factor

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Factor

A financial institution that buys a firm's accounts receivable and collects the accounts.

Factor

A third party that buys a firm's accounts receivable. If a firm is not confident in its ability to collect on its credit sales, it may sell the right to receive payment to the factor at a discount. The factor then assumes the credit risk associated with the accounts receivable. This provides the firm immediate access to working capital, which is important, especially if the firm has a cash flow problem. The price of factoring is determined by the creditworthiness of the firm's customer, not of the firm itself. It is also known as accounts receivable financing.

factor

A firm that purchases accounts receivable from another firm at a discount. The purchasing firm then attempts to collect the receivables.

factor

To sell accounts receivable to another party at a discount from face value. Thus, a firm in need of cash to pay down short-term debt may decide to factor its accounts receivable to another firm.

factor

  1. a firm that purchases TRADE DEBTS from client firms. See FACTORING.
  2. a firm that buys in bulk and performs a WHOLESALING function.
  3. an input (for example raw material, labour, capital) which is used to produce a good or provide a service.

factor

  1. 1a FACTOR INPUT that is used in production (see NATURAL RESOURCES, LABOUR, CAPITAL).
  2. a business that buys in bulk and performs a WHOLESALING function.
  3. a business that buys trade debts from client firms (at some agreed price below the nominal value of the debts) and then arranges to recover them for itself. See FACTOR MARKET, FACTORING.
References in periodicals archive ?
Keywords: P-Selectin, CD40 ligand, Beta thromboglobulin, Platelet factor 4, Heterozygous beta thalassemia.
The Blood sample was used for measurement of resting hematological parameters (Platelet count, RBC count and hemoglobin) and baseline platelet factor 4 (PF4) and beta thromboglobulin ([beta]TG) were measured by radio immunologic method.
4] Nonstandard abbreviations: CD40L, CD40 ligand; sCD40L, soluble CD40L; PCI, percutaneous coronary intervention; ACS, acute coronary syndrome; [beta]TG, [beta]-thromboglobulin; PF4, platelet factor 4; CTAD, citrate, theophylline, adenosine, and dipyridamole; PPP, platelet-poor plasma.
ABBREVIATIONS: DIC = disseminated intravascular coagulation; HELLP syndrome = microangiopathic hemolysis, elevated liver enzymes, and a low platelet count; HIT = heparin-induced thrombocytopenia; HUS = hemolyticuremic syndrome; HUS = hemolytic-uremic syndrome; ITP = immune thrombocytopenic purpura; PF4 = platelet factor 4; TAR = thrombocytopenia with absent radii; TTP = thrombotic thrombocytopenic purpura; ULVWF = unusually large von Willebrand factor; VWF = von Willebrand factor.
It can inactivate platelet-bound factor Xa and resist inhibition by platelet factor IV, which is released during clotting.
In vitro platelet activation has consequences for the evaluation of heparin activity as well (4) because activated platelets might release platelet factor 4 (PF4), inactivating heparin and leading to artifactual shortening of activated partial thromboplastin time (APTT) results.
Heterogeneity in storage pool deficiency: studies on granule-bound substances in 18 patients including variants deficient in [Alpha]-granules, platelet factor 4, [Beta]-thromboglobulin, and platelet-derived growth factor.
Immuno-globulin G from patients with heparin-induced thrombocytopenia binds to a complex of heparin and platelet factor 4.
1) The [alpha] granules contain platelet thrombospondin, fibrinogen, fibronectin, platelet factor 4, von Willebrand factor (VWF), [1] platelet-derived growth factor, [beta]-thromboglobulin, and coagulation factors V and VIII.
The use of citrate-theophylline-adenine-dipyridamol (CTAD) buffer rather than citrate decreased platelet activation as indicated by lowering the plasma concentrations of platelet factor 4 (12).
Platelet activation is measurable by quantifying thromboxanes, platelet factor 4, and thrombomodulin (TM).
In 1986, Knighton et al (7) showed that the accelerated epithelialisation of granulation tissue leading to complete repair of chronic non-healing ulcers is attainable by the use of autologous platelet factors.