Steroid isolation , depending on context, is the isolation of chemical matter required for chemical structure elucidation, derivitzation or degradation chemistry, biological testing, and other research needs (generally milligrams to grams, but often more  or the isolation of "analytical quantities" of the substance of interest (where the focus is on identifying and quantifying the substance (for example, in biological tissue or fluid). The amount isolated depends on the analytical method, but is generally less than one microgram.  [ page needed ] The methods of isolation to achieve the two scales of product are distinct, but include extraction , precipitation, adsorption , chromatography , and crystallization . In both cases, the isolated substance is purified to chemical homogeneity; combined separation and analytical methods, such as LC-MS , are chosen to be "orthogonal"—achieving their separations based on distinct modes of interaction between substance and isolating matrix—to detect a single species in the pure sample. Structure determination refers to the methods to determine the chemical structure of an isolated pure steroid, using an evolving array of chemical and physical methods which have included NMR and small-molecule crystallography .  : 10–19 Methods of analysis overlap both of the above areas, emphasizing analytical methods to determining if a steroid is present in a mixture and determining its quantity. 
In a larger series of 118 unrelated cases of Apert syndrome studied in Oxford, Moloney et al. (1996) found that 74 had the 934C-G mutation and 44 had the 937C-G mutation. Combined with the cases reported by Park et al. (1995) , the total experience indicated that 108 of 166 cases (65%) were of the 934C-G type, 57 of 166 cases (34%) were of the 937C-G type, and 1 case observed by Park et al. (1995) was of unknown mutational basis. Wilkie (1996) observed paternal age effect with both Apert mutations in 54 informative families; the mutation was of paternal origin in all cases. Limb malformation seemed to be more severe in the 937C-G mutation; cleft palate was more often present, and craniofacial abnormality was in general more severe with the 934C-G mutation ( Wilkie, 1996 ). Indeed, the severe craniofacial abnormality and cleft palate in association with milder involvement of the hands gave rise to the designation of Vogt cephalodactyly or Apert-Crouzon disease for the condition in the cases described by Vogt (1933) combining the hand and foot malformations characteristic of Apert disease with the facial characteristics of Crouzon disease; see 101200 .