difficulty in studying the ill-health effects of ETS has been assessing exposure, since this may occur in multiple settings with highly variable concentrations and exposure profiles may vary considerably during different age periods. Accurate and precise exposure assessment is crucial, since health effects of ETS are likely to be relatively small in magnitude. Appropriate exposure assessment is also needed for inferring causality and for risk assessment. In addition, exposure assessment is obviously necessary for development of preventive strategies.The purpose of this paper is to present a theoretical framework for assessment of exposure to ETS, and to review current methods of exposure assessment in order to provide guidelines for choice of appropriate methods for different types of study. General definitions and concepts of exposure and its assessment will be presented, followed by definitions and components of ETS. The principles for assessment of ETS exposure will then be presented. Current methods of assessment will be reviewed in terms of their advantages and disadvantages, followed by a very brief summary of the ill-health effects of ETS. This allows the criteria for selection of the appropriate method of assessing ETS exposure to be set in context, and to be formulated as user guidelines. Definitions of concentration, exposure and dose ConcentrationConcentration is the amount of a contaminant at a particular location in a particular medium [9]. For example, for an air pollutant it is the amount of the material contained in a specified volume of air. Air pollutant concentrations are usually expressed as mass per unit volume, e.g. µg·m -3 , and gaseous pollutants may also be expressed as a mixing ratio with air, e.g. parts per million (ppm) by volume. Air pollutant concentrations vary in time and space. ExposureExposure is defined as the contact of pollutant with a susceptible surface of the human body [9][10][11]. For ETS, this means contact with the eyes, the epithelium of the nose, mouth and throat, and the lining of the airways and alveoli. With respect to time, there are a number of possible formulations, including instantaneous exposure, peak exposure, average exposure over a specified time period, and cumulative exposure [11]. The best approach to assess ETS exposure will depend on the aim of the study, the health outcome, and the resources. Personal monitoring of nicotine or RSPs is the best method in studies of short-term health effects with small study samples. Stationary measurements of indoor air nicotine or RSPs are suitable for overall monitoring of ETS in different microenvironments over time. Questionnaires and interviews are suitable when studying health outcomes ...

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“…Polyclonal rabbit antisera was raised in 10-wk-old New Zealand White rabbits immunized three times at 6-wk intervals by intradermal injection of 200 g of the KLH-linked peptide. Antisera titer was tested for reactivity to rhVEGF by standard ELISA methods as described previously (22), with the exception that alkaline phosphatase conjugated mouse anti-rabbit gamma IgG together with p -nitrophenyl phosphate substrate system (Kirkegaard & Perry Laboratories Inc., Gaithersburg, MD) was used for the ELISA. Neutralizing antibody activity was tested by inhibition of 125 I-VEGF binding to recombinant human Flt-1 coated onto microtitre wells (see below).…”

Section: Recombinant Human Vegf and Neutralizing Vegf Antibodiesmentioning

confidence: 99%

“…The mouse with the highest serum level of anti-rhVEGF and neutralizing antibody activity was injected intravenously with an additional 30 g of immunogen in PBS, 21 d after the last immunization. 3 d later, spleen cells of the mouse were harvested for production of hybridomas to human recombinant VEGF using previously described techniques (22,23).…”

Section: Recombinant Human Vegf and Neutralizing Vegf Antibodiesmentioning

confidence: 99%

Vascular dysfunction induced by elevated glucose levels in rats is mediated by vascular endothelial growth factor.

Tilton¹,

Kawamura²,

Chang³

et al. 1997

J. Clin. Invest.

175

143

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The purpose of these experiments was to investigate a potential role for vascular endothelial growth factor (VEGF) in mediating vascular dysfunction induced by increased glucose flux via the sorbitol pathway. Skin chambers were mounted on the backs of Sprague-Dawley rats and 1 wk later, granulation tissue in the chamber was exposed twice daily for 7 d to 5 mM glucose, 30 mM glucose, or 1 mM sorbitol in the presence and absence of neutralizing VEGF antibodies. Albumin permeation and blood flow were increased two-to three-fold by 30 mM glucose and 1 mM sorbitol; these increases were prevented by coadministration of neutralizing VEGF antibodies. Blood flow and albumin permeation were increased ‫ف‬ 2.5-fold 1 h after topical application of recombinant human VEGF and these effects were prevented by nitric oxide synthase (NOS) inhibitors (aminoguanidine and N G -monomethyl L -arginine). Topical application of a superoxide generating system increased albumin permeation and blood flow and these changes were markedly attenuated by VEGF antibody and NOS inhibitors. Application of sodium nitroprusside for 7 d or the single application of a calcium ionophore, A23187, mimicked effects of glucose, sorbitol, and VEGF on vascular dysfunction and the ionophore effect was prevented by coadministration of aminoguanidine. These observations suggest a potentially important role for VEGF in mediating vascular dysfunction induced by "hypoxia-like" cytosolic metabolic imbalances (reductive stress, increased superoxide, and nitric oxide production) linked to increased flux of glucose via the sorbitol pathway. ( J. Clin. Invest. 1997. 99:2192-2202.)

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Stereospecific monoclonal antibodies to nicotine and cotinine and their use in enzyme-linked immunosorbent assays

Cited by 89 publications

References 13 publications

Long-Term Renal Effects of a Neutralizing RAGE Antibody in Obese Type 2 Diabetic Mice

Long-Term Renal Effects of a Neutralizing RAGE Antibody in Obese Type 2 Diabetic Mice

Assessment of exposure to environmental tobacco smoke

Vascular dysfunction induced by elevated glucose levels in rats is mediated by vascular endothelial growth factor.

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