Miracle-dz/UniFAR-FTUs huggingface dataset:
Gaining insight into the allometric scaling of trees by utilizing 3d reconstructed tree models - a SimpleForest study

Forestry utilizes volume predictor functions utilizing as input the diameter at breast height. Some of those functions take the power form Y = a ∗ Xb. In fact this function is fundamental for the biology field of allometric scaling theories founded round about a century ago. The theory describes the relationships between organs/body parts and the complete body of organisms. With digital methods we can generate 3d forest point clouds non destructively in short time frames. SimpleForest is one free available tool which generates fully automated ground and tree models from high resoluted forest plots. Generated topological ordered cylinder models are called commonly QSMs. We use SimpleForest QSMs an build a function which estimates the total supported wood volume at any given point of the tree. As input we use the supported soft wood volume for those query points. Instead of measuring directly the soft wood volume we use as a proxy the number of supported twigs. We argue with the pipe model theory for the correctness of the proxy. We can use the named relationship to also filter our QSMs made of an open data set of tree clouds. The filter corrects overestimated radii. And we compare the corrected QSM volume against the harvested reference data for 66 felled trees. We also found QSM data of TreeQSM, a competitive and broadly accepted QSM modeling tool. Our RMSE was less than 40% of the tree QSM RMSE. And for other error measures, the r2adj. and the CCC, the relative improvement looked even better with 27% and 21% respectively. We consider this manuscript as highly impactful because of the magnitude of quality improvement we do. The relation between soft volume and total volume distributions seems to be really strong and tree data can easily also be used as example data for the generic field of allometric scaling.
Generating variability from motor primitives during infant locomotor development

Motor variability is a fundamental feature of developing systems allowing motor exploration and learning. In human infants, leg movements involve a small number of basic coordination patterns called locomotor primitives, but whether and when motor variability could emerge from these primitives remains unknown. Here we longitudinally followed 10 neonates (∼4 days old) until walking onset (∼14 months old) and recorded the activity of their leg muscles during locomotor or rhythmic movements. Using unsupervised machine learning, we show that the structure of trial-to-trial variability changes during early development. In the neonatal period, infants own a minimal number of motor primitives but generate a maximal motor variability across trials thanks to variable activations of these primitives. A few months later, toddlers generate significantly less variability despite the existence of more primitives, due to more regularity within their activation. These results suggest that human neonates initiate motor exploration as soon as birth by variably activating a few basic locomotor primitives that later fraction and become more consistently activated by the motor system.
FIP-fve Stimulates Cell Proliferation and Enhances IL-2 Release by Activating MAP2K3/p38α (MAPK14) Signaling Pathway in Jurkat E6-1 Cells

FIP-fve, a fungal fruiting body protein from Flammulina velutipes, has potential immunomodulatory properties. Here, we investigated the immunomodulation mechanism of FIP-fve in Jurkat E6-1 cells by conducting a cell viability assay and IL-2 release assay. Kinase inhibitors experiment and proteomics analysis were also involved in the mechanism study. It was found that FIP-fve stimulated cell proliferation and enhanced IL-2 secretion in a dose-dependent manner in Jurkat E6-1 cells. Unbiased high-throughput proteomics analysis showed that 4 T cell immune activation markers, including ZAP-70, CD69, CD82, and KIF23, were upregulated in response to FIP-fve treatment. Further pathway analysis indicated that MAP2K3/p38 pathway-related proteins, including MAP2K, p38, ELK, AATF, FOS, and JUN-B, were unregulated. In addition, losmapimod (p38 inhibitor) and gossypetin (MAP2K3 inhibitor) inhibited FIP-fve enhanced cell proliferation and IL-2 release in Jurkat E6-1 cells. Our results demonstrate that FIP-fve stimulates cell proliferation and enhances IL-2 secretion through MAP2K3/p38α activation.
Dyssynchronous Left Ventricular Activation is Insufficient for the Breakdown of Wringing Rotation

Cardiac resynchronization therapy is a valuable tool to restore left ventricular function in patients experiencing dyssynchronous ventricular activation. However, the non-responder rate is still as high as 40%. Recent studies suggest that left ventricular torsion or specifically the lack thereof might be a good predictor for the response of cardiac resynchronization therapy. Since left ventricular torsion is governed by the muscle fiber orientation and the heterogeneous electromechanical activation of the myocardium, understanding the relation between these components and the ability to measure them is vital. To analyze if locally altered electromechanical activation in heart failure patients affects left ventricular torsion, we conducted a simulation study on 27 personalized left ventricular models. Electroanatomical maps and late gadolinium enhanced magnetic resonance imaging data informed our in-silico model cohort. The angle of rotation was evaluated in every material point of the model and averaged values were used to classify the rotation as clockwise or counterclockwise in each segment and sector of the left ventricle. 88% of the patient models (n = 24) were classified as a wringing rotation and 12% (n = 3) as a rigid-body-type rotation. Comparison to classification based on in vivo rotational NOGA XP maps showed no correlation. Thus, isolated changes of the electromechanical activation sequence in the left ventricle are not sufficient to reproduce the rotation pattern changes observed in vivo and suggest that further patho-mechanisms are involved.
LcNAC13 Is Involved in the Reactive Oxygen Species-Dependent Senescence of the Rudimentary Leaves in Litchi chinensis

Litchi is an important evergreen fruit tree. Floral formation in litchi is induced by low temperatures (LTs). However, unstable flowering is a challenge for litchi production in times of global warming and climate change. Previous studies have shown that the methyl viologen dichloride hydrate-generated reactive oxygen species (ROS) could promote flowering. Leaves in the panicles may affect the development of the inflorescence in litchi under high-temperature condition. In this study, potted litchi trees were transferred to growth chambers at LT and high temperature (HT). From a previous dataset of the RNA sequencing of the ROS-treated rudimentary leaves, a NAC transcription factor-encoding gene LcNAC13 was identified. By genetic transformation of LcNAC13 to Arabidopsis thaliana and tobacco, it was found that the ROS-induced senescence of the leaves was accelerated. Silencing LcNAC13 by virus-induced gene silencing (VIGS) delayed ROS-dependent senescence. Our results suggested that LcNAC13 regulates rudimentary leaf senescence. Our study provided a new target gene for the future molecular breeding of new cultivars that could flower under global warming conditions.
Hypoxic/Ischemic Inflammation, MicroRNAs and δ-Opioid Receptors: Hypoxia/Ischemia-Sensitive Versus-Insensitive Organs

Hypoxia and ischemia cause inflammatory injury and critically participate in the pathogenesis of various diseases in various organs. However, the protective strategies against hypoxic and ischemic insults are very limited in clinical settings up to date. It is of utmost importance to improve our understanding of hypoxic/ischemic (H/I) inflammation and find novel therapies for better prevention/treatment of H/I injury. Recent studies provide strong evidence that the expression of microRNAs (miRNAs), which regulate gene expression and affect H/I inflammation through post-transcriptional mechanisms, are differentially altered in response to H/I stress, while δ-opioid receptors (DOR) play a protective role against H/I insults in different organs, including both H/I-sensitive organs (e.g., brain, kidney, and heart) and H/I-insensitive organs (e.g., liver and muscle). Indeed, many studies have demonstrated the crucial role of the DOR-mediated cyto-protection against H/I injury by several molecular pathways, including NLRP3 inflammasome modulated by miRNAs. In this review, we summarize our recent studies along with those of others worldwide, and compare the effects of DOR on H/I expression of miRNAs in H/I-sensitive and -insensitive organs. The alternation in miRNA expression profiles upon DOR activation and the potential impact on inflammatory injury in different organs under normoxic and hypoxic conditions are discussed at molecular and cellular levels. More in-depth investigations into this field may provide novel clues for new protective strategies against H/I inflammation in different types of organs.
A Potential Target for Diabetic Vascular Damage: High Glucose-Induced Monocyte Extracellular Vesicles Impair Endothelial Cells by Delivering miR-142-5p

Endothelial dysfunction is a key accessory to diabetic cardiovascular complications, and the regulatory role of the extracellular vesicles (EVs) from the innate immune system is growing. We tested whether EVs derived from high glucose-induced monocytes could shuttle microRNAs and impair endothelial cells. EVs from high glucose- and basal glucose-treated THP-1 cells (HG-THP-1 EVs and BG-THP-1 EVs) were isolated and identified. After coculture with THP-1 EVs, human umbilical vein endothelial cells (HUVECs) were tested by proliferation, migration, reactive oxygen species (ROS) detection assays, and western blot for Nrf2/NLRP3 signaling. MiR-142-5p was predicted by miRNAs databases and further verified by RT–qPCR and dual-luciferase reporter gene assays that inhibit Nrf2 expression. The regulation of miR-142-5p in HUVECs was further evaluated. A type 1 diabetes mellitus (T1DM) mouse model was developed for miR-142-5p inhibition. Aorta tissue was harvested for hematoxylin-eosin staining and immunohistochemistry of interleukin-1β (IL-1β). Compared to BG-THP-1 EVs, HG-THP-1 EVs significantly reduced migration and increased ROS production in HUVECs but did not affect proliferation. HG-THP-1 EVs induced suppression of Nrf2 signaling and NLRP3 signaling activation. RT–qPCR results showed that HG-THP-1 EVs overexpressed miR-142-5p in HUVECs. The transfection of miR-142-5p mimics into HUVECs exhibited consistent regulatory effects on HG-THP-1 EVs, whereas miR-142-5p inhibitors demonstrated protective effects. The miR-142-5p antagomir significantly reduced the IL-1β level in T1DM aortas despite morphological changes. To conclude, miR-142-5p transferred by high glucose-induced monocyte EVs participates in diabetic endothelial damage. The inhibition of miR-142-5p could be a potential adjuvant to diabetic cardiovascular protection.
Ag Functionalized In2O3 Derived From MIL-68(In) as an Efficient Electrochemical Glucose Sensor

In this study, Ag@In2O3 modified nickel foam (NF) was reported for its role as a non-enzymatic glucose sensor. Ag@In2O3 was prepared by a simple two-step method; preparation of a metal-organic framework (MOF) MIL-68(In) by solvothermal method, entrapment of Ag + by adding AgNO3 then drying it for 2 h to complete the entrapment process and subsequent calcination at 650°C for 3 h. The Ag@In2O3 modified NF was employed as a non-enzymatic glucose sensor to determine glucose concentrations in an alkaline medium. Two linear ranges were obtained from Ag@In2O3 modified electrode, i.e., 10 μM to 0.8 mM and 0.8–2.16 mM with a sensitivity of 3.31 mA mM−1 cm−2 and 1.51 mA mM−1 cm−2 respectively, with a detection limit of 0.49 µM. Ag@In2O3 modified NF exhibited high selectivity for glucose, among other interfering agents.
Molecular Determinants of in vitro Plant Regeneration: Prospects for Enhanced Manipulation of Lettuce (Lactuca sativa L.)

In vitro plant regeneration involves dedifferentiation and molecular reprogramming of cells in order to regenerate whole organs. Plant regeneration can occur via two pathways, de novo organogenesis and somatic embryogenesis. Both pathways involve intricate molecular mechanisms and crosstalk between auxin and cytokinin signaling. Molecular determinants of both pathways have been studied in detail in model species, but little is known about the molecular mechanisms controlling de novo shoot organogenesis in lettuce. This review provides a synopsis of our current knowledge on molecular determinants of de novo organogenesis and somatic embryogenesis with an emphasis on the former as well as provides insights into applying this information for enhanced in vitro regeneration in non-model species such as lettuce (Lactuca sativa L.).
Cell Based Treatment of Autoimmune Diseases in Children

Mesenchymal stem cells have recently been recoined as medicinal signaling cells (MSC) for their ability to promote tissue homeostasis through immune modulation, angiogenesis and tropism. During the last 20 years, there has been a plethora of publications using MSC in adults and to lesser extent neonates on a variety of illnesses. In parts of the world, autologous and allogeneic MSCs have been purified and used to treat a range of autoimmune conditions, including graft versus host disease, Crohn’s disease, multiple sclerosis, refractory systemic lupus erythematosus and systemic sclerosis. Generally, these reports are not part of stringent clinical trials but are of note for good outcomes with minimal side effects. This review is to summarize the current state of the art in MSC therapy, with a brief discussion of cell preparation and safety, insights into mechanisms of action, and a review of published reports of MSC treatment of autoimmune diseases, toward the potential application of MSC in treatment of children with severe autoimmune diseases using multicenter clinical trials and treatment algorithms.
Design of a Helicopter Deployable Ground Robotic System for Hazardous Environments

The use of robotics in hazardous environments is becoming more common, where autonomy can handle the dull, dirty and dangerous jobs that humans have previously supported. This thesis focuses on the design of a helicopter deployable unmanned ground vehicle for use in hazardous environments, and presents the benefits of heterogeneous unmanned vehicle teams for operation in beyond line-of-site hazardous environments. The design of a ground robot that is capable of being flown on the undercarriage of a Yamaha RMAX unmanned air vehicle is presented. The robot is size, weight, and power limited and must be capable of traversing rough, unstructured terrain. The results of testing show that the design criteria for size, weight, and mobility are met. A path planning algorithm is developed using the A* search algorithm for the planning of optimal paths through rough terrain. The algorithm makes use of a vehicle/terrain interaction model to compute the cost of path traversal. In the CONOPS, the terrain model is generated real-time during a mission through the use of a stereovision system carried on the helicopter, which station-keeps above the ground robot. The algorithm simulates the robot on the terrain and presents the best feasible path to the operator to aid in teleoperated robot navigation. Simulations of the planning algorithm provided feasible paths over a rough terrain environment. A user study was conducted that evaluates the abilities of both monoand stereo-vision systems in providing the teleoperator with adequate situational awareness with the intent of proving that stereovision data is more effective at aiding the user in making timely navigation decisions. The results of the study showed that the helicopter-mounted stereovision system was more efficient than the monovision system with respect to navigation time, the number of invalid moves, and total moves required for navigation of a simulated rough terrain environment. To my loving wife Diane
Exploration of Potential Biomarker Genes and Pathways in Kawasaki Disease: An Integrated in-Silico Approach

Kawasaki disease (KD) is a common childhood systemic vasculitis with a special predilection for coronary arteries. Even after more than five decades of the initial description of the disease, the etiology of KD remains an enigma. This transcriptome data re-analysis study aimed to elucidate the underlying pathogenesis of KD using a bioinformatic approach to identify differentially expressed genes (DEGs) to delineate common pathways involved in KD. Array datasets from the Gene Expression Omnibus database were extracted and subjected to comparative meta-analysis for the identification of prominent DEGs. Fifteen hub genes with high connectivity were selected from these DEGs (IL1B, ITGAM, TLR2, CXCL8, SPI1, S100A12, MMP9, PRF1, TLR8, TREM1, CD44, UBB, FCER1G, IL7R, and FCGR1A). Of these 15 genes, five genes (CXCL8, FCGR1A, IL1B, TLR2, and TLR8) were found to be involved in neutrophil degranulation. To gain further insight into the molecular mechanism, a protein–protein network was established. Significantly enriched pathways based on the above-mentioned genes were mainly centered on biological regulation and signaling events. In addition, the pathway analysis also indicated that the majority of the DEGs in KD were enriched in systemic lupus erythematosus, suggesting a strong interplay between immunological and genetic factors in the pathogenesis of KD. These findings could significantly aid in identifying therapeutic targets and understanding KD biosignatures to design a biomarker panel for early diagnosis and severity of the disease.
PyRAT: An Open-Source Python Library for Animal Behavior Analysis

Here we developed an open-source Python-based library called Python rodent Analysis and Tracking (PyRAT). Our library analyzes tracking data to classify distinct behaviors, estimate traveled distance, speed and area occupancy. To classify and cluster behaviors, we used two unsupervised algorithms: hierarchical agglomerative clustering and t-distributed stochastic neighbor embedding (t-SNE). Finally, we built algorithms that associate the detected behaviors with synchronized neural data and facilitate the visualization of this association in the pixel space. PyRAT is fully available on GitHub: https://github.com/pyratlib/pyrat.
Fractal Correlation Properties of Heart Rate Variability as a Biomarker for Intensity Distribution and Training Prescription in Endurance Exercise: An Update

While established methods for determining physiologic exercise thresholds and intensity distribution such as gas exchange or lactate testing are appropriate for the laboratory setting, they are not easily obtainable for most participants. Data over the past two years has indicated that the short-term scaling exponent alpha1 of Detrended Fluctuation Analysis (DFA a1), a heart rate variability (HRV) index representing the degree of fractal correlation properties of the cardiac beat sequence, shows promise as an alternative for exercise load assessment. Unlike conventional HRV indexes, it possesses a dynamic range throughout all intensity zones and does not require prior calibration with an incremental exercise test. A DFA a1 value of 0.75, reflecting values midway between well correlated fractal patterns and uncorrelated behavior, has been shown to be associated with the aerobic threshold in elite, recreational and cardiac disease populations and termed the heart rate variability threshold (HRVT). Further loss of fractal correlation properties indicative of random beat patterns, signifying an autonomic state of unsustainability (DFA a1 of 0.5), may be associated with that of the anaerobic threshold. There is minimal bias in DFA a1 induced by common artifact correction methods at levels below 3% and negligible change in HRVT even at levels of 6%. DFA a1 has also shown value for exercise load management in situations where standard intensity targets can be skewed such as eccentric cycling. Currently, several web sites and smartphone apps have been developed to track DFA a1 in retrospect or in real-time, making field assessment of physiologic exercise thresholds and internal load assessment practical. Although of value when viewed in isolation, DFA a1 tracking in combination with non-autonomic markers such as power/pace, open intriguing possibilities regarding athlete durability, identification of endurance exercise fatigue and optimization of daily training guidance.
Regulation of Mitophagy by Sirtuin Family Proteins: A Vital Role in Aging and Age-Related Diseases

Sirtuins are protein factors that can delay aging and alleviate age-related diseases through multiple molecular pathways, mainly by promoting DNA damage repair, delaying telomere shortening, and mediating the longevity effect of caloric restriction. In the last decade, sirtuins have also been suggested to exert mitochondrial quality control by mediating mitophagy, which targets damaged mitochondria and delivers them to lysosomes for degradation. This is especially significant for age-related diseases because dysfunctional mitochondria accumulate in aging organisms. Accordingly, it has been suggested that sirtuins and mitophagy have many common and interactive aspects in the aging process. This article reviews the mechanisms and pathways of sirtuin family-mediated mitophagy and further discusses its role in aging and age-related diseases.
Analysing Visual Behaviour in Engineering Design by Eye Tracking Experiments

In the past few years several experiments in cognitive science, human-computer interaction and marketing research impressively showed that eye tracking is a powerful research method to gain deeper insights in human behaviour. However, until now in engineering design research only a small number of eye tracking experiments have been conducted. But even these experiments indicate that eye tracking technology can lead to highly important research results. This paper introduces four different fields, where eye tracking experiments can support engineering design research in order to better understand human behaviour in the context of (1) product representations, (2) engineering design expertise, (3) design creativity and (4) product application. The paper especially focuses on the first aspect by presenting eye tracking experiments, in which the scan path of several test persons analysing a technical drawing is recorded and evaluated in order to identify patterns in their visual behaviour. Based on the results, it finally is discussed how visual behaviour can be purposefully described in design research and how the engineering designer can be effectively supported in design practice.