Nitrogen and carbon removal from anaerobic digester effluents with low carbon to nitrogen ratios under feammox conditions.

Removal of nitrogen and carbon from anaerobic digester (AD) effluents is challenging for currently available technologies. Herein, effective treatment for real AD effluents was achieved via the feammox process by using a Multistage Feammox Bioreactor (MSFB). The reactor achieved the best performance with AD effluent of a low carbon to nitrogen (C/N) ratio of 2.5. A 6-day retention time reached removal efficiencies for NH4+ and COD at 99 % and 97 %, respectively, with a thorough conversion of NH4+ to N2. Accordingly, the MSFB achieved removal rates for N and C of 14 and 34 mg L-1 d-1, respectively. The C/N ratio of 2.5 is regarded to be the critical point above which the feammox is shifted to conventional iron reduction with organic carbon. Iron-reducing bacteria of the γ- Proteobacteria (Pseudomonas and Acinetobacter), and δ- Proteobacteria (Geobacter) were dominant in the MSFB and were supposed to drive the feammox process.

Addition of the BMP4 antagonist, noggin, disrupts avian inner ear development.

Bone morphogenetic protein 4 (BMP4) is known to regulate dorsoventral patterning, limb bud formation and axis specification in many organisms, including the chicken. In the chick developing inner ear, BMP4 expression becomes localized in two cell clusters at the anterior and posterior edges of the otic epithelium beginning at stage 16/17 and is expressed in presumptive sensory tissue at later stages. This restricted spatiotemporal pattern of expression occurs just prior to the otocyst's transition to a more complex three-dimensional structure. To further analyze the role of BMP4 in avian otic morphogenesis, cells expressing BMP4 or its antagonist, noggin, were grown on agarose beads and implanted into the periotic mesenchyme surrounding the chick otocyst. Although the BMP4-producing cells had no effect on the mature inner ear structure when implanted alone, noggin-producing cells implanted adjacent to the BMP4 cell foci prevented normal semicircular canal development. Beads implanted at the anterior BMP4 focus eliminated the anterior and/or the horizontal canals. Noggin cells implanted at the posterior focus eliminated the posterior canal. Canal loss was prevented by co-implantation of BMP4 cell beads next to noggin beads. An antibody to the chick hair cell antigen (HCA) was used to examine sensory cell distribution, which was abnormal only in the affected tissues of noggin-exposed inner ears. These data suggest a role for BMP4 in the accurate and complete morphological development of the semicircular canals.

Expression of Pax2 and patterning of the chick inner ear.

Early regionalized gene expression patterns within the otocyst appear to correlate with and contribute to development of mature otic structures. In the chick, the transcription factor Pax2 becomes restricted to the dorsal and entire medial side of the otocyst by stage 16/17. The dorsal region of the otocyst forms the endolymphatic duct and sac (ED/ES), and the cochlear duct is derived from the ventromedial region. In the mouse, however, Pax2 expression is reported only in the ventromedial and not the dorsal otocyst. In Pax2 null mice, the cochlea is missing or truncated, but vestibular structures differentiate normally. Here we demonstrate that in the chick, the emerging ED/ES express high levels of Pax2 even when the position of the emerging ED is altered with respect to its environment, either by 180 degrees otocyst rotations about the anterior/posterior axis or transplantation of the otocyst into the hindbrain cavity. However, the Pax2 expression pattern is plastic in the rest of the otic epithelium after 180 degrees rotation of the otocyst. Pax2 is upregulated on the medial side (formerly lateral), and downregulated on the lateral side (formerly medial and expressing Pax2) indicating that Pax2 expression is influenced by the environment. Although Pax2 is upregulated in the epithelium after 180 degrees rotations in the region that should form the cochlear duct, cochlear ducts are truncated or absent, and the ED/ES emerge in a new ventrolateral position. Ablation of the hindbrain at the placode or early otic pit stage alters the timing of regionalized Pax2 expression in the otocyst. The resulting otocysts and ears are generally smaller, vestibular structures are abnormal, ED/ES are missing but cochlear ducts are of normal length. The hindbrain and dorsal periotic mesenchyme provide unique trophic and patterning information to the dorsal otocyst. Our results demonstrate that the ED is the earliest structure patterned in the inner ear and that the hindbrain is important for its specification. We also show that, although normal Pax2 expression is required for cochlear duct development, it is downstream of ventral otocyst patterning events.