lncRNA USP30-AS1 sponges miR-765 and modulates the progression of colon cancer.

BACKGROUND: The incidence and mortality of colon cancer is increasing recently. It is necessary to identify effective biomarkers for the progression and prognosis of colon cancer. To assess the potential of lncRNA USP30-AS1 (USP30-AS1) in serving as the biomarker of colon cancer and unearth the underlying mechanism. METHODS: There were 123 colon cancer patients enrolled. The expression of USP30-AS1 was evaluated with PCR in tissue and cell samples. The clinical significance of USP30-AS1 was assessed with a series of statistical methods, while the CCK8 and Transwell assay were conducted to estimate its biological effect on the colon cancer cellular processes. In mechanism, the interaction of USP30-AS1 with miR-765 was evaluated with the dual-luciferase reporter assay. RESULTS: In colon cancer tissues, the USP30-AS1 downregulation and the miR-765 upregulation were observed, and there was a negative correlation between the USP30-AS1 expression level and the miR-765 expression level. The downregulation of USP30-AS1 related to the malignant progression and served as an adverse prognostic indicator of colon cancer. The overexpression of USP30-AS1 dramatically suppressed colon cancer cellular processes, which was alleviated by miR-765. CONCLUSIONS: USP30-AS1 predicts the malignancy and prognosis of colon cancer patients. USP30-AS1 suppressed the progression of colon cancer through modulating miR-765.

Connexin-based channels contribute to metabolic pathways in the oligodendroglial lineage.

Oligodendrocyte precursor cells (OPCs) undergo a series of energy-consuming developmental events; however, the uptake and trafficking pathways for their energy metabolites remain unknown. In the present study, we found that 2-NBDG, a fluorescent glucose analog, can be delivered between astrocytes and oligodendrocytes through connexin-based gap junction channels but cannot be transferred between astrocytes and OPCs. Instead, connexin hemichannel-mediated glucose uptake supports OPC proliferation, and ethidium bromide uptake or increase of 2-NBDG uptake rate is correlated with intracellular Ca(2+) elevation in OPCs, indicating a Ca(2+)-dependent activation of connexin hemichannels. Interestingly, deletion of connexin 43 (Cx43, also known as GJA1) in astrocytes inhibits OPC proliferation by decreasing matrix glucose levels without impacting on OPC hemichannel properties, a process that also occurs in corpus callosum from acute brain slices. Thus, dual functions of connexin-based channels contribute to glucose supply in oligodendroglial lineage, which might pave a new way for energy-metabolism-directed oligodendroglial-targeted therapies.

Catalpol Inhibits Ischemia-Induced Premyelinating Oligodendrocyte Damage through Regulation of Intercellular Calcium Homeostasis via Na⁺/Ca2+ Exchanger 3.

The heightened vulnerability of premyelinating oligodendrocytes (PreOLs) in response to hypoxia⁻ischemia may contribute to perinatal white matter injury and subsequent neurobehavioral dysfunction. Intracellular Ca2+ overload is considered a crucial mechanism predisposing PreOLs to ischemic injury. We previously reported that catalpol, an iridoid glycoside extracted from Rehmannia root, inhibits intracellular Ca2+ overload of PreOLs in an in vitro ischemia model. However, the exact underlying mechanisms remain elusive. In the present study, we aimed to investigate the protective effects of catalpol on PreOLs and to explore the underlying mechanisms involved in the modulation of intracellular Ca2+ homeostasis. Postnatal day 2 (P2) Sprague-Dawley (SD) rats subjected to bilateral common carotid artery ligation followed by exposure to 8% oxygen for 10 min were used as a rat model of neonatal hypoxia⁻ischemia. We found that catalpol significantly improved behavioral functions and prevented PreOL loss and myelination deficit after hypoxia⁻ischemia. Our in vitro studies also confirmed the direct effects of catalpol on oxygen-glucose deprivation (OGD)-induced cell death and arrested maturation of PreOLs. Moreover, we demonstrated that catalpol significantly inhibited intracellular Ca2+ overload and promoted the expression of Na⁺/Ca2+ exchanger 3 (NCX3). Finally, we found that catalpol significantly reduced mitochondrial damage and subsequent extracellular signal-regulated kinase 1/2 (ERK1/2) and poly-ADP-ribose polymerase-1 (PARP-1) activation. Treatment with NCX3-preferring inhibitor 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea (KB-R7943) significantly reversed the protective effects of catalpol on PreOLs under OGD. Overall, our data suggest that catalpol protects PreOLs from ischemic injury through regulation of intercellular Ca2+ homeostasis via upregulation of NCX3 activity.

Modified task-based learning program promotes problem-solving capacity among Chinese medical postgraduates: a mixed quantitative survey.

BACKGROUND: Despite great advances, China's postgraduate education faces many problems, for example traditional lecture-based learning (LBL) method provides fewer oppotunities to apply knowledge in a working situation. Task-based learning (TBL) is an efficient strategy for increasing the connections among skills, knowledge and competences. This study aimed to evaluate the effect of a modified TBL model on problem-solving abilities among postgraduate medical students in China. METHODS: We allocated 228 first-year postgraduate students at Third Military Medical University into two groups: the TBL group and LBL group. The TBL group was taught using a TBL program for immunohistochemistry. The curriculum consisted of five phases: task design, self-learning, experimental operations, discussion and summary. The LBL group was taught using traditional LBL. After the course, learning performance was assessed using theoretical and practical tests. The students' preferences and satisfaction of TBL and LBL were also evaluated using questionnaires. RESULTS: There were notable differences in the mean score rates in the practical test (P < 0.05): the number of high scores (>80) in the TBL group was higher than that in the LBL group. We observed no substantial differences in the theoretical test between the two groups (P > 0.05). The questionnaire results indicated that the TBL students were satisfied with teaching content, teaching methods and experiment content. The TBL program was also beneficial for the postgraduates in completing their research projects. Furthermore, the TBL students reported positive effects in terms of innovative thinking, collaboration, and communication. CONCLUSIONS: TBL is a powerful educational strategy for postgraduate education in China. Our modified TBL imparted basic knowledge to the students and also engaged them more effectively in applying knowledge to solve real-world issues. In conclusion, our TBL established a good foundation for the students' future in both medical research and clinical work.

Multifunctional uranyl hybrid materials: structural diversities as a function of pH, luminescence with potential nitrobenzene sensing, and photoelectric behavior as p-type semiconductors.

A series of uranyl-organic frameworks (UOFs), {[(UO2)2(H2TTHA)(H2O)]·4,4'-bipy·2H2O}n (1), {[(UO2)3(TTHA)(H2O)3]}n (2), and {[(UO2)5(TTHA) (HTTHA)(H2O)3]·H3O}n (3), have been obtained by the hydrothermal reaction of uranyl acetate with a flexible hexapodal ligand (1,3,5-triazine-2,4,6-triamine hexaacetic acid, H6TTHA). These compounds exhibited three distinct 3D self-assembly architectures as a function of pH by single-crystal structural analysis, although the used ligand was the same in each reaction. Surprisingly, all of the coordination modes of the H6TTHA ligand in this work are first discovered. Furthermore, the photoluminescent results showed that these compounds displayed high-sensitivity luminescent sensing functions for nitrobenzene. Additionally, the surface photovoltage spectroscopy and electric-field-induced surface photovoltage spectroscopy showed that compounds 1-3 could behave as p-type semiconductors.

Expression of Dbn1 during mouse brain development and neural stem cell differentiation.

Dbn1 is a newly discovered gene in the drebrin gene family of mice. Previous studies have reported that Dbn1 is specifically expressed in the mouse brain suggesting its potential role in brain development. However, a detailed analysis of Dbn1 expression during mouse brain development has not been demonstrated. Here, we describe the expression pattern of Dbn1 and the coexpression of Dbn1 and actin during the development of the mouse brain from embryonic day 14 (E14) to adulthood and during the differentiation of neural stem cells (NSCs), as determined using immunohistochemistry, double-labeling immunofluorescence, and quantitative real-time polymerase chain reaction. During mouse brain development, Dbn1 expression level was high at E14, attenuated postnatally, reached its highest point at postnatal day 7 (P7), and showed a very low level at adulthood. Imaging data showed that Dbn1 was mainly expressed in the hippocampus, ventricular zone, and cortex, where NSCs are densely distributed, and that the intracellular distribution of Dbn1 was predominantly located in the cytoplasm edges and neurites. Moreover, the signal for colocalization of Dbn1 with actin was intense at E14, P0, and P7, but it was weak at adulthood. During NSC differentiation, Dbn1 mRNA expression increased after the onset of differentiation and reached its highest point at 3days, followed by a decrease in expression. The imaging data showed that Dbn1 was increasingly expressed in the extending neurites in accordance with the cell morphological changes that occur during differentiation. Furthermore, obvious colocalization signals of Dbn1 with actin were found in the neurites and dendritic spines. Collectively, these results suggest that Dbn1 may play a key role in mouse brain development and may regulate NSC differentiation by filamentous actin.

Virtual microscopy system at Chinese medical university: an assisted teaching platform for promoting active learning and problem-solving skills.

BACKGROUND: Chinese medical universities typically have a high number of students, a shortage of teachers and limited equipment, and as such histology courses have been taught using traditional lecture-based formats, with textbooks and conventional microscopy. This method, however, has reduced creativity and problem-solving skills training in the curriculum. The virtual microscope (VM) system has been shown to be an effective and efficient educational strategy. The present study aims to describe a VM system for undergraduates and to evaluate the effects of promoting active learning and problem-solving skills. METHODS: Two hundred and twenty-nine second-year undergraduate students in the Third Military Medical University were divided into two groups. The VM group contained 115 students and was taught using the VM system. The light microscope (LM) group consisted of 114 students and was taught using the LM system. Post-teaching performances were assessed by multiple-choice questions, short essay questions, case analysis questions and the identification of structure of tissue. Students' teaching preferences and satisfaction were assessed using questionnaires. RESULTS: Test scores in the VM group showed a significant improvement compared with those in the LM group (p < 0.05). There were no substantial differences between the two groups in the mean score rate of multiple-choice questions and the short essay category (p > 0.05); however, there were notable differences in the mean score rate of case analysis questions and identification of structure of tissue (p < 0.05). The questionnaire results indicate that the VM system improves students' productivity and promotes learning efficiency. Furthermore, students reported other positive effects of the VM system in terms of additional learning resources, critical thinking, ease of communication and confidence. CONCLUSIONS: The VM system is an effective tool at Chinese medical university to promote undergraduates' active learning and problem-solving skills as an assisted teaching platform.

The Interactions between Ionic Liquids and Lithium Polysulfides in Lithium-Sulfur Batteries: A Systematic Density Functional Theory Study.

Ionic liquids (ILs) based on hybrid anions have recently garnered attention as beguiling alternative electrolytes for energy storage devices. This attention stems from the potential of these asymmetric anions to reduce the melting point of ILs and impede the crystallization of ILs. Furthermore, they uphold the advantages associated with their more conventional symmetric counterparts. In this study, we employed dispersion-corrected density functional theory (DFT-D) calculations to scrutinize the interplay between two hybrid anions found in ionic liquids [FTFSA]- and [MCTFSA]- and the [C4mpyr]+ cation, as well as in lithium polysulfides in lithium-sulfur batteries. For comparison, we also examined the corresponding ILs containing symmetric anions, [TFSA]- and [FSA]-. We found that the hybrid anion [MCTFSA]- and its ionic liquid exhibited exceptional stability and interaction strength. Additionally, our investigation unveiled a remarkably consistent interaction between ionic liquids (ILs) and anions with lithium polysulfides (and S8) during the transition from octathiocane (S8) to the liquid long-chain Li2Sn (4 ≤ n ≤ 8). This contrasts with the gradual alignment observed between cations and lithium polysulfides during the intermediate state from Li2S4 to the solid short-chain Li2S2 and Li2S1. We thoroughly analyzed the interaction mechanism of ionic liquids composed of different symmetry anions and their interactions with lithium polysulfides.

BNIP3 mediates pre-myelinating oligodendrocyte cell death in hypoxia and ischemia.

Developing oligodendrocytes, collectively termed 'pre-myelinating oligodendrocytes' (preOLs), are vulnerable to hypoxic or ischemic insults. The underlying mechanism of this vulnerability remains unclear. Previously, we showed that Bcl-2/E1B-19K-interacting protein 3 (BNIP3), a proapoptotic member of the Bcl-2 family proteins, induced neuronal death in a caspase-independent manner in stroke. In this study, we investigated the role of BNIP3 in preOL cell death induced by hypoxia or ischemia. In primary oligodendrocyte progenitor cell (OPC) cultures exposed to oxygen-glucose deprivation, we found that BNIP3 was upregulated and levels of BNIP3 expression correlated with the death of OPCs. Up-regulation of BNIP3 was observed in preOLs in the white matter in a neonatal rat model of stroke. Knockout of BNIP3 significantly reduced death of preOLs in the middle cerebral artery occlusion model in mice. Our results demonstrate a role of BNIP3 in mediating preOLs cell death induced by hypoxia or ischemia, and suggest that BNIP3 may be a new target for protecting oligodendrocytes from death after stroke. Pre-myelinating oligodendrocytes (preOLs) are known to be highly vulnerable to ischemic insults. It remains unclear, however, how preOLs die. This study shows that BNIP3, a proapoptotic member of the Bcl-2 family proteins, is a mediator of hypoxia/ischemia-induced preOLs death. The BNIP3 cell death pathway may therefore be a new target for protecting oligodendrocytes from death after stroke.

[Research progress in sperm mediated gene transfer technology].

With the rapid development of biotechnology, we can change the trait of organism using transgenetic technology. In recent years, there are growing interests in the establishment of sperm mediated gene transfer (SMGT) technology as an effective and convenient method to produce transgenic animals. SMGT technology is a transgenetic method, which is easy in operation and does little harm to the cell compared with the other transgenetic methods. In this review, we expound the background, development, mechanism, operation and application of SMGT.

A bioinformatics framework to identify the biomarkers and potential drugs for the treatment of colorectal cancer.

Colorectal cancer (CRC), a common malignant tumor, is one of the main causes of death in cancer patients in the world. Therefore, it is critical to understand the molecular mechanism of CRC and identify its diagnostic and prognostic biomarkers. The purpose of this study is to reveal the genes involved in the development of CRC and to predict drug candidates that may help treat CRC through bioinformatics analyses. Two independent CRC gene expression datasets including The Cancer Genome Atlas (TCGA) database and GSE104836 were used in this study. Differentially expressed genes (DEGs) were analyzed separately on the two datasets, and intersected for further analyses. 249 drug candidates for CRC were identified according to the intersected DEGs and the Crowd Extracted Expression of Differential Signatures (CREEDS) database. In addition, hub genes were analyzed using Cytoscape according to the DEGs, and survival analysis results showed that one of the hub genes, TIMP1 was related to the prognosis of CRC patients. Thus, we further focused on drugs that could reverse the expression level of TIMP1. Eight potential drugs with documentary evidence and two new drugs that could reverse the expression of TIMP1 were found among the 249 drugs. In conclusion, we successfully identified potential biomarkers for CRC and achieved drug repurposing using bioinformatics methods. Further exploration is needed to understand the molecular mechanisms of these identified genes and drugs/small molecules in the occurrence, development and treatment of CRC.

Cerebral Ischemic Preconditioning Aggravates Death of Oligodendrocytes.

Neurodegeneration can benefit from ischemic preconditioning, a natural adaptive reaction to sublethal noxious stimuli. Although there is growing interest in advancing preconditioning to preserve brain function, preconditioning is not yet considered readily achievable in clinical settings. One of the most challenging issues is that there is no fine line between preconditioning stimuli and lethal stimuli. Here, we show deleterious effect of preconditioning on oligodendrocyte precursor cells (OPCs). We identified Bcl-2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3), a mitochondrial BH3-only protein specifically involved in OPCs loss after preconditioning. Repeated ischemia stabilized BNIP3 and increased the vulnerability of OPCs to subsequent ischemic events. BNIP3 became mitochondrial-bound and was concurrent with the dysfunction of monocarboxylate transporter 1 (MCT1). Inhibition of BNIP3 by RNAi or necrostatin-1 (Nec-1) and knocking out of BNIP3 almost completely prevented OPCs loss and preserved white matter integrity. Together, our results suggest that the unfavorable effect of BNIP3 on OPCs should be noted for safe development of ischemic tolerance. BNIP3 inhibition appears to be a complementary approach to improve the efficacy of preconditioning for ischemic stroke.

Highly efficient downconversion white light in Tm³âº/Tb³âº/Mn²âº tridoped P2O5-Li2O-Sb2O3 glass.

Tm³âº/Tb³âº/Mn²âº tridoped phosphate glasses containing different Mn²âº ion concentrations were synthesized to explore new white-light-emitting material. Under 355 nm excitation, the CIE coordinates (x=0.328, y=0.337) of the Mn0.10 sample doped with 0.10 wt. % Mn²âº are close to the standard equal energy white-light illumination (x=0.333, y=0.333). The quantum efficiency of the Mn0.01 sample is very high (~72.32%). The concentration of Mn²âº ions has a great effect on the emission color, and the energy transitions from Tm³âº, Tb³âº to Mn²âº become more intense with an increase in Mn2+ ion concentrations. The phenomenon is reasonably interpreted based on the analysis of the luminescence lifetime.

Screening genes related to development and injury of the mouse optic nerve by cDNA microarrays.

The aim of this study was to screen genes related to the development and injury of the mouse optic nerve so as to provide possible target genes for gene-engineering therapy of central nervous system (CNS) injury. Gene expression was profiled by cDNA microarrays in the mouse superior colliculus at 8-time points during the development or following injury of the optic nerve; consequently, 1,095 highly expressed genes (ratio > or =2) were identified. Then, these genes were categorized functionally; there were 561 genes (51.19%) with unidentified functions and 534 genes (48.81%) with identified or partially identified functions. After discounting the overlapping genes, 486 genes with identified or partially identified functions were categorized into 17 functional groups. The 17 functional groups were as follows: I transcription regulation, II signal transduction, III protein synthesis, IV materials transporting, V RNA processing, VI metabolism-related genes, VII cell cycle or apoptosis-related genes, VIII extracellular matrix, IX protein folding and degradation, X cytoskeleton, XI histone metabolism, XII nervous system specific functional genes, XIII tumor related genes, XIV DNA replication and repair, XV axon growth and guidance, XVI immune response, and XVII cell adhesion. These genes may play key roles in the development, injury, and repairment of the optic nerve.

Manipulation of Mitophagy by "All-in-One" nanosensitizer augments sonodynamic glioma therapy.

Limited penetration of chemotherapeutic drugs through the blood brain barrier (BBB), and the increased chemo-resistance of glioma cells due to macroautophagy/autophagy, result in high tumor recurrence and extremely limited survival of glioma patients. Ultrasound-targeted microbubble destruction (UTMD) is a technique of transient and reversible BBB disruption, which greatly facilitates intracerebral drug delivery. In addition, sonodynamic therapy (SDT) based on ultrasound stimulation and a sonosensitizer, can be a safe and noninvasive strategy for treating glioma. We innovatively designed a smart "all-in-one" nanosensitizer platform by incorporating the sonoactive chlorin e6 (Ce6) and an autophagy inhibitor-hydroxychloroquine (HCQ) into angiopep-2 peptide-modified liposomes (designated as ACHL), which integrates multiple diagnostic and therapeutic functions. ACHL selectively accumulated in the brain tumors during the optimal time-window of transient UTMD-mediated BBB opening. The nanosensitizer then responded to a second ultrasonic stimulation, and simultaneously unloaded HCQ and generated ROS in the glioma cells. The sonotherapy triggered apoptosis as well as MAPK/p38-PINK1-PRKN-dependent mitophagy, in which the antioxidant relieved the sonotoxicity and MAPK/p38 activation, while the inhibition of MAPK/p38 attenuated the progression toward mitophagy by compromising redistribution of PRKN. Moreover, HCQ blocking autophagosome degradation, augmented intracellular ROS production and resulted in an oxidative-damage regenerative loop. ACHL-SDT treatment using this construct significantly inhibited the xenograft-tumor growth and prolonged the survival time of tumor-bearing mice, exhibiting an improved therapeutic efficiency. All together, we demonstrated a precision sonotherapy with simultaneous apoptosis induction and mitophagy inhibition, which served as an intelligently strategic sense of working alongside, providing new insights into the theranostics of brain tumors. ABBREVIATIONS: ACHL: Angiopep-2-modified liposomes loaded with Ce6 and hydroxychloroquine; ACL: Angiopep-2-modified liposomes loaded with Ce6; BBB: blood brain barrier; Ce6: chlorin e6; CHL: liposomes loaded with Ce6 and hydroxychloroquine; CL: liposomes loaded with Ce6; CNS: central nervous system; DDS: drug delivery system; EB: Evans blue; FUS: focused ultrasound; HCQ: hydroxychloroquine; LRP1: low density lipoprotein receptor-related protein 1; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MBs: microbubbles; MTG: MitoTracker Green; MTR: MitoTracker Red; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; PBS: phosphate-buffered saline; PDI: polydispersity index; PINK1: PTEN induced kinase 1; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; ROS: reactive oxygen species; SDT: sonodynamic therapy; SQSTM1: sequestome 1; TA: terephthalic acid; TEM: transmission electron microscopy; TUNEL: terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling; US: ultrasound; UTMD: ultrasound-targeted microbubble destruction.

Molecular characterization and pathogenicity of infectious bronchitis coronaviruses: complicated evolution and epidemiology in china caused by cocirculation of multiple types of infectious bronchitis coronaviruses.

OBJECTIVE: To monitor and study the molecular epidemiology, evolution and pathogenicity of infectious bronchitis viruses (IBVs) in China in recent years and further our knowledge of the evolution of IBVs. METHODS: Thirty-seven IBV isolates were isolated from commercial chickens in China. The isolates were characterized by RT-PCR, sequencing, typing and analyzing the entire S1 gene. In addition, 4 selected IBV isolates were used to experimentally infect the specific pathogen-free chickens to study their pathogenicity. RESULTS: Three types of IBV have been cocirculating in chicken flocks in China in recent years. Unique insertions and deletions in S1 protein regions were identified among different types of IBV. Moreover, a new IBV strain was isolated and identified in a layer hen. S1 gene analysis showed that a recombination event had occurred in the virus's evolutionary process. In addition, experimental infection has shown that IBV isolates have been nephropathogenic in China in recent years. CONCLUSION: Mutations, insertions, deletions and recombination of the S1 protein gene contribute to the genetic diversity of IBV in China. Cocirculation of multiple types of IBV in field conditions in China renders its epidemiology and evolution very complicated, indicating the necessity for development of new vaccines or vaccine strategies.

Evaluation of the protection conferred by commercial vaccines and attenuated heterologous isolates in China against the CK/CH/LDL/97I strain of infectious bronchitis coronavirus.

Avian infectious bronchitis virus (IBV) causes tremendous economic losses to the poultry industry worldwide. Different serotypes of this virus show little cross-protection. The present study investigated the genotypic relationship between CK/CH/LDL/97I-type strains and reference IBVs based on S1 gene comparisons and the protection provided by vaccination with commercial vaccines and attenuated homologous and heterologous strains. Phylogenetic analysis and the comparison of S1 showed that CK/CH/LDL/97I-type virus might be a new serotype compared to vaccine strains and other types of IBV isolates in China. Protection efficacy was evaluated by morbidity, mortality, and virus re-isolation from the challenged chicks. Complete protection by IBV vaccination was provided by the homologous strain but sufficient respiratory protection was not provided by the commercial vaccines. Heterologous strains against CK/CH/LDL/97I challenge and the development of a vaccine against CK/CH/LDL/97I-type IBV will be necessary to control infectious bronchitis disease in poultry. Further development of the attenuated CK/CH/LDL/97I strain may provide a valuable contribution towards this goal.

MicroRNA-193b acts as a tumor suppressor in colon cancer progression via targeting RAB22A.

To explore microRNA (miR)-193b expression and its potential role in colon cancer, reverse transcription-quantitative polymerase chain reaction was performed to detect the miR-193b expression levels in 62 colon cancer tissues and normal adjacent tissues. The miR-193b-overexpressed cell line SW620 was used to study the role of miR-193b in colon cancer. Subsequently, a Transwell assay and cell cycle assay were performed to observe the functional cell changes in the in vitro expression levels of miR-193b. Results indicated that miR-193b expression levels were significantly decreased in colon cancer tissues compared with adjacent normal tissue (P<0.001) and the expression of miR-193b was significantly correlated with TNM staging (P=0.03) and lymph node invasion (P=0.007). Furthermore, overexpression of miR-193b significantly decreased colon cancer cell cycle progression and its migration ability. In addition, the present findings suggested that the increased expression of miR-193b by RAB22A, inhibited downstream proteins involved in the Ras signaling pathway, including the Ras and extracellular signal-related kinase which may inhibit cancer proliferation and migration. In conclusion, the aim was to clarify the association of miR-193b expression with colon cancer, and to explore the mechanism of miR-193b in colon cancer proliferation and cell migration. The preliminary findings revealed that miR-193b may have an important role in the process in colon cancer cell cycle and migration by the RAB22A-Ras signaling pathway, thus providing a theoretical basis for miR-193b as a potential molecular target for colon cancer treatment.

MicroRNA 214 inhibits adipocyte enhancer-binding protein 1 activity and increases the sensitivity of chemotherapy in colorectal cancer.

The present study aimed to analyze adipocyte enhancer-binding protein 1 (AEBP1) expression in colorectal cancer (CRC), with a focus on its possible molecular mechanisms, in order to provide novel insight into the clinical treatment of CRC. Immunohistochemistry (IHC) was used to detect AEBP1 expression in 62 CRC tissues. Kaplan-Meier survival curves were used to analyze AEBP1 expression and the postoperative disease-free survival (DFS) and overall survival (OS) rates of CRC patients. HT-29 cells were treated with oxaliplatin to detect cell proliferation and apoptosis following a Cell Counting kit-8. Through bioinformatics prediction, microRNA 214 (miR214) was identified as an upstream microRNA of AEBP1 that regulates its expression. IHC revealed that the expression of AEBP1 in CRC tissues was significantly higher than that in adjacent healthy tissues, and that it is associated with Tumor-Node-Metastasis stage, recurrence and metastasis. The DFS and OS rates of patients with a low AEBP1 expression were significantly higher than those in patients with a high expression (P<0.05). Following depletion of AEBP1 and treatment with oxaliplatin, the HT-29 cell proliferation was lower than that of the blank control and the negative control groups. However, the cell apoptosis rate was higher than that of the control group at 72 h (P<0.05). Bioinformatics prediction revealed that miR-214 is negatively associated with AEBP1 expression, and co-transfection and luciferase report gene tests revealed that AEBP1 is a target gene of miR-214. Therefore, AEBP1 may become a novel treatment for CRC patients with chemoresistance and may act through the upstream miR-214 to participate in the progression of a tumor.

Photoluminescence enhancement in Yb(3+):Er(3+)co-doped eutectic Al(2)O(3): SiO(2) thin films by 980nm excitation.

Si nanocrystals (nc-Si) are addressed in the eutectic Al(2)O(3):SiO(2) thin films co-doped with Er(3+) and Yb(3+) by the laser-induced crystallization (LIC). The thin films are originally synthesized on a silica-on-silicon (SOS) substrate by the microwave electron cyclotron resonance (MW-ECR) plasma source enhanced RF sputtering. Raman spectroscopy has revealed that the strong crystallization occurs with the emergence of the nc-Si in the eutectic Al(2)O(3): SiO(2) layer during the liquid phase transformation. The dual wavelength energy transfer mechanism at 800nm and 980nm induced by 980nm excitation in nc-Si and Yb sensitized Er doped system has been proposed and demonstrated. A tenfold photoluminescence enhancement has been obtained from this mechanism.