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Index / Bioassays / QuantiChrom™ BCP Albumin Assay Kit, Quantitative determination of albumin by bromcresol purple BCP method at 610nm. Procedure 5 min. Kit size 250 tests. Detection limit 0.3 g_dL. Shelf life 12 mon / Product Detail : DIAP-250 QuantiChrom™ BCP Albumin Assay Kit, Quantitative determination of albumin by bromcresol purple BCP method at 610nm. Procedure 5 min. Kit size 250 tests. Detection limit 0.3 g_dL. Shelf life 12 mon
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#DIAP-250 QuantiChrom™ BCP Albumin Assay Kit, Quantitative determination of albumin by bromcresol purple BCP method at 610nm. Procedure 5 min. Kit size 250 tests. Detection limit 0.3 g_dL. Shelf life 12 mon

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Product name : QuantiChrom™ BCP Albumin Assay Kit, Quantitative determination of albumin by bromcresol purple BCP method at 610nm. Procedure 5 min. Kit size 250 tests. Detection limit 0.3 g_dL. Shelf life 12 mon

Catalog number : DIAP-250

Quantity: 250tests

Availability: Yes

Supplier name : Bioassays

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QuantiChrom™ BCP Albumin Assay Kit, Quantitative determination of albumin by bromcresol purple BCP method at 610nm. Procedure 5 min. Kit size 250 tests. Detection limit 0.3 g_dL. Shelf life 12 mon antibody storage GENTAUR recommends for long therm storage to freeze at -24 C. For short time storage up to 30 days we suggest fridge storage at 1 to 10 C. Prevent multiple freeze taw cycles of QuantiChrom™ BCP Albumin Assay Kit, Quantitative determination of albumin by bromcresol purple BCP method at 610nm. Procedure 5 min. Kit size 250 tests. Detection limit 0.3 g_dL. Shelf life 12 mon.
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For quantitative determination of albumin.
Method: OD610nm (BCP).
Samples: serum, plasma, urine, biological preparations.
Species: all.
Procedure: 5 min.
Size: 250 tests.
Detection limit: 0.3 g/dL.

DESCRIPTION
Albumin is the most abundant plasma protein in human. It accounts for
about 60% of the total serum protein. Albumin plays important
physiological roles, including maintenance of colloid osmotic pressure,
binding of key substances such as long-chain fatty acids, bile acids,
bilirubin, haematin, calcium, magnesium. It has anti-oxidant and
anticoagulant effects, and also acts as a carrier for nutritional factors and
drugs, as an effective plasma pH buffer. Serum albumin is a reliable
prognostic indicator for morbidity and mortality, liver disease, nephritic
syndrome, malnutrition and protein-losing enteropathies. High levels are
associated with dehydration.
Simple, direct and automation-ready procedures for measuring albumin
concentration in biological samples are becoming popular in Research
and Drug Discovery. BioAssay Systems' BCP albumin assay kit is
designed to measure albumin directly in biological samples without any
pretreatment. The improved method utilizes bromcresol purple that forms
a colored complex specifically with albumin. The intensity of the color,
measured at 610nm, is directly proportional to the albumin concentration
in the sample. The optimized formulation substantially reduces
interference by substances in the raw samples.
KEY FEATURES
Sensitive and accurate. Use as little as 20 μL samples. Detection range
0.3 g/dL (45μM) to 5 g/dL (750μM) albumin in 96-well plate assay.
Simple and high-throughput. The procedure involves addition of a
single working reagent and incubation for 5 min. Can be readily
automated as a high-throughput assay for thousands of samples per day.
Improved reagent stability and versatility. The optimized formulation has
greatly enhanced reagent and signal stability. Cuvet or 96-well plate assay.
Low interference in biological samples. No pretreatments are needed.
Assays can be directly performed on raw biological samples i.e., in the
presence of lipid and protein.
APPLICATIONS:
Direct Assays: albumin in serum, urine, biological preparations.
Drug Discovery/Pharmacology: effects of drugs on albumin metabolism.
KIT CONTENTS (250 tests in 96-well plates)
Reagent: 50 mL Albumin standard: 2 mL 5 g/dL BSA
Storage conditions. The kit is shipped at room temperature. Store
Reagent and standard at 4°C and -20°C, respectively. Shelf life: 12
months after receipt.
Precautions: reagents are for research use only. Normal precautions for
laboratory reagents should be exercised while using the reagents.

MATERIALS REQUIRED, BUT NOT PROVIDED
Pipeting devices and accessories (e.g. 5 μL).
Procedure using 96-well plate:
Clear bottom 96-well plates (e.g. Corning Costar) and plate reader.
Procedure using cuvette:
Spectrophotometer and cuvets for measuring OD at 610nm.

 

Sample type: urine, serum

Species: mouse

 

References: Maier, SM et al (2007) Proteinuria of Nonautoimmune Origin in Wild-type FVB/NJ Mice. Comp Med. 57(3) 255-266

Pubmed ID: 17605340

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=17605340

Abstract: FVB/NJ mice frequently are used as transgenic hosts, but the suitability of this genetic background for transgenic and congenic models of systemic autoimmunity have not been reported. In this study, FVB/NJ mice were evaluated for the presence of serum autoantibodies and autoimmune kidney pathology. Previously unreported albuminuria was observed in aged female FVB/NJ mice; however, serum autoantibody testing, light microscopic evaluation of differentially stained renal sections, and evaluation of renal sections for immunoglobulin deposits revealed that the albuminuria was not of autoimmune etiology. Anecdotally, multiple characteristics of the FVB/NJ strain, including albuminuria, cholesterolemia, mild podocyte foot process effacement in aged female FVB/NJ kidneys and predisposition to enhanced Th2 immune responses, is reminiscent of human minimal change nephrotic syndrome (MCNS). We propose that mapping of genetic polymorphisms that are responsible for these traits in FVB/NJ mice may lead to increased understanding of mild nephrotic syndromes including MCNS and other proteinurias. [PubMed - indexed for MEDLINE]

 

Sample type: urine

Species: human

 

References:  Yung, S et al (2009). Anti-DNA antibody induction of protein kinase C phosphorylation and fibronectin synthesis in human and murine lupus and the effect of mycophenolic acid. Arthritis Rheum. 60(7):2071-82.

Pubmed ID: 19565476

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=19565476

Abstract:

OBJECTIVE:  To examine fibronectin (FN) expression in human lupus nephritis and the effect of anti-DNA antibodies on transforming growth factor beta1 (TGFbeta1) and FN synthesis in cultured human mesangial cells. The effects of mycophenolic acid (MPA) on this pathway, and the effects of mycophenolate mofetil (MMF) treatment in (NZB x NZW)F(1)/J mice were also studied.

METHODS: Immunohistochemical analyses of renal biopsy samples from patients with active diffuse proliferative lupus nephritis were performed. Cultured human mesangial cells were incubated with human polyclonal anti-DNA antibodies, with or without MPA. (NZB x NZW)F(1)/J mice with active nephritis were randomized to receive either MMF (100 mg/kg/day) or vehicle treatment for 12 weeks.

RESULTS:  Glomerular FN expression was increased in patients with lupus nephritis, and it colocalized with IgG deposition. Anti-DNA antibodies induced protein kinase Calpha (PKCalpha), PKCbetaI, and PKCbetaII activation, increased levels of bioactive TGFbeta1, and increased FN synthesis in human mesangial cells (P < 0.001 for each comparison versus control conditions). Pretreatment of anti-DNA antibodies with exogenous DNA reduced their cellular binding and abrogated their induction of TGFbeta1 and FN synthesis. Inhibition of PKC activation in human mesangial cells prior to anti-DNA antibody stimulation had no effect on cell proliferation, but resulted in significantly reduced antibody-mediated TGFbeta1 secretion and FN synthesis. MPA treatment down-regulated PKCalpha, PKCbetaI, and PKCbetaII phosphorylation, reduced levels of TGFbeta1 bioactivation, and decreased FN synthesis and deposition into the extracellular matrix. MMF treatment in (NZB x NZW)F(1)/J mice resulted in a reduction in glomerular IgG deposition, PKC activation, and FN expression, as well as an amelioration of proteinuria.

CONCLUSION: Human polyclonal anti-DNA antibodies induce TGFbeta1 and FN synthesis in human mesangial cells through PKC activation, which is inhibited by MPA. [PubMed - indexed for MEDLINE]

 

 

Sample Type: serum

Species: fish

 

References: Sharifuzzaman, SM and Austin, B (2010). Kocuria SM1 controls vibriosis in rainbow trout (Oncorhynchus mykiss, Walbaum). J Appl Microbiol. 108(6): 2162 – 2170.

Pubmed ID: 19929950

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=19929950

Abstract:

AIMS: To develop probiotics for the control of vibriosis caused by Vibrio anguillarum and Vibrio ordalii in finfish.

METHODS AND RESULTS: Kocuria SM1, isolated from the digestive tract of rainbow trout, was administered orally to rainbow trout (Oncorhynchus mykiss) for 2 weeks at a dose equivalent to c. 10(8) cells per g of feed and then challenged intraperitoneally with V. anguillarum and V. ordalii. Use of SM1 led to a reduction in mortalities to 15-20% compared to 74-80% mortalities in the controls. SM1 stimulated both cellular and humoral immune responses in rainbow trout, by elevation of leucocytes (5.5 +/- 0.8 x 10(6) ml(-1) from 3.7 +/- 0.8 x 10(6) ml(-1)), erythrocytes (1.2 +/- 0.1 x 10(8) ml(-1) from 0.8 +/- 0.1 x 10(8) ml(-1)), protein (23 +/- 4.4 mg ml(-1) from 16 +/- 1.3 mg ml(-1)), globulin (15.7 +/- 0.2 mg ml(-1) from 9.9 +/- 0.1 mg ml(-1)) and albumin (7.3 +/- 0.2 mg ml(-1) from 6.1 +/- 0.1 mg ml(-1)) levels, upregulation of respiratory burst (0.05 +/- 0.01 from 0.02 +/- 0.01), complement (56 +/- 7.2 units ml(-1) from 40 +/- 8.0 units ml(-1)), lysozyme (920 +/- 128.8 units ml(-1) from 760 +/- 115.3 units ml(-1)) and bacterial killing activities.

CONCLUSIONS: Kocuria SM1 successfully controlled vibriosis in rainbow trout, and the mode of action reflected stimulation of the host innate immune system.

SIGNIFICANCE AND IMPACT OF THE STUDY: Probiotics can contribute a significant role in fish disease control strategies, and their use may replace some of the inhibitory chemicals currently used in fish farms.

[PubMed - indexed for MEDLINE]

 

Sample Type: plasma

Species: rat

 

References: Kelly, E et al (2011). Redistribution of labile plasma zinc during mild surgical stress in the rat. Transl Res. 157(3):139-49.

Pubmed ID: 21316030

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21316030

Abstract: Zinc is an essential trace element and cofactor for many cellular processes. Uptake of ionized divalent zinc (Zn(2+)) in peripheral tissues depends on its total content in the circulation and on mechanisms facilitating delivery to tissues in its labile form. Understanding mechanisms of Zn(2+) delivery has been hindered by the absence of techniques to detect labile Zn(2+) in the circulation. In this study, we report the use of the fluorescent zinc-binding dye (ZnAF-2) to detect changes in labile Zn(2+) in the circulating plasma of the rat under standardized conditions, including exogenous infusions to increase plasma Zn(2+) and an infusion of the chelator, citrate, to decrease labile Zn(2+) in the plasma without altering total Zn(2+) content. In a model of mild surgical stress (unilateral femoral arterial ligation), plasma levels of total and labile Zn(2+) decreased significantly 24 h after the operation. Ultrafiltration of plasma into high- and low-molecular weight macromolecule fractionations indicated that binding capacity of zinc in the high-molecular weight fraction is impaired for the entire 24-h interval after induction of mild surgical stress. Affinity of the filtrate fraction was rapidly and reversibly responsive to anesthesia alone, decreasing significantly at 4 h and recovering at 24 h; in animals subjected to moderate surgical stress, this responsiveness was lost. These findings are the first reported measurements of labile Zn(2+) in the circulation in any form of mild systemic stress. Zinc undergoes substantial redistribution in the plasma as a response to surgical stress, leading to increased availability in lower molecular weight fractions and in its labile form.

Copyright © 2011 Mosby, Inc. All rights reserved.

 [PubMed - indexed for MEDLINE] PMCID: PMC3073749 [Available on 2012/3/1]

 

Sample Type: blood

Species: human

 

References: Shin, SY et al (2009). Local production of total IgE and specific antibodies to the house dust mite in adenoid tissue. Pediatr Allergy Immunol. 20(2):134-41.

Pubmed ID: 18657051

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=18657051

Abstract: Adenoids are known as immunosecretory organs and those in atopic children present cellular and cytokine profiles different from those of non-atopic children. We hypothesized that locally produced total IgE and allergen-specific antibodies could be involved in the inflammatory responses in adenoid tissue. Local productions of total IgE and Dermatophagoides pteronyssinus (DP)-specific IgE, IgA, IgG1, and IgG4 antibodies were evaluated, as well as their relationships with the markers of allergic inflammation within adenoid tissue. Eighteen atopic subjects, who were sensitized to more than one common aeroallergen, and 22 non-atopic subjects undergoing adenotonsillectomy, were recruited. Immunoassays using adenoid tissue homogenate were performed to quantify the levels of total IgE, eosinophil cationic protein (ECP), and mast cell tryptase. DP-specific IgE, IgA, IgG1, and IgG4 antibodies, soluble IL-2 receptors (sIL-2R), soluble CD23 (sCD23), and IL-6 were measured by ELISA. All parameters measured in adenoid tissue homogenate were presented as a ratio to the albumin level found in the adenoid. Median level of total IgE in adenoid tissue homogenate was significantly higher in atopic individuals than in non-atopic individuals. Median values of DP-specific IgE and IgA antibodies were significantly higher in atopics than in non-atopics (p = 0.001, p = 0.006, respectively), while no differences were seen in DP-specific IgG1 and IgG4 antibodies. ECP and sCD23 levels in adenoid homogenate were significantly higher in atopics than in non-atopics (p = 0.026, p = 0.048, respectively), while no significant differences were noted in tryptase, sIL-2R, and IL-6 levels. The levels of DP-specific IgE, IgA, IgG1, and IgG4 antibodies in adenoid homogenate correlated significantly with ECP levels, but not with those of sIL-2R, sCD23, and IL-6. The presence of total IgE and DP-specific antibodies in adenoid tissue was confirmed to be more prominent in atopics. In conclusion, locally-produced total IgE and DP-specific antibodies may contribute to eosinophilic inflammation in adenoid tissue in atopic children.

[PubMed - indexed for MEDLINE]

 

Sample Type: serum

Species: human

 

References: Shin, SY et al (2009). IgE response to staphylococcal enterotoxins in adenoid tissues from atopic children. Laryngoscope. 119(1):171-5.

Pubmed ID: 19117319

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=19117319

Abstract:

OBJECTIVES/HYPOTHESIS: To evaluate local production of staphylococcal superantigen (SAg)-specific IgE in adenoid tissue and to compare its prevalence with that in the tonsil and serum, as well as its relationship with markers of allergic inflammation within adenoid tissue.

STUDY DESIGN: Prospective randomized study.

METHODS: We recruited 18 atopic children who had rhinitis symptoms and were sensitized to more than one common aeroallergen, and 22 nonatopic children undergoing adenotonsillectomy. Immunoassays were performed using adenoid tissue homogenate to quantify the levels of three staphylococcal SAg-specific IgE (SEA, SEB, and TSST-1), total IgE, eosinophil cationic protein (ECP), mast cell tryptase, and soluble CD23.

RESULTS: Three kinds of SAg-specific IgE were detected in the adenoid and tonsil tissues of atopic patients, but not in those of nonatopic patients. In atopic children, the prevalence of SEA-, SEB-, and TSST-1-specific IgE in adenoid tissues (61.1%, 27.8%, 33.3%, respectively) were higher than those in tonsil tissues (38.9%, 5.6%, 11.1%, respectively) and in sera (11.1%, 27.8%, 16.7%, respectively). Subjects with high SEA levels showed significantly higher serum and adenoid total IgE, with higher eosinophilia. Significant correlations were noted between SAg-specific IgE levels and tryptase levels in adenoid tissue.

CONCLUSIONS: Local specific IgE response to staphylococcal SAgs, especially SEA may contribute to ongoing allergic inflammation in adenoid tissue from atopic children.

 [PubMed - indexed for MEDLINE]

 

Sample Type: tissue

Species: human

 

References: Shin, SY et al (2009). Immunological investigation in the adenoid tissues from children with chronic rhinosinusitis. Otolaryngol Head Neck Surg. 141(1):91-6.

Pubmed ID: 19559965

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=19559965

Abstract:

OBJECTIVE: Chronic rhinosinusitis (CRS) is characterized by persistent inflammation and tissue remodeling of the nasal mucosa. Adenoidectomy is an effective surgical treatment in pediatric CRS. To evaluate the effect of pediatric CRS on the severity and characteristics of adenoid inflammation, the authors evaluated the expressions of inflammatory cell activation markers and tissue remodeling in adenoid tissues associated with cytokines tissue-remodeling-associated cytokines in adenoid tissues.

STUDY DESIGN AND SETTING: A prospective controlled study on 40 pediatric patients admitting for adenotonsillectomy.

SUBJECTS AND METHODS: Immunoassays were performed on adenoid tissues homogenates from 16 children with CRS and from 24 children without CRS to quantify the levels of inflammatory cell activation markers, such as soluble interleukin (IL)-2 receptor (sIL-2R), soluble CD23 (sCD23), IL-6, eosinophilic cationic protein (ECP), and tryptase, and the levels of cytokines associated with tissue remodeling, such as transforming growth factor (TGF)-beta1, matrix metalloproteinase (MMP) 2 and 9, and tissue inhibitor of metalloproteinase (TIMP)-1.

RESULTS: The mean levels (the ratio to albumin level) of sIL-2R, TGF-beta1, MMP-2, MMP-9, and TIMP-1 were significantly higher in adenoid tissues of patients with CRS (27.31+/-30.32, 4894.65+/-2388.77, 500.13+/-604.59, and 23.06+/-10.37, respectively) than those without it (16.27+/-10.93, 2635.51+/-1448.63, 120.87+/-321.50, 16.74+/-11.10, and 7.39+/-3.12, respectively; all P<0.05). Regarding the severity of CRS, ECP level was significantly higher in patients with severe CRS than in those with mild to moderate CRS (P=0.033).

CONCLUSIONS: Adenoid tissues in pediatric CRS patients had higher levels of tissue-remodeling-associated cytokines, which may explain the relationship between pediatric CRS and adenoid inflammation.

 [PubMed - indexed for MEDLINE]

 

Sample Type: blood

Species: zebrafish

 

References: Olsen, AS et al (2010). Limb regeneration is impaired in an adult zebrafish model of diabetes mellitus. Wound Repair Regen. 18(5):532-42.

Pubmed ID: 20840523

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=20840523

Abstract: The zebrafish (Danio rerio) is an established model organism for the study of developmental processes, human disease, and tissue regeneration. We report that limb regeneration is severely impaired in our newly developed adult zebrafish model of type I diabetes mellitus. Intraperitoneal streptozocin injection of adult, wild-type zebrafish results in a sustained hyperglycemic state as determined by elevated fasting blood glucose values and increased glycation of serum protein. Serum insulin levels are also decreased and pancreas immunohistochemisty revealed a decreased amount of insulin signal in hyperglycemic fish. Additionally, the diabetic complications of retinal thinning and glomerular basement membrane thickening (early signs of retinopathy and nephropathy) resulting from the hyperglycemic state were evident in streptozocin-injected fish at 3 weeks. Most significantly, limb regeneration, following caudal fin amputation, is severely impaired in diabetic zebrafish and nonspecific toxic effects outside the pancreas were not found to contribute to impaired limb regeneration. This experimental system using adult zebrafish facilitates a broad spectrum of genetic and molecular approaches to study regeneration in the diabetic background.

© 2010 by the Wound Healing Society.

[PubMed - indexed for MEDLINE] PMCID: PMC2941236

 

 

 

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Bioassays \ QuantiChrom™_BCP_Albumin_Assay_Kit,_Quantitative_determination_of_albumin_by_bromcresol_purple_BCP_method_at_610nm._Procedure__5_min._Kit_size__250_tests._Detection_limit__0.3_g_dL._Shelf_life__12_mon \ DIAP_250
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