Daunorubicin
One pathway starts from Daunorubicin, a common byproduct found in fermentation, since it is relatively easily available and already structurally similar to the product (only requiring minor alterations). Firstly, the amine group is protected using trifluoroacetic acid to stop it from further reactions. Next the hydroxyl group needs to be changed from an equatorial position to an axial, this is achieved by firstly oxidizing an intermediate sulfoxy salt to a keto group (losing the optical center) followed by a stereo-specific reduction using sodium borohydride to give the hydroxide group in the axial position. Secondly, the focus shifts to carbon number 13 where it is necessary to add a hydroxide group which is achieved by bromination followed by a reaction with an alkali salt of formic acid and water to give the final product. There is an older variant of this pathway which involves first splitting the Daunorubicin, into daunomycin one and daunosamine methyl ether, using methanol. Analogous reactions are performed to get the two hydroxyl groups onto their positions and the rings are then recombined and the protecting groups released. The drawbacks are more chemicals are used and daunomycin one and daunosamine need to be separated first. 13-daunorubicinol
The second pathway startsfrom 13-daunorubicinol (hydroxyl group on carbon 13 instead of Daunorubicins keto group). Firstly, the amine group is protected using trifluoroacetic acid then both the hydroxyl groups at positions 4 and 13 are oxidized simultaneously to keto groups again using DMSO, but a different alkylating agent.
The diffuse leprosy of Lucio and Latapí, also known as diffuse lepromatous leprosy or "pretty leprosy" is a clinical variety of lepromatous leprosy. It was first described by Lucio and Alvarado in 1852 and re-identified by Latapí in 1936. It is common in Mexico (23% of leprosy cases) and in Costa Rica and very rare in other countries. History
The spotted or lazarine leprosy was first described by Ladislao de la Pascua in 1844. Lucio and Alvarado published a description of the disease with the same names in 1852. Latapí re-described it in 1938 and reported it as spotted leprosy of Lucio in 1948. It was named the diffuse leprosy of Lucio and Latapí in 1963 by Frenken. The underlying pathology was explained by Chévez-Zamora as a diffuse generalised cutaneous infiltration. He named it pure and primitive diffuse lepromatosis, upon which necrotising lesions develop. He proposed the name Fenómeno de Lucio or erythema necrotisans for these lesions. Clinical features
This condition is characterized by:
a diffuse infiltration of all the skin which never transforms into nodule
a complete alopecia of eyebrows and eyelashes and body hair
an anhydrotic and dysesthesic zones of the skin
a peculiar type of lepra reaction named Lucios phenomenon or necrotic erythemaLucios phenomenon consists of well-shaped erythematous spots which later become necrotic with scabs, ulcerations and scars. These lesions are usually located on the lower extremities and may be extensive. They are frequently painful and rarely fatal. Pathology
The main pathological features of this disease are a vasculitis affecting all cutaneous vessels.