SUMMARYHere we discuss proteomic analyses of whole cell preparations of the mosquito stages of malaria parasite development (i.e. gametocytes, microgamete, ookinete, oocyst and sporozoite) of Plasmodium berghei. We also include critiques of the proteomes of two cell fractions from the purified ookinete, namely the micronemes and cell surface. Whereas we summarise key biological interpretations of the data, we also try to identify key methodological constraints we have met, only some of which we were able to resolve. Recognising the need to translate the potential of current genome sequencing into functional understanding, we report our efforts to develop more powerful combinations of methods for the in silico prediction of protein function and location. We have applied this analysis to the proteome of the male gamete, a cell whose very simple structural organisation facilitated interpretation of data. Some of the in silico predictions made have now been supported by ongoing protein tagging and genetic knockout studies. We hope this discussion may assist future studies.
. (1976). Archives of Disease in Childhood, 51, 771. Biopterin derivatives in normal and phenylketonuric patients after oral loads of L-phenylalanine, L-tyrosine, and L-tryptophan. Plasma biopterin derivatives studied in 10 normal and 21 phenylketonuric children showed a significantly high concentration in the latter group. Biopterin derivatives correlated with plasma phenylalanine concentration, but in normal adults given an oral phenylalanine load the rate of increase with phenylalanine differed from that in phenylketonuric patients.A patient with hyperphenylalaninaemia, not due to phenylketonuria, had an abnormal biopterin derivatives response to phenylalanine distinct from that of patients with classical phenylketonuria. This may be a useful investigation to differentiate some variants of phenylketonuria.Patients with hyperphenylalaninaemia do not necessarily have phenylketonuria, due to an almost total deficiency of the hepatic enzyme phenylalanine hydroxylase, and diagnosis is complicated by the several variants or atypical forms of phenylketonuria. These variants are currently identified by criteria including plasma phenylalanine concentrations lower than those found in classical phenylketonuria; an increased tolerance to administered phenylalanine over a few hours; and the ability of a patient to sustain a diet containing about 250-500 mg phenylalanine per day rather than 150-250 mg/day in classical phenylketonuria.
concentrations of 37-60 .Lg/lOO ml, levels previously accepted as harmless.Children with blood lead concentrations greater than 60 tug/100 ml show radiological evidence of lead intoxication, and treatment for this should be considered when blood lead concentration exceeds 37 Fg/100 ml. Children presenting with unexplained encephalopathy should be radiographed for evidence of lead intoxication.
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