HPV16 infection promotes the malignant transformation of the esophagus and progression of esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) may be correlated with HPV infection, and the mechanism underlying the ESCC formation induced by HPV16 infection remains elusive. Here, we overexpressed HPV16 E6 and E7 and coordinated the overexpression of these two genes in EPC2 and ESCC cells. We found that E7 and coordinated expression of E6 and E7 promoted the proliferation of EPC2 cells, and upregulation of shh was responsible for cell proliferation since the use of vismodegib led to the failure of organoid formation. Meanwhile, overexpression of E6 and E7 in ESCC cells promoted cell proliferation, migration, and invasion in vitro. Importantly, E6 and E7 coordinately increased the capability of tumor growth in nude mice, while vismodegib slowed the growth of tumors in NCG mice. Moreover, a series of genes and proteins changed in cell lines after overexpression of the E6 and E7 genes, the potential biological processes and pathways were systematically analyzed using a bioinformatics assay. Together, these findings suggest that the activation of the hedgehog pathway induced by HPV16 infection may initially transform basal cells in the esophagus and promote following malignant processes in ESCC cells. The application of hedgehog inhibitors may represent a therapeutic avenue for ESCC treatment.

MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis.

SWI/SNF related, matrix associated, actin-dependent regulator of chromatin, subfamily a, member 4 (SMARCA4, also known as BRG1), an ATPase subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, plays an important regulatory role in many cytogenetic and cytological processes during cancer development. However, the biological function and mechanism of SMARCA4 in oral squamous cell carcinoma (OSCC) remain unclear. The present study aimed to investigate the role of SMARCA4 in OSCC and its potential mechanism. Using a tissue microarray, SMARCA4 expression was found to be highly upregulated in OSCC tissues. In addition, SMARCA4 upregulate expression led to increased migration and invasion of OSCC cells in vitro, as well as tumor growth and invasion in vivo. These events were associated with the promotion of epithelial-mesenchymal transition (EMT). Bioinformatic analysis and luciferase reporter assay confirmed that SMARCA4 is a target gene of microRNA miR-199a-5p. Further mechanistic studies showed that the miR-199a-5p regulated SMARCA4 can promote the invasion and metastasis of tumor cells through EMT. These findings indicate that the miR-199a-5p- SMARCA4 axis plays a role in tumorigenesis by promoting OSCC cell invasion and metastasis through EMT regulation. Our findings provide insights into the role of SMARCA4 in OSCC and the mechanism involved, which may have important implications for therapeutic purposes.

Impact Forces of Water Drops Falling on Superhydrophobic Surfaces.

A falling liquid drop, after impact on a rigid substrate, deforms and spreads, owing to the normal reaction force. Subsequently, if the substrate is nonwetting, the drop retracts and then jumps off. As we show here, not only is the impact itself associated with a distinct peak in the temporal evolution of the normal force, but also the jump-off, which was hitherto unknown. We characterize both peaks and elucidate how they relate to the different stages of the drop impact process. The time at which the second peak appears coincides with the formation of a Worthington jet, emerging through flow focusing. Even low-velocity impacts can lead to a surprisingly high second peak in the normal force, even larger than the first one, namely when the Worthington jet becomes singular due to the collapse of an air cavity in the drop.

Anisotropic Fracture of Graphene Revealed by Surface Steps on Graphite.

The anisotropic fracture toughness G(θ) is an intrinsic feature of graphene and is fundamental for fabrication, functioning, and robustness of graphene-based devices. However, existing results show significant discrepancies on the anisotropic factor, i.e., the ratio between zigzag (ZZ) and armchair (AC) directions, G_{ZZ}/G_{AC}, both qualitatively and quantitatively. Here, we investigate the anisotropic fracture of graphene by atomic steps on cleaved graphite surfaces. Depending on the relation between the peeling direction and local lattice orientation, two categories of steps with different structures and behaviors are observed. In one category are straight steps well aligned with local ZZ directions, while in the other are steps consisting of nanoscale ZZ and AC segments. Combined with an analysis on fracture mechanics, the microscale morphology of steps and statistics of their directions provides a measurement on the anisotropic factor of G_{ZZ}/G_{AC}=0.971, suggesting that the ZZ direction has a slightly lower fracture toughness. The results provide an experimental benchmark for the widely scattered existing results, and offer constraints on future models of graphene fracture.

HnRNPA2B1 promotes the proliferation of breast cancer MCF-7 cells via the STAT3 pathway.

HnRNPA2/B1 is highly expressed in many tumors. However, the role of hnRNPA2/B1 in breast cancer is not clear. In this study, we found the proliferation rate was decreased after knockout of hnRNPA2/B1 by CRISPR-CAS9 in MCF-7 cells, as demonstrated by the reduced expression of CDK4 and p-AKT, and the increased expression of P27. Besides this, the western blot results showed that knockout of hnRNPA2/B1 increased the rate of apoptosis and declined autophagy. By in vivo assay, we found that knockout of hnRNPA2/B1 suppressed tumor growth in a xenograft mouse model. Immunohistochemical staining results confirmed knockout of hnRNPA2/B1 impaired tumor angiogenesis, as illustrated by downregulated expression of VEGF-A. Besides this, interacting proteins with hnRNPA2/B1 were identified by mass spectrometry and the PPI network was constructed. GO analysis suggests that the Interacting proteins are mainly enriched in the Wnt signaling pathway, tumor necrosis factor-mediated signaling pathway, translation, and so on. We then identified hnRNPA2/B1 interacted with signal transducer and activator of transcription 3 (STAT3), as supported by the colocalization of hnRNPA2/B1 and STAT3. Meanwhile, knockout of hnRNPA2/B1 inhibited the phosphorylation of STAT3. Collectively, our results demonstrate that hnRNPA2/B1 promotes tumor cell growth in vitro and in vivo by activating the STAT3 pathway, regulating apoptosis and autophagy.

Effects of Geometric Confinement on Zero-Gravity Droplets between Two Parallel Planes.

Investigation of geometric effects on confined droplets is important for the fundamental understanding of the ubiquitous wetting phenomena in nature as well as for a variety of practical applications. In this study, the effect of geometric confinement on the wetting behavior of a droplet confined between two parallel rigid planes was investigated. The closed solutions of the Young-Laplace equation were derived through an analytical method. These solutions are applicable for arbitrary values of the contact angles and the ratio of the size of the droplet to the separation of the planes. For completely nonwetting and wetting cases, an asymptotic method was employed, and the sophisticated analytical solutions of the Laplace pressure, droplet volume, surface energy, and capillary force were expressed as functions of the size and the separation of the droplet in a simple way. In order to check the applicability of the results, experiments were designed to counteract the gravity of the droplets. The asymptotic results not only quantitatively agree well with the theoretical and experimental results over a large range of the parameter space, but also provide a straightforward view for reflecting the effect of the geometric confinement on the wetting behaviors of droplets.

Temperature-regulated adhesion of impacting drops on nano/microtextured monostable superrepellent surfaces.

The monostable Cassie state is a favorable wetting state for superhydrophobic materials, in which water drops can automatically transfer from the Wenzel wetting state to the Cassie wetting state, such that as a consequence the water repellency can be maintained. Drop impact phenomena are ubiquitous in nature and of critical importance in industry, and previous works show that the efficiency of self-cleaning and dropwise condensation could benefit from drop impact on monostable surfaces. However, whether such a feature is sufficiently robust remains unclear when the temperature of the surface is taken into consideration. Here, we report that there exists a lower bound of the temperature of the surface, under which a transition from the Cassie wetting state to the Wenzel wetting state arises. By varying the temperature of the surface, it is found that the solid-liquid wetting region could be regulated. Based on thermodynamics, we propose a model to predict the controllable wetting region, and we show that the gradual transition of the wetting state is a result of the accumulation of droplets on the nanoscale. Connections between the dynamics occurring at the solid-liquid interfaces on the microscale and the condensation occurring in the nanotextures are constructed. These results deepen our understanding of the breakdown of superhydrophobicity under dynamic impinging in high humidity. Moreover, this study will shed new light on the applications for controllable liquid deposition and surface decoration, such as catalysts on the superhydrophobic surfaces.

FNDC3B circular RNA promotes the migration and invasion of gastric cancer cells via the regulation of E-cadherin and CD44 expression.

Circular RNAs (circRNAs) are a new class of RNAs, and many studies have identified thousands of circRNAs in tumor cells. Fibronectin type III domain-containing protein 3B (FNDC3B) circular RNA (circFNDC3B, circBase ID: hsa_circ_0006156) circularizes with exons 5 and 6. Gibson Assembly DNA technology was used to construct a circFNDC3B expression vector without a splice site and restriction enzyme site. We showed that circFNDC3B increased migration and invasion in gastric cancer (GC). Ectopic expression of circFNDC3B reduced the level of E-cadherin protein to promote the epithelial-mesenchymal transition in GC. RNA immunoprecipitation assays and RNA pull-down assays confirmed that circFNC3B increased CD44 expression, which was associated with cell adhesion, via the formation of a ternary complex of circFNDC3B-IGF2BP3-CD44 mRNA. These results indicated that circFNDC3B was associated with the degree of malignancy to highlight the specific characteristics of cell invasion.

Rotational Instability in Superlubric Joints.

Surface and interfacial energies play important roles in a number of instability phenomena in liquids and soft matter, but rarely have similar effects in solids. Here, a mechanical instability is reported which is controlled by surface and interfacial energies and is valid for a large class of materials, in particular two-dimensional layered materials. When sliding a top flake cleaved from a square microscale graphite mesa by using a probe acting on the flake through a point contact, it was observed that the flake moved unrotationally for a certain distance before it suddenly transferred to a rotating-moving state. The theoretical analysis was consistent with the experimental observation and revealed that this mechanical instability was an interesting effect of the structural superlubricity (a state of nearly zero friction). Further analysis showed that this type of instability was applicable generally for various sliding joints on different scales, as long as the friction was ultralow. Thus, the uncovered mechanism provides useful knowledge for manipulating and controlling these sliding joints, and can guide the design of future superlubricity-based devices.

Epigenetic regulation of integrin ß6 transcription induced by TGF-ß1 in human oral squamous cell carcinoma cells.

Overexpression of integrin αvß6 is believed to play an important role in the invasion and metastasis of oral squamous cell carcinoma (OSCC). However, little is known about the molecular mechanisms leading to αvß6 upregulation in OSCC. As the integrin ß6 (ITGB6) is the only partner with αv, the expression of αvß6 is dependent on ITGB6, it is, therefore, pivotal to investigate the mechanisms underlying ITGB6 overexpression in OSCC. We previously reported the cloning and characterization of human ITGB6 gene. In the current study, we further investigated the molecular mechanisms of ITGB6 expression and the upregulation by carcinogenesis related cytokine-transforming growth factor-ß1 (TGF-ß1) in OSCC cells. We first demonstrated that TGF-ß1 can induce ITGB6 mRNA and protein express in a time and concentration dependent manner, and the induced-ITGB6 mRNA was not due to increase the mRNA stability, but regulated at transcriptional level. By using a luciferase reporter assay, site-mutation, RNA interference, and chromatin immunoprecipitation assay, we revealed for the first time that JunB, a member of the activator protein-1 (AP-1) family, is involved in the positive regulation to the ITGB6 transcription induced by TGF-ß1 in OSCC cells. Furthermore, our data also demonstrated that histone acetyltransferase (HAT) CBP mediated histone H3 and H4 hyperacetylation, and RNA Polymerase II recruitment to ITGB6 promoter, facilitated the binding of transcription factor JunB to ITGB6 promoter after TGF-ß1 stimulation. Collectively, these findings demonstrate that JunB and CBP-mediated histone hyperacetylation are responsible for TGF-ß1 induced ITGB6 transcription in OSCC cells, suggesting that epigenetic mechanisms are responsible for the active transcription expression of ITGB6 induced by TGF-ß1 in OSCC cells.

Thrombin Induces CCL2 Expression in Human Lung Fibroblasts via p300 Mediated Histone Acetylation and NF-KappaB Activation.

Thrombin has been shown to play a key role in lung diseases such as pulmonary fibrosis via the induction of fibrotic cytokine- chemokine (CC motif) ligand-2 (CCL2) expression. We previously reported that transcription factor nuclear factor-κB (NF-κB) is responsible for thrombin-induced CCL2 expression in human lung fibroblasts (HLFs). Here, we extended our study to investigate the epigenetic regulation mechanism for thrombin-induced CCL2 expression in HLFs. HLFs were cultured in F-12 medium. CCL2 protein and mRNA levels were detected by ELISA and quantitative real-time PCR, respectively. Histone, histone acetyltransferases, and NF-κB binding to CCL2 promoter were detected by ChIP assay. NF-κB activation was detected by Western blotting. We revealed that increased binding of histone acetyltransferase p300 and acetylated histone H3 and H4 to CCL2 promoter are responsible for thrombin induced CCL2 expression in HLF cells. In addition, p300 inhibition attenuates both thrombin induced-CCL2 expression and histone H3 and H4 acetylation in HLFs, suggesting that p300 is involved in thrombin-induced CCL2 expression via hyperacetylating histone H3 and H4. Our data further showed that p300 also regulates CCL2 expression via interaction with NF-κB p65, as depletion of p300 inhibits both NF-κB p65 activation and its binding to CCL2 promoter. The findings strongly suggest that epigenetic dysregulation and the interaction between histone acetyltransferase and transcription factor may be responsible for thrombin induced-CCL2 expression in HLFs. Increased understanding of the epigenetic mechanisms of CCL2 regulation may provide opportunities for identifying novel molecular targets for therapeutic purposes. J. Cell. Biochem. 118: 4012-4019, 2017. © 2017 Wiley Periodicals, Inc.

Relocation of NPM Affects the Malignant Phenotypes of Hepatoma SMMC-7721 Cells.

Nucleophosmin(NPM), heavily implicated in diverse solid tumors, is an important multifunctional protein mainly located in the nucleolus. Our previous study confirmed that NPM can also localize and accumulate in the cytoplasm of liver cancer cells. However, the role of cytoplasmic NPM (NPMc +) is unclear. Here, we showed that both nucleolar NPM and NPMc+ could promote cell proliferation, although the effect of NPMc+ was weaker than that of NPM. Cell adhesion ability of hepatoma cells was significantly reduced to a greater extent by NPMc+ expression. Nucleolar NPM enhanced cell migration and invasion, whereas NPMc+ impeded cell migration and invasion. The investigation of NPM interactional proteins by proteomic method demonstrated that the NPM was involved in multiple biological processes. By contrast, the interactional proteins of NPMc+ were mainly implicated in tRNA amino acylation regulation. The interactional network of NPMc+ was significantly small and simple. These results suggested that relocation of NPM altered its interactional network and consequently disturbed the primary functions, including cell proliferation, adhesion, migration, and invasion. NPM plays a promotional role in cancer and the reducing relocation may be a potential therapeutic target for hepatocellular carcinoma. J. Cell. Biochem. 118: 3225-3236, 2017. © 2017 Wiley Periodicals, Inc.

Nucleophosmin Regulates Intracellular Oxidative Stress Homeostasis via Antioxidant PRDX6.

Reactive oxygen species (ROS) play both deleterious and beneficial roles in cancer cells. Nucleophosmin (NPM) is heavily implicated in cancers of diverse origins, being its gene over-expression in solid tumors or frequent mutations in hematological malignancies. However, the role and regulatory mechanism of NPM in oxidative stress are unclear. Here, we found that NPM regulated the expression of peroxiredoxin 6 (PRDX6), a member of thiol-specific antioxidant protein family, consequently affected the level and distribution of ROS. Our data indicated that NPM knockdown caused the increase of ROS and its relocation from cytoplasm to nucleoplasm. In contrast, overexpression or cytoplasmic localization of NPM upregulated PRDX6, and decreased ROS. In addition, NPM knockdown decreased peroxiredoxin family proteins, including PRDX1, PRDX4, and PRDX6. Co-immunoprecipitation further confirmed the interaction between PRDX6 and NPM. Moreover, NSC348884, an inhibitor specifically targeting NPM oligomerization, decreased PRDX6 and significantly upregulated ROS. These observations demonstrated that the expression and localization of NPM affected the homeostatic balance of oxidative stress in tumor cells via PRDX6 protein. The regulation axis of NPM/PRDX/ROS may provide a novel therapeutic target for cancer treatment. J. Cell. Biochem. 118: 4697-4707, 2017. © 2017 Wiley Periodicals, Inc.

Exacerbated experimental colitis in TNFAIP8-deficient mice.

The TNF-α-induced protein 8 (TNFAIP8 or TIPE) is a risk factor for cancer and bacterial infection, and its expression is upregulated in a number of human cancers. However, its physiologic and pathologic functions are unclear. In this study, we describe the generation of TIPE-deficient mice and their increased sensitivity to colonic inflammation. TIPE-deficient mice were generated by germ line gene targeting and were born without noticeable developmental abnormalities. Their major organs, including lymphoid organs and intestines, were macroscopically and microscopically normal. However, after drinking dextran sodium sulfate-containing water, TIPE-deficient mice developed more severe colitis than wild type mice did, as demonstrated by decreased survival rates, increased body weight loss, and enhanced leukocyte infiltration, bacterial invasion, and inflammatory cytokine production in the colon. Bone marrow chimeric experiments revealed that TIPE deficiency in nonhematopoietic cells was responsible for the exacerbated colitis in TIPE-deficient mice. Consistent with this result, TIPE-deficient intestinal epithelial cells had increased rate of cell death and decreased rate of proliferation as compared with wild type controls. These findings indicate that TIPE plays an important role in maintaining colon homeostasis and in protecting against colitis.

[Response of radial growth of different timberline species to climate change in Yading Nature Reserve, Sichuan, China]. / å››å·äºšä¸è‡ªç„¶ä¿æŠ¤åŒºä¸åŒæž—çº¿æ ‘ç§å¾„å‘ç”Ÿé•¿å¯¹æ°”å€™å˜åŒ–çš„å“åº”.

The radial growth of trees in alpine timberline is particularly sensitive to climate change. We sampled and disposed tree-ring cores of three coniferous tree species including Juniperus saltuaria, Abies forrestii, and Larix potaninii at alpine timberline in Yading Nature Reserve. The standard tree-ring chronology was used to explore the response of radial growth of different timberline species to climate change. The results showed that radial growth of L. potaninii increased after 2000, while that of A. forrestii declined after 2002, and J. saltuaria showed a significant decreasing growth trend in the past 10 years. Such results indicated divergent growth responses to climate factors among the three tree species at alpine timberline. The radial growth of J. saltuaria was sensitive to temperature, and was positively correlated with the minimum temperature from previous October to current August, the mean tempera-ture from previous November to current April and from current July to October, but was negatively associated with the relative humidity from current July to October. The radial growth of A. forrestii showed negative correlation with mean temperature and the maximum temperature from May to June in the current year, while it exhibited positive association with the relative humidity and the Palmer drought severity index from May to June in the current year. L. potaninii radial growth was positively associated with mean temperature and the maximum temperature of November-December in the previous year, the maximum temperature of current March and mean temperature of current August. The temporal stability of climate-growth relationship varied among different timberline species. The positive correlation between radial growth of A. forrestii and J. saltuaria and temperature gradually decreased, while the posi-tive relationship of L. potaninii radial growth and temperature gradually increased. Under the background of climate warming, rapid rise in surface air temperatures may promote the radial growth of L. potaninii, while inhibit that of J. saltuaria and A. forrestii, which may change the position of regional timberline.

[Response of radial growth of Pinus wallichiana to climate change in Mount Qomolangma, Tibet, China]. / è¥¿è—ç å³°åœ°åŒºä¹”æ¾å¾„å‘ç”Ÿé•¿å¯¹æ°”å€™å˜åŒ–çš„å“åº”.

Global warming would significantly impact tree growth in the Tibetan Plateau. However, the specific effects of climate change on the radial growth of Pinus wallichiana in Mount Qomolangma are still uncertain. To investigate the responses of radial growth of P. wallichiana to climate change, we analyzed tree-ring samples in Mount Qomolangma. We removed the age-related growth trends and established three chronologies by using the modified negative exponential curve, basal area index, and regional curve standardization, and conducted Pearson correlation and moving correlation analyses to examine the association between radial growth of P. wallichiana and climatic factors. The results showed that this region had experienced a significant upward trend in temperature and that the Palmer drought severity index (PDSI) indicated a decreasing trend since 1980s, while the relative humi-dity changed from a significant upward to a downward trend around 2004, implying the climate shifted toward warmer and drier. Results of Pearson correlation analysis indicated a significant and positive relationship between the radial growth of P. wallichiana and the minimum temperature of April-June and July-September, and precipitation of January-April in the current year. The radial growth of P. wallichiana was significantly and negatively associated with the relative humidity of June, July, and August in the current year. As temperature rose after 1983, the relationship between radial growth of P. wallichiana and the minimum temperature in July and September of the current year increased from a non-significant association to a significant and positive association, while the relationship between radial growth of P. wallichiana and relative humidity in August and precipitation in September of the current year changed from non-significant correlation to a significant and negative correlation. Results of the moving correlation analysis suggested that the radial growth of P. wallichiana showed a significant and stable correlation with the July-September minimum temperature of the current year. Under the background of climate warming, the rapid increases of temperature would accelerate the radial growth of P. wallichiana in Mount Qomolangma.

Tensile cracks can shatter classical speed limits.

Brittle materials fail by means of rapid cracks. Classical fracture mechanics describes the motion of tensile cracks that dissipate released elastic energy within a point-like zone at their tips. Within this framework, a "classical" tensile crack cannot exceed the Rayleigh wave speed, [Formula: see text]. Using brittle neo-hookean materials, we experimentally demonstrate the existence of "supershear" tensile cracks that exceed shear wave speeds, [Formula: see text]. Supershear cracks smoothly accelerate beyond [Formula: see text], to speeds that could approach dilatation wave speeds. Supershear dynamics are governed by different principles than those guiding "classical" cracks; this fracture mode is excited at critical (material dependent) applied strains. This nonclassical mode of tensile fracture represents a fundamental shift in our understanding of the fracture process.

How frictional slip evolves.

Earthquake-like ruptures break the contacts that form the frictional interface separating contacting bodies and mediate the onset of frictional motion (stick-slip). The slip (motion) of the interface immediately resulting from the rupture that initiates each stick-slip event is generally much smaller than the total slip logged over the duration of the event. Slip after the onset of friction is generally attributed to continuous motion globally attributed to 'dynamic friction'. Here we show, by means of direct measurements of real contact area and slip at the frictional interface, that sequences of myriad hitherto invisible, secondary ruptures are triggered immediately in the wake of each initial rupture. Each secondary rupture generates incremental slip that, when not resolved, may appear as steady sliding of the interface. Each slip increment is linked, via fracture mechanics, to corresponding variations of contact area and local strain. Only by accounting for the contributions of these secondary ruptures can the accumulated interface slip be described. These results have important ramifications both to our fundamental understanding of frictional motion as well as to the essential role of aftershocks within natural faults in generating earthquake-mediated slip.

Improving predictions and understanding of primary and ultimate biodegradation rates with machine learning models.

This study aimed to develop machine learning based quantitative structure biodegradability relationship (QSBR) models for predicting primary and ultimate biodegradation rates of organic chemicals, which are essential parameters for environmental risk assessment. For this purpose, experimental primary and ultimate biodegradation rates of high consistency were compiled for 173 organic compounds. A significant number of descriptors were calculated with a collection of quantum/computational chemistry software and tools to achieve comprehensive representation and interpretability. Following a pre-screening process, multiple QSBR models were developed for both primary and ultimate endpoints using three algorithms: extreme gradient boosting (XGBoost), support vector machine (SVM), and multiple linear regression (MLR). Furthermore, a unified QSBR model was constructed using the knowledge transfer technique and XGBoost. Results demonstrated that all QSBR models developed in this study had good performance. Particularly, SVM models exhibited high level of goodness of fit (coefficient of determination on the training set of 0.973 for primary and 0.980 for ultimate), robustness (leave-one-out cross-validated coefficient of 0.953 for primary and 0.967 for ultimate), and external predictive ability (external explained variance of 0.947 for primary and 0.958 for ultimate). The knowledge transfer technique enhanced model performance by learning from properties of two biodegradation endpoints. Williams plots were used to visualize the application domains of the models. Through SHapley Additive exPlanations (SHAP) analysis, this study identified key features affecting biodegradation rates. Notably, MDEO-12, APC2D1_C_O, and other features contributed to primary biodegradation, while AATS0v, AATS2v, and others inhibited it. For ultimate biodegradation, features like No. of Rotatable Bonds, APC2D1_C_O, and minHBa were contributors, while C1SP3, Halogen Ratio, GGI4, and others hindered the process. Also, the study quantified the contributions of each feature in predictions for individual chemicals. This research provides valuable tools for predicting both primary and ultimate biodegradation rates while offering insights into the mechanisms.

Influences of environment, human activity, and climate on the invasion of Ageratina adenophora (Spreng.) in Southwest China.

With economic and social globalization, invasive alien species have significantly threatened local ecological security. Identifying the invasive mechanisms of invasive alien species can aid in preventing species invasions and protecting local ecological and economic security. As a globally invasive plant, Ageratina adenophora (Asteraceae) has spread to many parts of the world and had a seriously impacted the ecology and economy of its invaded areas. Using observational data and Landsat OLI images in an arid valley region in southwest China, this study examined how climate, human activity and environmental factors influence the invasion of A. adenophora and its underlying mechanism. Our results showed that the invasion abundance of A. adenophora was significantly affected by environmental factors (the relative importance was 87.2%), but was less influenced by human activity and climate factors (the relative importance was 2% and 10.8%, respectively). The A. adenophora abundance significantly decreased with aspect, community canopy density, shrub layer coverage, herb layer coverage, Simpson diversity index of shrub and herb layers, the shortest distance to residential areas and temperature seasonality, whereas it increased with soil moisture, temperature annual range, precipitation of wettest month and precipitation of driest month. We conclude that biotic competition is the most influential factor in the invasion of this plant in the arid valley regions. Our results are of great significance for invasion prevention and forest conservation and management in southwest China. Our work emphasized that optimizing the community structure, such as by increasing canopy and shrub coverage and species biodiversity, may help control and mitigate the A. adenophora invasion in southwest China.