Biology subjects

Shiraishi, M.

Publications and source records attributed to Shiraishi, M..

6 recordsLinked to original sources

bioRxiv2026

DiverScan: attention-guided exploratory analysis of animal behaviour across diverse comparative experiments

High-throughput tracking yields rich time-series data of animal behaviour, yet extracting biological insight remains a bottleneck, even for simple control--treatment comparisons. Existing analyses struggle to pinpoint the multiple, nonlinearly intertwined differences hidden in the data and fail to generalise across diverse recording set-ups. Here we present DiverScan, a deep-learning framework for attention-guided exploratory analysis of behavioural time series. DiverScan disentangles condition-dependent behavioural differences by pairing a loss function tailored to data exploration with an attention-branch architecture, and highlights condition-specific behavioural features visually and with explanatory text generated by a large language model. DiverScan is validated on a synthetic benchmark and on datasets from seven laboratories spanning multiple species and both single- and multi-animal behaviour. Beyond recovering known phenotypes, we demonstrate that DiverScan helps researchers generate new hypotheses across these diverse datasets. Available as Jupyter notebooks with a graphical user interface and flexible input formats, DiverScan can integrate into existing behavioural-analysis pipelines.

animal behavior and cognition↗

bioRxiv2026

Avoidance of simultaneous patch use in Japanese large-footed bats

Group foraging can enhance prey detection, but depending on resource availability, it may also generate conflicts among conspecifics. To understand how animals balance these benefits and costs, foraging performance must be evaluated together with inter-individual interactions. However, under fully natural conditions, it remains challenging to quantify both simultaneously. Here, we investigated how individual foraging efficiency and pairwise interactions are shaped when more than one individuals simultaneously exploit the same foraging patch, using the Japanese large-footed bat (Myotis macrodactylus) as a model system. We monitored an entire pond functioning as a natural foraging patch using two thermal cameras and an eight-channel microphone array, and reconstructed the arrival, prey-attack, and exit times of individual bats. Using a Poisson generalized linear mixed model (GLMM), we found that prey-attack rates were approximately 25% lower during paired flights than during solitary flights. We then constructed a null model in which arrival, attack, and departure events followed independent Poisson processes parameterized from the empirical data. Compared with null-model predictions, both the total duration and the duration of individual paired flights in the empirical data were significantly shorter, indicating that bats limited the time spent co-using the same patch relative to solitary foraging. In addition, the probability that the first exiting individual was the one that arrived earlier or later did not deviate from chance levels, providing no evidence for a prior residence advantage. Together, these results demonstrate that simultaneous patch use avoidance occurs independently of arrival order and coincides with reduced prey-attack rate, suggesting that bats leave shared patches and move to alternative foraging sites to mitigate losses in prey-attack efficiency. Our findings highlight bats as an excellent model system for non-invasively linking individual behavior and foraging performance via echolocation, and for elucidating the dynamics of foraging behavior and sensory interference in the wild.

animal behavior and cognition↗

bioRxiv2024

Self-organized acoustic behavior in bats arises from simple rules

Although self-organized behavior has been extensively studied in the movement of group-behaving animals, such as fish or birds, far less attention has been paid to vocal behavior in animal groups, especially in mammals. Here, by testing the vocal response of echolocating bats (Miniopterus fuliginosus) to the playback of jamming stimuli in the lab, we discovered a mathematical model that can well describe vocal frequency control by bats in response to jamming stimuli mimicking echolocation sounds emitted in a group of bats. We then extended the model to a group of flying bats and observed frequency-adjusting behavior by which the frequency differences for the group increased overall, similar to a previous observation on group-flying bats. Further, we showed the frequency-adjusting behavior led to less potential misdetections by echolocation in a group. Our findings suggest this frequency-adjusting behavior is a self-organized vocal behavior that mitigates conflicts within a group, one achieved via simple behavioral rules, as in other types of collective animal behavior.

animal behavior and cognition↗

bioRxiv2024

Experimental method for creating skin with acquired appendage dysfunction

Mammalian skin appendages, such as hair follicles and sweat glands, are essential for both esthetic and functional purposes. Conditions such as burns and ulcers can lead to dysfunction or loss of skin appendages and result in hair loss and dry skin, posing challenges in their regeneration. Existing animal models are insufficient for studying acquired dysfunction of skin appendages without underlying genetic causes. This study aimed to develop more clinically relevant mouse models by evaluating two approaches: keratinocyte transplantation and grafting of skin at varying thicknesses. GFP-expressing keratinocytes were transplanted into ulcers on nude mice, leading to re-epithelialization with minimal skin appendages at 4 weeks after transplantation. However, the re-epithelialized area was largely derived from recipient cells, with the grafted cells contributing to only 1.31% of the area. In the skin grafting model, donor skin from GFP transgenic mice was grafted onto nude mice at three thicknesses: full thickness, 10/1000 inch, and 5/1000 inch. The grafted area of the 5/1000-inch grafts remained stable at 89.5% of its original size 5 weeks after transplantation, ensuring a sufficiently large skin area. The 5/1000-inch grafts resulted in a significant reduction in skin appendages, with a mean of only 3.73 hair follicles per 5 mm, compared with 69.7 in the control group. The 5/1000-inch skin grafting in orthotopic autologous transplantation also showed the achievement of skin surfaces with a minimal number of skin appendages. Therefore, a mouse model with skin grafting demonstrated stability in producing large areas of skin with minimal appendages. In conclusion, these two models with acquired skin appendage dysfunction and no underlying genetic causes provide valuable tools for researching skin appendage regeneration, offering insights into potential therapeutic strategies for conditions involving skin appendage loss.

bioengineering↗

bioRxiv2024

Unveiling reversibility and plasticity in cardiac hypertrophy: insights from a transverse aortic constriction-release model

Transverse aortic constriction (TAC) is a well-established animal model used to study the pathomechanisms of pressure overload-induced heart failure. A number of studies have shown that treatment of the heart failure in this model may reverse the associated hypertrophy and fibrosis. However, because no TAC-release model in which hemodynamics improve upon alleviation of the physical stenosis has yet been established, the histologic changes and regulatory molecular biological mechanisms underlying the reversibility of cardiac hypertrophy and fibrosis are unknown. This study was conducted to establish an animal TAC-release model and thereby investigate the mechanisms that govern reversibility and plasticity of myocardial hypertrophy, fibrosis, and angiogenesis. TAC surgery was performed on rats, and 4 weeks later TAC release was achieved by cutting the constricting threads. TAC-subjected heart exhibited severe myocardial hypertrophy, fibrosis, and increased angiogenesis, along with diastolic dysfunction. Heart released from TAC showed reduced hypertrophy and fibrosis and improved diastolic function. Gene expression analysis uncovered regulator of calcineurin 1 (Rcan1) as a key player in cardiac function and histologic changes after TAC release. Rcan1 knockdown exacerbated myocardial hypertrophy and fibrosis in heart released from TAC. The left ventricular afterload relief model revealed that increased oxidative stress and Rcan1 upregulation, which suppresses the calcineurin-NFAT pathway, are key to structural and functional recovery from pressure overload-induced cardiac hypertrophy.

molecular biology↗

bioRxiv2021

Reparative macrophages regulate fibrosis in the infarcted myocardium by attenuating apoptosis and senescence of fibroblasts

RATIONALEAppropriate fibrotic tissue formation after myocardial infarction (MI) is crucial to maintenance of the hearts structure. Reparative or M2-like macrophages play a vital role in post-MI fibrosis by activating cardiac fibroblasts. However, the mechanism by which post-MI cardiac fibrosis is regulated is not fully understood. OBJECTIVEWe investigated the cellular and molecular mechanisms of post-MI fibrotic tissue formation, especially those related to regulation of cellular senescence and apoptosis. METHODS AND RESULTSIn vivo and in vitro experiments were used to investigate the molecular and cellular mechanisms through which post-MI fibrosis occurs, with a focus on the role of M2-like macrophages. Microarray analysis revealed that CD206+F4/80+CD11b+ M2-like macrophages collected from mouse hearts on post-MI day 7 showed increased expression of neuregulin 1 (Nrg1). Nrg1 receptor epidermal growth factor receptor ErbB was expressed on cardiac fibroblasts in the infarct area. In cardiac fibroblasts in which hydrogen peroxide-induced senescence, M2-like macrophage-derived Nrg1 suppressed both senescence and apoptosis of the fibroblasts, whereas blockade of ErbB function significantly accelerated. M2-like macrophage-derived Nrg1/ErbB/PI3K/Akt signaling, which was shown to be related to anti-senescence, was activated in damaged cardiac fibroblasts. Interestingly, systemic blockade of ErbB function in MI model mice enhanced senescence and apoptosis of cardiac fibroblasts and exacerbated inflammation. Further, increased accumulation of M2-like macrophages resulted in excessive progression of fibrosis in post-MI murine hearts. The molecular mechanism underlying regulation of fibrotic tissue formation in the infarcted myocardium was shown in part to be attenuation of apoptosis and senescence of cardiac fibroblasts by activation of Nrg1/ErbB/PI3K/Akt signaling. CONCLUSIONSM2-like macrophage-mediated regulation of Nrg1/ErbB signaling, have a substantial effect on fibrotic tissue formation in the infarcted adult mouse heart, is critical for suppressing the progression of senescence and apoptosis of cardiac fibroblasts.

molecular biology↗