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This paper explores the role that tropical storms (TS) of the eastern North Pacific play in the rainfall climatology of western Mexico. It uses an 18-station rainfall grid, along with a data base of storm tracks (1949 -1997). TS rainfall is defined by a distance threshold, so that for each station in the grid, daily rainfall recorded when a TS is located within 550 km of the station is considered as TS-derived; rainfall recorded in the absence of a TS or when a storm is beyond 550 km from a station is by default 'non-TS' rainfall. A variety of statistics are presented to demonstrate the static associations that exist between TS activity and regional rainfall patterns. In sum, they clearly suggest that improved seasonal forecasts of TS activity in the eastern North Pacific will be critical to advancing seasonal climate prediction for Mexico. This study also addresses the interannual variability in TS and non-TS rainfall. Principal component analysis is used to define the region's primary modes of rainfall variation. Considering the temporal behaviour of the rainfall modes, analyses reveal no statistically significant trends in TS rainfall. In contrast, non-TS rainfall modes exhibit significant trends. This study provides support for the idea that these trends are partly tied to long-period fluctuations in the ocean-atmosphere system. The results also indicate that while TS rainfall is not subject to trend behaviour, its year-to-year fluctuations, apparently, are linked to large-scale processes like El Niñ o-Southern Oscillation (ENSO) and the state of North Pacific sea-surface temperatures (SSTs). Copyright

The global climate during 1998 was affected by opposite extremes of the ENSO cycle, with one of the strongest Pacific warm episodes (El Nino) in the historical record continuing during January-early May and Pacific cold episode (La Nina) conditions occurring from July-December. In both periods, regional temperature, rainfall, and atmospheric circulation patterns across the Pacific Ocean and the Americas were generally consistent with those observed during past warm and cold episodes.

Chicken anemia virus (CAV) causes cytopathogenic effects in chicken thymocytes and cultured transformed mononuclear cells via apoptosis. Early after infection of chicken mononuclear cells, the CAV-encoded protein VP3 exhibits a finely granular distribution within the nucleus. At a later stage after infection, VP3 forms aggregates. At this point, the cell becomes apoptotic and the cellular DNA is fragmented and condensed. By immunogold electron microscopy VP3 was shown to be associated with apoptotic structures. In vitro, expression of VP3 induced apoptosis in chicken lymphoblastoid T cells and myeloid cells, which are susceptible to CAV infection, but not in chicken embryo fibroblasts, which are not susceptible to CAV. Expression of a C-terminally truncated VP3 induced much less pronounced apoptosis in the chicken lymphoblastoid T cells. Chicken anemia virus (CAV) transiently causes severe anemia due to destruction of erythroblastoid cells and immunodeficiency due to depletion of cortical thymocytes in young chickens (10, 38). Jeurissen et al. (11) have provided evidence that the observed depletion of the thymocytes occurs via CAV-induced apoptosis. Apoptosis is considered to be a physiological process of cell depletion that is part of the homeostatic regulation of normal tissues (5). CAV in addition to several other viruses, such as human immunodeficiency virus type 1 (2) and parvovirus B19 (19), seems to use apoptosis to exert its cytopathogenic effect. CAV is a small virus with a diameter of about 23 nm and contains a circular single-stranded DNA of 2.3 kb (27). CAV multiplies via a circular double-stranded DNA replicative intermediate, which was recently cloned (18, 21). The cloned CAV genome was proven to be representative for CAV isolates collected worldwide (23, 29). A polycistronic polyadenylated mRNA (22) which comprises three overlapping open reading frames encoding proteins VP1 (51.6 kDa), VP2 (24.0 kDa), and VP3 (13.6 kDa) is transcribed from the CAV

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