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Zuniga, A.

Publications and source records attributed to Zuniga, A..

2 recordsLinked to original sources

Operando Failure Diagnosis and Performance Dynamics in Microbial Fuel Cells Treating Mine Waste

Bench-scale microbial fuel cells (MFCs) treating mining wastewater frequently exhibit operational variability and uncharacterized degradation that obscure true biocatalytic performance. To decouple genuine biological treatment effects from mechanical failures, this paper presents an integrated diagnostic framework validated on two bench-scale systems treating heavy-metal-rich gold mine tailings. The first system evaluates Micractinium inermum algal bio-augmentation (System 1), while the second compares Psychrobacter alimentarius- and Trichococcus patagoniensis-dominated anodic consortia (System 2). To overcome single-reactor constraints, the framework integrates paired time-series statistical modeling, an adaptive percentile-floor change-point detector, equivalent-circuit modeling, and baseline-corrected spectroscopy (XRD/FTIR). Applying the framework to these systems uncovers previously masked dynamics: statistical analysis demonstrates that algal biocatalysis provides no voltage advantage under stable operation (+0.17%) but increases output by 27.54% under diurnal perturbation, while periodicity analysis links these diurnal shifts to the chamber photoperiod. Furthermore, heavy-metal remediation (up to 97.7%) is governed by system-level physicochemical mechanisms rather than algal-specific processes. The change-point detector successfully isolates distinct failure modes, distinguishing a recoverable excursion from terminal structural collapse. Finally, equivalent-circuit modeling reveals that the superior power density of Trichococcus consortia is driven by combined improvements in internal resistance and open-circuit voltage. Ultimately, pairing statistical controls with automated fault detection resolves operational ambiguity, offering a scalable baseline for health monitoring in bio-electrochemical wastewater treatment.

bioengineering

TGF(beta) Mediated Structural Remodeling Facilitates Optic Fissure Fusion And The Necessity Of BMP Antagonism In This Process

The optic fissure is a transient gap in the developing vertebrate eye, which must be closed as development proceeds. A persisting optic fissure, coloboma, is a major cause for blindness in children. Multiple factors are genetically linked to coloboma formation. However, especially the process of optic fissure fusion is still largely elusive on a cellular and molecular basis.\n\nWe found a coloboma phenotype in mice with a targeted inactivation of the transforming growth factor 2 (TGF{beta}2). Here the optic fissure margins got in touch, however, failed to fuse. Transcriptomic analyses indicated TGF{beta} mediated ECM remodeling during optic fissure fusion. For functional analyses, we switched model systems and made use of zebrafish. We found TGF{beta} ligands expressed in the developing zebrafish eye, and the ligand binding receptor in the optic fissure. Using a new in vivo TGF{beta} signaling reporter, we also found active TGF{beta} signaling in the margins of the optic fissure. We addressed the function of Cadherin 6 (cdh6), one of the TGF{beta} regulated genes, by knock down experiments in zebrafish and found a prominent coloboma phenotype. Cdh6 was often found involved in processes of epithelial to mesenchymal transition (EMT), strengthening our hypothesis that an EMT-like process is also necessary for optic fissure fusion. Furthermore, we found Gremlin 2b (grem2b) and Follistatin a (fsta), homologs of TGF{beta} regulated bone morphogenetic protein (BMP) antagonists, expressed in the optic fissure margins, indicating the necessity of a localized inhibition of BMP signaling. Finally, we show that induced BMP expression is sufficient to inhibit optic fissure fusion. Together with our previous findings this indicates a dual role of BMP signaling during optic fissure closure.\n\nSummary statementTGF{beta} is crucial for optic fissure fusion, involving cdh6. TGF{beta} mediated optic fissure fusion is potentially hampered by BMP signaling, which is blocked by TGF{beta} induced BMP antagonists within the optic fissure margins.

developmental biology