Fetuin A ELISA Kit (DEIA1984)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
serum, plasma, cell culture supernatant, tissues extractsion, urine
Species Reactivity
Human
Intended Use
This ELISA (enzyme-linked immunosorbent assay) kit is intended for measurement of human Fetuin-A, also known as alpha-2-HS glycoprotein (AHSG), in serum, plasma, cell culture supernatant, tissue extraction and urine.
Contents of Kit
1. Fetuin-A Antibody Coated Microplate
2. Fetuin-A Tracer Antibody
3. Tracer Antibody Diluent
4. Fetuin-A Assay Buffer Concentrate
5. ELISA Wash Concentrate
6. ELISA HRP Substrate Solution
7. ELISA Stop Solution
8. Fetuin-A Standards
9. Fetuin-A Controls
Storage
This test kit must be stored at 2-8°C upon receipt. For more detailed information, please download the following document on our website.
Standard Curve

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References


Cellular and Molecular Mechanisms of Kidney Injury in 2,8-Dihydroxyadenine Nephropathy

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY

Authors: Klinkhammer, Barbara Mara; Djudjaj, Sonja; Kunter, Uta; Palsson, Runolfur; Edvardsson, Vidar Orn; Wiech, Thorsten; Thorsteinsdottir, Margret; Hardarson, Sverrir; Foresto-Neto, Orestes; Mulay, Shrikant R.; Moeller, Marcus Johannes; Jahnen-Dechent, Wilhelm; Floege, Juergen; Anders, Hans-Joachim; Boor, Peter

Background Hereditary deficiency of adenine phosphoribosyltransferase causes 2,8-dihydroxyadenine (2,8-DHA) nephropathy, a rare condition characterized by formation of 2,8-DHA crystals within renal tubules. Clinical relevance of rodent models of 2,8-DHA crystal nephropathy induced by excessive adenine intake is unknown. Methods Using animal models and patient kidney biopsies, we assessed the pathogenic sequelae of 2,8-DHA crystal-induced kidney damage. We also used knockout mice to investigate the role of TNF receptors 1 and 2 (TNFR1 and TNFR2), CD44, or alpha2-HS glycoprotein (AHSG), all of which are involved in the pathogenesis of other types of crystal-induced nephropathies. Results Adenine-enriched diet in mice induced 2,8-DHA nephropathy, leading to progressive kidney disease, characterized by crystal deposits, tubular injury, inflammation, and fibrosis. Kidney injury depended on crystal size. The smallest crystals were endocytosed by tubular epithelial cells. Crystals of variable size were excreted in urine. Large crystals obstructed whole tubules. Medium-sized crystals induced a particular reparative process that we term extratubulation. In this process, tubular cells, in coordination with macrophages, overgrew and translocated crystals into the interstitium, restoring the tubular luminal patency; this was followed by degradation of interstitial crystals by granulomatous inflammation. Patients with adenine phosphoribosyltransferase deficiency showed similar histopathological findings regarding crystal morphology, crystal clearance, and renal injury. In mice, deletion of Tnfrl significantly reduced tubular CD44 and annexin two expression, as well as inflammation, thereby ameliorating the disease course. In contrast, genetic deletion of Tnfr2, Cd44, or Ahsg had no effect on the manifestations of 2,8-DHA nephropathy. Conclusions Rodent models of the cellular and molecular mechanisms of 2,8-DHA nephropathy and crystal clearance have clinical relevance and offer insight into potential future targets for therapeutic interventions.

Study of 15 protein polymorphisms in a sample of the Turkish population

HUMAN BIOLOGY

Authors: Brega, A; Scacchi, R; Cuccia, M; Kirdar, B; Peloso, G; Corbo, RM

Anatolia, because of its geographic position and its use as an area of settlement, was also a land of transit that accommodated a succession of populations. The last important invasion occurred in the Middle Ages with the arrival of the Turks, an Altaic-speaking nomadic population descended from the Oguz tribes and originating in Mongolia. Although the Turks imposed their culture, their genetic contribution seems to have been modest. To validate this hypothesis, we studied the genetic structure of the Turkish population by examining 15 genetic markers in a sample of 93 subjects. The allele frequencies observed were HP*1 = 0.240; GLO1*1 = 0.344, ESD*2 = 0.134, GC*1S = 0.613, GC*1F = 0.129, PGM1*2S = 0.322, PGM1*2F = 0.041, PGM1*1F = 0.027, F13B*1 = 0.762, F13B*2 = 0.101, ORM1*S = 0.327, AHSG*2 = 0.181, C6*B = 0.239, C7*1 = 0.983, APOC2*1 = 1.0, APOE*3 = 0.868, APOE*2 = 0.063, BF*F = 0.258, BF*S07 = 0.017, BF*SQ0 = 0.011, C4A*Q0 = 0.145, C4A*2 = 0.070, C4A*5 = 0.012, C4A*6 = 0.023, C4B*Q0 = 0.101, C4B*2 = 0.048, C4B*3 = 0.005, and C4B*11 = 0.005. The present Turkish population was compared to other European, Middle Eastern, and North African populations by means of correspondence analysis. Turks cluster with Turkomans, who share the ancient Turks' derivation from the Oguz tribe. Moreover, Turks clearly belong to European groups and resemble the populations of neighboring countries. Therefore the present data support the hypothesis that the ancient Turkish tribes, who started to enter Anatolia 1000 years ago, contributed little to the gene pool of the preexisting Anatolian populations. Alternatively, if the genetic structure of the invading Turks resembled that of the ancient Anatolians, it will be impossible to find traces of their admixture with the autochthonous inhabitants of Anatolia. However, further analysis of other samples from Turkey and from populations living in the homelands of the Turkish tribes, namely, the eastern area of the Caspian Sea and Mongolia, is needed.

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