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Background: There are limited studies designed by matching related factors to compare clinical outcomes and return to sport (RTS) between patients undergoing revision anterior cruciate ligament reconstruction (R-ACLR) and primary ACLR (P-ACLR). Purpose: (1) To compare the outcomes between R-ACLR and P-ACLR in a matched-pair analysis with 3- to 5-year follow-up and (2) to evaluate patient-reported factors for not returning to preinjury-level sport. Study Design: Cohort study; Level of evidence, 4. Methods: Patients who underwent R-ACLR between September 2016 and November 2018 were propensity matched by age, sex, body mass index, passive anterior tibial subluxation, and generalized hypermobility in a 1:1 ratio to patients who underwent P-ACLR during the same period. By combining in person follow-up at 2 years postoperatively and telemedicine interview at the final follow-up (January 2022), knee stability and clinical scores were compared, including International Knee Documentation Committee (IKDC), Lysholm, and Tegner. Status of RTS was requested, specifically whether the patient returned to preinjury level of sport. Patient-reported reasons for not returning were analyzed. Results: There were 63 matched pairs in the present study. Knee stability was similar in terms of KT-2000 arthrometer, Lachman test, and pivot-shift test results between the groups at 2 years of follow-up. At the final follow-up, no significant difference was found between groups for postoperative clinical scores (IKDC, Tegner, and Lysholm) ( P > .05). There was a significant difference in total RTS: 53 (84.1%) in the P-ACLR cohort and 41 (65.1%) in the R-ACLR cohort ( P = .014). No significant difference was shown in terms of RTS at the same level: 35 (55.6%) in P-ACLR and 31 (49.2%) in R-ACLR ( P = .476). Significantly more patients showed fear of reinjury: 26 of 32 (81.3%) in the R-ACLR group as compared with 15 of 28 (53.5%) in the P-ACLR group ( P < .021). Conclusion: R-ACLR resulted in similar clinical scores (IKDC, Tegner, and Lysholm) but significantly lower RTS versus P-ACLR at 3 to 5 years of follow-up. Fear of reinjury was the most common factor that caused sport changes in patients with R-ACLR.

Background and Aims Soil heterogeneity can be caused by plant-soil feedback (PSF), but little is known about how such PSF-mediated soil heterogeneity affects plant growth and the distribution of roots. Moreover, as invasive and native plant species frequently differ in PSF and in root-foraging ability, they may also differ in their responses to PSF-mediated soil heterogeneity.Methods We first conditioned soils by 16 plant species (eight pairs of invasive alien and native species). Then, we grew each species in a homogeneous treatment with unconditioned soil and in three heterogeneous treatments with patches filled with two of the following three soils: unconditioned soil (control soil), soil conditioned by the target species (home soil) or soil conditioned by the other species in a pair (foreign soil).Results Invasive species were more negatively affected by the heterogeneous treatment with control-soil and home-soil patches than natives. In the heterogeneous treatment with home-soil and foreign-soil patches, root mass of the invasive species was much greater in the foreign-soil than in the home-soil patches, whereas the reverse was true for natives.Conclusion Although invasive species suffered more from conspecific PSF, root foraging allowed them to avoid home soil. In the long term, this could potentially help invasive species gain a competitive advantage over natives.

The aim of this study was to evaluate the correlation between tibial tuberosity-trochlear groove distance (TT-TG) and body height or knee size, and to find height-related pathologic thresholds of increased TT-TG.One-hundred and fifty-three patients with recurrent patellar instability and 151 controls were included. The TT-TG was measured on axial computed tomography (CT) images. Femora width and tibial width were selected to represent knee size. The correlation of TT-TG and gender, body height, femora width, and tibial width was evaluated. The height-related pathologic threshold of increased TT-TG was produced according to Dejour's method. To combine TT-TG with body height and knee size, three new indexes were introduced, ratio of TT-TG to body height (RTH), ratio of TT-TG to femoral width (RTF), and ratio of TT-TG to tibial width (RTT). The ability to predict patellar instability was assessed by the receiver-operating characteristic (ROC) curve, odds ratios (ORs), sensitivity, and specificity.In patients with patellar instability, TT-TG showed significantly correlation with patient height, femoral width, and tibial width respectively (range r = 0.266-0.283). This correlation was not found in the control group. The pathologic threshold of TT-TG was 18 mm in patients 169 cm (53%), and the mean TT-TG was 21 mm in patients ≥ 169 cm (54%). There was significant difference in RTH, RTF, and RTT between the two groups. RTH, RTF and RTT have similar large area under the curve (AUC) with TT-TG.TT-TG showed significant correlation with body height and knee size, respectively. The pathologic threshold of increased TT-TG was suggested to be 21 mm for patients [Formula: see text] 169 cm and 18 mm for patients [Formula: see text] 169 cm. Body height-related pathologic threshold provided a supplement for indications of tibial tuberosity medialization.IV.

IntroductionThe factors that determine the growth and spread advantages of an alien plant during the invasion process remain open to debate. The genetic diversity and differentiation of an invasive plant population might be closely related to its growth adaptation and spread in the introduced range. However, little is known about whether phenotypic and genetic variation in invasive plant populations covary during the invasion process along invaded geographic distances.MethodsIn a wild experiment, we examined the genetic variation in populations of the aggressively invasive species Erigeron annuus at different geographical distances from the first recorded point of introduction (FRPI) in China. We also measured growth traits in the wild and common garden experiments, and the coefficient of variation (CV) of populations in the common garden experiments.Results and discussionWe found that E. annuus populations had better growth performance (i.e., height and biomass) and genetic diversity, and less trait variation, in the long-term introduced region (east) than in the short-term introduced region (west). Furthermore, population growth performance was significantly positively or negatively correlated with genetic diversity or genetic variation. Our results indicate that there was parallel genetic and phenotypic differentiation along the invaded geographic distance in response to adaptation and spread, and populations that entered introduced regions earlier had consistently high genetic diversity and high growth dominance. Growth and reproduction traits can be used as reliable predictors of the adaptation and genetic variation of invasive plants.

Functional traits are frequently proposed to determine the invasiveness of alien species. However, few empirical studies have directly manipulated functional traits and tested their importance in the invasion success of alien species into native plant communities, particularly under global change. We manipulated clonal integration (a key clonal functional trait) of four alien clonal plants by severing inter-ramet connections or keeping them intact and simulated their invasion into native plant communities with two levels of species diversity, population density and nutrient availability. High community diversity and density impeded the invasion success of the alien clonal plants. Clonal integration of the alien plants promoted their invasion success, particularly in the low-density communities associated with low species diversity or nutrient addition, which resulted in a negative correlation between the performance of alien plants and native communities, as expected under global change. Thus, clonal integration can favor the invasion success of alien clonal plants into degraded resident communities with a high degree of disturbance and eutrophication. Our findings confirm the role of clonal functional traits in facilitating alien plant invasions into native plant communities and suggest that clonal functional traits should be considered to efficiently restore degraded communities heavily invaded by alien clonal plants.摘要 功能性状常常被认为是决定外来物种入侵性的关键因素。然而，迄今很少有实证研究直接操控功能性状来检验其在外来物种成功入侵本地植物群落中的重要性，尤其是在全球变化的背景下。克隆整合是克隆植物最重要的功能性状之一。通过切断或不切断分株之间的连接，我们操控了4种外来入侵克隆植物的克隆整合，并模拟它们入侵两种不同物种多样性水平、两种不同密度和两种不同养分可用性的本地植物群落。高群落物种多样性和高群落密度阻碍了外来克隆植物的成功入侵。外来入侵植物的克隆整合可以显著促进其对本地植物群落的成功入侵，这种效应在物种多样性低或具有高养分水平的低密度群落中尤为明显，并导致外来植物与本地群落生长之间呈显著的负相关。因此，克隆整合有助于外来克隆植物成功入侵遭受高度干扰和富营养化的退化本地群落。本项研究成果证实了克隆功能性状在促进外来植物入侵本地植物群落中的作用，表明为有效恢复被外来克隆植物严重入侵的退化群落，我们应考虑外来入侵物种克隆功能性状。.

Heavy metal (HM) contamination resulting from industrialization and urbanization during the Anthropocene along with plant invasion can severely threaten the growth and adaptation of local flora. Invasive alien plant species generally exhibit a growth pattern consistent with their functional traits in non-contaminated environments in the introduced range. However, it remains unclear whether invasive alien plants have an advantage over native plants in contaminated environments and whether this growth pattern is dependent on the adaptation of their leaf functional traits. Here, we selected two congeneric pairs of invasive alien and native grasses that naturally co-exist in China and are commonly found growing in contaminated soil. To evaluate the effect of cadmium (Cd) on the structural and physiological leaf traits, we grew all four species in soil contaminated without or with 80 mg/kg Cd. Invasive plants contained significantly higher concentrations of Cd in all three organs (leaf, stem, and root). They displayed a higher transfer factor and bioconcentration factor (BCF) of shoot and root than natives, indicating that invasive species are potential Cd hyperaccumulators. Invasive plants accumulated polyphenol oxidase (PPO) to higher levels than natives and showed similar patterns of leaf structural and physiological traits in response to changes in Cd bioconcentration. The quantifiable leaf structural traits of invasive plants were significantly greater (except for stomatal density and number of dead leaves) than native plants. Leaf physiological traits, chlorophyll content, and flavonoid content were also significantly higher in invasive plants than in natives under Cd stress conditions after 4 weeks, although nitrogen balance index (NBI) showed no significant difference between the two species. Chlorophyll fluorescence parameters decreased, except for the quantum yield of photosystem II (ΦPSII) and the proportion of open photosystem II (qP), which increased under Cd stress conditions in both species. However, invasive plants exhibited higher fluorescence parameters than natives under Cd stress, and the decrement observed in invasive plants under Cd stress was greater than that in natives. High Cd adaptation of invasive grasses over natives suggests that invasive plants possess optimal leaf structural and physiological traits, which enable them to adapt to stressful conditions and capture resources more quickly than natives. This study further emphasizes the potential invasion of alien plants in contaminated soil environments within the introduced range. To a certain extent, some non-invasive alien plants might adapt to metalliferous environments and serve as hyperaccumulator candidates in phytoremediation projects in contaminated environments.

Aberrant differentiation of keratinocytes disrupts the skin barrier and causes a series of skin diseases. However, the molecular basis of keratinocyte differentiation is still poorly understood. In the present study, we examined the expression of C7ORF41 using tissue microarrays by immunohistochemistry and found that C7ORF41 is specifically expressed in the basal layers of skin epithelium and its expression is gradually decreased during keratinocytes differentiation. Importantly, we corroborated the pivotal role of C7ORF41 during keratinocyte differentiation by C7ORF41 knockdown or overexpression in TPA-induced Hacat keratinocytes. Mechanismly, we first demonstrated that C7ORF41 inhibited keratinocyte differentiation mainly through formatting a complex with IKKα in the cytoplasm, which thus blocked the nuclear translocation of IKKα. Furthermore, we also demonstrated that inhibiting the PKCα/ERK signaling pathway reversed the reduction in C7ORF41 in TPA-induced keratinocytes, indicating that C7ORF41 expression could be regulated by upstream PKCα/ERK signaling pathway during keratinocyte differentiation. Collectively, our study uncovers a novel regulatory network PKCα/ERK/C7ORF41/IKKα during keratinocyte differentiation, which provides potential therapeutic targets for skin diseases.

Background Liver cancer stem cells (LCSCs) are a small subset of cells characterized by unlimited self-renewal, cell differentiation, and uncontrollable cellular growth. LCSCs are also resistant to conventional therapies and are thus believed to be held responsible for causing treatment failure of hepatocellular carcinoma (HCC). It has been recently found that long non-coding RNAs (lncRNAs) are important regulators in HCC. This present study aims to explore the underlying mechanism of how lncRNA DLX6-AS1 influences the development of LCSCs and HCC. Methods A microarray-based analysis was performed to initially screen differentially expressed lncRNAs associated with HCC. We then analyzed the lncRNA DLX6-AS1 levels as well as CADM1 promoter methylation. The mRNA and protein expression of CADM1, STAT3, CD133, CD13, OCT-4, SOX2, and Nanog were then detected. We quantified our results by evaluating the spheroid formation, proliferation, and tumor formation abilities, as well as the proportion of tumor stem cells, and the recruitment of DNA methyltransferase (DNMT) in LCSCs when lncRNA DLX6-AS1 was either overexpressed or silenced. Results LncRNA DLX6-AS1 was upregulated in HCC. The silencing of lncRNA DLX6-AS1 was shown to reduce and inhibit spheroid formation, colony formation, proliferation, and tumor formation abilities, as well as attenuate CD133, CD13, OCT-4, SOX2, and Nanog expression in LCSCs. Furthermore, downregulation of lncRNA DLX6-AS1 contributed to a reduction in CADM1 promoter methylation via suppression of DNMT1, DNMT3a, and DNMT3b in LCSCs and inactivating the STAT3 signaling pathway. Conclusion This study demonstrated that down-regulated lncRNA DLX6-AS1 may inhibit the stem cell properties of LCSCs through upregulation of CADM1 by suppressing the methylation of the CADM1 promoter and inactivation of the STAT3 signaling pathway. Electronic supplementary material The online version of this article (10.1186/s13046-019-1239-3) contains supplementary material, which is available to authorized users.

To compare the long-term clinical outcomes of single-bundle anterior cruciate ligament reconstruction (SBR) and double-bundle anterior cruciate ligament reconstruction (DBR) in patients with isolated anterior cruciate ligament (ACL) rupture, presenting no meniscus injury and no obvious preoperative cartilage degeneration. One hundred and three patients (38.6 ± 9.5 years) with a median follow-up of 151.6 months (range, 144–189 months) completed the retrospective study (SBR group: n = 51; DBR group: n = 52). Clinical outcomes were evaluated with physical examinations, KT-2000 anterior and posterior stability measurement with the knee in 30o of flexion, International Knee Documentation Committee (IKDC) subjective score, Tegner score, Lysholm score; magnetic resonance imaging (MRI) (3.0 T) was performed, and International Cartilage Repair Society (ICRS) cartilage degeneration grades were determined. Multivariate analysis was performed to identify factors associated with cartilage degeneration. There were significant differences in the pre- and postoperative IKDC, Lysholm and Tegner scores between the SBR and DBR groups. The SBR group had over double the rate of positive pressure/rub patellar test results (SBR vs DBR, 43.1% vs. 19.2%, p

Epilepsy is a prevalent neurological disorder and it is a significant health risk, affecting >50 million people worldwide. The development of novel and appropriate strategies is required for ameliorating the progression and/or limiting the detrimental consequences of epilepsy. In the current study, kainic acid (KA), a neurotoxin, was used to induce seizures in mice. The flavonoid quercetin has recently been reported to have neuroprotective effects. Therefore, the effects of quercetin on KA-induced epilepsy and the potential underlying molecular mechanisms were examined. It was noted that quercetin attenuated the KA-induced seizure score and proinflammatory cytokine production, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and activation of nuclear factor κB (NF-κB) in mice. Quercetin attenuated KA-induced proinflammatory cytokine (TNF-α and IL-1β) release from microglia cells, as well as activation of NF-κB and ionized calcium binding adapter molecule 1 in microglia cells. Therefore, quercetin inhibited KA-induced epilepsy by microglia cell inactivation and the production of NF-κB, TNF-α and IL-1β.

Hypericum patulum has been used as a folk medicine for its varied therapeutic effects including antifungal, wound-healing, spasmolytic, stimulant, hypotensive activities. The water decoction is drank as tea could treat cold, infantile malnutrition. The present study aims to isolate the constituents of the plant and investigate their effects on the glucose consumption in insulin-resistant HepG2 cells, furthermore, lipid metabolism in oleic acid (OA)-treated HepG2 cells was also studied. The phytochemical investigation of the plant led to the isolation of eleven compounds, and their structures were identified by spectroscopic analysis as n-dotriacontanol (1), shikimic acid (2), 1-O-caffeoylquinic acid methyl ester (3), 5-O-caffeoylquinic acid methyl ester (4), 5-O-coumaroylquinic acid methyl ester (5), 5-O-caffeoylquinic acid butyl ester (6), quercetin-3-O-α-L-rhamnoside (7), quercetin (8), quercetin-3-O-(4״-methoxy)-α-L-rahmnopyranosyl (9), hyperoside (10), and rutin (11). The results revealed that compounds 7, 9, and 10 could enhance glucose consumption significantly in hyperglycemia induced HepG2 cells and insulin-resistant HepG2 cells. In addition, the western blotting analysis result exhibited that compounds 7, 9, and 10 in high concentration (5 μM, H) group could dramatically upregulate the expression of PPARγ protein, and even the effect of them had no significant difference compared with that of rosiglitazone. Furthermore, compounds 9 and 10 in middle concentration (2.5 μM, M) group and H group could dramatically promote triglyceride metabolism and decrease TG content in OA-treated HepG2 cells, and even in H group, reactive oxygen species (ROS) level were significantly decreased compared with model group. PRACTICAL APPLICATIONS: Hypericum patulum is a well-known plant of the genera Hypericum for its varied preventive and therapeutic potential activities. To study the chemical constituents and their effects on glucose and lipid metabolism in vitro, we detected glucose consumption in insulin-resistant HepG2 cells, triglyceride content and reactive oxygen species level in OA-treated HepG2 cells. In addition, PPARγ protein was also detected by western blotting analysis in the study. Compounds 1, 2, 3, 5, 6, 9, 10, and 11 were isolated from the plant for the first time. Quercetin-3-O-(4"-methoxy)-α-L-rahmnopyranosyl (9) and hyperoside (10) had potential therapeutic benefit against glucose and lipid metabolic disease. Therefore, this study might have certain guiding significance for further research and development of H. patulum.

The hot deformation behavior of as-solutionized Mg–8Sn–2Zn–0.5Cu (TZC820) alloy was investigated experimentally and numerically via isothermal compression tests at 250–400 °C and strain rate range of 0.01–3 s−1 on a Gleeble–1500D thermomechanical simulator. Results show that the deformation temperature and strain rate significantly affected flow stress and material constants. In addition, the strain-compensated constitutive relationship was established on the basis of true stress–strain curves. The main deformation mechanism for this alloy was the dynamic recrystallization (DRX), and the DRX degree was effectively enhanced with an increase in deformation temperature and a decrease in strain rate. Moreover, the cellular automaton method was used to simulate the microstructure evolution during hot compression. In addition, the processing maps were established, and the optimum deformation parameters for the as-solutionized TZC820 alloy are at 370–400 °C and 0.01 s−1, and at 320–360 °C and 1–3 s−1.

Pancreatic cancer is a lethal malignancy with relatively few effective therapies. Recent investigations have highlighted the role of microRNAs (miRNAs) as crucial regulators in various tumor processes including tumor progression. Hence the current study aimed to investigate the role of bone marrow mesenchymal stem cell (BMSC)-derived exosomal microRNA-126-3p (miR-126-3p) in pancreatic cancer. Initially, miRNA candidates and related genes associated with pancreatic cancer were screened. PANC-1 cells were transfected with miR-126-3p or silenced a disintegrin and a metalloproteinase-9 (ADAM9) to examine their regulatory roles in pancreatic cancer cells. Additionally, exosomes derived from BMSCs were isolated and co-cultured with pancreatic cancer cells to elucidate the effects of exosomes in pancreatic cancer. Furthermore, the effects of overexpressed miR-126-3p derived from BMSCs exosomes on proliferation, migration, invasion, apoptosis, tumor growth, and metastasis of pancreatic cancer cells were analyzed in connection with lentiviral packaged miR-126-3p in vivo. Restored miR-126-3p was observed to suppress pancreatic cancer through downregulating ADAM9. Notably, overexpressed miR-126-3p derived from BMSCs exosomes inhibited the proliferation, invasion, and metastasis of pancreatic cancer cells, and promoted their apoptosis both in vitro and in vivo. Taken together, the key findings of the study indicated that overexpressed miR-126-3p derived from BMSCs exosomes inhibited the development of pancreatic cancer through the downregulation of ADAM9, highlighting the potential of miR-126-3p as a novel biomarker for pancreatic cancer treatment. Keywords: bone marrow mesenchymal stem cells, exosomes, microRNA-126-3p, a disintegrin and a metalloproteinase-9, pancreatic cancer, invasion, metastasis

A worth noticing pattern in current invasive biology is the clonal ability of many of the world's worst invasive plants. Selective placement of ramets (i.e. foraging behavior) can intensify ramet performance and allocation, and place more ramets in the more favorable microhabitats, which can maximum utilize resource and share risk in heterogeneous environments. Still little is known about whether invasive alien and native clonal plants differ in the selective placement patterns of ramets in invasive clonal plants or not. We used five congeneric pairs of naturally co-occurring invasive alien and native clonal plant species in China. In a glasshouse, we grew all species in pots under a homogeneous and three heterogeneous conditions (i.e. light, soil nutrients or water) subjected to resource-high or -low patches. All biomass parameters and number of ramets significantly increased in resource-high patches in all three types of heterogeneous environments. Interestingly, growth of invasive alien plants benefited significantly more from resource-high patches than native plants in all heterogeneous environments. Overall, invasive had higher biomass parameters per ramet than natives. Ramet parameters of invasive plants also benefited more from resource-low patches than natives. Three different selective placement patterns of ramets in resource-low patches were exhibited in invasive plants: ramet increasing shoot investment (above pattern), increasing root investment (below pattern) and increasing both investments (complete pattern) in the light, soil water and nutrient heterogeneity, respectively. Investment on less, larger ramet was the adaptive strategy of invasive plants in resource-poor patches. The results suggest that adaptively selective placement patterns of ramets promote a higher morphology plasticity and performance in invasive clonal plants over natives. When alien clonal plants spread new areas with light, soil nutrients or water heterogeneity, selective placement patterns of ramets might play an important role in plant performance and competitive superior by capitalizing more on additional resources.

Long noncoding RNAs, including HOTAIR, are involved in the pathogenesis of a wide range of diseases. This study aimed to explore the mechanism underlying the involvement of HOTAIR in neonatal bronchial hyperresponsiveness (BHR). A total of 105 newborns were recruited in this study to collect their peripheral blood mononuclear cell and serum samples, which were then divided into different genotype groups based on the genotypes of rs4759314, rs874945, and rs7958904. The real-time polymerase chain reaction, western blot analysis, computational analyses, and luciferase assays were performed to establish the regulatory relationships between the HOTAIR, microRNA-126 (miR-126), and interleukin-13 (IL-13). The level of HOTAIR, miR-126, and IL-13 among rs4759314 AA, AG, and GG groups, as well as among rs874945 GG, AG, and AA groups was similar. However, the level of HOTAIR was increased in the rs7958904 GG group, accompanied by a decreased level of miR-126 and IL-13. In addition, the level of airway responsiveness was comparable among rs4759314 AA, AG, and GG groups, as well as among rs874945 GG, AG, and AA groups. However, the airway responsiveness in the groups rs7958904 CG and CC was much stronger than that of the GG group. We also demonstrated that, by directly binding to miR-126, HOTAIR reduced the expression of miR-126, which in turn decreased the expression of IL-13. In summary, we demonstrated the role of HOTAIR-induced downregulation of miR-126 and IL-13 in the development of BHR in neonates.

Clonal integration, i.e. resource sharing between interconnected ramets, can help clonal plants tolerate abiotic stress. However, few studies have directly examined the ecological significance of clonal integration in the ability of clonal plants to tolerate biotic stress such as herbivory. We grew clonal fragments of an invasive clonal plant Alternanthera philoxeroides, each consisting of an apical part (relatively young) and a basal part (relatively old), at two levels (low and high) of soil nitrogen (N). For each fragment, the apical part was subjected to either no herbivory or herbivory for 2 weeks by a specialist insect, Agasicles hygrophila, and was either connected with or disconnected from the basal part not subjected to herbivory. Herbivory in the apical part severely reduced leaf growth (leaf mass, leaf number or leaf area) and ramet production of both apical and basal parts, and increased root to shoot ratio of the apical part. Irrespective of herbivory and soil N, stem connection between the apical and the basal part decreased root to shoot ratio of the apical part, but did not change its growth measures. Meanwhile, connection increased stem N concentration of the apical part growing under high-N supply and decreased stem carbon (C) concentration of the apical part under low-N supply. By contrast, connection increased root to shoot ratio of the basal part, but reduced its leaf and ramet production. Connection also increased leaf and stem C concentrations of the basal part under low-N supply. Thus, clonal integration can be beneficial for the early development of young A. philoxeroides ramets, but not for their local adaptation to herbivory damage by A. hygrophila.

Aims We aimed to explore the impact of long noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) on cell proliferation, invasion, and migration of glioma. Methods Differentially expressed genes were screened out from Gene Expression Omnibus data set based on the microarray analysis. The expression levels of lncRNA NEAT1, miR-139-5p, and CDK6 in glioma cells and tissues were examined by quantitative reverse transcription polymerase chain reaction, and the protein level of CDK6 in glioma cells was determined by western blot and immunohistochemistry. Glioma cell viability, cell cycle, and apoptosis were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) and flow cytometry, respectively, whereas cell invasion and migration were analyzed by transwell assay. The target relationships among NEAT1, miR-139-5p, and CDK6 were confirmed by dual-luciferase reporter gene assay. The effects of lncRNA NEAT1 on tumor growth were further testified through glioma xenografts in nude mice. Results LncRNA NEAT1 and CDK6 were highly expressed in glioma tissues and cells, whereas miR-139-5p was lowly expressed. There were target relationships and correlations on expressions between miR-139-5p and NEAT1/ CDK6. NEAT1 and CDK6 could promote cell proliferation and metastasis of glioma cells and impeded cell apoptosis, whereas miR-139-5p exerted suppressive effects on the biological functions of glioma cells. NEAT1 regulated CDK6 to affect glioma growth through sponging miR-139-5p. Conclusions LncRNA NEAT1 promotes cell proliferation, invasion, and migration of glioma through regulating miR-139-5p/CDK6 pathway.

Many invasive alien plant species are clonal and can greatly propagate and spread through clonal integration (sharing resources between connected ramets) in heterogeneous and variable environments. Here, we tested whether water variability influences clonal integration of invasive alien plant species and consequently facilitates their growth and dominance in a native community. We selected four typical invasive clonal plant species in China. Connected (with clonal integration) and disconnected (without clonal integration) clonal fragments were established either under constant watering or variable watering condition in an experimental native plant community consisting of three naturally co-occurring grassland species. Proximal part of the container received high nutrient and distal part received low nutrient. Clonal integration significantly increased biomass, aboveground mass and belowground mass of invasive alien plants in the proximal ramets, the distal ramets and the whole clone and decreased the growth of native community. Interestingly, clonal integration significantly increased the growth of invasive plants in variable watering. The positive effect of clonal integration was stronger in variable watering than in constant watering. Invasive plants with clonal integration had high biomass proportion (>0.6) in the whole community. Our results suggest that invasive clonal plants benefit more from clonal integration in variable water environments when established in a native community, and to some extent, clonal integration potentially contribute greatly to the invasiveness of alien clonal plants when they enter a new community with resource variability.

The fruits of Swietenia macrophylla King have been processed commercially to a variety of health foods and healthcare products and exhibited antidiabetic, anti-inflammatory, antimutagenicity, antitumor activity, and so on. This study was aimed to examine the glucose consumption in human hepatoma HepG2 cells and the expression of PPARγ of limonoids isolated from the fruits of S. macrophylla. The phytochemical investigation of the fruits led to the isolation of ten limonoids which structures were elucidated by spectroscopic analysis as swietenine (1), khayasin T (2), 6-deoxyswietenine (3), 3-O-tigloylswietenolide (4), swietenolide (5), 3,6-O,O-diacetylswietenolide (6), 7-deacetoxy-7-oxogedunin (7), fissinolide (8), proceranolide (9), 7-deacetoxy-7α-hydroxygedunin (10), and compound 10 was isolated from this plant for the first time. The glucose consumption assay revealed that compounds 1, 2, 3, 5, and 9 could promote glucose consumption significantly in normal hyperglycemia-induced HepG2 cells, furthermore, compounds 1, 5, and 9 had a better effect on promoting glucose consumption in insulin-resistant HepG2 cells. In addition, compounds 1 and 5 could dramatically enhance the expression of PPARγ protein in insulin-resistant HepG2 cells according to the western blotting analysis result. PRACTICAL APPLICATIONS: Swietenia macrophylla King belongs to the family Meliaceae and the fruits have been exhibited a wide range of biological activities, such as antidiabetic, anti-inflammatory, antimutagenicity, antitumor activity, and so on. Phytochemical investigations of S. macrophylla have revealed that limonoids and triterpenoids were effective antidiabetic agents. However, the mechanism of these limonoids to antidiabetic activity is unclear. In this study, limonoids were isolated from the fruit of S. macrophylla and their effects on the glucose consumption of insulin-resistant HepG2 cells were studied. The results showed that compounds 1 and 5 could dramatically enhance the expression of PPARγ protein in insulin-resistant HepG2 cells, which will give aid to explore the mechanism of these limonoids in the treatment of type 2 diabetes. Therefore, this research might facilitate further research and development of S. macrophylla.

Purpose The purpose of the present study was to analyze the anatomic landmarks of Schottle’s point and establish a locating method for identification. Methods From 2013 to 2016, patients undergoing medial patellofemoral ligament (MPFL) reconstruction for patellofemoral instability were enrolled. Inclusion criteria: at least 2 episodes of patellar dislocation. Exclusion criteria: previous knee surgeries, open physes, severe trochlear dysplasia， tibial tuberosity lateralization, or patella alta. Group A: From January 2013 to December 2013, preoperative 3-dimensional computed tomography (3D-CT) images were obtained. Anatomic features of Schottle’s point were measured on the 3D-CT images. A Schottle’s point locating method with 2 distinct landmarks was established. Group B: From January 2014 to January 2016, consecutive MPFL reconstructions were performed. The placement of Schottle’s point was following the established method without fluoroscopy. The accuracy of femoral tunnel positions was assessed on the 3D-CT images postoperatively. Results CT images of 53 knees were obtained in group A. Forty-seven MPFL reconstructions were performed in group B. No significant difference was found between the 2 groups regarding to demographic characteristics. The intraclass correlation coefficients were excellent for all measures (r = 0.97). In group A, Schottle’s point was 8.1 ± 0.2 mm (95% confidence interval [CI], 7.7-8.5) distal to the apex of the adductor tubercle and 8.0 ± 0.3 mm (95% CI, 7.4-8.6) anterior to the posterior edge. Apex of the adductor tubercle was defined as the most convex point, and posterior edge was defined as the edge of the posteromedial cortex in the transition area between the medial condyle and femoral shaft. In group B, 44 of 47 femoral tunnels (93.6%) were considered localized in the proper zone. Conclusions Schottle’s point was approximately 8 mm distal to the apex of the adductor tubercle and 8 mm from the posterior edge. Schottle’s point locating method without fluoroscopy had high accuracy. Level of Evidence Level IV, case series.

Eupatorium adenophorum is an alien species that threatens community stability and diversity in karst areas. Arbuscular mycorrhizal (AM) fungi form interconnected mycorrhizal network, connecting adjacent plants and plant species. How mycorrhizal networks affect the competition for nutrients between invasive and native plants in karst habitat remains unclear at present. An experiment was conducted using a compartmental growing device, which was composed of two planting compartments (for the invasive E. adenophorum or native Artemisia annua) and a competitive compartment (for the interconnected mycorrhizal network). The experiment contained mycorrhizal fungus treatments, with AM fungi (M+) and without AM fungi (M−) using the species Claroideoglomus etunicatum, and the nutrient utilization treatments using nylon mesh to interconnective mycorrhizal networks, including common utilization (Cu), single utilization (Su), and non-utilization (Nu). The results showed as follows: AM fungi differentially increased biomass, nitrogen (N) acquisition and phosphorus (P) acquisition and significantly reduced N/P ratio of the invasive E. adenophorum and native A. annua under Cu, Su, and Nu conditions. Additionally, the biomass, N acquisition and P acquisition of E. adenophorum was greater than A. annua and the N/P ratio of E. adenophorum was significantly lower than A. annua under Cu condition, which AM fungi promoted the accumulation of biomass, N and P for E. adenophorum and A. annua, and E. adenophorum experienced a greater reduction of P limitation than A. annua via the interconnected mycorrhizal network. In conclusion, we suggest that AM fungi endow invasive plants greater alleviation of P limitation and enhancement of nutrient competition than native plants via mycorrhizal network in low-P karst soil.

Development of effective therapeutic drugs for Parkinson's disease (PD) is of great importance. Aberrant microRNA (miRNA) expression has been identified in postmortem human PD brain samples, in vitro and in vivo PD models. However, the role of miR-342-3p in PD has been understudied. The study explores the effects of miR-342-3p on expression of glutamate (Glu) transporter, and dopaminergic neuron apoptosis and proliferation by targeting p21-activated kinase 1 (PAK1) through the Wnt signaling pathway in PD mice. After establishment of PD mouse models, gain- or loss-of-function assay was performed to explore the functional role of miR-342-3p in PD. Number of apoptotic neurons and Glu concentration was then determined. Subsequently, PC12 cells were treated with miR-342-3p mimic, miR-342-3p inhibitor, dickkopf-1 (DKK1), and miR-342-3p inhibitor + DKK1. The expression of miR-342-3p, PAK1, the Wnt signaling pathway-related and apoptosis-related genes, Glutamate transporter subtype 1 (GLT-1), l-glutamate/ l-aspartate transporter (GLAST), tyrosine hydroxylase (TH) was measured. Also, cell viability and apoptosis were evaluated. PD mice exhibited increased miR-342-3p, while decreased expression of PAK1, GLT-1, GLAST, TH, and the Wnt signaling pathway-related and antiapoptosis genes. miR-342-3p downregulation could promote expression of PAK1, the Wnt signaling pathway-related and antiapoptosis genes. GLT-1, GLAST, and TH as well as cell viability, but reduce cell apoptosis rate. The results indicated that suppression of miR-342-3p improves expression of Glu transporter and promotes dopaminergic neuron proliferation while suppressing apoptosis through the Wnt signaling pathway by targeting PAK1 in mice with PD.

Broadband low-voltage power line communication (PLC) has many advantages including less investment cost, construction speed, and convenient access. Since the orthogonal frequency division multiplexing (OFDM) technology has strong anti-jamming and anti-frequency selective fading characteristics naturally it becomes a better low voltage power line communication solution. We proposed an OFDM channel estimation method based on compressed sensing (CS) technique according to the channel characteristics of low-voltage power lines. CS algorithm in OFDM system was discussed and an orthogonal matching pursuit (OMP) algorithm was applied to reconstruct the PLC channel information. The simulation results showed that the communication channel estimation method based on CS technique was feasible in PLC system, and the validity of information transmission in OFDM systems can be enhanced.

In the large majority of papers utilizing the Gurtin-Murdoch (G-M) model of a material surface, the complete model is avoided in favor of various modified versions often because they lead to simpler representations of the corresponding stress boundary condition. We propose in this paper an integral-type stress boundary condition for the plane deformations of a bulk-interface composite system which allows for an equally simple implementation of the complete G-M model. Since the mechanical behavior of such composite systems is often analyzed using complex variable methods, we formulate our ideas accordingly, in this context. Remarkably, in contrast to what is often believed to be the case, we find that boundary value problems based on our formulation of the stress boundary condition offer no added difficulty when utilizing the complete G-M model versus its various simplified counterparts. This new representation of the stress boundary condition is concise in form and will prove to be extremely useful in, for example, the calculation of the elastic field in the vicinity of nano-inhomogeneities of irregular shape.

This study was designed to explore the relationship between miR-1275 and SERPINE1 and its effects on glioma cell proliferation, migration, invasion and apoptosis. Differentially expressed miRNAs and mRNAs in glioma tissues were screened out by bioinformatic analysis. Dual-luciferase reporter gene assay was used to validate the targeted relationship between miR-1275 and SERPINE1. qRT-PCR was used to detect the expression of miR-1275 and SERPINE1 in glioma tissues. The expressions of SERPINE1 and p53 pathway-related proteins in glioma cells were detected by western blot. Glioma cell proliferation, apoptosis, migration and invasion were respectively detected by CCK-8 assay, flow cytometry, wound healing assay and transwell assay. Tumour xenograft model was developed to study the influence of miR-1275 and SERPINE1 on glioma growth in vivo. The results of microarray analysis, qRT-PCR and western blot showed that miR-1275 was low-expressed while SERPINE1 was high-expressed in glioma. Dual-luciferase assay showed that miR-1275 could bind to SERPINE1. Overexpression of miR-1275 could promote the p53 pathway-related proteins' expression. Highly expressed miR-1275 could repress the migration, proliferation and invasion of glioma cells while highly expressed SERPINE1 had inverse effects. Tumour xenograft showed that up-regulated miR-1275 or down-regulated SERPINE1 could repress glioma growth in vivo. Up-regulation of miR-1275 activated p53 signalling pathway via regulating SERPINE1 and therefore suppressed glioma cell proliferation, invasion and migration, whereas promoted cell apoptosis.

Graves' disease is an autoimmune process in which the thyroid gland is triggered by autoantibodies, resulting in hyperthyroidism. The purpose of the present study is to elucidate whether exon-1 49 A/G and promoter region 318C/T polymorphisms in the CTLA-4 gene. This study consisted of 653 eligible patients with Graves' disease. After receiving 131I radionuclide therapy, these patients were classified into the remission and non-remission groups. A logistic regression-based model was used to analyze independent factors affecting the patient response to 131I radionuclide therapy. The results showed that CTLA-4 49 A/G was closely related to the efficacy of 131 I treatment for Graves' disease (AG + GG vs. AA: OR = 6.543, 95%CI = 2.611 ∼ 16.40, P

The loss of pancreatic islet β-cell function represents the classical feature in the pathogenesis of type 2 diabetes mellitus (T2DM). Previous evidence has highlighted the involvement of the activated JNK pathway in relation to islet β-cell apoptosis. Hence, during the present study a streptozotocin-induced DM mice model was established in a bid to ascertain as to whether microRNA-30d (miR-30d) plays a regulatory role in the JNK pathway in relation to islet β-cell dysfunction. The collection and identification of the islet β cells from streptozotocin-induced mice was performed. Islet β cells with elevated or suppressed levels of miR-30 as well as knocked down SOCS3 were established in order to verify the regulatory mechanisms by which miR-30d governs SOCS3 in vitro. We found miR-30d was overexpressed among tissue samples obtained form streptozotocin-induced mice and their islet β cells, as well as increasing miR-30d expression when the JNK pathway was activated were found to promote islet β cell growth and cell cycle entry, and inhibit apoptosis. SOCS3, confirmed to be a miR-30d target, was decreased in the islet β cells following the promotion of miR-30d, while the JNK pathway was inhibited following SOCS3 knocdown. Furthermore, the effect of miR-30d inhibition was lost in islet β cells when SOCS3 was knocked down. The data of the present study support the notion that miR-30d-mediated direct suppression of SOCS3 acts to protect pancreatic β-cell functions through the JNK signaling pathway, emphasizing the potential of miR-30d as a novel pharmacological target for treatment and intervention of DM.

Epilepsy is a group of neurological disorders characterized by epileptic seizures. In this study, we aim to explore the role of microRNA-421 (miR-421) in hippocampal neurons of epilepsy mice via the TLR/MYD88 pathway. Forty mice were randomly served as the normal and model (established as epilepsy model) groups. Hippocampal neurons were assigned into seven groups with different transfections. The RT-qPCR and western blotting were conducted to examine the expression of miR-421 TLR2, TLR4, MYD88, Bax, Bcl-2, p53, Beclin-1, and LC3II/LC3I. Cell proliferation and apoptosis were detected by MTT and flow cytometry.MYD88 is a target gene of miR-421. Model mice showed elevated expression of TLR2, TLR4, MYD88, Bax, p53, Beclin-1, and LC3II/LC3I but reduced expression of miR-421 and Bcl-2. In vitro experiments reveals that overexpression of miR-421 inhibited the TLR/MYD88 pathway. Besides, overexpressed miR-421 declined cell apoptosis but increased cell proliferation. It reveals that miR-421 targeting MYD88 could inhibit the apoptosis and autophagy of hippocampal neurons in epilepsy mice by down-regulating the TLR/MYD88 pathway.

Hypoxia–ischaemia (HI) remains a major cause of foetal brain damage presented a scarcity of effective therapeutic approaches. Dexmedetomidine (DEX) and microRNA‐140‐5p (miR‐140‐5p) have been highlighted due to its potentially significant role in the treatment of cerebral ischaemia. This study was to investigate the role by which miR‐140‐5p provides cerebral protection using DEX to treat hypoxic–ischaemic brain damage (HIBD) in neonatal rats via the Wnt/β‐catenin signalling pathway. The HIBD rat models were established and allocated into various groups with different treatment plans, and eight SD rats into sham group. The learning and memory ability of the rats was assessed. Apoptosis and pathological changes in the hippocampus CA1 region and expressions of the related genes of the Wnt/β‐catenin signalling pathway as well as the genes responsible of apoptosis were detected. Compared with the sham group, the parameters of weight, length growth, weight ratio between hemispheres, the rate of reaching standard, as well as Bcl‐2 expressions, were all increased. Furthermore, observations of increased levels of cerebral infarction volume, total mortality rate, response times, total response duration, expressions of Wnt1, β‐catenin, TCF‐4, E‐cadherin, apoptosis rate of neurons, and Bax expression were elevated. Following DEX treatment, the symptoms exhibited by HIBD rats were ameliorated. miR‐140‐5p and si‐Wnt1 were noted to attenuate the progression of HIBD. Our study demonstrates that miR‐140‐5p promotes the cerebral protective effects of DEX against HIBD in neonatal rats by targeting the Wnt1 gene through via the negative regulation of the Wnt/β‐catenin signalling pathway.

In this study, we aim to investigate the role of tanshinone IIA in myocardial infarction (MI), especially in left ventricular remodelling (VR) and the underlying mechanism involving the TLR4/MyD88/NF-κB signalling pathway. Sprague-Dawley (SD) rats (n = 96) were selected, and 12 of them underwent sham surgery. The remaining 84 rats were subjected to MI modelling. HE and MT staining were carried out to estimate infract size, histopathological changes and fibrosis degree. Macrophage infiltration and cardiomyocyte apoptosis were evaluated by immunohistochemistry and TUNEL staining. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to determine the expression levels of TLR4, MyD88 and NF-κB. Serum levels of IL-2, IL-6, IL-8, TNF-a, procollagen I Cpropeptide (PICP), and procollagen III N-propeptide (PIIINP) were measured using enzyme-linked immunosorbent assay (ELISA). The heart weight/body weight, mean arterial pressure (MAP), left ventricular end-systolic pressure (LVESP), +dP/dt and -dP/dt increased while the ventricular function and the left ventricular end-diastole pressure (LVEDP) decreased in MI rats. Compared with the rats undergoing sham surgery, MI rats showed larger infarct size, severer fibrosis, higher expression levels of TLR4, NF-κB-P65, MyD88, IL-2, IL-6, IL-8, TNF-a, PICP and PIIINP as well as enhanced macrophage infiltration, cardiomyocyte apoptosis. After treatment with tanshinone IIA combined with LPS for 4 weeks, the rats showed better condition than those treated with only LPS. These results indicate that tanshinone IIA attenuates MI and prevents left VR. Importantly, inhibition of TLR4/MyD88/NF-κB signalling pathway is a key step in this process.

This study investigates the protective effects of miR-431 against cerebral ischemia-reperfusion injury through the Rho/Rho-kinase signaling pathway. SD rats were randomly classified into normal, sham, and model (middle cerebral artery occluded) groups. Rho expression and cerebral infarction were visualized by immunohischemistry and TTC staining, respectively. qRT-PCR and western blotting were used to measure mRNA and protein expression of miR-431 and Rho/Rho-kinase signaling pathway-related genes. Hippocampal neurons were extracted and assigned into normal, blank, negative control (NC), miR-431 mimics, miR-431 inhibitors, siRNA-Rho, and miR-431 inhibitors + siRNA-Rho groups. Proliferation and apoptosis were detected by MTT and flow cytometry, respectively. Compared with the normal group, the model group showed elevated Rho expression, area of cerebral infarction, and expressions of Rho/Rho-kinase related genes but reduced miR-431 expression. Compared with the blank group, expression of Rho, Rho-kinase α, and Rho-kinase β decreased and miR-431 expression increased in the miR-431 mimics and siRNA-Rho groups, and the tendency reversed in the miR-431 inhibitors group. Enhanced proliferation and inhibited apoptosis were exhibited in the miR-431 mimics and siRNA-Rho groups while results in the miR-431 inhibitors group reversed. Findings obtained from this study indicated that miR-431 confers protection against cerebral ischemia-reperfusion injury through negatively regulating the Rho/Rho-kinase signaling pathway.

The study aimed to investigate whether S100A9 gene silencing mediating the IL‐17 pathway affected the release of pro‐inflammatory cytokines in acute pancreatitis (AP). Kunming mice were assigned to the normal, AP, AP + negative control (NC), AP + shRNA, AP + IgG and AP + anti IL‐17 groups. ELISA was applied to measure expressions of AMY, LDH, CRP, TNF‐α, IL‐6 and IL‐8. The cells were distributed into the control, blank, NC, shRNA1 and shRNA2 groups. MTT assay, flow cytometry, RT‐qPCR and Western blotting were used to evaluate cell proliferation, cell cycle and apoptosis, and expressions of S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12 in tissues and cells. Compared with the normal group, the AP group displayed increased expressions of AMY, LDH, CRP, TNFα, IL‐6, IL‐8, S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12. The AP + shRNA and AP + anti IL‐17 groups exhibited an opposite trend. The in vivo results: Compare with the control group, the blank, NC, shRNA1 and shRNA2 groups demonstrated increased expressions of S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12, as well as cell apoptosis and cells at the G1 phase, with reduced proliferation. Compared with the blank and NC groups, the shRNA1 and shRNA2 groups had declined expressions of S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12, as well as cell apoptosis and cells at the G1 phase, with elevated proliferation. The results indicated that S100A9 gene silencing suppressed the release of pro‐inflammatory cytokines through blocking of the IL‐17 pathway in AP.

We explored the effect of S100A12 gene on serum levels of anti-inflammatory/pro-inflammatory cytokines in septic rats by activating the extracellular signal-regulated kinase (ERK) signaling pathway. A total of 180 specific pathogen-free (SPF) rats were purchased to establish cecal ligation and puncture (CLP) model. Rats were assigned into the sham, model, empty vector, S100A12 siRNA, epidermal growth factor (EGF), and S100A12 siRNA + EGF groups. The expressions of S100A12, ERK-1, ERK-2, cPLA2, and NF-κB in liver tissues of rats among six groups were detected by RT-qPCR and western blotting. ELISA was used to determine serum levels of IL-1β, IL-10, TNF-α, procalcitonin (PCT), and C-reactive protein (CRP). Pearson correlation analysis was conducted to measure correlations. Cell apoptosis of rats among six groups was detected by Tunel staining. The expressions of S100A12, ERK-1, ERK-2, cPLA2, and NF-κB decreased in the S100A12 siRNA group while increased in the EGF group compared with the model group. S100A12 mRNA expression was positively correlated with mRNA expressions of related genes in the ERK signaling pathway (ERK-1, ERK-2, cPLA2, and NF-κB) in the model and empty vector groups. Expressions of IL-1β, IL-6, TNF-α, PCT, and CRP in the EGF group were higher than those in the model group, but were lower than those in the S100A12 siRNA group. Compared with the model group, cell apoptosis decreased in the S100A12 siRNA group but that increased in the EGF group. We demonstrates that S100A12 gene silencing decreases serum levels of anti-inflammatory/pro-inflammatory cytokines in septic rats by inhibiting the ERK signaling pathway.

Background/Aims: Parkinson’s disease (PD) is a neurodegenerative movement disease with a high annual incidence. Accumulating evidence demonstrates that microRNAs play important roles in the pathogenesis of multiple neurological disorders, including PD. This study aims to investigate how microRNA-200a (miR-200a) regulates striatal dopamine receptor D2 (DRD2) to affect apoptosis of striatum in rats with PD and to explore the associated mechanism. Methods: After successfully establishing a PD model by 6-hydroxydopamine injections, PD rats were mainly treated with miR-200a mimics, inhibitors, Forskolin or a combination of miR-200a inhibitors and Forskolin. High-performance liquid chromatography-electrochemical detection (HPLC-ECD) was employed to detect the levels of dopamine, 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and chemistry colorimetric methods were applied to detect the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). A TUNEL assay and immunocytochemical staining were performed to observe apoptosis and tyrosine hydroxylase (TH)-positive cells in the striatum. The expression of miR-200a, DRD2, Bad, Bax, Bcl-2, cAMP and PKA was determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot assays. Results: In the cellular experiments, after transfection with the inhibitor of miR-200a, decreased levels of Bax, GSH-Px, SOD, dopamine, DOPAC and HVA but increased levels of MDA and Bcl-2 were found along with a reduced apoptosis rate and increased TH-positive cell number. In addition, downregulating miR-200a resulted in lower expression of AKT, cAMP and PKA but higher expression of DRD2 and CREB, indicating that the downregulation of miR-200a increases DRD2 expression, which blocks the cAMP/PKA signaling pathway. Conclusion: This study provides evidence that the inhibition of miR-200a can repress apoptosis in the striatum via inhibition of the cAMP/PKA signaling pathway by upregulating DRD2 expression in PD rats.

Background/Aims: MiRNAs are involved in phenotype modulation of neural cells after peripheral nerve injury. However, the roles of miRNAs on the survival of dorsal root ganglion (DRG) neurons have not yet been fully understood. Methods: In this study, the expression of miR-142-3p was measured in rat DRGs (L4-L6) during the initial 24 hours post sciatic nerve transection by microarray profiling and quantitative PCR. The functional assays including the cell viability, colony formation, cell cycle and apoptosis assays were performed in miR-142-3p mimic or inhibitor transfected cell lines. Results: MiR-142-3p was identified to be siginificantly upregulated in rat DRGs (L4-L6) during the initial 24 hours post sciatic nerve transection. MiR-142-3p mimic enhanced cell viability by promoting cell cycle and inhibiting cell apoptosis in cultured DRG neurons. In addition, cyclin-dependent kinase inhibitor 1B (CDKN1B, also known as p27/Kip1) and tissue inhibitor of metalloproteinase 3 (TIMP3) were identified as targets of miR-142-3p. Furthermore, knockdown of CDKN1B or TIMP3 by specific siRNAs could reverse the effect of miR-142-3p. Conclusions: In the conclusion, the results showed that miR-142-3p could promote neuronal cell cycle and inhibit apoptosis at least partially through suppressing CDKN1B and TIMP3 after peripheral nerve injury.

Ornamental plant trees possess multiple ecosystem roles, retain ambient quality and have pleasant landscape effects, whereas urbanization also induce many environmental changes compared with rural areas and these changes affect the plants leaf functional traits. In response to these stresses, functional traits of plants may change. Here, we studied leaf functional traits and plasticity for three ornamental species growing under various levels of urban environment stresses. The results showed that leaf and stomatal traits varied between trees growing under different environment stresses. For all three species, as environment stresses increased, LT (leaf thickness), SLI (single leaf area), FAA (fluctuating asymmetry based on leaf area) and FAW (fluctuating asymmetry based on leaf width) decreased. Spatial distribution maps for SLA (specific leaf area) showed a high spatial variation, corresponding with the level of urbanization. These results suggest that stomatal traits of ornamentals tree species may potentially be used as indicators for urban habitat quality.

Previous studies suggested that lower vitamin D might be a risk factor for autism spectrum disorders (ASDs). The aim of this study was to estimate the prevalence of ASDs in 3-year-old Chinese children and to examine the association between neonatal vitamin D status and risk of ASDs. We conducted a study of live births who had taken part in expanded newborn screening (NBS), with outpatient follow-up when the children 3-year old. The children were confirmed for ASDs in outpatient by the Autism Diagnostic Interview-Revised and Diagnostic and Statistical Manual of Mental Disorders (DSM)-5 criteria. Intellectual disability (ID) status was defined by the intelligence quotient (IQ < 80) for all the participants. The study design included a 1:4 case to control design. The concentration of 25-hydroxyvitamin D3 [25(OH)D3] in children with ASD and controls were assessed from neonatal dried blood samples. A total of 310 children were diagnosed as having ASDs; thus, the prevalence was 1.11% (95% CI, 0.99% to 1.23%). The concentration of 25(OH)D3 in 310 ASD and 1240 controls were assessed. The median 25(OH)D3 level was significantly lower in children with ASD as compared to controls (p < 0.0001). Compared with the fourth quartiles, the relative risk (RR) of ASDs was significantly increased for neonates in each of the three lower quartiles of the distribution of 25(OH)D3, and increased risk of ASDs by 260% (RR for lowest quartile: 3.6; 95% CI, 1.8 to 7.2; p < 0.001), 150% (RR for second quartile: 2.5; 95% CI, 1.4 to 3.5; p = 0.024), and 90% (RR for third quartile: 1.9; 95% CI, 1.1 to 3.3; p = 0.08), respectively. Furthermore, the nonlinear nature of the ID-risk relationship was more prominent when the data were assessed in deciles. This model predicted the lowest relative risk of ID in the 72rd percentile (corresponding to 48.1 nmol/L of 25(OH)D3). Neonatal vitamin D status was significantly associated with the risk of ASDs and intellectual disability. The nature of those relationships was nonlinear. © 2017 American Society for Bone and Mineral Research.

Objective : This study aims to explore the neuroprotective effects of dexmedetomidine (Dex) in rats suffering from traumatic brain injury (TBI) via the PI3K/Akt/mTOR signaling pathway. Methods A weight drop model was performed for TBI model establishment. A total of 150 Sprague Dawley rats were selected and assigned into control, sham, TBI, TBI + Dex, TBI + LY294002 (LY) and TBI + Dex + LY groups. Modified Neurological Severity Score (mNSS) was conducted in order to evaluate the neurological injury. The water content in brain tissues was measured. The expressions of PI3K/Akt/mTOR signaling pathway-related proteins, tight junction proteins (ZO-1 and Claudin-5) and autophagy proteins (LC3 I/II and Beclin-1) were detected using Western blot assay. A TUNEL assay was applied for cell apoptosis, immunofluorescence was employed for the detection of the positive expression of LC3, and ELISA was applied for detection of levels of inflammatory factors [tumor necrosis factor-alph (TNF-a), interleukin-1β (IL-1β), interferon-γ (INF-γ) as well as IL-6], respectively. Results Compared with the control group, the other four groups exhibited increased mNSS, brain water content, expression of LC3, TNF-a, IL-1β, INF-γ and IL-6, and positive expression of LC3, expression of LC3 I/II and Beclin-1, but decreased expression of pp-PI3K/t-PI3K, p-Akt/t-Akt, p-mTOR/t-mTOR, ZO-1 and Claudin-5. Compared with the TBI group, the TBI + Dex group exhibited reduced mNSS, brain water content, expression of LC3, TNF-a, IL-1β, INF-γ and IL-6, positive expression of LC3, as well as expression of LC3 I/II and Beclin-1 but demonstrated an elevated expression of pp-PI3K/t-PI3K, p-Akt/t-Akt, p-mTOR/t-mTOR, ZO-1 and Claudin-5, while opposite trends were observed in the TBI + LY group. The TBI + Dex group exhibited reduced mNSS, brain water content, expression of LC3, TNF-a, IL-1β, INF-γ and IL-6, positive expression of LC3, as well as expression of LC3 I/II and Beclin-1 but demonstrated an elevated expression of pp-PI3K/t-PI3K, p-Akt/t-Akt, p-mTOR/t-mTOR, ZO-1 and Claudin-5, while opposite trends were observed in the TBI + LY group, as compared with the TBI + Dex + LY group. Conclusion The data shows that Dex exerts a neuroprotective effect via the activation of the PI3K/Akt/mTOR signaling pathway in rats with TBI.

// Yong-Jian Wang 1, * , Zi-Feng Zhang 1, * , Shao-Hua Fan 1 , Juan Zhuang 1, 2, 3 , Qun Shan 1 , Xin-Rui Han 1 , Xin Wen 1 , Meng-Qiu Li 1 , Bin Hu 1 , Chun-Hui Sun 1 , Bin Qiao 4 , Qian Tao 4 , Dong-Mei Wu 1 , Jun Lu 1 and Yuan-Lin Zheng 1 1 Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China 2 School of Environment Science and Spatial Informatics, China University of Mining and Technology, Xuzhou 221008, P.R. China 3 Jiangsu Key Laboratory for Eco-Agricultural Biotechnology around Hongze Lake, School of Life Sciences, Huaiyin Normal University, Huaian 223300, P.R. China 4 Department of Oral and Maxillofacial Surgery, Guanghua School and Hospital of Stomatology, Guangdong Provincial Key Laboratory of Oral Diseases, Sun Yat-Sen University, Guangzhou 510055, P.R. China * These authors have contributed equally to this work Correspondence to: Dong-Mei Wu, email: wdm8610@jsnu.edu.cn Jun Lu, email: lu-jun75@163.com Yuan-Lin Zheng, email: ylzheng@jsnu.edu.cn Keywords: oral squamous cell carcinoma; SCC-9 cell; microRNA-433; FAK; ERK Received: March 01, 2017 Accepted: October 05, 2017 Published: October 27, 2017 ABSTRACT We investigated the involvement of microRNA-433 (miR-433) in the proliferation, migration, and invasiveness of oral squamous cell carcinoma (OSCC). Totally 108 OSCC tissues and adjacent normal tissues from patients with OSCC were collected. Also, transplanted tumor formation experiment in nude mice was conducted to verify the effect of miR-433 and FAK on subcutaneous transplanted tumor. The CD44 + stem cell from SCC-9 were collected and assigned into the blank, miR-433 mimics, mimics control, miR-433 inhibitors, inhibitors control, siFAK and miR-433 inhibitors + siFAK groups. The qRT-PCR and western blotting were used to detect miR-433, FAK, ERK, MEK, pERK and pMEK after transfection. Flow cytometry, MTT assay, scratch test and Transwell assay were performed to determine the cell proportion, growth, migration and invasion of SCC-9 cells. In cell line SCC-9, expression of CD133, Oct-4, and BIM-1 was greater in CD44 + cells than CD44 - cells, indicating that CD44 + cells had characteristics of tumor stem cells. Expression of FAK, ERK, MEK, p-ERK and p-MEK was decreased in tumor tissues from the CD44 - , miR-433, and siFAK groups. Expression of MiR-433 mRNA was elevated, while levels of FAK, ERK, MEK, p-ERK, and p-MEK mRNA were all decreased in the miR-433 mimics group. In the miR-433 mimics and siFAK groups, cell proliferation, migration, and invasion were all decreased, while the opposite trends were seen in the miR-433 inhibitor group. These results indicate that miR-433 downregulates FAK through the ERK/MAPK signaling pathway to inhibit the proliferation, migration, and invasiveness of SCC-9 OSCC cells.