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Pulmonary arterial hypertension (PAH) is a progressive disease with a complex aetiology and high mortality. Functional and structural changes in the small pulmonary arteries lead to elevated pulmonary arterial pressure, resulting in right heart failure. The pathobiology of PAH is not fully understood, and novel treatment targets in PAH are desperately needed. The renin-angiotensin system is critical for maintaining homeostasis of the cardiovascular system. The system consists of the angiotensin converting enzyme (ACE)-angiotensin (Ang) II-angiotensin type 1 receptor (AT1R) axis and the ACE2-Ang-(1–7)-Mas receptor axis. The former, the ACE-Ang II-AT1R axis, is involved in vasoconstrictive and hypertensive actions along with cardiac and vascular remodelling. The latter, the ACE2-Ang-(1–7)-Mas axis, generally mediates counterbalancing effects against those mediated by the ACE-Ang II-AT1R axis. Based on established functions, the ACE2-Ang-(1–7)-Mas axis may represent a novel target for the treatment of PAH. This review focuses on recent advances in pulmonary circulation science and the role of the ACE2-Ang-(1–7)-Mas axis in PAH.

Activation of transient receptor potential vanilloid 4 (TRPV4) induces neuronal injury. TRPV4 activation enhances inflammatory response and promotes the proinflammatory cytokine release in various types of tissue and cells. Hyperneuroinflammation contributes to neuronal damage in epilepsy. Herein, we examined the contribution of neuroinflammation to TRPV4-induced neurotoxicity and its involvement in the inflammation and neuronal damage in pilocarpine model of temporal lobe epilepsy in mice. Icv. injection of TRPV4 agonist GSK1016790A (GSK1016790A-injected mice) increased ionized calcium binding adapter molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) protein levels and Iba-1-positive (Iba-1+) and GFAP-positive (GFAP+) cells in hippocampi, which indicated TRPV4-induced microglial cell and astrocyte activation. The protein levels of nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome components NLRP3, apoptosis-related spotted protein (ASC) and cysteinyl aspartate-specific protease-1 (caspase-1) were increased in GSK1016790A-injected mice, which indicated NLRP3 inflammasome activation. GSK1016790A also increased proinflammatory cytokine IL-1β, TNF-α and IL-6 protein levels, which were blocked by caspase-1 inhibitor Ac-YVAD-cmk. GSK1016790A-induced neuronal death was attenuated by Ac-YVAD-cmk. Icv. injection of TRPV4-specific antagonist HC-067047 markedly increased the number of surviving cells 3 d post status epilepticus in pilocarpine model of temporal lobe epilepsy in mice (pilocarpine-induced status epilepticus, PISE). HC-067047 also markedly blocked the increase in Iba-1 and GFAP protein levels, as well as Iba-1+ and GFAP+ cells 3 d post-PISE. Finally, the increased protein levels of NLRP3, ASC and caspase-1 as well as IL-1β, TNF-α and IL-6 were markedly blocked by HC-067047. We conclude that TRPV4-induced neuronal death is mediated at least partially by enhancing the neuroinflammatory response, and this action is involved in neuronal injury following status epilepticus.

Colorectal carcinoma (CRC) is one of the most common malignant tumors. The present study aimed to investigate a non-invasive molecular marker that can evaluate the diagnosis and potential molecular mechanism of CRC. Microarray assays and reverse transcription-quantitative PCR analysis demonstrated that microRNA (miR)-325-3p expression was significantly increased in both tissues and serum samples of patients with CRC. In addition, miR-325-3p expression in the tissues and serum was significantly associated with differentiation, TNM stage and lymph node metastasis. The results of the dual-luciferase reporter assay and western blot analysis revealed that cytokeratin 18 (CK18) is a target gene of miR-325-3p. Furthermore, treatment with transforming growth factor (TGF)-β increased miR-325-3p expression in a time-dependent manner. Conversely, TGF-β decreased CK18 expression at 48 and 72 h. Western blot analysis demonstrated that TGF-β1 significantly decreased the expression of the epithelial marker, CK18, and increased the expression of the mesenchymal markers, α-SMA and vimentin. Notably, these effects were reversed following inhibition of miR-325-3p expression. Taken together, the results of the present study suggest that miR-325-3p is a key regulator of TGF-β-induced CK18 downregulation. Thus, elevated levels of miR-325-3p is an important factor affecting epithelial-to-mesenchymal transition, and is likely to be a molecular marker in the progression of CRC and act as a potential therapeutic target.

BackgroundThe white-backed planthopper (WBPH),Sogatella furcifera(Horváth) (Hemiptera, Delphacidae), is a migratory pest of rice in Asia. Shandong Province, in northern China, is located on the migration pathway of WBPH between southern and northeast China. The potential sources of WBPH in northern China are poorly understood. We studied the sources of WBPH in Shandong Province by determining the population genetic structure of WBPH in 18 sites distributed in Shandong and in six regions of the Greater Mekong Subregion (GMS). We used mitochondrial gene and single-nucleotide polymorphism (SNP) markers for analysis.ResultsAll of the WBPH populations studied in the seven regions had low genetic diversity. Pairwise FSTvalues based on mtDNA ranged from − 0.061 to 0.285, while FSTbased on SNP data ranged from − 0.007 to 0.009. These two molecular markers revealed that 4.40% (mtDNA) and 0.19% (SNP) genetic variation could be explained by the interpopulation variation, while the rest came from intrapopulation variation. The populations in the seven geographic regions comprised four hypothetical genetic clusters (K = 4) not associated with geographic location. Eighty-four of 129 individuals distributed across the given area were designated as recent migrants or of admixed ancestry. Although the substantial migration presented, a weak but significant correlation between genetic and geographic distances was found (r = 0.083, P = 0.004).ConclusionThe Greater Mekong Subregion was the main genetic source of WBPH in Shandong, while other source populations may also exist. The genetic structure of WBPH is shaped by both migration and geographic barriers.These results help clarify the migration route and the source of WBPH in northern China.

PurposeSalusin-β, a multifunctional vasoactive peptide, has a potentially important function in the pathological development of hypertension. However, the exact functional role of salusin-β and the underlying mechanism in this process are still not fully understood. The current study aimed to investigate the effects of silencing salusin-β on vascular function and vascular remodeling, as well as its signaling pathways in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).MethodsSilencing salusin-β was performed by caudal vein injection of adenovirus expressing salusin-β short hairpin RNA (shRNA). Acetylcholine (ACh)-induced endothelium-dependent relaxation was used to evaluate vasodilator function, and high K+ solution-induced constriction was used to evaluate vasoconstriction function.ResultsSalusin-β levels in plasma and its protein expression in mesenteric artery (MA), coronary artery (CA), and pulmonary artery (PA) of SHR were higher than those in WKY. The salusin-β level and expression were decreased effectively by salusin-β shRNA. Knockdown of salusin-β decreased arterial blood pressure (ABP) and high K+ solution-induced vascular constrictions, and improved the endothelium-dependent relaxation and vascular remodeling in SHR. The improved effect of silencing salusin-β on ACh-induced relaxation in SHR was almost blocked by the nitric oxide synthase (NOS) inhibitor L-NAME. Compared to WKY, the endothelial NOS (eNOS) activity and level, and nitric oxide (NO) level were decreased, while NAD(P)H oxidase activity and reactive oxygen species (ROS) levels in MA, CA, and PA of SHR were increased, which were all redressed by salusin-β knockdown.ConclusionThese results indicate that knockdown of salusin-β improves endothelium-dependent vascular relaxation and vascular remodeling and decreases ABP and vasoconstriction in SHR, which might be accomplished by increasing eNOS activation and NO release while inhibiting NAD(P)H oxidase derived-ROS generation. Scavenging salusin-β improves vascular function and then prevents the development and progression of vasculopathy of hypertension.

Attenuated vasodilatation of small arteries is a hallmark feature of hypertension. Salusin-β, which is a TOR2A gene product and an important vasoactive peptide, has a close relationship with cardiovascular disease. This study aimed to determinate the roles of salusin-β in vasodilatation, and its signal pathways in Wistar–Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Isometric tension experiments were performed. Vasodilatation was induced by acetylcholine (ACh) or sodium nitroprusside (SNP). Plasma salusin-β levels and their protein expressions in coronary artery (CA), mesenteric artery (MA), and pulmonary artery (PA) of SHR were much higher than that of WKY. Intravenous injection of salusin-β increased arterial blood pressure in SHR, while anti-salusin-β IgG decreased it. Salusin-β further deteriorated, while anti-salusin-β IgG improved, the attenuated ACh-induced relaxation, the decreased nitric oxide (NO) level, and endothelial nitric oxide synthase (eNOS) activity in arteries of SHR, and salusin-β had no significant effect on SNP-induced relaxation. The NAD(P)H oxidase activity and reactive oxygen species (ROS) level in arteries of SHR were much higher than that of WKY, which was further increased by salusin-β but reduced by anti-salusin-β IgG. ROS scavenger NAC or antioxidant apocynin significantly inhibited, while SOD inhibitor DETC aggravated, the effects of salusin-β, and the eNOS inhibitor L-NAME inhibited the effects of anti-salusin-β IgG. These results indicated that enhanced salusin-β activity is involved in attenuated endothelium-dependent vasodilatation pathogenesis in SHR by activating NAD(P)H oxidase derived ROS generation and inhibiting eNOS activation and NO release.

Background The white-backed planthopper (WBPH), Sogatella furcifera (Horváth) (Hemiptera, Delphacidae), is a migratory pest of rice in Asia. Shandong Province, in northern China, is located on the migration pathway of WBPH between southern and northeast China. The potential sources of WBPH in northern China are poorly understood. We studied the sources of WBPH in Shandong Province by determining the population genetic structure of WBPH in 18 sites distributed in Shandong and in six regions of the Greater Mekong Subregion (GMS). We used mitochondrial gene and single-nucleotide polymorphism (SNP) markers (2b-RAD sequencing) for analysis.Results All of the WBPH populations studied in the seven regions had low genetic diversity. Pairwise FST values ranged from − 0.061 to 0.285, while FST based on SNP data ranged from − 0.007 to 0.009. These two molecular markers revealed that 4.40% (mtDNA) and 0.19% (SNP) genetic variation could be explained by the interpopulation variation, while the rest came from intrapopulation variation. The populations in the seven geographic regions comprised four hypothetical genetic clusters (K = 4) not associated with geographic location. Eighty-four of 129 individuals distributed across the given area were designated as recent migrants or of admixed ancestry. Although the substantial migration presented, a weak but significant correlation between genetic and geographic distances was found (r = 0.083, P = 0.004).Conclusion GMS was the main source of WBPH in Shandong, while other source populations may also exist. The genetic structure of WBPH is shaped by both migration and geographic barriers. These results help clarify the migration route and the source of WBPH in northern China.

IAV regulates inflammatory signaling via glucose metabolism., In this study, we demonstrated an essential function of the hexosamine biosynthesis pathway (HBP)–associated O-linked β-N-acetylglucosamine (O-GlcNAc) signaling in influenza A virus (IAV)–induced cytokine storm. O-GlcNAc transferase (OGT), a key enzyme for protein O-GlcNAcylation, mediated IAV-induced cytokine production. Upon investigating the mechanisms driving this event, we determined that IAV induced OGT to bind to interferon regulatory factor–5 (IRF5), leading to O-GlcNAcylation of IRF5 on serine-430. O-GlcNAcylation of IRF5 is required for K63-linked ubiquitination of IRF5 and subsequent cytokine production. Analysis of clinical samples revealed that IRF5 is O-GlcNAcylated, and higher levels of proinflammatory cytokines correlated with higher levels of blood glucose in IAV-infected patients. We identified a molecular mechanism by which HBP-mediated O-GlcNAcylation regulates IRF5 function during IAV infection, highlighting the importance of glucose metabolism in IAV-induced cytokine storm.

A laboratory bioassay was conducted to determine the allelopathic potentials of aqueous extracts from either roots or leaves of seventeen sweet potato [Ipomoea batatas L. (Lam)] cultivars (SP0, SP1, SP2, SP3, SP4, SP5, SP6, SP7, SP9, SP10, SP11, SP13, SP14, SP15, SP16, SP18, and SP19). Most inhibitory rates on Lactuca sativa calculated for leaf or root extracts from the seventeen sweet potato cultivars exhibited positive values and significantly increased with increasing concentration. Germination was totally inhibited at a concentration of 0.05 g·mL−1 for leaf water extracts of SP13, SP15, SP18 and at a concentration of 0.05 g·mL−1 for both leaf and root water extracts of SP19. Inhibition of root length was clearly greater than inhibition of shoot length for both leaf and root water extracts. Biomass inhibition increased with increasing concentration, but some cultivars showed stimulatory effects at low concentrations, and inhibition was generally more pronounced for root water extracts than for leaf water extracts. Moreover, most synthetical inhibitory rates for both leaf and root water extracts from the seventeen cultivars exhibited positive values and significantly increased with increasing concentration. Comparing the synthetical inhibitory rates for both leaf and root water extracts among the seventeen cultivars, SP19, SP6, SP11, and SP7 had the highest allelopathic inhibition. The inhibitory activity on germination index was the greatest, followed by germination rate, root length, biomass, and shoot length in all bioassays. Inhibition by leaf water extracts was generally greater than inhibition by root water extracts, except in the case of shoot length or biomass. Overall, we conclude that all seventeen sweet potato cultivars have strong inhibitory effects on L. sativa, but that these effects vary with cultivar and plant part, with SP19, SP6, SP11, and SP7 exhibiting the highest rates of allelopathic inhibition.

Background and aims Major vault protein (MVP) is up-regulated during infections with hepatitis B virus (HBV) and hepatitis C virus (HCV). Here, we found that MVP deficiency inhibited hepatocellular carcinoma (HCC) development induced by diethylnitrosamine, hepatitis B X protein, and HCV core. Approach and results Forced MVP expression was sufficient to induce HCC in mice. Mechanistic studies demonstrate that the ubiquitin ligase human double minute 2 (HDM2) forms mutual exclusive complexes either with interferon regulatory factor 2 (IRF2) or with p53. In the presence of MVP, HDM2 is liberated from IRF2, leading to the ubiquitination of the tumor suppressor p53. Mouse xenograft models showed that HBV and HCV promote carcinogenesis through MVP induction, resulting in a loss of p53 mediated by HDM2. Analyses of clinical samples from chronic hepatitis B, liver cirrhosis, and HCC revealed that MVP up-regulation correlates with several hallmarks of malignancy and associates with poor overall survival. Conclusions Taken together, through the sequestration of IRF2, MVP promotes an HDM2-dependent loss of p53 that promotes HCC development.

Glucose metabolism and innate immunity evolved side-by-side. It is unclear if and how the two systems interact with each other during hepatitis B virus (HBV) infections and, if so, which mechanisms are involved. Here, we report that HBV activates glycolysis to impede retinoic acid-inducible gene I (RIG-I)-induced interferon production. We demonstrate that HBV sequesters MAVS from RIG-I by forming a ternary complex including hexokinase (HK). Using a series of pharmacological and genetic approaches, we provide in vitro and in vivo evidence indicating that HBV suppresses RLR signaling via lactate dehydrogenase-A-dependent lactate production. Lactate directly binds MAVS preventing its aggregation and mitochondrial localization during HBV infection. Therefore, we show that HK2 and glycolysis-derived lactate have important functions in the immune escape of HBV and that energy metabolism regulates innate immunity during HBV infection., RIG-I is a cytosolic antiviral nucleic acid sensor that signals via MAVS to produce type 1 interferons. Here the authors show that hepatits B virus can repress this pathway by activating glycolysis and lactate production, enabling accumulated lactate to bind MAVS and prevent its mitochondrial localization.

Hepatitis B virus X protein (HBx) critically contributes to the development of hepatocellular carcinoma (HCC). However, the mechanisms by which HBx promotes HCC remain unclear. In the present study, using a combination of gene expression profiling and immunohistochemistry, we found higher levels of SH2 domain–containing 5 (SH2D5) in liver tissue from HBV-associated HCC (HBV-HCC) patients than in adjacent nontumor tissues. Moreover, HBV infection elevated SH2D5 levels, and we observed that HBx plays an important role in SH2D5 induction. We also found that HBx triggers SH2D5 expression through the NF-κB and c-Jun kinase pathways. Employing SH2D5 overexpression or knockdown, we further demonstrate that SH2D5 promotes HCC cell proliferation both in vitro and in vivo. While investigating the mechanism of SH2D5-mediated stimulation of HCC cell proliferation, we noted that HBV induces SH2D5 binding to transketolase (TKT), a pentose phosphate pathway enzyme, thereby promoting an interaction between and signal transducer and activator of transcription 3 (STAT3). Furthermore, HBx stimulated STAT3 phosphorylation at Tyr-705 and promoted the activity and downstream signaling pathway of STAT3 via the SH2D5–TKT interaction. Taken together, our results suggest that SH2D5 is an HBV-induced protein capable of binding to TKT, leading to induction of HCC cell proliferation.

Background and objectives Sweet potato [Ipomoea batatas (L.) Lam] is an important locally grown cash crop in China; it was demonstrated to suppress the invasive plant Mikania micrantha (M. micrantha) H.B.K through strong competitiveness, but its allelopathic effects on this weed were unknown. The present study aimed to explore the allelopathic potential of sweet potato on M. micrantha. Materials and methods The allelopathic effects of water extracts and soil incorporation from leaves of three sweet potato cultivars (SP1, SP0 and SP9) on the sprout seedling growth of invasive plant M. micrantha in Yunnan Province, China, were studied under laboratory and greenhouse conditions. Results Stem length, root biomass, aboveground biomass and total biomass of M. micrantha were significantly reduced with increasing concentration in both leaf water extracts and leaf soil incorporation of three sweet potato cultivars. Among these, SP1 had the strongest inhibition and the next highest impact was from SP0 with the lowest effect from SP9. The highest inhibition rates were seen for root biomass, followed by total biomass, whereas the lowest impact was on aboveground biomass. The strong correspondence between results for both leaf water extracts and leaf soil incorporation provided a good demonstration that compounds produced by sweet potato have allelopathic effects on M. micrantha. The general inhibition of M. micrantha by sweet potato followed the order among the three sweet potato cultivars tested as SP1, SP0 and SP9. Moreover, the synthetical allelopathic indices of leaf soil incorporation of three cultivars on M. micrantha were generally higher than these of leaf water extracts. Conclusion Competition and allelopathy have primarily been seen as separate ecological weed management tools, but as these have demonstrated in the case of sweet potato where both mechanisms inhibit weed growth, there is potential for synergism between competition and allelopathy in the reduction of weed infestations.

Numerous microRNAs (miRNA/miRs) have been reported to be associated with the initiation and progression of non‑small cell lung cancer (NSCLC). The aim of the present study was to examine the expression and biological role of miR‑939 in human NSCLC, in vitro. Reverse transcription‑quantitative polymerase chain reaction analysis was used to evaluate the expression of miR‑939 in NSCLC tissues. Cell Counting Kit‑8, 5‑ethynyl‑29‑deoxyuridine and Transwell assays were also used to determine the effects of miR‑939 on tumor cell proliferation and invasion in two human NSCLC cell lines (H1299 and SPCA1). Furthermore, tissue inhibitor of metalloproteinases 2 (TIMP2) was confirmed to be a target of miR‑939 by luciferase reporter assay, western blotting and bioinformatics analysis. Following downregulation of miR‑939 expression, cell proliferative and invasive abilities were significantly suppressed. Collectively, these findings indicated that the knockdown of miR‑939 may inhibit cell proliferation and invasion by regulating the expression of TIMP2 in NSCLC cells. Thus, miR‑939 may be a potential target in the treatment of NSCLC, although this requires further investigation.

Apple is one of the most important fruits in China, and both yield and quality are greatly affected by insect pests. According to surveys, there are more than 200 species of natural enemies in apple orchards. Few, however, have been closely studied. Major natural enemies including parasitoids, predators and pathogens are briefly described in this review, especially focusing on two parasitoids of Trichogramma dendrolimi Matsumura and Aphelinus mali Haldeman, predatory mites and a pathogenic fungus of Beauveria bassiana (Balsamo) Vuillemin as case studies. Augmentation, one important strategy of biological control, supplements the natural control provided by the existing natural enemy community in apple orchards, and greatly increases their efficiency in controlling pests. Conservation biological control is also widely applied in four major apple-producing areas. Based on habitat manipulation, the ground cover planting system helps regulate the microclimate and enhance the biodiversity of apple orchards, effectively conserving the richness and diversity of beneficial insect species. Certain achievements have been made in the main biological control strategies including successful introduction of some exotic natural enemies such as A. mali and Typhlodromus occidentalis Nesbitt, augmentative production and application of biological control agents such as T. dendrolimi , B. bassiana and Bacillus thuringiensis , and further research in conservation of establishing adaptive ground cover planting patterns to local environment. Challenges, however, still exist. Biological control of insect pests in apple orchards is an important part of integrated pest management programs, requiring more research and application in China.

A study on the survival of Lecanicillium lecanii conidia in storage at room temperature was carried out. Firstly, drying methods of conidia powder were compared. Vacuum-freeze drying (VFD) was more suitable for drying conidia as compared to vacuum drying (VD) at room temperature. Vacuum-freeze drying for 24-h resulted in a water content of 5.4%, and a viability, determined as germination of conidia in 2% glucose solution after16 h, was 90.3% and the infection in greenhouse whitefly, Trialeurodes vaporariorum was about 94.7% at a dose of 1×108 conidia/mL. Secondly, the factors influencing viability of conidia stored at room temperature were evaluated in the laboratory. Temperature was the most critical factor influencing conidial storage stability, among the tested factors affecting survival of conidia stored at room temperature for 6 months. Both conidial germination and infection of hosts decreased with storage temperature increasing from 15 to 35°C, and at 35°C the survival of stored conidia fo...

Background As a means of biologically controlling Mikania micrantha H.B.K. in Yunnan, China, the influence of sweet potato [Ipomoea batatas (L.) Lam.] on its reproductive characteristics was studied. The trial utilized a de Wit replacement series incorporating six ratios of sweet potato and M. micrantha plants in 25 m2 plots over 2 years. Results Budding of M. micrantha occurred at the end of September; flowering and fruiting occurred from October to February. Flowering phenology of M. micrantha was delayed (P

Central blockade of mineralocorticoid receptors (MRs) or angiotensin II type 1 receptors (AT1Rs) attenuates aldosterone (aldo)-salt induced hypertension. We examined the role of the subfornical organ (SFO), aldo synthesized locally in the brain, and MR and AT1R specifically in the paraventricular nucleus (PVN) in aldo-salt hypertension. Wistar rats were treated with subcutaneous aldo (1 μg/h) plus saline as drinking fluid, and gene expression was assessed by real-time qPCR. Other sets of rats received chronic intra-cerebroventricular (icv) infusion of aldo synthase (AS) inhibitor FAD286, MR blocker eplerenone or vehicle, electrolytic or sham lesions of the SFO, or intra-PVN infusion of AAV-MR-siRNA or AAV-AT1aR-siRNA. Infusion of aldo had no effect on 11βHSD2, MR and AT1R mRNA in different nuclei but increased CYP11B2 mRNA in the SFO, and serum and glucocorticoid-kinase 1 (Sgk1) and epithelial sodium channel (ENaC) γ subunit mRNA in the SFO and supraoptic nucleus (SON). MR-siRNA decreased both MR and AT1R mRNA in the PVN by ∼ 60%, but AT1aR-siRNA only decreased AT1R mRNA. SFO lesion, blockade of brain AS or MR, or knockdown of MR or AT1R in the PVN similarly attenuated aldosterone-induced saline intake by ∼ 50% and hypertension by ∼ 70%. These results suggest that an increase in circulating aldosterone may via MR and AT1R in the SFO increase local aldosterone production in hypothalamic nuclei such as the SON and PVN, and via MR enhance AT1R signaling in the PVN. This central aldosterone-MR-AT1R neuro-modulatory pathway appears to play a major role in the progressive hypertension.

Background There are a variety of ways of increasing crop diversity to increase agricultural sustainability and in turn having a positive influence on nearby natural ecosystems. Competitive crops may provide potent management tools against invasive plants. To elucidate the competitive mechanisms between a sweet potato crop (Ipomoea batatas) and an invasive plant, mile-a-minute (Mikania micrantha), field experiments were carried out in Longchuan County of Yunnan Province, Southwest China, utilizing a de Wit replacement series. The trial incorporated seven ratios of sweet potato and mile-a-minute plants in 25 m2 plots. Results In monoculture, the total biomass, biomass of adventitious root, leafstalk length, and leaf area of sweet potato were all higher than those of mile-a-minute, and in mixed culture the plant height, branch, leaf, stem node, adventitious root, flowering and biomass of mile-a-minute were suppressed significantly (P