Two different methods for the direct application of indigo dye were developed in England in the 18th century and remained in use well into the 19th century. One of these, known as china blue, involved iron(II) sulfate. After printing an insoluble form of indigo onto the fabric, the indigo was reduced to leuco-indigo in a sequence of baths of ferrous sulfate (with reoxidation to indigo in air between immersions). The china blue process could make sharp designs, but it could not produce the dark hues of other methods. In the second half of the 1850s ferrous sulfate was used as a photographic developer for collodion process images. Hydrates
Iron(II) sulfate can be found in various states of hydration, and several of these forms exist in nature. FeSO4·H2O (mineral: szomolnokite, relatively rare)
FeSO4·4H2O (mineral: rozenite, white, relatively common, may be dehydratation product of melanterite)
FeSO4·5H2O (mineral: siderotil, relatively rare)
FeSO4·6H2O (mineral: ferrohexahydrite, relatively rare)
FeSO4·7H2O (mineral: melanterite, blue-green, relatively common)
The tetrahydrate is stabilized when the temperature of aqueous solutions reaches 56.6 °C (133.9 °F). At 64.8 °C (148.6 °F) these solutions form both the tetrahydrate and monohydrate.Mineral forms are found in oxidation zones of iron-bearing ore beds, e.g. pyrite, marcasite, chalcopyrite, etc. They are also found in related environments, like coal fire sites. Many rapidly dehydrate and sometimes oxidize. Numerous other, more complex (either basic, hydrated, and/or containing additional cations) Fe(II)-bearing sulfates exist in such environments, with copiapite being a common example.
Pathophysiology
Regardless of the underlying cause of purpura fulminans, the mechanism of disease is similar with deficiency in protein C concentration or decrease in protein C activity which promotes blood clotting (thrombosis).In cases of severe sepsis, there is widespread activation of the acute systemic inflammatory response, including activation of the coagulation and complement pathways, as well as endothelial dysfunction. Activated protein C helps regulate the systemic inflammatory response. During sepsis, signalling by the inflammatory cytokines, interleukin-1 and tumour necrosis factor, mediate altered protein transcription in the systemic inflammatory response, resulting in decreased synthesis of the regulatory proteins antithrombin, protein C and protein S, with increased synthesis of prothrombotic proteins Factor VIII, von Willebrand factor, and fibrinogen. Activated protein C binds to endothelial protein C receptor and subsequently cleaves the endothelial cell protease activated receptor-1, not only altering coagulation profiles but down-regulating pro-inflammatory and pro-apoptotic mediators, up-regulation of anti-inflammatory and anti-apoptotic pathways and stabilization of the endothelial cell barrier functions.Systemic coagulation activation may lead to depletion of circulating coagulation factors and platelets, which subsequently lead to bleeding. In early purpura fulminans, lesion progression correlates with the histological appearance of blockage of small skin blood vessels with blood clots causing capillary dilation and congestion with red blood cells.