Miracle-dz/UniFAR-FTUs huggingface dataset:
Extreme and Highly Heterogeneous Microclimates in Selectively Logged Tropical Forests

Microclimate within forests influences ecosystem fluxes and demographic rates. Anthropogenic disturbances such as selective logging can affect within-forest microclimate through effects on forest structure, leading to indirect effects on forests beyond the immediate impact of logging. However, the scope and predictability of these effects remains poorly understood. Here we use a microclimate thermal proxy (sensitive to radiative, convective, and conductive heat fluxes) measured at the forest floor in three 1-ha forest plots spanning a logging intensity gradient in Malaysian Borneo. We show 1) that thermal proxy ranges and spatiotemporal heterogeneity are doubled between old growth and heavily logged forests, with extremes often exceeding 45°C, 2) that nearby weather station air temperatures provide estimates of maximum thermal proxy values that are biased down by 5-10°C, and 3) that lower canopy density, higher canopy height, and higher biomass removal are associated with higher maximum temperatures. Thus, logged forests are less buffered from regional climate change than old growth forests, and experience much higher microclimate extremes and heterogeneity. Better predicting the linkages between regional climate and its effects on within-forest microclimate will be critical for understanding the wide range of conditions experienced within tropical forests.
Intratracheal transplantation of mesenchymal stem cells attenuates hyperoxia-induced lung injury by down-regulating, but not direct inhibiting formyl peptide receptor 1 in the newborn mice

Formyl peptide receptor 1 (FPR1) has been shown to be a key regulator of inflammation. However, its role in bronchopulmonary dysplasia (BPD) has not been delineated yet. We investigated whether FPR1 plays a pivotal role in regulating lung inflammation and injuries, and whether intratracheally transplanted mesenchymal stem cells (MSCs) attenuate hyperoxic lung inflammation and injuries by down-regulating FPR1. Newborn wild type (WT) or FPR1 knockout (FPR1-/-) C57/BL6 mice were randomly exposed to 80% oxygen or room air for 14 days. At postnatal day (P) 5, 2×105 MSCs were intratracheally transplanted. At P14, mice were sacrificed for histopathological and morphometric analyses. Hyperoxia significantly increased lung neutrophils, macrophages, and TUNEL-positive cells, while impairing alveolarization and angiogenesis, along with a significant increase in FPR1 mRNA levels in WT mice. The hyperoxia-induced lung inflammation and lung injuries were significantly attenuated, with the reduced mRNA level of FPR1, in WT mice with MSC transplantation and in FPR1-/- mice, irrespective of MSCs transplantation. However, only MSC transplantation, but not the FPR1 knockout, significantly attenuated the hyperoxia-induced increase in TUNEL-positive cells. Our findings indicate that FPR1 play a critical role in regulating lung inflammation and injuries in BPD, and MSCs attenuate hyperoxic lung inflammation and injuries, but not apoptosis, with down regulating, but not direct inhibiting FPR1.
Serratia liquefaciens KM4 Improves Salt Stress Tolerance in Maize by Regulating Redox Potential, Ion Homeostasis, Leaf Gas Exchange and Stress-Related Gene Expression

High salinity mitigates crop productivity and quality. Plant growth-promoting soil rhizobacteria (PGPR) improve plant growth and abiotic stress tolerance via mediating various physiological and molecular mechanisms. This study investigated the effects of the PGPR strain Serratia liquefaciens KM4 on the growth and physiological and molecular responsiveness of maize (Zea mays L.) plants under salinity stress (0, 80, and 160 mM NaCl). High salinity significantly reduced plant growth and biomass production, nutrient uptake, leaf relative water content, pigment content, leaf gas exchange attributes, and total flavonoid and phenolic contents in maize. However, osmolyte content (e.g., soluble proteins, proline, and free amino acids), oxidative stress markers, and enzymatic and non-enzymatic antioxidants levels were increased in maize under high salinity. On the other hand, Serratia liquefaciens KM4 inoculation significantly reduced oxidative stress markers, but increased the maize growth and biomass production along with better leaf gas exchange, osmoregulation, antioxidant defense systems, and nutrient uptake under salt stress. Moreover, it was found that all these improvements were accompanied with the upregulation of stress-related genes (APX, CAT, SOD, RBCS, RBCL, H+-PPase, HKT1, and NHX1), and downregulation of the key gene in ABA biosynthesis (NCED). Taken together, the results demonstrate the beneficial role of Serratia liquefaciens KM4 in improving plant growth and salt stress tolerance in maize by regulating ion homeostasis, redox potential, leaf gas exchange, and stress-related genes expression.
A paediatric case of cutaneous larva migrans acquired in the UK

Cutaneous larva migrans (CLM) is the clinical term for a human ectoparasitosis caused by animal hookworm larvae. CLM is generally acquired in tropical and subtropical climates, as warm and moist conditions are favourable for the parasites to mature. The larvae are typically found in sandy soil, where the parasite eggs have been excreted in the stool of their natural animal hosts. The eggs mature in the soil from first to third stage larvae (filariform larvae), at which point they are capable of infecting other animal hosts through penetration of their skin. Cats and dogs are the most commonly affected hosts, with Ancylostoma caninum and Ancylostoma brazillense being the most commonly implicated hookworm species. Humans are ‘accidental’ hosts and experience only superficial infection as the filariform larvae are unable to penetrate the upper dermis. Infection manifests as erythematous serpiginous tracks at exposed sites, which are usually intensely pruritic. A 3-year-old white boy presented in an Urgent Care Centre in August 2017 with an evolving erythematous serpiginous eruption just above the left lateral malleolus (Fig. 1). This had first been noticed the previous month, but had failed to resolve with multiple courses of oral antibiotics and topical steroids prescribed in primary care. The patient’s mother described the rash as initially presenting as a small ‘red spot’, which then progressed into a meandering track, and had become increasingly itchy and erythematous. Other than well-controlled asthma, the patient was perfectly well and normally attended nursery three times a week. A month prior to the lesion presenting itself, the patient had been on a family holiday in Devon where he had played in the sand bare-footed. He had also more recently spent time in a woodland area in the English countryside. He had never been overseas. He lived at home with his parents and a pet cat. Following review by a dermatologist, a diagnosis of CLM was made. Three doses of topical mebendazole were trialled, but the lesion failed to respond. Oral albendazole was then prescribed but was unavailable from pharmacy, and there were subsequently dispensing issues with ivermectin. By this point, however (6 weeks after the initial presentation), the eruption regressed, in keeping with the natural history of this disease. CLM is typically acquired in warmer latitudes and therefore when diagnosed in the UK, it is seen most commonly in travellers returning from the tropics. CLM acquired in the UK is rare. The few cases listed in the literature have been attributed to various exposures, including running in muddy areas frequented by infected animals, gardening, prolonged contact with clothing infected by cat and dog faeces, exposure to sand on a Cornish beach, grassland on the west coast of Scotland and to puppies that had not received hookworm prophylaxis. Cases of autochthonous CLM have also been reported in Germany and France, which have a similar climate to the UK. Correspondence: Dr Lucy Howard, Great Western Hospital, Marlborough Road, Swindon, Wiltshire, SN3 6BB, UK E-mail: lucy.howard3@nhs.net
Myeloid HMG-CoA (3-Hydroxy-3-Methylglutaryl-Coenzyme A) Reductase Determines Atherosclerosis by Modulating Migration of Macrophages

Objective— Inhibition of HMGCR (3-hydroxy-3-methylglutaryl-coenzyme A reductase) is atheroprotective primarily by decreasing plasma LDL (low-density lipoprotein)-cholesterol. However, it is unknown whether inhibition of HMGCR in myeloid cells contributes to this atheroprotection. We sought to determine the role of myeloid HMGCR in the development of atherosclerosis. Approach and Results— We generated mice with genetically reduced Hmgcr in myeloid cells (Hmgcrm−/m−) using LysM (Cre) and compared various functions of their macrophages to those of Hmgcrfl/fl control mice. We further compared the extent of atherosclerosis in Hmgcrm−/m− and Hmgcrfl/fl mice in the absence of Ldlr (LDL receptor). Hmgcrm−/m− macrophages and granulocytes had significantly lower Hmgcr mRNA expression and cholesterol biosynthesis than Hmgcrfl/fl cells. In vitro, Hmgcrm−/m− monocytes/macrophages had reduced ability to migrate, proliferate, and survive compared with Hmgcrfl/fl monocytes/macrophages. However, there was no difference in ability to adhere, phagocytose, store lipids, or polarize to M1 macrophages between the 2 types of macrophages. The amounts of plasma membrane–associated small GTPase proteins, such as RhoA (RAS homolog family member A), were increased in Hmgcrm−/m− macrophages. In the setting of Ldlr deficiency, Hmgcrm−/m− mice developed significantly smaller atherosclerotic lesions than Hmgcrfl/fl mice. However, there were no differences between the 2 types of mice either in plasma lipoprotein profiles or in the numbers of proliferating or apoptotic cells in the lesions in vivo. The in vivo migration of Hmgcrm−/m− macrophages to the lesions was reduced compared with Hmgcrfl/fl macrophages. Conclusions— Genetic reduction of HMGCR in myeloid cells may exert atheroprotective effects primarily by decreasing the migratory activity of monocytes/macrophages to the lesions.
Toxicological Implications of Platinum Nanoparticle Exposure: Stimulation of Intracellular Stress, Inflammatory Response, and Akt Signaling In Vitro

Due to their distinctive physicochemical properties, platinum nanoparticles (PtNPs) have emerged as a material of interest for a number of biomedical therapeutics. However, in some instances NP exposure has been correlated to health and safety concerns, including cytotoxicity, activation of cellular stress, and modification to normal cell functionality. As PtNPs have induced differential cellular responses in vitro, the goal of this study was to further characterize the behavior and toxicological potential of PtNPs within a HepG2 liver model. This study identified that a high PtNP dosage induced HepG2 cytotoxicity. However, lower, subtoxic PtNP concentrations were able to elicit multiple stress responses, secretion of proinflammatory cytokines, and modulation of insulin-like growth factor-1 dependent signal transduction. Taken together, this work suggests that PtNPs would not be overtly toxic for acute exposures, but sustained cellular interactions might produce long term health consequences.
Dopamine Signaling Modulates the Stability and Integration of Intrinsic Brain Networks

Dopaminergic projections are hypothesized to stabilize neural signaling and neural representations, but how they shape regional information processing and large-scale network interactions remains unclear. Here we investigated effects of lowered dopamine levels on within-region temporal signal variability (measured by sample entropy) and between-region functional connectivity (measured by pairwise temporal correlations) in the healthy brain at rest. The acute phenylalanine and tyrosine depletion (APTD) method was used to decrease dopamine synthesis in 51 healthy participants who underwent resting-state functional MRI (fMRI) scanning. Functional connectivity and regional signal variability were estimated for each participant. Multivariate partial least squares (PLS) analysis was used to statistically assess changes in signal variability following APTD as compared to the balanced control treatment. The analysis captured a pattern of increased regional signal variability following dopamine depletion. Changes in hemodynamic signal variability were concomitant with changes in functional connectivity, such that nodes with greatest increase in signal variability following dopamine depletion also experienced greatest decrease in functional connectivity. Our results suggest that dopamine may act to stabilize neural signaling, particularly in networks related to motor function and orienting attention towards behaviorally-relevant stimuli. Moreover, dopaminedependent signal variability is critically associated with functional embedding of individual areas in large-scale networks.
Exosome-Mediated Transfer of ACE (Angiotensin-Converting Enzyme) From Adventitial Fibroblasts of Spontaneously Hypertensive Rats Promotes Vascular Smooth Muscle Cell Migration

Migration of vascular smooth muscle cells (VSMCs) is pivotal for vascular remodeling in hypertension. Vascular adventitial fibroblasts (AFs) are important in the homeostasis of vascular structure. This study is designed to investigate the roles of AF exosomes (AFE) in VSMC migration and underling mechanism. Primary VSMCs and AFs were obtained from the aorta of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. VSMC migration was evaluated with Boyden chamber assay and wound healing assay. AFE from WKY rats and SHR were isolated and identified. AFE from SHR promoted but AFE from WKY rats had no significant effect on VSMC migration. The effects of AFE on VSMC migration were prevented by an exosome inhibitor GW4869, an AT1R (Ang II [angiotensin II] type 1 receptor) antagonist losartan, or an inhibitor of ACE (angiotensin-converting enzyme) captopril. ACE contents and activity were much higher in AFE from SHR than those from WKY rats. There were no significant difference in Ang II and AT1R mRNA and protein levels between AFE from SHR and AFE from WKY rats. AFE from SHR increased Ang II and ACE contents and ACE activity in VSMCs of WKY rats and SHR. The changes of Ang II contents and ACE activity were prevented by captopril. ACE knockdown in AFs reduced ACE contents and activity in AFE from SHR and inhibited AFE-induced migration of VSMCs of WKY rats and those of SHR. These results indicate that exosomes from AFs of SHR transfer ACE to VSMCs, which increases Ang II levels and activates AT1R in VSMCs and thereby promotes VSMC migration.
Hippo Pathway Looms Large for the Function of the JCAD (Junctional Protein Associated With Coronary Artery Disease) on Endothelial Cells.

Endothelial cells (ECs) are central to the development and progression of coronary artery disease (CAD). ECs form the interface between blood and tissue, and, therefore, mediate response to hemodynamic forces, inflammation, and cellular infiltration of the blood vessel wall. EC dysfunction is observed in lesion-prone areas of the arterial vasculature. Reduced production of nitric oxide in these cells results in loss of normal vascular reactivity and impaired regulation of inflammation. Other dysfunctional EC phenotypes, such as apoptosis, neovascularization, impaired migration, and compromised barrier function, may contribute to atherosclerosis. The causal link between these pathways and human disease remains unclear, and, therefore, they have not been prioritized for treatment.
Data-driven Analysis of Complex Networks and their Model-generated Counterparts

Data-driven analysis of complex networks has been in the focus of research for decades. An important question is to discover the relation between various network characteristics in real-world networks and how these relationships vary across network domains. A related research question is to study how well the network models can capture the observed relations between the graph metrics. In this paper, we apply statistical and machine learning techniques to answer the aforementioned questions. We study 400 real-world networks along with 2400 networks generated by five frequently used network models with previously fitted parameters to make the generated graphs as similar to the real network as possible. We find that the correlation profiles of the structural measures significantly differ across network domains and the domain can be efficiently determined using a small selection of graph metrics. The goodness-of-fit of the network models and the best performing models themselves highly depend on the domains. Using machine learning techniques, it turned out to be relatively easy to decide if a network is real or model-generated. We also investigate what structural properties make it possible to achieve a good accuracy, i.e. what features the network models cannot capture.
Evaluation of Synthetic Video Data in Machine Learning Approaches for Parking Space Classification

Most modern computer vision techniques rely on large amounts of meticulously annotated data for training and evaluation. In close-to-market development, this demand is even higher since numerous common and—more important—less common situations have to be tested and must hence be covered datawise. However, gathering the necessary amount of data ready-labeled for the task at hand is a challenge of its own. Depending on the complexity of the objective and the chosen approach, the required amount of data can be vast. At the same time, the effort to capture all possible cases of a given problem grows with their variability. This makes recording new video data unfeasible, even impossible at times. In this work, we regard parking space classification as an exemplary application to target the imbalance of cost and benefit w.r. t. image data creation for machine learning approaches. We rely on a fully-fledged park deck simulation created with Unreal Engine 4 for data creation and replace all conventionally recorded and hand-labeled training data by automatically-annotated synthetic video data. We train several of-the-shelf classifiers with a common choice of feature inputs on synthetic images only and evaluate them on two realworld sequences of different outdoor car parks. We reach a classification performance that matches our previous work on this task in which all classifiers were developed solely with real-life video data.
Antitumor effect of ginsenoside Rg3 on gallbladder cancer by inducing endoplasmic reticulum stress-mediated apoptosis in vitro and in vivo

Recent studies have highlighted the importance of the endoplasmic reticulum (ER) in apoptotic processes. In the present study, the traditional herbal medicine ginsenoside Rg3 was used to treat gallbladder cancer in vitro and in vivo. The underlying signaling mechanisms were investigated using various molecular biology techniques, including flow cytometry, western blot analysis, ELISA and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). It was indicated that Rg3 exerted pro-apoptotic activity against the gallbladder cancer cell line GBC-SD through the ER stress-mediated signaling pathway. This was demonstrated by increased expression of phosphorylation of eukaryotic translation-initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein homologous protein and lipocalin 2. In addition, eIF2α and ATF4 knockdown attenuated the pro-apoptotic effect of Rg3 by inhibiting reactive oxygen species. Furthermore, the results of RT-qPCR analysis indicated that long intergenic non-protein coding RNA-p21 was significantly upregulated following Rg3 treatment. In conclusion, the results of the present study demonstrated that Rg3 inhibited tumor growth in a GBC-SD gallbladder cancer xenograft, by upregulating the ER stress-mediated signaling pathway. Therefore, ER stress activation is suggested to mediate the antitumor effect of Rg3 in gallbladder cancer activity in vitro and in vivo.
A Dirty Dozen Ways to Die: Metrics and Modifiers of Mortality Driven by Drought and Warming for a Tree Species

Tree mortality events driven by drought and warmer temperature, often amplified by pests and pathogens, are emerging as one of the predominant climate change impacts on plants. Understanding and predicting widespread tree mortality events in the future is vital as they affect ecosystem goods and services provided by forests and woodlands, including carbon storage needed to help offset warming. Additionally, if extensive enough, tree die-off events can influence not only local climate but also climate and vegetation elsewhere via climate teleconnections. Consequently, recent efforts have focused on improving predictions of tree mortality. The most commercially important genera of trees is Pinus, and the most studied species for tree mortality is the pinon pine, Pinus edulis. Numerous metrics have been developed in association with predicting mortality thresholds or variations in mortality for this species. In this Mini Review we compiled metrics associated with drought and warming related mortality that were developed for P. edulis or for which P. edulis was a key example species used in a calculation or prediction. We grouped these metrics into four categories: (i) those related to simple climate variables, (ii) those related to physiological responses, (iii) those that require multi-step calculations or modeling using climate, ecohydrological, and/or ecophysiological data, and (iv) modifiers of rates or sensitivities of mortality. We identified the spatial-temporal scale of each of these metrics. The metrics to predict mortality include empirical ones which often have implicit linkages to expected mechanisms, and more mechanistic ones related to physiological drivers. The metrics for P. edulis have similarities with those available for other species of Pinus. Expected future mortality events will provide an opportunity to observationally and experimentally test and compare these metrics related to tree mortality for P. edulis via near-term ecological forecasting. The metrics for P. edulis may also be useful as potential analogs for other genera. Improving predictions of tree mortality for this species and others will be increasingly important as an aid to move towards anticipatory management.
Using Time-to-React based on Naturalistic Traffic Object Behavior for Scenario-Based Risk Assessment of Automated Driving

The steady improvement of advanced driving assistance systems (ADAS) and the leap towards automated driving (AD) require novel methods for assessing the safety of those, which is a major subject for current research. Different proposals cope with the massive testing effort to assure the safety of such systems. These proposals include virtualization of testing, usage of stochastic methods and reduction of the necessary real world driving tests. Despite these different approaches, they all rely on the same basis: The behavior assessment of the vehicle under test, which results in a measurement of risk. This paper presents a novel approach to measure the criticality of a given driving scenario fitted on the requirements of testing. A Monte-Carlo simulation, which uses the input of a motion prediction model as variation parameters, determines the possible evolutions of a scenario at every time step. The distributions of these parameters have been fitted to data obtained by a large-scale field tests. These evolutions are then analyzed individually by considering the Time-To-React (TTR) measure. Finally a single value of accident risk between 0 and 1 can be assigned to the scenario.