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Anna, I hope the technique now is a little more automated than Malcolm grinding away for hours. I was thinking more of an underpaid research assistant staring at thousands of piles of seeds on a table stretching off to infinity and wishing he'd gone into library science instead. And how did Mollyredone know that the blue socks ARE on the right????

What do you all mean - 'I don't know how they HAD the time'!? Go into the present tense. Anti-A1 lectin is still being made......

... and it will always be the last one you pick ... (because of the general contrariness of the universe and also that you stop looking once you've found it}

Geoff Daniels quotes no less than 7 papers in the 3rd edition of his book Human Blood Groups. They are: Yasuda H, Nollet K, Ohto H. A review of hemolytic disease of the fetus and newborn due to MN incompatibility in Japan. Vox Sang 2009; 97 (Suppl. 1): 125 (Abstract). Stone B, Marsh WL. Haemolytic disease of the newborn caused by anti-M. Br J Haematol 1959; 5: 144-147. Macpherson CR, Zartman ER. Anti-M antibody as a cause of intrauterine death. A follow-up. Am J Clin Path 1965; 43: 544-547. Yoshida Y, Yoshida H, Tatsumi K, et al. Successful antibody elimination in severe M incompatible pregnancy. New Eng J Med 1981; 305: 460-461. Duguid JKM, Bromilow IM, Entwistle CD, Wilkinson R. Haemolytic disease of the newborn due to anti-M. Vox Sang 1995; 68: 195-196. Furukawa K, Nakajima, T, Kogure T, et al. Example of a woman with multiple intrauterine deaths due to anti-M who delivered a live child after plasmapheresis. Exp Clin Immunogenet 1993; 10: 161-167. Kantra T, Yuce K, Ozcebe OI. Hydrops fetalis and intrauterine deaths due to anti-M. Acta Obstet Gynecol Scand 1996; 75: 415-417. Hinchliffe RF, Nolan B, Vora AJ, Stamps R. Neonatal pure red cell aplasia due to anti-M. Arch Dis Child fetal Neonatal Ed 2006; 91: F467-F468. Wikman A, Edner A, Gryfelt G, Jonsson B, Henter J-I. Fatal hemolytic anemia and intrauterine death caused by anti-M immunization. Transfusion 2007; 47: 911-917. Geoff speculates that anti-M could have a similar aetiology to anti-K, in that it attacks very early erythroblasts, leading to a sort of suppression of erythropoiesis, hence the neonatal pure red cell aplasia.

What do you use as a cut-off point for an aPTT to reflex to a mixing study? Our current policy is to perform a mixing study on every pre-surgical patient with an "elevated" PTT. Elevated = anything above the normal cutoff. So with 36 seconds being our high end of normal, a 36.1 is reflexing a mixing study. I haven't had much luck finding what other's are doing.....