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To obtain a more detailed insight into the structure of PcRu (1), an EXAFS investigation has been carried out on amorphous PcRu and compared with the bisubstituted PcRu(n-BuNH 2 ) 2 (2). From the obtained atomic distances around the metal center, it was possible to deduce detailed structural models for both compounds. For 1, the dimeric structure was confirmed; for 2, the EXAFS measurements led to an unusual structure in which both n-butylamine groups are located on one side of the PcRu ring.

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The apoprotein composition of the main lipoprotein fractions (VLDL, LDL‐1, LDL‐2 and HDL) was studied initially in 15 patients with Broad‐β disease. Analytical isoelectric focusing of urea‐soluble apo‐VLDL and apo LDL‐1 demonstrated a variant pattern of the polymorphic Apoprotein E with a deficient Apo E‐III band in all patients. The Apo E‐III deficiency pattern was seen in only six out of 304 hyperlipidaemic controls. These six Apo E‐III deficient controls had characteristic signs of Broad+ disease, and thus represented patients not previously recognized as having the disorder. The Apo E focusing patterns were constant on repeated examinations and were stable under different metabolic conditions. The data show that Apo E‐III deficiency in VLDL is a specific qualitative marker for Broad‐β disease, allowing an unequivocal diagnosis that had not been possible previously. Indirect evidence suggests that Apo E‐III deficiency is the basic lipoprotein abnormality underlying the familial dyslipoproteinaemia.

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