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The hypersensitivity of anammox bacteria toward fluctuating temperature (seasonal) conditions significantly limits its real-world application. Biomass immobilization alleviates the impact of environmental shocks on the anammox process. In this study (291 d), a sequencing batch reactor engaging dishwashing scrubbers as model waste biocarriers and an amalgamation of activated, anaerobic, and anammox sludge (1:1:0.5 ratio) as inoculum (at influent pH 8.0) were deployed for the startup of the anammox process. Intriguingly, the SBR was run at ambient temperature (6–37 °C) at varying nitrogen loading rates (g N m−3 d−1) of 20, 30, 40, 46.4, 58, 60, 81.2, 92.8, and 116. Notably, anammox activation took place at ⁓247 d wherein the reactor performance improved and exhibited stable nitrogen removal (NH4+–N, NO2−–N and total nitrogen removals were 100, 99, and 72.04%, respectively). Additionally, post 279 days of reactor operation (280 – 291 d), the reactor demonstrated an average total nitrogen removal rate (g N m−3 d−1) of 88.2 at a maximum nitrogen loading rate (g N m−3 d−1) of 116. The 16S rRNA gene sequencing results revealed that Anammox bacteria predominated in the reactor, highlighting the fact that the reported increase in the percentage abundance of Candidatus Kuenenia at 266 d was exorbitantly higher (41.69%) than inoculum sludge (0.18%). Nitrospira (23.9%) and Nitrosomonas (4.32%), in addition to anammox, were found in high concentrations, suggesting presence of dissolved oxygen in the system. [ABSTRACT FROM AUTHOR]

DNA mismatch repair (DMR) functions to maintain genome stability. Prokaryotic and eukaryotic cells deficient in DMR show a microsatellite instability (MSI) phenotype characterized by repeat length alterations at microsatellite sequences. Mice deficient in Pms2, a mammalian homolog of bacterial mutL, develop cancer and display MSI in all tissues examined, including the male germ line where a frequency of ~10% was observed. To determine the consequences of maternal DMR deficiency on genetic stability, we analyzed [F.sub.1] progeny from [Pms2.sup.-/-] female mice mated with wild-type males. Our analysis indicates that MSI in the female germ line was ~9%. MSI was also observed in paternal alleles, a surprising result since the alleles were obtained from wild-type males and the embryos were therefore DMR proficient. We propose that mosaicism for paternal alleles is a maternal effect that results from Pms2 deficiency during the early cleavage divisions. The absence of DMR in one-cell embryos leads to the formation of unrepaired replication errors in early cell divisions of the zygote. The occurrence of postzygotic mutation in the early mouse embryo suggests that Pms2 deficiency is a maternal effect, one of a limited number identified in the mouse and the first to involve a DNA repair gene.