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The first sporadic cases of Fujian/411/02-lineage viruses were recorded in Finland in winter 2001-2002. The first protracted but low-intensity outbreak occurred here during the first half of 2003, and the second outbreak early in autumn 2003, after detection of sporadic influenza A cases in the summer. The calculated incidence of influenza A in the Finnish army was 515/10000 during the first outbreak and 2066/10000 during the second outbreak. During the 2003-2004 epidemic season, the isolates fell into three groups for their haemagglutinin (HA1) sequences. In groups I and II, the strains were reassortants which differed for their neuraminidase (NA) sequences from the viruses of the previous spring. Group II viruses, which predominated in Finland during the 2003-2004 season, were characterized by loss of the glycosylation site at position 126 in HA1. The relevance of this loss to the epidemiology is discussed, as well as the frequent appearance of codominant amino acid mixtures at position 151 lining the catalytic cavity of the NA. Group III viruses, genetically related to Wellington/1/2004, the drift variant predominant in 2004 in the southern hemisphere, caused some localized outbreaks in Finland towards the end of the 2003-2004 epidemic. The antigenic match between the vaccine virus (Panama/2007/99) and the Fujian-lineage epidemic viruses in winter 2003-2004 was far from optimal. Nevertheless, high levels of prevaccination and postvaccination antibodies to the predomi- nant group II virus were recorded. Lower antibody levels were detected to the group III virus, which turned out to be a herald strain that reappeared in Finland during the following epidemic season.

The clinical trials of glioma patients at the Finnish boron neutron capture therapy (BNCT) facility (FiR 1) started in May 1999. The doses of the patient in tumour, target volume and sensitive tissues are calculated individually. The calculated doses are calibrated to the reference monitor units according to the ratio of the independently measured and calculated 197Au(n,g) reactions rates at the depth of 20 mm on the central axis of a cylindracal PMMA phantom chosen as the reference geometry. Absorbed doses to the head and body are monitored individually using in vivo dosimeters. In BNCT the total dose is the weighted sum of the absorbed doses originating from the neutron and gamma interactions in tissues. The material compositions of the head model for the neutron-gamma transport calculation and kema factors are based on the ICRU report 46. The doses in the clinical research of BNCT should be reported in such a way that the doses are comparable, traceable and can be recalculated, if underlying information, like weighting factors for dose components, are replaced by new ones. The minimum, average and reference doses are reported for the tumour, target and normal brain. In addition to the total weighted doses the dose components (boron, gamma, nitrogen, and fast neutron dose), weighting factors and estimated boron concentration in these tissues are reported. There are no international recommendations available for BNCT dose calculation or reporting. Therefore the BNCT doses reported in the literature may not be comparable and a careless use of values can lead to over- or underdosing. There is an obvious need for standardisation in the medical application of BNCT. In this paper the methods of dose calculation and reporting of the glioma patients at FiR 1 are described.

The Finnish boron neutron capture therapy (BNCT) facility at the FiR 1 nuclear research reactor in Espoo, Otaniemi is ready for patient trials. The performance of the epithermal neutron beam has been verified in an extensive dosimetric campaign. The Finnish beam has the best therapeutic characteristics among the existing BNCT facilities. The reactor building has been converted into a BNCT research and treatment facility. A patient positioning and fixation system has been designed and constructed.