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F-specific RNA (FRNA) bacteriophages can be assayed in wastewater by simple and rapid methods. Their inactivation by UV radiation follows first-order kinetics and relatively simple formulas can describe the effect of UV absorbance by wastewater and the wavelength-dependent killing efficiency of polychromatic lamps. Because the organisms can be grown in high concentrations, biological calibration of full-scale reactors requires only relatively small volumes of phage culture. Naturally occurring FRNA-phages were more resistant to UV than somatic coliphages, Escherichiacoli and faecal streptococci. The inactivation rate constant was almost equal to that of reoviruses, which underlines the suitability of FRNA-phages as a process indicator for UV inactivation of viruses. A pure culture of MS2 was inactivated at a rate which was almost twice that of naturally occurring FRNA-phages, indicating the necessity of designing reactors for practical applications on field-data rather than laboratory experiments.

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Epidemiological studies have indicated that malnutrition during early life may programme chronic degenerative disease in adulthood. In an animal model of fetal malnutrition, rats received an isoenergetic, low-protein (LP) diet during gestation. This reduced fetal b-cell proliferation and insulin secretion. Supplementation during gestation with taurine prevented these alterations. Since proteases are involved in secretion and proliferation, we investigated which proteases were associated with these alterations and their restoration in fetal LP islets. Insulin secretion and proliferation of fetal control and LP islets exposed to different protease modulators were measured. Lactacystin and calpain inhibitor I, but not isovaleryl-L-carnitine, raised insulin secretion in control islets, indicating that proteasome and cysteinyl cathepsin(s), but not m-calpain, are involved in fetal insulin secretion. Insulin secretion from LP islets responded normally to lactacystin but was insensitive to calpain inhibitor I, indicating a loss of cysteinyl cathepsin activity. Taurine supplementation prevented this by restoring the response to calpain inhibitor I. Control islet cell proliferation was reduced by calpain inhibitor I and raised by isovaleryl-L-carnitine, indicating an involvement of calpain. Calpain activity appeared to be lost in LP islets and not restored by taurine. Most modifications in the mRNA expression of cysteinyl cathepsins, calpains and calpastatin due to maternal protein restriction were consistent with reduced protease activity and were restored by taurine. Thus, maternal protein restriction affected cysteinyl cathepsins and the calpain-calpastatin system. Taurine normalised fetal LP insulin secretion by protecting cysteinyl cathepsin(s), but the restoration of LP islet cell proliferation by taurine did not implicate calpains.