Multifaced roles of PLAC8 in cancer

The role of PLAC8 in tumorigenesis has been gradually elucidated with the development of research. Although there are common molecular mechanisms that enforce cell growth, the impact of PLAC8 is varied and can, in some instances, have opposite effects on tumorigenesis. To systematically understand the role of PLAC8 in tumors, the molecular functions of PLAC8 in cancer will be discussed by focusing on how PLAC8 impacts tumorigenesis when it arises within tumor cells and how these roles can change in different stages of cancer progression with the ultimate goal of suppressing PLAC8-relevant cancer behavior and related pathologies. In addition, we highlight the diversity of PLAC8 in different tumors and its functional output beyond cancer cell growth. The comprehension of PLAC8’s molecular function might provide new target and lead to the development of novel anticancer therapies.

Switch-level dynamic fault modeling for resistive short and open faults in nanometre technologies

Modeling the dynamic behaviour of resistive shorts and opens at switch-level dictates the characterization o enhanced delay attributable to these faults with referenc to the input combinations, fault sites, defect resistance and CMOS technology variation. Resistive physical failures make the output voltage fluctuate between intermediate ranges by disturbing the propagation time of the logic, without adversely changing the functional output. To determine the impact of logic propagation delay (tp) on the output voltage (Vout) of a gate, a switch-level fault analysis on CMOS primitive gates is executed for CMOS technologies 350 nm, 180 nm, and 90 nm in comparison with nanometre technologies 45 nm and 32 nm. To understand the nature and effect of actual resistive faults in silicon, static faults in static primitive gates are reviewed after altering the defect resistance. Delay and output voltage changes induced by these variations are determined for CMOS 32 nm technology.

Switch-level dynamic fault modeling for resistive short and open faults in nanometre technologies

Modeling the dynamic behaviour of resistive shorts and opens at switch-level dictates the characterization o enhanced delay attributable to these faults with referenc to the input combinations, fault sites, defect resistance and CMOS technology variation. Resistive physical failures make the output voltage fluctuate between intermediate ranges by disturbing the propagation time of the logic, without adversely changing the functional output. To determine the impact of logic propagation delay (tp) on the output voltage (Vout) of a gate, a switch-level fault analysis on CMOS primitive gates is executed for CMOS technologies 350 nm, 180 nm, and 90 nm in comparison with nanometre technologies 45 nm and 32 nm. To understand the nature and effect of actual resistive faults in silicon, static faults in static primitive gates are reviewed after altering the defect resistance. Delay and output voltage changes induced by these variations are determined for CMOS 32 nm technology.

Role of neuronal positioning in jaw motor circuit function in zebrafish

Development of the vertebrate nervous system involves substantial cell migration, where immature neurons move to specific locations to generate functional circuits. Precise neuronal migration and positioning are essential for proper brain architecture and function. Abnormal neuronal migration can contribute to neurological disorders such as lissencephaly, autism and schizophrenia. However, the consequences of abnormal neuronal migration for circuit organization and functional output are poorly understood. To provide some insight, I used the facial branchiomotor (FBM) neurons in zebrafish as a model system to analyze the effects of aberrant neuronal migration on circuit function. The FBM neurons are a subset of the branchiomotor neurons, which are generated in the vertebrate hindbrain and innervate facial and jaw muscles. During development in zebrafish and mice, FBM neurons migrate caudally from rhombomere 4 (r4) to r6 to form the facial motor nucleus and innervate jaw and gill muscles (in fish). In order to examine the consequences of aberrant neuronal migration, one must first characterize the normal functional output of the FBM circuit that drives jaw movements. In collaboration with colleagues in the MU Department of Computer Science, we developed an automated image analysis system to extract motion features from video recordings of jaw movement, enabling rapid and accurate high-throughput analysis. We used this software to examine the emergence of jaw movement in zebrafish larvae between 3-9 days post fertilization (dpf). While gape, the displacement of the lower jaw to form the mouth opening, was minimal at 3 dpf, gape frequency increased sharply by 5 dpf, and stabilized by 7 dpf. A detailed analysis of branchiomotor axons and neuromuscular junctions (NMJs) on jaw muscles suggest that this "maturation" of branchiomotor circuit output may be driven by changes in presynaptic structures at the jaw NMJs. To evaluate the consequences of defective neuronal migration on circuit output, I examined whether jaw movement was affected in the zebrafish off-limits (olt) mutant in which FBM neurons fail to migrate out of r4. In olt mutants, the increase in gape frequency occurred normally between 3-5 dpf. However, the average gape frequency was [approximately] 50 [percent] lower than wildtype siblings from 5-9 dpf while gape amplitude was unaffected. Given the jaw movement defect in olt mutants, I evaluated food intake, an independent measure of jaw movement and another functional output of the branchiomotor circuit. Olt mutants ate poorly compared to their wildtype siblings, consistent with their reduced jaw movement. I then tested several potential mechanisms that could generate the functional deficits in olt mutants. While fzd3a, the gene inactivated in olt mutants, is ubiquitously expressed in neural and non-neural tissues, jaw cartilage and muscle developed normally in olt mutants, and muscle function also appeared to be unaffected. Although FBM neurons were mispositioned in olt mutants, axon pathfinding to jaw muscles were unaffected. Moreover, neuromuscular junctions established by FBM neurons on jaw muscles were similar between wildtype siblings and olt mutants. Interestingly, FBM axons innervating the interhyoideus jaw muscle were frequently defasciculated in olt mutants. Furthermore, GCaMP imaging revealed that mutant FBM neurons were less active than their wildtype counterparts. These data suggest that aberrant positioning of FBM neurons in olt mutants results in subtle defects in fasciculation and neuronal activity, potentially generating defective functional outputs. In the future, we will examine modulatory inputs from other brain regions to the branchiomotor neurons and examine their roles in impacting circuit output in olt mutants.

Steganography Technique Inspired by Rook

A steganographic technique inspired by rook is presented in this paper to ensure privacy and secrecy. In this approach, the cover image is partitioned into n × 1 pixel blocks and converted equivalent n × 8 binary bit planes. Then the functional output of each block is calculated on the basis of the number of rook positions, which are attacked by opponent rooks. The rook is a chess piece that moves only forward and backward in a straight line. In binary bit plane, 0 and 1 are considered as a black and white opponent rook, respectively. The secret information is considered as stream of binary bits. The binary bits of secret information are compared with the functional output of the corresponding block. If it is equal to the functional output of the corresponding block, then nothing needs to be done. In case of inequality, the small number of bits needs to be flipped in such a way that the functional output of the corresponding block becomes equal to the corresponding secret binary bits and the distortion of the cover is minimized.

Structural and Functional Maturation of Rat Primary Motor Cortex Layer V Neurons

Rodent neocortical neurons undergo prominent postnatal development and maturation. The process is associated with structural and functional maturation of the axon initial segment (AIS), the site of action potential initiation. In this regard, cell size and optimal AIS length are interconnected. In sensory cortices, developmental onset of sensory input and consequent changes in network activity cause phasic AIS plasticity that can also control functional output. In non-sensory cortices, network input driving phasic events should be less prominent. We, therefore, explored the relationship between postnatal functional maturation and AIS maturation in principal neurons of the primary motor cortex layer V (M1LV), a non-sensory area of the rat brain. We hypothesized that a rather continuous process of AIS maturation and elongation would reflect cell growth, accompanied by progressive refinement of functional output properties. We found that, in the first two postnatal weeks, cell growth prompted substantial decline of neuronal input resistance, such that older neurons needed larger input current to reach rheobase and fire action potentials. In the same period, we observed the most prominent AIS elongation and significant maturation of functional output properties. Alternating phases of AIS plasticity did not occur, and changes in functional output properties were largely justified by AIS elongation. From the third postnatal week up to five months of age, cell growth, AIS elongation, and functional output maturation were marginal. Thus, AIS maturation in M1LV is a continuous process that attunes the functional output of pyramidal neurons and associates with early postnatal development to counterbalance increasing electrical leakage due to cell growth.

Automated design of synthetic microbial communities

In naturally occurring microbial systems, species rarely exist in isolation. There is strong ecological evidence for a positive relationship between species diversity and the functional output of communities. The pervasiveness of these communities in nature highlights that there may be advantages for engineered strains to exist in cocultures as well. Building synthetic microbial communities allows us to create distributed systems that mitigates issues often found in engineering a monoculture, especially when functional complexity is increasing. Here, we demonstrate a methodology for designing robust synthetic communities that use quorum sensing to control amensal bacteriocin interactions in a chemostat environment. We explore model spaces for two and three strain systems, using Bayesian methods to perform model selection, and identify the most robust candidates for producing stable steady state communities. Our findings highlight important interaction motifs that provide stability, and identify requirements for selecting genetic parts and tuning the community composition.