Biology subjects

Sato, F.

Publications and source records attributed to Sato, F..

4 recordsLinked to original sources

bioRxiv2026

Reducing the Risk of Gradient Induced EEG Hardware Heating During Simultaneous EEG-fMRI

Simultaneous electroencephalography (EEG) and functional MRI (fMRI) has the potential to provide a more complete characterisation of brain function. Acquiring these data simultaneously requires the EEG hardware to be MR safe, since the EEG cap, amplifiers and powerpacks must be located within the MR environment. Placing them in this environment exposes them to both static and varying (radiofrequency (RF) and gradient) magnetic fields, presenting a potential heating risk. Previous studies have typically positioned the amplifiers and powerpacks outside of the bore, meaning that this risk is largely limited to the EEG cap. However, current guidelines recommend positioning the amplifiers within the bore. This reduces the distance between the EEG electrodes and amplifier, improving EEG signal quality and reducing risks of RF heating at the electrodes, but presents a potential heating risk for the amplifiers and powerpacks from the varying magnetic field gradients. In this study, we demonstrate that placing the amplifiers and powerpacks in the bore presents a significant heating risk, both at 7T and 3T. At 7T, we show that EPI sequences with a slew rate of at least 88 T/m/s resulted in significant heating of the EEG amplifiers. This heating effect could be negated by reducing the slew rate to 61 T/m/s. At 3T, we replicate the EEG amplifier heating and show that an alternative approach to reducing the gradient slew rates experience by the hardware is to increase the distance between the EEG amplifier/powerpacks and the isocentre of the magnet. Increasing the distance between the EEG hardware and MR isocentre by 30 cm mitigates the heating risk to the amplifiers and powerpacks, regardless of sequence parameters (e.g., slew rate). Therefore, whilst reducing the distance between the electrodes and amplifiers may improve EEG signal quality and reduce the potential for electrode RF heating, we show that risk of heating of hardware by gradient switching is greatly increased. This is particularly important to consider with the faster gradient slew rates available on modern MRI scanners, desired to increase spatial resolution. Experimenters must make careful decisions about hardware placement to ensure that the EEG-fMRI setup they use is safe, taking account of the varying risks that are posed by different approaches.

neuroscience↗

bioRxiv2026

Pathway-specific short-term synaptic dynamics and lateral inhibition shape frequency-dependent input integration and population-level pattern separation in the dentate gyrus

The dentate gyrus (DG) decorrelates overlapping entorhinal inputs into distinct granule-cell representations, a computation central to pattern separation and to reducing interference in episodic memory. The three excitatory pathways to granule cells -- the lateral perforant path (distal dendrites), the medial perforant path (middle dendrites), and proximal inputs -- carry distinct short-term synaptic dynamics, but how these combine with lateral inhibition to set the frequency dependence of DG integration and pattern separation remains unclear. Here we integrate mechanism, function, and robustness into a single computational modeling study spanning three complementary model tiers, using Tsodyks-Markram short-term synaptic parameters grounded in prior slice electrophysiology. In a biophysically detailed 37-compartment granule-cell model (Tier 1), the distal (lateral) pathway facilitates at low frequency, the middle (medial) pathway depresses, and the proximal pathway is mixed, producing frequency- and pathway-dependent integration; three-pathway summation is mildly sublinear, and a direct granule-cell-to-granule-cell lateral inhibition -- a shunting connection emulating disynaptic feedforward inhibition without an explicit interneuron -- further attenuates it. In a reduced leaky-integrate-and-fire network with the same dynamics (Tier 2), pattern separation is frequency-dependent, rising to a gamma-band maximum at 40 Hz that is reproducible across independently wired networks, whereas the basket-cell-inhibition magnitude varies with the random connectivity. In a three-layer population network (Tier 3), pattern separation is robust: although single granule-cell spike counts are highly sensitive to input noise, the population-level separation code is nearly noise-invariant (a roughly 60-fold dissociation), and separation is governed by the magnitude of local lateral inhibition rather than its targeting. Two claims that hold at the single-cell scale -- a microsecond spike-timing-precision requirement and an advantage of finely targeted inhibition -- do not survive at the network scale. Pathway-specific synaptic dynamics and lateral inhibition thus shape frequency-dependent integration and noise-robust population pattern separation in the DG. Author SummaryThe dentate gyrus (DG) performs pattern separation: it takes overlapping cortical inputs and makes their DG representations more distinct, a computation thought to reduce memory interference. How does the DG do this? We approach the question across three scales in a single computational study. First (mechanism), we show in a biophysically detailed granule-cell model that the three anatomical input pathways carry different short-term synaptic dynamics -- the distal (lateral perforant path) input facilitates, the middle (medial perforant path) input depresses, and the proximal input is mixed -- so that the cells response depends on input frequency and pathway. Second (function), in a reduced network model we show that these dynamics, combined with lateral inhibition, tune pattern separation in a frequency-selective way. Third (robustness), we find that although a single granule cells spike count is highly sensitive to input noise, the population-level separation code is nearly noise-invariant -- a "noise paradox" in which population coding rescues what is fragile at the single-cell level. We also show that two claims that appear at the single-cell scale -- a microsecond spike-timing-precision requirement, and an advantage of finely targeted inhibition -- do not survive at the network scale: what matters is the amount of local inhibition, not how it is distributed. The synaptic parameters are grounded in prior slice recordings; the model integrates the mechanism.

neuroscience↗

bioRxiv2021

Transport engineering for improving production and secretion of valuable alkaloids in Escherichia coli

Metabolic engineering of microorganisms to produce specialized plant metabolites has been established. However, these methods are limited by low productivity and the intracellular accumulation of metabolites. Here, we aimed to use transport engineering for producing reticuline, an important intermediate in the alkaloid biosynthetic pathway. We established a reticuline-producing Escherichia coli strain and introduced a multidrug and toxic compound extrusion transporter, Arabidopsis AtDTX1, into it. AtDTX1 was selected due to its suitable expression in E. coli and its reticuline-transport activity. Expression of AtDTX1 significantly enhanced reticuline production by 11-fold; produced reticuline was secreted into the medium. AtDTX1 expression conferred high plasmid stability, and up- or downregulated genes associated with biological processes including metabolic pathways for reticuline biosynthesis, leading to a high production and secretion of reticuline. The successful application of a transporter for alkaloid production suggests that the transport engineering approach may improve the biosynthesis of specialized metabolites via metabolic engineering.

synthetic biology↗

bioRxiv2019

Estrogen induces mammary ductal dysplasia.

Mammary ductal dysplasia is a phenotype observed in precancerous lesions and early-stage breast cancer. However, the mechanism of dysplasia formation remains elusive. Here we show, by establishing a novel dysplasia model system, that estrogen, a female hormone, has the potential to cause mammary ductal dysplasia. We injected estradiol (E2), the most active form of estrogen, daily into scid mice with a defect in nonhomologous end joining repair and observed dysplasia formation with cell proliferation at day 30. Moreover, we found that isoflavones inhibited E2-induced dysplasia formation. Our dysplasia model system provides insight into the mechanistic understanding of breast tumorigenesis, and the development of breast cancer prevention.

cancer biology↗