Human Factor V Matched Antibody Pair (ABPR-L005)

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

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Sufficient reagent for 5 x 96 well plates
Species Reactivity
Intended Use
This antibody pair set comes with matched antibody pair to detect and quantify protein level of Human Factor V
Contents of Kit
1. Capture Antibody (yellow): 0.5 ml of polyclonal affinity purified anti-FV antibody for coating plates.
2. Detecting Antibody (red): 0.5 ml of polyclonal anti-FV antibody for detection of captured FV.
Note: Reagents are sufficient for at least 5×96 well plates using recommended protocols. Antibodies are supplied in a 50% (v/v) glycerol solution for storage at –10 to -20°C. Keep vials tightly capped. Do not store in frost-free freezers.
-10 to -20°C
General Description
Factor V (formerly referred to as accelerator globulin and labile factor) is a large glycoprotein (320 kDa) that is produced in the liver. The gene that encodes factor V (F.V) is located on chromosome 1. A congenital deficiency of F.V is a hemorrhagic disorder inherited as an autosomal recessive disease. The concentration of F.V in plasma is typically 10 μg/ml. F.V is a pro-cofactor that is activated through limited proteolysis by thrombin, or by activated factor X in the presence of phospholipid surface. Other physiologic activators of F.V include plasmin, neutrophil elastase and platelet calpain. The activated cofactor (F.Va) is an essential component of the prothrombin activator complex, which consists of F.Va, activated factor X, calcium and anionic phospholipid surface. The intact prothrombinase complex activates prothrombin to thrombin at a rate 300,000-fold greater than activated factor X alone. In a positive feedback loop, the thrombin generated accelerates its own generation by activating more F.V to F.Va. Thrombin also acts to down-regulate F.Va indirectly by activating Protein C, which inactivates F.Va cofactor activity.


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Phenotypic and genotypic characterization of enterotoxigenic Escherichia coli isolated from diarrheic calves in Argentina


Authors: Gonzalez Pasayo, Ramon A.; Sanz, Marcelo E.; Padola, Nora L.; Moreira, Ana R.

Enterotoxigenic Escherichia coli (ETEC) is the most common and global cause of neonatal calf diarrhea, but there is a little information regarding calf ETEC strains in Argentina. In this study, five ETEC isolates from diarrheic dairy calves (2-10 d old) from Buenos Aires and Cordoba, Argentina were characterized on the basis of virulence gene (VG) pattern, O:H serotyping, hemolytic phenotype, phylogenetic group affiliation, antimicrobial (AM) resistance profile, and presence of integron class 1 and 2. The five isolates were examined by polymerase chain reaction (PCR) for the presence of 18 bovine VGs and showed the following genotypes: F5(+)/F41(+)/sta(+) (D242), F5(+)/sta(+) (D158), F5(+)/sta(+) (D157), F5(+) (D151-9), and F5(+)/iucD(+) (D151-5). These VGs confer pathogenic potential and most of them are associated with the ETEC pathotype. The five isolates showed a non-hemolytic phenotype, belonged to five different serotypes: O101:H-, O141:H-, O60:H-, ONT:H10, and ONT: H-, and were assigned to the phylogenetic group A by the quadruplex Clermont PCR method. The AM resistance of the three isolates D242, D157, and D151-5 was determined by agar disk diffusion method for 24 AMs and they exhibited a multi-resistance phenotype (resistance to four different AM classes: Cephalosporins, Penicillins, Macrolides, and Ansamycins). In addition, class 1 integrons were found in the isolate D151-5 containing the dfrA17-aadA5 gene cassette and in the bovine ETEC reference strain FV10191 containing the dfrA1-aadA1 gene cassette. The present study revealed for the first time the occurrence of multi-resistant ETEC associated with neonatal diarrhea in dairy calves in Argentina. This finding may be used for diagnostic and therapeutic purposes.



Authors: Leonetti, Paolo; Tringali, Salvatore

Let P(N) be the power set of N. We say that a function mu* : P(N) -> R is an upper density if, for all X, Y subset of N and h, k is an element of N+, the following hold: (F1) mu* (N) = 1; (F2) mu* (X) <= mu* (Y) if X subset of Y; (F3) mu (X boolean OR Y) <= mu* (X) + mu* (Y); (F4) mu* (k . X) = (1/k)mu* (X), where k . X := {kx : x is an element of X}; and (F5) mu* (X + h) = mu* (X). We show that the upper asymptotic, upper logarithmic, upper Banach, upper Buck, upper Palya and upper analytic densities, together with all upper a-densities (with alpha a real parameter >= -1), are upper densities in the sense of our definition. Moreover, we establish the mutual independence of axioms (F1)-(F5), and we investigate various properties of upper densities (and related functions) under the assumption that (F2) is replaced by the weaker condition that mu* (X) <= 1 for every X subset of N. Overall, this allows us to extend and generalize results so far independently derived for some of the classical upper densities mentioned above, thus introducing a certain amount of unification into the theory.

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