Abstract Colorectal cancer (CRC) is one of the most prevalent tumors worldwide. Recently, long noncoding RNAs (lncRNAs) have been recognized as key regulators in postgenomic biology. Numerous lncRNAs have been identified as diagnostic biomarkers and therapeutic targets. However, the molecular mechanisms underlying the role of lncRNAs in CRC progression are not fully understood. Differentially expressed lncRNAs and messenger RNAs were investigated using a microarray approach in five paired primary CRC tumor tissues and the corresponding nontumor tissues and confirmed in an additional 116 paired tissues and 21 inflammatory bowel disease tissues and 15 adjacent normal tissues by a quantitative real‐time polymerase chain reaction. We also performed comprehensive transcriptome profiling analysis on Gene Expression Omnibus and The Cancer Genome Atlas datasets. We identified LINC02595 and evaluated its clinical significance as a plasma biomarker. The function of LINC02595 was evaluated using a panel of in vivo and vitro assays, including cell counting kit‐8, colony formation, cell cycle, apoptosis, RNA fluorescence in situ hybridization, luciferase reporter, immunohistochemistry, and CRC xenografts. We found that LINC02595 is upregulated in tumor tissues and blood samples of patients with CRC and CRC cell lines. Functional research found that LINC02595 promotes CRC cell growth, influences the cell cycle, and reduces apoptosis in vitro and vivo. Mechanistically, LINC02595 promoted BCL2‐like 1 (BCL2L1) expression through miR‐203b‐3p sponging. Our research demonstrated that LINC02595 is an oncogene in CRC and established the presence of a LINC02595‐miR‐203b‐BCL2L1 axis in CRC, which might provide a new diagnostic biomarker and therapeutic targets for the treatment of this disease.
According to the WHO (World Health Organization), infectious diseases continue to one of the leading causes of death worldwide. Since the core microbiota flora of humans is largely diverse and HGT (Horizontal Gene Transfer), it is very challenging to determine whether a particular bacterial strain is commensal or pathogenic to humans. With the latest advances in NGS (Next-Generation Sequencing) technology, bioinformatics tools and techniques using NGS data have increasingly been used for the diagnosis and monitoring of infectious diseases. Even if the biological background is not available, the machine learning method can still infer the pathogenic phenotype from the NGS readings, independent of the database of known organisms, and being studied intensively. However, previous methods have not considered opportunistic pathogenic and interpretability of black box model, are not well suited for clinical requirements.
To modify polyethyleneimine (PEI) nanoparticles using hyaluronic acid (HA) to prepare a novel nonviral vector and use it to coat Atoh1-EGFP plasmid to detect its translocation in living guinea pig cochlea dyeing efficiency. Atoh1-EGFP plasmid was extracted and characterized using a Zetasizer particle size analyzer. HA/PEI/DNA complexion was characterized and introduced into the round window membrane. EGFP green fluorescence carried in the Atoh1 plasmid was observed by confocal microscopy. The transfection results were verified by Western blot and reverse transcription polymerase chain reaction (RT-PCR) from the perspective of protein and nucleic acid to verify its expression results. In this study, HA-modified PEI nanoparticles are negatively-charged nanoscale gene carrier complexes. After the Atoh1-EGFP plasmid was introduced into the cochlea, the results of confocal microscopy showed that the inner and outer hair cells of the basement membrane could be detected in green fluorescent protein. The transfection efficiency of basement membrane is as high as 81.7±4.71%, while the transversion is 33.8±9.02%. Western Blot and RT-PCR also confirmed that the Atoh1 gene can be successfully transfected on the basement membrane. The gene transfection of cochlea may be achieved by HA-modified PEI nanoparticle gene vector with no obvious toxicity to basement membrane cells. It is also an ideal inner-end gene transfection vector owing to its simple synthesis method and low cost.
This study is aimed to investigate the intervention effect and possible mechanism of ophiopogonin D( OPD) in protecting cardiomyocytes against ophiopogonin D'( OPD')-induced injury,and provide reference for further research on toxicity difference of saponins from ophiopogonins. CCK-8 assay was used to evaluate the effect of OPD and OPD' on cell viability. The effect of OPD on OPD'-induced cell apoptosis was measured by flow cytometry. Morphologies of endoplasmic reticulum were observed by endoplasmic reticulum fluorescent probe. PERK,ATF-4,Bip and CHOP mRNA levels were detected by Real-time quantitative polymerase chain reaction( PCR) analysis. ATF-4,phosphorylated PERK and e IF2α protein levels were detected by Western blot assay. RESULTS:: showed that treatment with OPD'( 6 μmol·L-1) significantly increased the rate of apoptosis; expressions of endoplasmic reticulum stress related genes were increased. The morphology of the endoplasmic reticulum was changed. In addition,different concentrations of OPD could partially reverse the myocardial cell injury caused by OPD'. The experimental results showed that OPD'-induced myocardial toxicity may be associated with the endoplasmic reticulum stress,and OPD may modulate the expression of CYP2 J3 to relieve the endoplasmic reticulum stress caused by OPD'.
Novel H7N9 influenza virus transmitted from birds to human and, since March 2013, it has caused five epidemic waves in China. Although the evolution of H7N9 viruses has been investigated, the evolutionary changes associated with codon usage are still unclear. Herein, the codon usage pattern of two surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA), was studied to understand the evolutionary changes in relation to host, epidemic wave, and pathogenicity. Both genes displayed a low codon usage bias, with HA higher than NA. The codon usage was driven by mutation pressure and natural selection, although the main contributing factor was natural selection. Additionally, the codon adaptation index (CAI) and deoptimization (RCDI) illustrated the strong adaptability of H7N9 to Gallus gallus. Similarity index (SiD) analysis showed that Homo sapiens posed a stronger selection pressure than Gallus gallus. Thus, we assume that this may be related to the gradual adaptability of the virus to human. In addition, the host strong selection pressure was validated based on CpG dinucleotide content. In conclusion, this study analyzed the usage of codons of two genes of H7N9 and expanded our understanding of H7N9 host specificity. This aids into the development of control measures against H7N9 influenza virus.
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Abstract Background Ginkgo biloba extract (EGb) has been widely applied in the treatment of cerebrovascular and neurological diseases. However, the effect of EGb761 on ovarian hyperstimulation syndrome (OHSS), a vascular disorder and life-threatening complication of In vitro fertilization and Intracytoplasmic sperm injection therapy (IVF/ICSI), has not been evaluated. MethodsForty female Wistar rats aged 22-days old (D22) were divided into eight groups: Control rats received intraperitoneal injection of saline for 5 consecutive days (D22-D26); OHSS-model group received 10 IU equine chorionic gonadotropin (eCG) for 4 consecutive days (D22-D25) and 30 IU of human chorionic gonadotropin (hCG) on the 5th day (D26); Prophylactic treatment group received three doses of EGb761 (50mg/kg/d, 100mg/kg/d, 200mg/kg/d) one hour before injection of eCG (hCG) for 7 consecutive days; Therapeutic treatment group received three doses of EGb761 (50mg/kg/d, 100mg/kg/d, 200mg/kg/d) 48 hours after injection of eCG (hCG) for 7 consecutive days. ResultsWe found the therapeutic treatment group exhibited the lowest ovarian and renal mass index, vascular permeability, estradiol and progesterone concentrations, vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor (VEGFR) protein expression. ConclusionsEGb761 decreases vascular permeability in OHSS rat model by inhibiting VEGF and VEGFR expression, which may contribute to the prevention and treatment of OHSS. Furthermore, therapeutic medication is superior to prophylactic medication.
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