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Reuter, D.

Publications and source records attributed to Reuter, D..

2 recordsLinked to original sources

Practically Error-Free Junctions Enable Solving Large Instances of Exact Cover Problems Using Network-Based Biocomputation

Network-based biocomputing (NBC) presents an energy-efficient, parallel computing approach for solving nondeterministic polynomial time (NP) complete problems by leveraging motor-driven cytoskeletal filaments that explore all possible solutions through nanofabricated networks in a massively parallel fashion. However, guiding errors at pass junctions, where filaments deviate from their intended path, currently limit the scalability of NBC systems. In this study, we addressed this critical challenge by fabricating sub-200 nm channel geometries using modified electron-beam-lithography and reactive-ion-etching protocols to physically constrain the trajectories of kinesin-driven microtubules and enhance path fidelity. Investigating junction designs with varying channel widths, we demonstrate that reducing channel width significantly lowers junction error rates. Practically error-free junction performance was achieved by scaling down the entire network geometry by a factor of two. These optimized junctions were incorporated into NBC networks that successfully solved 24- and 25-set instances of the Exact Cover problem, representing solution spaces of approximately 16 million and 33 million, respectively. This work establishes a new benchmark in NBC performance and represents a computational scale far beyond what has been achieved in prior demonstrations.

bioengineering↗

EARLY AND MID-GESTATION ZIKA VIRUS (ZIKV) INFECTION IN THE OLIVE BABOON (PAPIO ANUBIS) LEADS TO FETAL CNS PATHOLOGY BY TERM GESTATION

Zika virus (ZIKV) infection in pregnancy can produce catastrophic teratogenic damage to the developing fetus including microcephaly and congenital Zika syndrome (CZS). We previously described fetal CNS pathology occurring by three weeks post-ZIKV infection in Olive baboons at mid-gestation, including neuroinflammation, loss of radial glia (RG), RG fibers, neuroprogenitor cells (NPCs) resulting in disrupted NPC migration. In the present study, we explored fetal brain pathologies at term gestation resulting from ZIKV infection during either first or second trimester in the Olive baboon. In all dams, viremia resolved after 7 days post infection (dpi). One first trimester infected dam aborted at 5 dpi. All dams developed IgM and IgG response to ZIKV with ZIKV IgG detected in fetal serum. Substantial placental pathology and inflammation was observed including disruption of syncytiotrophoblast layers, delayed villous maturation, partially or fully thrombosed vessels, calcium mineralization and fibrin deposits. In the uterus, ZIKV was detected in [3/4] first trimester but not in second trimester infected dams. While ZIKV was not detected in any fetal tissue at term, all fetuses exhibited varying degrees of neuropathology. Fetal brains from ZIKV infected dams exhibited a range of gross brain pathologies including irregularities of the major gyri and sulci of the cerebral cortex and cerebellar pathology. Frontal cortices of ZIKV fetuses showed a general disorganization of the six-layered cortex with degree of disorganization varying among the fetuses from the two groups. Frontal cortices from first but not second trimester infections exhibited increased microglia and astrocyte numbers (white matter) in both trimester infections. In the cerebellum, increased microglia were observed in both first and second trimester infected fetuses and decreased oligodendrocyte precursor cell populations in the cerebellar white matter in first trimester infections. In general, our observations are in accordance with those described in human ZIKV infected fetuses.

pathology↗