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This study investigates the effect of extended laminectomy (EL) on spinal cord injury (SCI) caused by spinal shortening, and further, the timing and the optimal length of removal. Dogs received spinal column shortening at T13 segment, following which the control group underwent regular laminectomy while other groups underwent laminectomy with an additional 1-lamina length removed 6h after shortening ("1-lamina EL 6 h"), an extra 1.5-lamina length resected at 6 h or 12 h after shortening ("1.5-lamina EL 6 h" and "1.5-lamina EL 12 h"), and an extra 2-lamina length removed at 6 or 12 h after shortening ("2-lamina EL 6 h" and 2-lamina EL 12 h"), respectively. Somatosensory evoked potential (SSEP) and neurological function were recorded periodically; spinal cord blood flow (SCBF) and nerve cell apoptosis were detected. The results showed that resection of an additional 1-lamina length appeared inadequate to relieve the sharp kinking of the spinal cord, whereas the kinking disappeared with an additional 2-lamina length resection. The "1-lamina EL 6 h" and "1.5-lamina EL 12 h" groups showed no significant differences from the control in latency of SSEP, SCBF, hindlimb function and apoptosis. By contrast, significant recovery of SSEP, SCBF and hindlimb function as well as reduction of apoptosis were presented in other three groups. The "2-lamina EL 6 h" group, in particular, showed the most prominent recovery. In conclusion, an additional resection of two laminae at 6 h after shortening showed the best effect in alleviating SCI. Timely and adequately extended laminectomy could be a potential therapeutic strategy for SCI attributable to spinal shortening.

Background: Pulmonary embolism (PE) is extremely rare after shoulder arthroscopy. However, early identification of the situation deserves attention due to its potential risk of causing death. By now, it is still difficult to detect the PE without symptoms and clear sources during the perioperative period. Case presentation: We report here two cases of asymptomatic PE, both happening within 24 h after shoulder arthroscopy, without any detected deep venous thrombosis of extremities. It is suspected the cases were due to the abnormal decrease in partial pressures of oxygen and arterial oxygen saturation, and were confirmed by computed tomography pulmonary angiography. We also discuss the reason why the patients showed no related symptoms when PE occurred and perform a review of PE following shoulder arthroscopy. Conclusions: This report highlights that PE could occur in the early phase after shoulder arthroscopy. An unexplained decrease in partial pressure of oxygen or arterial oxygen saturation should be considered seriously. The symptoms of PE might be masked due to patients’ tolerance to hypoxia., Pulmonary embolism (PE) could occur in the early phase after shoulder arthroscopy. An unexplained decrease in partial pressure of oxygen or arterial oxygen saturation should be considered seriously. The symptoms of PE might be masked due to patients’ tolerance to hypoxia.

RNAs are closely associated with human diseases; however, immune-related genes (IRGs) and their potential regulatory networks in relation to spinal cord injury (SCI) are still poorly understood. Here, we investigated the key IRGs as well as the competing endogenous RNA (ceRNA) mechanisms that are associated with SCI pathogenesis based on microarray datasets and the use of a rat SCI model. Specifically, four independent SCI microarray datasets from Gene Expression Omnibus (GEO) database were analyzed and, thereafter, differentially expressed IRGs were annotated via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Furthermore, based on the GEO datasets, differentially expressed RNAs (DERNAs), including DEcircRNAs, DEmiRNAs, and DEmRNAs were identified and interactions between them were also predicted using online databases, and to construct a circular RNA (circRNA) mediated ceRNA network, candidate RNAs were also identified. Furthermore, the support vector machine (SVM) and least absolute shrinkage and selection operator (LASSO) methods were used for the identification of critical DERNAs, while differential gene expression was validated using the GSE20907 dataset. Our results were as follows. In the SCI microarray datasets, 32, 58, and 74 DEIRGs, DEcircRNAs, and DEmiRNAs were identified, respectively. In addition, GO and KEGG analyses showed that the DEIRGs were primarily enriched in neutrophil-mediated immunity and nuclear factor-kappa B (NF-κB) and hypoxia-inducible factor-1 (HIF-1) signaling pathways, and based on LASSO and SVM screening, PLXNB2 was identified as a DEIRG, while hsa_circ_0026646 was identified as the key circRNA, showing a higher SCI expression. Furthermore, our results proved that PLXNB2 and hsa_circ_0026646 were upregulated in SCI, whereas miR-331-3p was downregulated, and, interestingly, similar expression profiles were confirmed using the rat SCI model. Furthermore, fluorescent reporter assay indicated that both hsa_circ_0026646 and PLXNB2 have miR-331-3p target sites, and the ceRNA hypothesis suggested the dysregulation of hsa_circ_0026646, miR-331-3p, and PLXNB2 in SCI. Thus, our results suggested that in SCI pathogenesis, hsa_circ_0026646 correlates with PLXNB2 by targeting miR-331-3p.

Ribosomal protein L38 (RPL38) was found upregulated in osteoarthritic peripheral blood mononuclear cells, however, its role in progression of osteoarthritis has not been characterized.The protein levels of RPL38 and SOCS2 in cartilage tissues from OA patients and controls were detected with Western blotting. IL-1β was used to stimulate primary chondrocytes to establish an OA cell model, and RPL38 siRNA (si-RPL38) was transfected into chondrocytes to investigate the effect of RPL38 knockdown on cell viability, apoptosis, inflammatory factor secretion and extracellular matrix degradation. Then, the mechanism that RPL38 regulate the SOCS2 expression and SOCS2-induced chondrocyte dysfunction was explored. The methyltransferase-like 3 (METTL3)-mediated m6A modification of SOCS2 mRNA was confirmed, and the interaction of RPL38 and METTL3 was verified. Moreover, the effects of SOCS2 overexpression on IL-1β-induced chondrocyte dysfunction and SOCS2 knockdown on the restoration of chondrocyte function by siRPL38 were investigated. Finally, RPL38 was knocked down in vivo and its role in OA progression was validated.RPL38 was upregulated and SOCS2 was downregulated in OA cartilages. RPL38 knockdown or SOCS2 overexpression either attenuated IL-1β-induced chondrocyte apoptosis, inflammatory cytokine secretion, and ECM degradation. RPL38 directly interacted with METTL3 and it inhibited SOCS2 expression through METTL3-mediated m6A modification. SOCS2 knockdown activated the JAK2/STAT3 proinflammatory pathway and reversed the effects of RPL38 knockdown on IL-1β-induced chondrocyte apoptosis, inflammation and ECM degradation. RPL38 knockdown alleviated cartilage tissue damage and ECM degradation in OA mice.RPL38 knockdown inhibited osteoarthritic chondrocyte dysfunction and alleviated OA progression through promoting METTL3-m6A-mediated SOCS2 expression.

Objective. Methane saline (MS) can be used to treat many diseases via its anti-inflammatory, antiapoptotic, and antioxidative activities. However, to date, there is no published evidence as to whether MS has any effect on traumatic brain injury (TBI). The Wnt signalling pathway regulates cell proliferation, differentiation, migration, and apoptosis; however, whether the Wnt signalling pathway regulates any effect of MS on TBI is unknown. This study was designed to explore the role of MS in the treatment of TBI and whether the Wnt pathway is involved. Methods. Sprague-Dawley rats were randomly divided into five groups: sham, TBI, TBI+10 ml/kg MS, TBI+20 ml/kg MS, and TBI+30 ml/kg MS. After induction of TBI, MS was injected intraperitoneally once daily for seven consecutive days. Neurological function was evaluated by the Neurological Severity Score (NSS) at 1, 7, and 14 days after TBI. Haematoxylin-eosin (HE) staining, inflammatory factors, neuron-specific enolase (NSE) staining, oxidative stress, and cell apoptosis were measured and compared 14 d after TBI to identify the optimal dose of MS and to investigate the effect of MS on TBI. In the second experiment, Sprague-Dawley rats were randomly divided into four groups: sham, TBI, TBI+20 ml/kg MS, and TBI+20 ml/kg MS+Dickkopf-1 (DKK-1, a specific inhibitor of the Wnt pathway). NSE, caspase-3, superoxide dismutase (SOD), Wnt3a, and β-catenin were detected by real-time PCR and Western blotting. The results from each group were compared 14 d after TBI to determine the regulatory role of the Wnt pathway. Results. Methane saline significantly inhibited inflammation, oxidative stress, and cell apoptosis, thus protecting neurons within 14 days of TBI. The best treatment effect against TBI was obtained with 20 ml/kg MS. When the Wnt pathway was inhibited, the treatment effect of MS was impaired. Conclusion. Methane saline ameliorates TBI through its anti-inflammatory, antiapoptotic, and antioxidative effects via activation of the Wnt signalling pathway, which plays a part but is not the only mechanism underlying the effects of MS. Thus, MS may be a novel strategy for treating TBI.

Objectives: Spinal cord injury (SCI) is an acute traumatic lesion of neurons in the spinal cord which has a high prevalence in the world, and has no effective surgical treatment. HSP70 is a molecular chaperone protein, serves a protective role in several different models of nervous system injury. The aim of the present study was to investigate the anti-inflammatory role of HSP70 in spinal cord injury and explore its mechanism. Methods: In vivo and in vitro models were constructed to mimic SCI. The Basso Mouse Scale (BMS) was applied to assess SCI degrees of the mouse model. Immunofluorescence (IF) was used for visualizing HSP70 and Iba1 in the spinal cord. Western blot assay was employed to quantify HSP70 and p65, and ELISA was for IL-1β and TNF-α. Results: The results showed that HSP70 expression decreased after SCI. HSP70 and Iba1 showed a decrease of co-localization in SCI mice. Further studies revealed that p65 was upregulated during the process of SCI. Overexpression of HSP70 inhibited the expression of p65 both in vitro and in vivo, and promoted the recovery of SCI mice. Conclusions: HSP70 was involved in the pathological process of spinal cord injury, HSP70 alleviated the spinal cord injury via inhibiting NF-κB signaling pathway.

In this paper, a nesting cell-based smoothed radial point interpolation method with two-level smoothed strains (CS-RPIM-N) is presented for static, free and forced vibration analysis of solids. In the present method, displacement fields are constructed using the radial basis function augmented by polynomial. To improve the accuracy of the CS-RPIM, two-level sub-domains based on the triangular background integration cells are designed and used to construct the two-level smoothed strains. Each two-level sub-domains includes the triangular background cell itself and four equal-area triangular sub-cells. The discretized system equations are constructed by the Generalized smoothed Galerkin (GS-Garlerkin) weak form and Richardson extrapolation method. The accuracy, efficiency and stability of the present method are assessed by virtue of several numerical examples for the problems involving static, free and forced vibration analysis of solids. The numerical results reveal that the CS-RPIM-N stands out and achieves better performance compared to other existing approaches in the literature.

Introduction Rare-earth nanoparticles in the environment and human body pose a potential threat to human health. Although toxic effects of rare-earth nanoparticles have been extensively studied, the effects on the early development are not well understood. In this study, we attempted to explain the toxic effects of neodymium oxide (Nd2O3) nanoparticles on early development. Methods We added the Nd2O3 nanoparticles at different concentrations and recorded the mortality and malformation rate per 24 hrs under a microscope. The live embryos treated with Nd2O3 nanoparticles were imaged as movies and Z step lapses with a confocal microscope, and heart rates were counted for 30 s to measure the cardiac function. The live Tg (Flk1:EGFP) transgenic embryos exposed to Nd2O3 nanoparticles were observed under confocal microscope to measure the cerebrovascular development. Subsequently, we extracted the total protein for Western blot at 5 days post-fertilisation (dpf). Embryos were collected to undergo TUNEL staining for apoptosis detection. Results Nd2O3 nanoparticles disturbed embryo development at high concentrations (>200 μg/mL). The mortality and malformation rate gradually increased in a dose-dependent manner by morphological observation, while the Nd2O3 median lethal concentration (LD50) was 203.4 μg/mL at 120 hrs post-fertilisation (hpf). Furthermore, the Nd2O3-treated embryos showed severe arrhythmia and reduced heart rate. We also observed the markedly cerebrovascular disappearance at middle concentration (100 and 200 μg/mL). The downregulated autophagy flux in brain blood vessels and increased apoptosis level in neurons might affect vessels sprouting and contribute to the vanished cerebrovascular. Conclusion The results suggested that the embryos exposed to Nd2O3 activated the apoptosis pathway and induced toxicity and abnormal cardiac/cerebrovascular development.

Cerium oxide (CeO2), one of many engineered nanomaterials (ENMs), is composed primarily of metal oxides, such as cerium oxide (CeO2). CeO2-containing materials are widely used as a polishing agent for glass mirrors, plate glass, television tubes, ophthalmic lenses, and precision optics. The widespread use of this nanomaterial (NM) resulted in increased environmental contamination levels and consequent human exposure. However, the influence of Ce on humans remains to be determined. The aim of this study was to expose female ICR mice to varying nanoparticle sizes of 35 nm, 300 nm as well as a mixture of 1-5 µM CeO2 particles through intranasal (i.n.) instillation at 40 mg/kg dose on day 1, 3 and 5, and the experiment terminated on day 7. Histopathology findings demonstrated that hydropic degeneration was prominently associated with hemorrhage in renal cortex and medulla in all CeO2-administered groups. In liver of CeO2-exposed mice, hydropic degeneration was also prominent. Serum chemistries also indicated signs of renal and hepatic lesion as evidenced by significantly decreased serum levels of total bilirubin (TBIL) and total phosphate (TP) and activity of alkaline phosphatase (ALP). ICP-MS analysis group demonstrated that Ce levels were not significantly higher in liver and kidneys of mice exposed to 35 nm CeO2. An increase in Ce content was observed in hepatic and renal tissues of mice exposed to 300 nm or 1-5 µM CeO2. The levels of Ce were similar in these two groups suggesting a threshold level of Ce was attained regardless of NP size. Data thus demonstrated that i.n. instillation of different-sized CeO2 particles translocated to liver and kidney and that size difference of CeO2 particles did not exert significant in the observed histopathology responses.

Objective: To discuss the clinical study on Fengshi Qutong capsules combined with diclofenac sodium in the treatment of ankylosing spondylitis. Methods: 80 patients who were treated for ankylosing spondylitis from June 2019 to June 2020 were selected and divided into two groups. The experimental group was treated with Fengshi Qutong capsules combined with diclofenac sodium, and the control group was treated with sulfasalazine enteric-coated tablets. Results: The treatment efficacy, VAS score, BASDAI score, BASFI score, CRP level, TNF-? level, IL-I? level, and the incidence of adverse reactions between the two groups were significantly different (P

Although substantial progress has been made in early detection and treatment of GC, this disease remains a major burden worldwide. CircRNAs have potential as prognostic and diagnostic biomarkers in tumorigenesis. Therefore, we aimed to clarify the role and mechanism of circACC1 in GC cell proliferation. The expression levels of circACC1, miR-29c-3p and FOXP1 were validated in GC tissue samples and adjacent tissue samples. The impact of circACC1 and miR-29c-3p on overall survival was evaluated in GC specimens. A functional study was performed on MKN-45 and BGC823 cells transfected with different vectors. Cell proliferation was assayed by CCK-8 and colony formation assays. The interactions among circACC1, miR-29c-3p and FOXP1 were tested by RNA immunoprecipitation and luciferase reporter assays. This study demonstrated that circACC1 is upregulated in GC tissues, and its upregulation predicts poorer OS in GC patients. Upregulation of circACC1 promoted GC cell proliferation, as indicated by CCK-8 and colony formation assays. A mechanistic study revealed that the pro-oncogenic effect of circACC1 was mainly caused by binding to miR-29c-3p, thus regulating expression of its downstream target FOXP1. The circACC1/miR-29c-3p/FOXP1 network plays a key role in gastric cancer by regulating cell proliferation.

A growing number of individuals are now exposed to neodymium (Nd) owing to its extensive applications. However, the biological effects of Nd on humans, especially on learning and memory, remain elusive. To investigate whether Nd exposure affects learning and memory, in this study female ICR mice were exposed to nano Nd2 O3 via intranasal instillation at doses of 50, 100, and 150 mg/kg body weight, daily for 45 days. According to Morris water maze data, learning and memory parameters were significantly reduced in the 150 mg/kg nano-Nd2 O3 group than the sham control. Furthermore, inductively coupled plasma-mass spectroscopy analysis revealed that Nd levels were significantly higher in the hippo campus of the 100 and 150 mg/kg exposed group than the sham control; however, no significant differences were observed in the hippocampal histopathology between these groups. Furthermore, reactive oxygen species were elevated in hippocampal tissues of experimental groups than the sham control, 447.3 in high dose group and 360.0 in control group; however, malondialdehyde levels were significantly increased and superoxide dismutase activities were decreased only in mice exposed to 100 and 150 mg/kg Nd2 O3 . High-performance liquid chromatography data demonstrated that levels of glutamic acid, glycine, and gamma-aminobutyric acid were higher in the hippocampus of mice exposed to 150 mg/kg Nd2 O3 than the sham control. Our findings indicated that the neuronal injury was induced by disruption of the oxidation-antioxidation homeostasis and altered amino acid neurotransmitter levels in the hippocampus, which could result in the poor cognitive performance demonstrated by exposed mice.

The estimated number of new cases of colorectal cancer (CRC) will increase to 140 250 in 2018 worldwide. The long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has recently been shown to be dysregulated in CRC, which plays an important role in the progression of CRC. However, the biological role and the underling mechanism of UCA1 in the carcinogenesis of CRC remain unclear. Herein, we found that UCA1 was aberrantly upregulated in two CRC cell lines (SW620 and HT29) compared to colorectal cell CCD-18Co. UCA1 knockdown inhibited the apoptosis, growth and autophagy of CRC cell lines in vitro. Furthermore, UCA1 could act as an endogenous sponge by directly interacting with miR-185-5p and downregulation miR-185-5p expression. In addition, UCA1 could reverse the inhibitory effect of miR-185-5p on the growth and autophagy of CRC cells, which might be involved in the derepression of member 1 (WNT1)-inducible signaling pathway protein 2 (WISP2, a target gene of miR-185-5p) expression and the activation of the WISP2/β-catenin signaling pathway. In vivo, the present study elucidates a novel UCA1-miR-185-5p-WISP2-Wnt/β-catenin axis in CRC, which may help us to understand the pathogenesis and the feasibility of lncRNA-directed diagnosis and therapy of CRC.

Primary brainstem haemorrhage (PBH) is characterized by acute onset, rapid deterioration, many complications, and poor prognosis. Its treatment has been controversial. This study aimed to explore the clinical risk factors of postoperative survival and neurological function recovery of stereotactic aspiration in the treatment of PBH. The clinical data of 65 patients with severe brainstem haemorrhage from February 2019 to February 2020 in the First Hospital of Hebei Medical University were reviewed. All patients were treated with stereotactic haematoma aspiration. We determined the survival status of patients at 30 days after the operation and the recovery of neurological function at 90 days. The modified Rankin Scale score (mRS) was used to assess the survival status. The 30-day mortality rate was 23.1% (15 patients). The proportion of patients with good neurological recovery at 90 days after the operation was 32.3% (21 patients). According to the multivariate logistic regression analysis, the haematoma classification was an independent risk factor for postoperative survival (OR = 0.197, 95% CI: 0.016–0.385, p = 0.046) and recovery of neurological function 90 days after surgery (OR = 0.019, 95% CI: 0.001–0.267, p = 0.003). The haematoma classification is an independent risk factor for 30-day mortality and recovery of neurological function 90 days after surgery. Massive and basal-tegmental haematomas were associated with higher mortality. The prognosis of patients with unilateral and bilateral tegmental haematoma was better than that of patients with other haematoma types.

Introduction Spinal cord impact is a mature method for building models of spinal cord injury (SCI). However, a common problem is that the degree of elicited paralysis may not be identical even though animals receive the same impact. We hypothesize that this difference may be caused by the difference in the secondary injury mechanism of SCI and there might be an impact dosage named “median paralyzing dose (PD50)”, similar as the “median lethal dose (LD50)” in pharmacology. In addition, since SCI is a result of multiple mechanisms, we hypothesize that it is more suitable to employ multiple regression analysis to analyze the related factors for complete paraplegia. So the present study aimed to calculate the existence of PD50 and analyze the related factors of SCI-induced complete paralysis using logistic regression under the PD50 which represents identical primary injury. Material and methods Rat models of SCI were built using the weight-drop method under PD50. PD50 was calculated by Karber’s method. Rats were allocated into two groups according to whether they developed complete or incomplete paralysis 2 weeks after injury. Cavity and spared tissues in the two groups were compared. Neuronal preservation, microglia/macrophage reaction, T-lymphocyte infiltration, astrocyte activation and neuronal apoptotic were compared by immunohistochemistry. The logistic regression model was constructed and significant related factors of complete paralysis were selected. Results Of the two groups, the cavity in the injured spinal cord of the complete-paralysis rats was significantly larger and the spared white matter volume (SWMV%) was obviously smaller. Whereas, the spared grey matter volume was not different between groups. Macrophage reaction, T-lymphocyte infiltration and neuronal apoptosis were significantly more severe in the complete-paralysis rats. Astrocyte activation and neuronal preservation showed no difference between groups. Logistic regression analysis showed that cavity volume, SWMV%, microglia/macrophage reaction and neuronal apoptosis were significantly correlated with SCI-induced complete paralysis. Conclusion As a non-mainstream method, it is feasible to analyze the secondary factors of SCI-induced complete paralysis using multiple regression analysis in the condition of identical primary injury (PD50). SWMV% and microglia/macrophage reaction are important factors that contribute to complete paralysis at the early phase of severe SCI.

Cerium oxide (CeO

In this study, we investigated the expression, correlation to clinical outcomes and biological functions of microRNA-15a-3p (miR-15a-3p) in human osteosarcoma. MiR-15a-3p expressions in osteosarcoma cell lines and clinical tissues of osteosarcoma patients were measured by qPCR. Relevance of endogenous miR-15a-3p to osteosarcoma patients' clinicopathological factors or overall survival was statistically analyzed. In addition, the independence of miR-15a-3p predicting cancer patients' overall survival was analyzed by Cox regression method. Furthermore, in osteosarcoma cell lines, Saos-2 and HOS cells, miR-15a-3p was overexpressed through stable lentiviral transduction. The functional regulations of miR-15a-3p overexpression on cancer ell proliferation and migration were then analyzed. MiR-15a-3p was significantly downregulated in osteosarcoma cell lines and human osteosarcoma tumors. Downregulation of endogenous miR-15a-3p in osteosarcoma tumors was significantly associated with cancer patient's poor clinical outcomes and low survival rate. Also, endogenous miR-15a-3p was confirmed to be an independent biomarker for predicating cancer patients' survival. In Saos-2 and HOS cells, lentivirus-induced miR-15a-3p overexpression had significantly tumor suppressing functions, by inhibiting both proliferation and migration. Significant downregulation of miR-15a-3p in osteosarcoma may be an independent biomarker to predicting cancer patients' poor prognosis. Overexpression miR-15a-3p may be an efficient functional meaning to suppress osteosarcoma development.

Introduction Rare-earth nanoparticles in the environment and human body pose a potential threat to human health. Although toxic effects of rare-earth nanoparticles have been extensively studied, the effects on the early development are not well understood. In this study, we attempted to explain the toxic effects of neodymium oxide (Nd2O3) nanoparticles on early development. Methods We added the Nd2O3 nanoparticles at different concentrations and recorded the mortality and malformation rate per 24 hrs under a microscope. The live embryos treated with Nd2O3 nanoparticles were imaged as movies and Z step lapses with a confocal microscope, and heart rates were counted for 30 s to measure the cardiac function. The live Tg (Flk1:EGFP) transgenic embryos exposed to Nd2O3 nanoparticles were observed under confocal microscope to measure the cerebrovascular development. Subsequently, we extracted the total protein for Western blot at 5 days post-fertilisation (dpf). Embryos were collected to undergo TUNEL staining for apoptosis detection. Results Nd2O3 nanoparticles disturbed embryo development at high concentrations (>200 μg/mL). The mortality and malformation rate gradually increased in a dose-dependent manner by morphological observation, while the Nd2O3 median lethal concentration (LD50) was 203.4 μg/mL at 120 hrs post-fertilisation (hpf). Furthermore, the Nd2O3-treated embryos showed severe arrhythmia and reduced heart rate. We also observed the markedly cerebrovascular disappearance at middle concentration (100 and 200 μg/mL). The downregulated autophagy flux in brain blood vessels and increased apoptosis level in neurons might affect vessels sprouting and contribute to the vanished cerebrovascular. Conclusion The results suggested that the embryos exposed to Nd2O3 activated the apoptosis pathway and induced toxicity and abnormal cardiac/cerebrovascular development.

The estimated number of new cases of colorectal cancer (CRC) will increase to 140 250 in 2018 worldwide. The long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has recently been shown to be dysregulated in CRC, which plays an important role in the progression of CRC. However, the biological role and the underling mechanism of UCA1 in the carcinogenesis of CRC remain unclear. Herein, we found that UCA1 was aberrantly upregulated in two CRC cell lines (SW620 and HT29) compared to colorectal cell CCD-18Co. UCA1 knockdown inhibited the apoptosis, growth and autophagy of CRC cell lines

To reveal the controlling mechanism of urban polluted river,four trophic level urban river was studied. The change of distribution of organic matter and nitrogen in the sediment was studied while the organic matter was disposed. High level of organic matter is the significant feature of urban city rivers. the humin (HM) was the major fraction of humus, accounting for more than 65% of OM. The most proportion of the total nitrogen (TN) was organic nitrogen which accounted for more than 50%. The amount of organic matter removal increased after the sediment adsorbed the saturated ammonia, which suggested ammonia as the main limited factor for the decomposition of organic matter. The most of Ammonia was adsorbed onto unstable humins. The HM was more stable than other organic matter which was disposed by Hydrogen peroxide (H

AISI 304L austenite stainless steel was irradiated by a high-current pulsed electron beam (HCPEB) source in different process. The microstructures were investigated in detail by electron microscopy. The relationship between corrosion resistance and the microstructures has been established. Our experimental results suggest that much abundant defect structures were formed within the irradiated surface which promoted the formation of a compact and thick passive layer during the process of corrosion experiment in simulated sea water. This passive layer effectively prevented corrosive anionic species from passing through the surface oxidation layer and delayed the corrosion process, leading to the improvement of irradiated materials’ corrosion performance. However, the craters on the treated surfaces may be turn into new active points on the metal surface which favored local pitting. Our experimental results demonstrate the potential of proper HCPEB processing for improving the corrosion resistance of metallic materials.