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Cortical slow waves are hallmark oscillations of deep sleep and certain anesthetic conditions, yet the neurobiological mechanisms controlling their dynamics remain incompletely understood. Here, we investigated the effects of local near-infrared (NIR) stimulation on slow-wave activity in ketamine/xylazine-anesthetized rats. Using a silicon-based multimodal optrode, we simultaneously delivered NIR light and recorded local field potentials (LFPs) and multi-unit activity (MUA) across cortical layers in the primary somatosensory (S1Tr) and parietal association (PtA) cortices. NIR stimulation induces local tissue heating, resulting in reproducible and reversible changes in the properties of slow waves. Specifically, up-state durations were shortened, down-states prolonged, and MUA amplitudes during up-states increased, with steeper slopes at state transitions, indicative of enhanced neuronal synchronization. LFP amplitude and spectral changes varied across cortical regions: PtA exhibited increased slow wave (0.5–2 Hz) and high delta (2–4 Hz) band activity, while S1Tr showed a trend toward reduction. Our findings demonstrate that local infrared stimulation can reliably modulate cortical slow-wave dynamics, likely through temperature-mediated changes in neuronal excitability. This approach provides a minimally invasive method for precise, local manipulation of cortical network activity and offers new insights into the biophysical regulation of slow oscillations.

Infrared neural stimulation has consistently shown that temperature is a critical neuronal state variable. However, a comprehensive understanding of the biophysical background is essential. In this study, using high-density laminar electrode recordings, we investigated the impact of pulsed and continuous-wave infrared illumination on cortical neurons in anesthetized rats ( ). By analyzing the infrared (IR) stimulation-related responses of more than 7500 single units, we found that elevating tissue temperature with IR stimulation resulted in a significant increase in the number of cells affected, including a substantial rise in the number of inhibited cells. Pulsed stimulation affected an average of of units, resulting primarily in increased activity. In contrast, continuous stimulation significantly increased the percentage of affected cells to , with single units tending to be suppressed. Furthermore, when analyzing cell types, a higher percentage of principal cells displayed increased firing rates ( ) compared to suppressed activity ( ). Meanwhile, more interneurons were suppressed ( ) than showed increased activity ( ). On average, the firing rate of neurons reached 90% of the maximal activation within approximately 36 seconds after the onset of infrared stimulation. The proportion of neurons with suppressed activity decreased with cortical depth, while the proportion of neurons with elevated activity increased in deeper layers. These results provide valuable data to understand the mechanism of infrared neural stimulation in the living brain.

Infrared neuromodulation (INM) is a promising neuromodulation tool that utilizes pulsed or continuous-wave near-infrared (NIR) laser light to produce an elevation of the background temperature of the neural tissue. The INM-based cortical heating has been proven as an effective modality to induce changes in neuronal activities. In this paper, we investigate the effect of INM-based cortical heating on the characteristics of interictal epileptiform discharges (IEDs) induced by penicillin in anesthetized rats. Cortical heating was conducted using a NIR laser light guided through a needle-like silicon-based waveguide probe. We detected penicillin-induced cortical IEDs from preprocessed micro-electrocorticography ( μ ECoG) recordings, then we assessed changes in various temporal and spectral features of IEDs due to INM. Our findings show that the fast cortical heating phase obtained with continuous-wave NIR light is highly associated with a reduction of IED amplitudes, small but significant changes in the negative amplitude of IEDs compared with the baseline, and a proportional increase in the power of frequency bands related to delta/theta (2–8 Hz) and gamma (28–80 Hz) oscillations. Furthermore, a low rate of cortical heating with pulsed NIR illumination has a more inhibitory impact on the sharp negative polarity of IEDs. Our findings do not indicate a clear reduction in the frequency of IEDs in anesthetized rodents. In contrast, 2–4 min of continuous laser illumination leads to a notable increase in IED frequency. This effect of INM could potentially restrict its use in therapeutic applications related to epilepsy. However, the thermal effect of INM on cortical neurons induces changes in other characteristics of IEDs, which could prove beneficial for future applications.

This paper details the compilation of data and application of quality assurance procedures for constructing a 157‐year snow and sleet series for the Greater Dublin Area, Ireland. Snowfall is particularly sensitive to climate variability in temperate regions, and long‐term records are essential for understanding changes in winter weather extremes over time. The dataset integrates observations from six sites and provides a regional snow and sleet frequency dataset at monthly, seasonal (October–May) and annual resolutions. Data sources include archived meteorological records, digitised station logs and synoptic weather reports. A brief analysis offers insights into long‐term snowfall climatology in the Greater Dublin region from 1867 to 2024, revealing substantial interannual and decadal variability, as well as notable reductions in snow frequency in recent decades. This dataset provides a valuable baseline for assessing historical trends in snowfall and contributes to broader efforts in climate reconstruction and climate change impact studies in Ireland and beyond. This study presents a 157‐year dataset of monthly snow and sleet frequencies for the Greater Dublin Area. Based on historical and modern observations, it offers high‐resolution insight into long‐term snowfall and sleet variability in Ireland and supports climate impact research through a quality‐assured, openly accessible dataset.

In the current climate change context and the potential to extend exotic crops in Romania, sweet potato could become an option for extensive areas with optimum ecophysiological conditions to provide economic and ecological benefits and assure food security. This study aimed to validate the suitability, photosynthetic performance, yield productivity, and sugar content of three sweet potato cultivars, KSC, Koretta, and Hayanmi, in Central Romania. Three key phenophases were selected: the beginning of flowering (P1), 50% tuber formation/full flowering (P2), and total tuber formation/leaves and stems bleached and dry (P3), respectively. At the beginning of flowering, extreme heat and moisture stress showed a reduced effect on the sweet potato development and photosynthetic parameters. The only exception was the assimilation rate for Hayanmi, which was markedly lower, with the highest relative chlorophyll content and leaf dry biomass. Koretta registered increased values for stomatal features. A higher tuber weight was registered for Hayanmi in P2 due to slightly increased rainfall and elevated evapotranspiration. In P3, the temperatures dropped sharply, rainfall exceeded evapotranspiration, and KSC accumulated a seven times higher value for tuber weight. The total biomass was 2–3 times higher for KSC in P3. Sugar content was negatively correlated with tuber weight, and Hayanmi had 1% higher values compared with KSC and Koretta. Sweet potato showed a variety-specific response to ecophysiological conditions, and for each variety, these physiological features suggest potential advantages for different cropping scenarios.

High-density microelectrode arrays have opened new possibilities for systems neuroscience, but brain motion relative to the array poses challenges for downstream analyses. We introduce DREDge (Decentralized Registration of Electrophysiology Data), a robust algorithm for the registration of noisy, nonstationary extracellular electrophysiology recordings. In addition to estimating motion from action potential data, DREDge enables automated, high-temporal-resolution motion tracking in local field potential data. In human intraoperative recordings, DREDge’s local field potential-based tracking reliably recovered evoked potentials and single-unit spike sorting. In recordings of deep probe insertions in nonhuman primates, DREDge tracked motion across centimeters of tissue and several brain regions while mapping single-unit electrophysiological features. DREDge reliably improved motion correction in acute mouse recordings, especially in those made with a recent ultrahigh-density probe. Applying DREDge to recordings from chronic implantations in mice yielded stable motion tracking despite changes in neural activity between experimental sessions. These advances enable automated, scalable registration of electrophysiological data across species, probes and drift types, providing a foundation for downstream analyses of these rich datasets. DREDge is a software tool for motion correction of high-density electrophysiology recordings. It can handle action potential or local field potential data and is demonstrated on a variety of acute or chronic recordings from humans, nonhuman primates and mice.

Extensive research work has been carried out to define the exact significance and contribution of regulated necrosis-like cell death program, such as necroptosis to cardiac ischemic injury. This cell damaging process plays a critical role in the pathomechanisms of myocardial infarction (MI) and post-infarction heart failure (HF). Accordingly, it has been documented that the modulation of key molecules of the canonical signaling pathway of necroptosis, involving receptor-interacting protein kinases (RIP1 and RIP3) as well as mixed lineage kinase domain-like pseudokinase (MLKL), elicit cardioprotective effects. This is evidenced by the reduction of the MI-induced infarct size, alleviation of myocardial dysfunction, and adverse cardiac remodeling. In addition to this molecular signaling of necroptosis, the non-canonical pathway, involving Ca2+/calmodulin-dependent protein kinase II (CaMKII)-mediated regulation of mitochondrial permeability transition pore (mPTP) opening, and phosphoglycerate mutase 5 (PGAM5)–dynamin-related protein 1 (Drp-1)-induced mitochondrial fission, has recently been linked to ischemic heart injury. Since MI and HF are characterized by an imbalance between reactive oxygen species production and degradation as well as the occurrence of necroptosis in the heart, it is likely that oxidative stress (OS) may be involved in the mechanisms of this cell death program for inducing cardiac damage. In this review, therefore, several observations from different studies are presented to support this paradigm linking cardiac OS, the canonical and non-canonical pathways of necroptosis, and ischemia-induced injury. It is concluded that a multiple therapeutic approach targeting some specific changes in OS and necroptosis may be beneficial in improving the treatment of ischemic heart disease.

Immune Mediators and Modulators in Reducing the Size and Inducing Stability of Atherosclerotic Plaques in the Carotid Artery Devendra Agrawal Western University of Health Sciences, Pomona, CA, USA Abstract Prevention of atherosclerotic plaque formation, reduction in plaque burden and stabilization of a vulnerable plaque are of therapeutic significance in decreasing the incidence of acute events. The findings supported the critical role of TLR4 and TREM-1 in underlying pathophysiology of chronic inflammation, atherosclerotic plaque formation and plaque instability. [...]we examined the effect of the selective inhibitors of TREM-1 (LR-12) and TLR4 (TAK242) in a microswine model of carotid artery atherosclerosis. Positive effects of hydrogen gas have previously been reported in cardiac arrest settings in animals and humans. [...]a preventive effect was observed on syndecan-1 release in a rat model of haemorrhagic shock. [...]SZV-2649, similar to amiodarone, has antiarrhythmic effects based on its multiple ion channel blocking properties.

Body composition, bone mineral density, and cardiopulmonary exercise testing (CPET) are commonly used to assess aerobic fitness in athletes, but their interrelationships remain unclear. This study compared these parameters by sex and examined their associations in elite athletes. Our study included 145 youth water polo players (age: 15.7 ± 1.6 years; male: 75). Body composition was measured by DEXA, and treadmill CPET was performed using a sport-specific protocol. We analysed the correlations between the following factors by multivariate linear regression: lean body mass (LBM, LBMindex); body fat mass (BFM); percent body fat (PBF); bone mineral content (BMC); lumbar, femoral, and radial bone mineral density (LBMD, FNBMD, FTBMD, RBMD); exercise time; absolute and relative maximal oxygen uptake (VO2absmax, VO2relmax); maximal ventilation (VEmax). Exercise time was found to be negatively correlated with BFM, while VO2relmax was found to be negatively correlated with BFM and PBF. VO2absmax was found to be positively correlated with BFM, LBM, BMC, FNBMD, and RBMD. VEmax was found to be positively correlated with LBM and LBMindex. In males, VO2absmax and VEmax were found to be positively correlated with LBMD and FTBMD. Correlations between bone density and CPET proved to be stronger in males. Our results indicate that body composition and bone density parameters influence CPET parameters, and their complex evaluation can support personalized diagnostics and athletes’ health.

Introduction Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are associated with osteoporosis. There have not been many peripheral quantitative computed tomography (QCT) studies in patients receiving biologics. We assessed volumetric and areal bone mineral density (BMD) by forearm QCT and dual-energy X-ray absorptiometry (DXA), respectively in addition to laboratory biomarkers in these arthritides. Methods Forty RA and AS patients treated with either etanercept (ETN) or certolizumab pegol (CZP) were undergoing follow-ups for one year. Volumetric and areal BMD, as well as parathyroid hormone (PTH), osteocalcin, RANKL, 25-hydroxyvitamin D (VITD), P1NP, CTX, sclerostin (SOST), Dickkopf 1 (DKK-1) and cathepsin K (CATHK) were determined. Results We did not observe any further bone loss during the 12-month treatment period. Volumetric and areal BMD showed significant correlations with each other (p<0.017 after Bonferroni’s correction). Trabecular QCT BMD at baseline (p=0.015) and cortical QCT BMD after 12 months (p=0.005) were inversely determined by disease activity at baseline in the full cohort. Trabecular QCT BMD at baseline also correlated with CTX (p=0.011). In RA, CRP negatively (p=0.014), while SOST positively (p=0.013) correlated with different QCT parameters. In AS, RANKL at baseline (p=0.014) and after 12 months (p=0.007) correlated with cortical QCT BMD. In the full cohort, 12-month change in QTRABBMD was related to TNF inhibition together with elevated VITD-0 levels (p=0.031). Treatment and lower CATHK correlated with QCORTBMD changes (p=0.006). In RA, TNF inhibition together with VITD-0 (p<0.01) or CATHK-0 (p=0.002), while in AS, treatment and RANKL-0 (p<0.05) determined one-year changes in QCT BMD. Conclusions BMD as determined by QCT did not change over one year of anti-TNF treatment. Disease activity, CATHK, RANKL and VITD may be associated with the effects of anti-TNF treatment on QCT BMD changes. RA and AS may differ in this respect.