Plant viruses have important global impacts on crops, and identifying their centre and date of emergence is important for planning control measures. Turnip mosaic virus (TuMV) is a member of the genus Potyvirus in the family Potyviridae and is a major worldwide pathogen of brassica crops. For two decades, we have collected TuMV isolates, mostly from brassicas, in Turkey and neighbouring countries. This region is thought to be the centre of emergence of this virus. We determined the genomic sequences of 179 of these isolates and used these to estimate the timescale of the spread of this virus. Our Bayesian coalescent analyses used synonymous sites from a total of 417 novel and published whole-genome sequences. We conclude that TuMV probably originated from a virus of wild orchids in Germany and, while adapting to wild and domestic brassicas, spread via Southern Europe to Asia Minor no more than 700 years ago. The population of basal-B group TuMVs in Asia Minor is older than all other populations of this virus, including a newly discovered population in Iran. The timescale of the spread of TuMV correlates well with the establishment of agriculture in these countries.

We have analyzed two unrelated Japanese patients with carbonic anhydrase II deficiency born to consanguineous parents. We have identified the same mutation as that reported to be homozygous in a Belgian family and compound heterozygous in an American family. It comprises to C-to-T transition that results in the amino acid substitution of Tyr (TAT) for His (CAT) at position 107. This point mutation creates an AccI site that can be conveniently screened by the polymerase chain reaction/restriction fragment length polymorphism method using a restriction enzyme for gene tracking. Our patients exhibit severe mental retardation, not seen in the Belgian and American patients.

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We have analyzed two unrelated Japanese patients with carbonic anhydrase II deficiency born to consanguineous parents. We have identified the same mutation as that reported to be homozygous in a Belgian family and compound heterozygous in an American family. It comprises to C-to-T transition that results in the amino acid substitution of Tyr (TAT) for His (CAT) at position 107. This point mutation creates an AccI site that can be conveniently screened by the polymerase chain reaction/restriction fragment length polymorphism method using a restriction enzyme for gene tracking. Our patients exhibit severe mental retardation, not seen in the Belgian and American patients.

The prenatal therapy is described of a patient with vitamin B12-responsive methylmalonic acidaemia during the last 10 days of gestation with oral administration of vitamin B12 (20 mg/day) given to a mother did not normalize her urinary excretion of methylmalonic acid (MMA), which was 14.5 mmol/mol creatinine at 32 weeks of gestation. Before delivery, the mother was excreting 18.9 +/- 3.3 mmol MMA/mol creatinine (mean value at 7 days after vitamin B12 therapy), as well as at 32-37 weeks of gestation with no therapy. After birth, the level of MMA in the infant's urine was remarkably elevated (500-700 mmol/mol creatinine); the level of MMA in maternal urine decreased dramatically after delivery. Compared with two previous reports, the length of administration was not sufficient to reduce maternal MMA excretion. In future, the length of the therapy, route of administration and total dose of vitamin B12 to maintain an efficient level of vitamin B12 in an affected fetus should be considered.