An investigation of moving bed biofilm reactor nitrification during long-term exposure to cold temperatures.

Biological treatment is the most common and economical means of ammonia removal in wastewater; however, nitrification rates can become completely impeded at cold temperatures. Attached growth processes and, specifically, moving bed biofilm reactors (MBBRs) have shown promise with respect to low-temperature nitrification. In this study, two laboratory MBBRs were used to investigate MBBR nitrification rates at 20, 5, and 1 degree C. Furthermore, the solids detached by the MBBR reactors were investigated and Arrhenius temperature correction models used to predict nitrification rates after long-term low-temperature exposure was evaluated. The nitrification rate at 5 degrees C was 66 +/- 3.9% and 64 +/- 3.7% compared to the rate measured at 20 degrees C for reactors 1 and 2, respectively. The nitrification rates at 1 degree C over a 4-month exposure period compared to the rate at 20 degrees C were 18.7 +/- 5.5% and 15.7 +/- 4.7% for the two reactors. The quantity of solids detached from the MBBR biocarriers was low and the mass of biofilm per carrier did not vary significantly at 20 degrees C compared to that after long-term exposure at 1 degree C. Lastly, a temperature correction model based on exposure time to cold temperatures showed a strong correlation to the calculated ammonia removal rates relative to 20 degrees C following a gradual acclimatization period to cold temperatures.

Smad7 is a transforming growth factor-beta-inducible mediator of apoptosis in granulosa cells.

OBJECTIVE: To determine the functional role of Smad7 in granulosa cells. DESIGN: Granulosa cell culture and molecular biological techniques were used to investigate regulation and function of Smad7. SETTING: Research laboratory. ANIMAL(S): C57bl/j hybrid mouse. INTERVENTION(S): Primary mouse granulosa cells were isolated and grown in culture for all messenger RNA expression experiments. Smad7 promoter constructs were evaluated with a luciferase reporter system in SIGC cells to determine sites activating Smad7 expression. MAIN OUTCOME MEASURE(S): Overexpression (Smad7 complementary DNA) and downregulation (Smad7 small interfering RNA) of Smad7 in primary mouse granulosa cells were used to evaluate the functional role of Smad7 in granulosa cells. RESULT(S): Smad7 expression was upregulated by treatment with transforming growth factor-ß (TGF-ß) but not activin or activation of the cyclic adenosine monophosphate pathway. The promoter of Smad7 was activated by TGF-ß. Truncation of the promoter or mutation of the Smad response element at -141 eliminated TGF-ß activation of the promoter. Smad3 was not specifically required for TGF-ß-stimulated expression of Smad7, though activation of the TGFBR1 receptor was. When Smad7 was overexpressed in granulosa cells, apoptosis was markedly increased. When Smad7 expression was reduced with small interfering RNA, then the TGF-ß-induced apoptosis was blocked. CONCLUSION(S): Smad7 mediates apoptosis induced by TGF-ß in mouse granulosa cells, suggesting that dysregulation of Smad7 could impair folliculogenesis.