Rain water chemistry at Calypsobyen, Svalbard

Measurements of pollutants scavenged from air masses over southern Svalbard in summer precipitation are presented. Rainfall was sampled in July and August 2002 at Calypsobyen, Bellsund. Specific conductivity (SpC) and pH were measured and ion con− centrations were determined by ion chromatography. Ions of marine origin were subtracted, assuming that all chlorides were of marine origin. The FLEXTRA trajectory model was ap− plied to discover the sources of air masses arriving at Svalbard and track the paths of pollut− ant transport. Average (v/w) rainfall pH was 4.94, mean SpC amounted to 34.8 μS cm−1. To− tal dissolved solids concentration (TDS) ranged from 12.6 to 67 mg L−1, with ions of marine origin (Cl−, Na+, Mg2+) prevailing. Rains with the highest percentage of marine salts oc− curred with winds from the East at above average velocities. Non−sea salt (nss) sulphate concentrations ranged from 0.5 μeq L−1 to 23 μeq L−1, (v/w) average was 17 μeq L−1. Nitrate concentrations ranged from 0 to 24 μeq L−1. The highest concentrations of nss−SO4 2− and NO3 − were measured on 25 August, when the highest rainfall occurred (27 mm) and pH was the lowest (4.65). Rainfall at Calypsobyen deposited 194 kg km−2 of acidifying anions and 263 kg km−2 of base cations over the recording period. The polluted air masses were mostly from northern and central Europe. Rainfalls scavenging air masses formed over Greenland and Norwegian Seas displayed similar concentrations, being probably polluted by SOx and NOx from ship emissions

Article Organic Pollution in Surface Waters from the Fuglebekken Basin in Svalbard, Norwegian Arctic

sensor

Expression of a constitutively active mutant of heat shock factor 1 under the control of testis-specific hst70 gene promoter in transgenic mice induces degeneration of seminiferous epithelium.

Heat shock activates in somatic cells a set of genes encoding heat shock proteins which function as molecular chaperones. The basic mechanism by which these genes are activated is the interaction of the specific transcription factor HSF1 with a regulatory DNA sequence called heat shock element (HSE). In higher eukaryotes HSF1 is present in unstressed cells as inactive monomers which, in response to cellular stress, aggregate into transcriptionally competent homotrimers. In the present paper we showed that the expression of a transgene encoding mutated constitutively active HSF1 placed under the control of a spermatocyte-specific promoter derived from the hst70 gene severely affects spermatogenesis. We found the testes of transgenic mice to be significantly smaller than those of wild-type males and histological analysis showed massive degeneration of the seminiferous epithelium. The lumen of tubules was devoid of spermatids and spermatozoa and using the TUNEL method we demonstrated a high rate of spermatocyte apoptosis. The molecular mechanism by which constitutively active HSF1 arrests spermatogenesis is not known so far. One can assume that HSF1 can either induce or repress so far unknown target genes involved in germ cell apoptosis