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Drought can greatly impact the biodiversity of an ecosystem and play a crucial role in regulating its functioning. However, the specific mechanisms by which drought mediate the biodiversity effect (BE) on community biomass in above- and belowground through functional traits remain poorly understood. Here, we conducted a common garden experiment in a greenhouse, which included two plant species richness levels and two water addition levels, to analyze the effects of biodiversity on aboveground biomass (AGB), belowground biomass (BGB) and total biomass (TB), and to quantify the relationship between BEs and functional traits under drought conditions. Our analysis focused on partitioning BEs into above- and belowground complementarity effect (CE) and selection effect (SE) at the species level, which allowed us to better understand the impacts of biodiversity on community biomass and the underlying mechanisms. Our results showed that plant species richness stimulated AGB, BGB and TB through CEs. Drought decreased AGB, BGB and TB, simultaneously. In addition, the aboveground CE was positively associated with the variation in plant height. SEs in above- and belowground were negatively correlated with the community mean plant height and root length, respectively. Furthermore, drought weakened the aboveground CE by decreasing variation in plant height, resulting in a reduction in AGB and TB. Our findings demonstrate that the complementarity of species is an important regulator of community biomass in above- and belowground, the dynamics of biomass under environmental stress are associated with the response of sensitive compartments. [ABSTRACT FROM AUTHOR]

Dopamine (DA) is a neurotransmitter synthesized in the human body that acts on multiple organs throughout the body, reaching them through the blood circulation. Neurotransmitters are special molecules that act as messengers by binding to receptors at chemical synapses between neurons. As ligands, they mainly bind to corresponding receptors on central or peripheral tissue cells. Signalling through chemical synapses is involved in regulating the activities of various body systems. Lack of DA or a decrease in DA levels in the brain can lead to serious diseases such as Parkinson's disease, schizophrenia, addiction and attention deficit disorder. It is widely recognized that DA is closely related to neurological diseases. As research on the roles of brain‐gut peptides in human physiology and pathology has deepened in recent years, the regulatory role of neurotransmitters in digestive system diseases has gradually attracted researchers' attention, and research on DA has expanded to the field of digestive system diseases. This review mainly elaborates on the research progress on the roles of DA and DRs related to digestive system diseases. Starting from the biochemical and pharmacological properties of DA and DRs, it discusses the therapeutic value of DA‐ and DR‐related drugs for digestive system diseases. [ABSTRACT FROM AUTHOR]

Ion channels and transporters are ubiquitously expressed on cell membrane, which involve in a plethora of physiological process such as contraction, neurotransmission, secretion and so on. Ion channels and transporters is of great importance to maintaining membrane potential homeostasis, which is essential to absorption of nutrients in gastrointestinal tract. Most of nutrients are electrogenic and require ion channels and transporters to absorb. This review summarizes the latest research on the role of ion channels and transporters in regulating nutrient uptake such as K+ channels, Ca2+ channels and ion exchangers. Revealing the mechanism of ion channels and transporters associated with nutrient uptake will be helpful to provide new methods to diagnosis and find potential targets for diseases like diabetes, inflammatory bowel diseases, etc. Even though some of study still remain ambiguous and in early stage, we believe that ion channels and transporters will be novel therapeutic targets in the future. [ABSTRACT FROM AUTHOR]

Nitrogen deposition and biodiversity alter plant flowering phenology through abiotic factors and functional traits. However, few studies have considered their combined effects on flowering phenology. A common garden experiment with two nitrogen addition levels (0 and 6 g N m−2 year−1) and five species richness levels (1, 2, 4, 6, and 8) was established. We assessed the effects of nitrogen addition and plant species richness on three flowering phenological events of Medicago sativa L. via changes in functional traits, soil nutrients, and soil moisture and temperature. The first flowering day was delayed, the last flowering day advanced, and the flowering duration shortened after nitrogen addition. Meanwhile, the last flowering day advanced, and flowering duration shortened along plant species richness gradients, with an average of 0.64 and 0.95 days change per plant species increase, respectively. Importantly, it was observed that plant species richness affected flowering phenology mainly through changes in plant nutrient acquisition traits (i.e., leaf nitrogen and carbon/nitrogen ratio). Our findings illustrate the non-negligible effects of intraspecific variation in functional traits on flowering phenology and highlight the importance of including functional traits in phenological models to improve predictions of plant phenology in response to nitrogen deposition and biodiversity loss. [ABSTRACT FROM AUTHOR]

Background and Aims Nitrogen enrichment affects biodiversity, plant functional traits and ecosystem functions. However, the direct and indirect effects of nitrogen addition and biodiversity on the links between plant traits and ecosystem functions have been largely overlooked, even though multidimensional characteristics of plant functional traits are probably critical predictors of ecosystem functions. Methods To investigate the mechanism underlying the links between plant trait identity, diversity, network topology and above- and below-ground biomass along a plant species richness gradient under different nitrogen addition levels, a common garden experiment was conducted in which those driving factors were manipulated. Key Results The study found that nitrogen addition increased above-ground biomass but not below-ground biomass, while species richness was positively associated with above- and below-ground biomass. Nitrogen addition had minor effects on plant trait identity and diversity, and on the connectivity and complexity of the trait networks. However, species richness increased above-ground biomass mainly by increasing leaf trait diversity and network modularity, and enhanced below-ground biomass through an increase in root nitrogen concentration and network modularity. Conclusions The results demonstrate the mechanistic links between community biomass and plant trait identity, diversity and network topology, and show that the trait network architecture could be an indicator of the effects of global changes on ecosystem functions as importantly as trait identity and diversity. [ABSTRACT FROM AUTHOR]

Natural infrastructure is essential in reducing thermal discomfort caused by the urban heat island (UHI) effect. Optimizing and planning green and blue spaces can help establish nature-based urban heat mitigation strategies that benefit sustainable urban development. Most current studies on urban heat mitigation have focused on the single heat reduction effect of green space or blue space, while there has been a lack of research on the combined cooling effects of blue and green spaces. Moreover, existing heat mitigation models and methods cannot directly guide the optimization of blue–green spatial patterns at the urban scale. This has led to an unclear relationship between heat mitigation effects and blue–green spatial patterns. Based on land use data, meteorological data, and biophysical information as inputs, this paper utilized the InVEST urban cooling model (UCM) and scenario analysis method to simulate urban heat mitigation patterns by setting up different blue–green space configuration scenarios. The relative contribution of blue–green space changes to the variation of heat mitigation benefits was quantitatively estimated using the difference comparison method, and the relationship between heat reduction effects and urban blue–green spatial patterns was elucidated using spatial analysis methods. The results show that the InVEST UCM captured some of the variability in the surface thermal response of Wuhan and can be applied to the modeling of urban heat mitigation patterns. Furthermore, they show that consideration of the cooling effect of water evaporation can improve the simulation accuracy to some extent. In Wuhan, there were regional differences in heat mitigation patterns and the heat mitigation effect was significantly higher in the suburbs than in the city. Additionally, urban parks, lakes, and mountains with surface or block distribution had noticeable cooling benefits. Finally, the scenario simulation results demonstrate that green space was more efficient at mitigating heat, while blue space was more critical for the geographical partitioning of the UHI. These findings can provide a reference for the planning and optimal management of urban blue and green spaces, as well as for the design of heat reduction policies. [ABSTRACT FROM AUTHOR]

P2X receptors (P2XRs) are trimeric, non-selective cation channels activated by extracellular ATP and widely distributed in the digestive system. P2XRs have an important role in the physiological function of the digestive system, such as neurotransmission, ion transports, proliferation and apoptosis, muscle contraction, and relaxation. P2XRs can be involved in pain mechanisms both centrally and in the periphery and confirmed the association of P2XRs with visceral pain. In the periphery, ATP can be released as a result of tissue injury, visceral distension, or sympathetic activation and can excite nociceptive primary afferents by acting at homomeric P2X(3)R or heteromeric P2X(2/3)R. Thus, peripheral P2XRs, and homomeric P2X(3) and/or heteromeric P2X(2/3)R in particular, constitute attractive targets for analgesic drugs. Recently studies have shown that P2XRs have made significant advances in inflammation and cancer. P2X7R mediates NLRP3 inflammasome activation, cytokine and chemokine release, T lymphocyte survival and differentiation, transcription factor activation, and cell death. The P2X7R is a potent stimulant of inflammation and immunity and a promoter of cancer cell growth. This makes P2X7R an appealing target for anti-inflammatory and anti-cancer therapy. It is believed that with the further study of P2XRs and its subtypes, P2XRs and its specific antagonists will be expected to be widely used in the treatment of human digestive diseases in the future. [ABSTRACT FROM AUTHOR]

Neurotransmitters are special molecules that serve as messengers in chemical synapses between neurons, cells, or receptors, including catecholamines, serotonin, dopamine, and other neurotransmitters, which play an important role in both human physiology and pathology. Compelling evidence has indicated that neurotransmitters have an important physiological role in various digestive diseases. They act as ligands in combination with central or peripheral receptors, and transmits signals through chemical synapses, which are involved in regulating the physiological and pathological processes of the digestive tract organs. For instance, neurotransmitters regulate blood circulation and affect intestinal movement, nutrient absorption, the gastrointestinal innate immune system, and the microbiome. In this review, we will focus on the role of neurotransmitters in the pathogenesis of digestive tract diseases to provide novel therapeutic targets for new drug development in digestive diseases. [ABSTRACT FROM AUTHOR]

Substantial research has revealed that peroxisome proliferator-activated receptor-gamma (PPARG) plays a critical role in glucose homeostasis and lipid metabolism, and recent studies have shown different effects in the progression of different tumors. However, the role of PPARG and its target gene in clear cell renal cell carcinoma (ccRCC) are incompletely understood. Clinical data revealed abnormal glucolipid metabolism in primary ccRCC samples. In addition, transcriptional profiling indicated that PPARG expression was positively correlated, whereas Six2 expression was negatively correlated with the overall survival of ccRCC patients. Staining showed that PPARG was mainly expressed in tumor cell cytoplasm, and Six2 was localized to the nuclei. In a ccRCC cell line, PPARG activation promoted cell apoptosis, inhibited cell migration and proliferation, and reduced Six2 expression. Mechanistically, overexpressing Six2 downregulated E-cadherin expression and cell apoptosis, but PPARG activation reversed those effects. Taken together, PPARG promotes apoptosis and suppresses the migration and proliferation of ccRCC cells by inhibiting Six2. These findings reveal that the PPARG/Six2 axis acts as a central pathobiological mediator of ccRCC formation and as a potential therapeutic target for the treatment of patients with ccRCC. [ABSTRACT FROM AUTHOR]

It has been generally accepted that alternatively activated macrophages (M2), which can be induced by type 2 cytokines such as IL-4, is responsible for tissue repair. However, the function of JNK in IL-4-induced M2 macrophage polarization remains unclear. Here, we demonstrated that M0 macrophages can be polarized into M2 status in response to IL-4 stimulation with the increased expression of the M2-specific molecular markers. We also found that IL-4 induced higher expression of JNK and transcription factor c-Myc in M2 macrophages. Our Q-PCR and Western blot results showed that JNK increased the expression of c-Myc and M2 markers Arg1, Mrc1. We also demonstrated c-Myc was the downstream of IL-4-JNK pathway. Further, the depletion of c-Myc, Arg1 and Mrc1 could inhibit the migration ability of M2 macrophages. Taken together, our data establishes a new role for JNK signaling in IL-4-induced alternative activation of macrophages and may provide a novel strategy for immune therapy. [ABSTRACT FROM AUTHOR]

The purpose of our study is to clarify the effects of microRNA-129-5p (miR-129-5p) in cellular processes correlated with cancer development and progression of Glioblastoma (GBM) cell by regulating FNDC3B. MiR-129-5p and FNDC3B expression in GBM tissues and tumor adjacent tissues were tested by quantitative real-time PCR. We validated the target relationship between miR-129-5p and FNDC3B by dual luciferase reporter gene system. MTT, colony formation, flow cytometry, Transwell and wound healing assays were used to analyze cell viability, proliferation, apoptosis, invasiveness and migration. The level of FNDC3B protein expression was detected by Western Blot. MiR-129-5p was downregulated in GBM tissues and cell lines, while FNDC3B was upregulated in GBM tissues. The result of luciferase reporter gene assay demonstrated that miR-129-5p could target FNDC3B by binding to the 3′ UTR. The overexpression of miR-129-5p or the inhibition of FNDC3B can both inhibit U87 cell viability, proliferation, migration and invasion, while promote cell apoptosis. Our results suggested that miR-129-5p could directly suppress FNDC3B, which might be one of potential mechanisms in inhibiting cell processes including viability, proliferation, migration and invasiveness of U87 cells. [ABSTRACT FROM AUTHOR]

Duty cycle is a key factor for analyzing exposure to the electromagnetic field from the wireless local area network (WLAN). In this letter, we provide an analytical method for calculating the duty cycle of WLAN in a busy period. It relates to the medium access control (MAC) mode, durations of frames, and the random back-off time. We investigate the rate change rules for calculating the durations of control frames. These durations are also crucial to the parameter setting of the instrument in measurement. We propose a calculation method of the random back-off time for a common scenario, where retransmission always occurs due to collisions or interferences. The duty cycles and the average exposure levels are analyzed and compared between two MAC modes for different transmission rates. Our study can be applied to the extrapolation and the measurement of exposure to WLAN, and compliance testing with safety guidelines. [ABSTRACT FROM PUBLISHER]

Non-small cell lung cancer (NSCLC) is the major cause of cancer-related lethality among human cancer patients globally, and the poor prognosis of this cancer is mainly explained by metastasis, so it is essential to find out the molecule mechanisms and a novel therapeutic for NSCLC. A disintegrin and metalloprotease with thrombospondin motif 5 (ADAMTS5) belongs to the protease family. It has been reported to participate in tumor migration and invasion. In this study, we showed that the expression of ADAMTS5 was higher in lung cancer tissues by Western blot. The immunohistochemistry analysis was performed in 140 NSCLC cases, and the result indicated that ADAMTS5 was significantly associated with clinical pathologic variables. The Kaplan-Meier curve showed that the high expression of ADAMTS5 was related to poor prognosis of lung cancer patients. Wound healing assays and transwell migration assays revealed that the high expression of ADAMTS5 promoted the migration and invasion of NSCLC. In a word, our findings suggest that ADAMTS5 can regulate the migration and invasion of NSCLC and it may be a useful target of therapy in NSCLC. [ABSTRACT FROM AUTHOR]