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Abstract Objective MicroRNA-29a-3p has been reported in a variety of cancers, but its role in hypopharyngeal cancer remains unclear. This study was to determine the role of microRNA-29a-3p in the occurrence and development of hypopharyngeal cancer. Methods 40 patients with hypopharyngeal cancer who underwent surgery in the Affiliated Hospital of Jining Medical University from April 2013 to November 2017 were selected for this study. The cancer tissue samples of the patients were collected, and the patients were followed up for three years. The expression of microRNA-29a-3p in tissue samples was detected by in situ hybridization with fluorescent probe, and the relationships among microRNA-29a-3p and clinicopathological factors, postoperative recurrent-metastasis, survival time were studied. Immunohistochemical was used to detect the expression of Ki67 and E-cadherin in tissue samples. Results Combined with HE staining results showed that microRNA-29a-3p expression was relatively high in non-cancer tissue cells (red blood cells and fibroblasts in tumor interstitial vessels), but was relatively low in cancer tissue and cells. According to the follow-up data of 40 patients with hypopharyngeal cancer, tumor size, T-stage, tumor differentiation, postoperative recurrent-metastasis of hypopharyngeal cancer patients were significantly negatively correlated with microRNA-29a-3p (p< 0.05). Immunohistochemica results further confirmed that microRNA-29a-3p was negatively correlated with the expression of Ki67 and E-cadherin. The survival time of patients positively related with microRNA-29a-3p expression (p< 0.05). Moreover, ROC curve analysis showed that the area under the curve of the combined detection of miRNA-29a-3p+Ki67+E-cadherin was larger than that of the single detection of the three indexes. Conclusions The expression of microRNA-29a-3p is closely related to the occurrence, development and prognosis of hypopharyngeal cancer, and it affects the proliferation and invasion. This indicates that microRNA-29a-3p serves as a therapeutic target for the occurrence and development of hypopharyngeal cancer. The evidence of study designs of this study is IV using "Oxford Centre for Evidence-Based Medicine 2011 Levels of Evidence".
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italic>Tussilago farfara L. is a perennial herb of Tussilago genus in the Compositae family. Its dried buds and leaves have good biological activities and have a long history of medicinal use in China and Europe. In this paper, we investigated the whole chloroplast genome characteristics, sequence duplication, structural variation and phylogeny of the Tussilago farfara L. After sequencing the Tussilago farfara L. chloroplast genome using Illumination technology, the complete Tussilago farfara L. chloroplast genome was further obtained by assembly and annotation, followed by a series of inverted repeat-large single copy/small single copy region contraction and expansion analysis, genome sequence variation, etc. The sequences of 13 homologous plants downloaded from NCBI were used to construct a neighbor-joining phylogenetic tree. The results showed that the total GC content of the chloroplast genome was 37.4% and the length was 150 300 bp; 125 genes were annotated, including 82 protein-coding genes, 35 tRNAs and 8 rRNAs; 148 (simple sequence repeats, SSR) loci were detected, and the relative synonymous codon usage showed that 31 codons out of 64 codons had a usage of >1. In the phylogenetic analysis, the chloroplast genomes of the seven species of Asteraceae, including the Yulin Tussilago farfara L., were highly conserved, and the sequence variation of the (large single-copy, LSC) and (small single-copy, SSC) regions was higher than that of the (inverted repeat, IR) region. This is in general agreement with the reported phylogeny of Yulin Tussilago farfara L. In this study, we obtained a high quality chloroplast genome and analyzed its genome characteristics, codon preference, SSR characteristics, SC/IR boundary, sequence variation and phylogeny, which can provide a basis for species identification, genetic diversity analysis and resource development of this medicinal plant.
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Netrin-1 may protect and repair the damage caused by cerebral infarction, in terms of inhibiting apoptosis and inflammatory, and promoting angiogenesis and axon regeneration, etc. Netrin-1 may associate with the pathogenesis and outcome of cerebral infarction. The application of Netrin-1 in clinic needs more researches.
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Aloin is a small-molecule drug well known for its protective actions in various models of damage. Traumatic brain injury (TBI)-induced cerebral edema from secondary damage caused by disruption of the blood-brain barrier (BBB) often leads to an adverse prognosis. Since the role of aloin in maintaining the integrity of the BBB after TBI remains unclear, we explored the protective effects of aloin on the BBB using in vivo and in vitro TBI models. Adult male C57BL/6 mice underwent controlled cortical impact injury, and mouse brain capillary endothelial bEnd.3 cells underwent biaxial stretch injury, then both received aloin treatment. In the animal experiments, we found 20 mg/kg aloin to be the optimum concentration to decrease cerebral edema, decrease disruption of the BBB, and improve neurobehavioral performance after cortical impact injury. In the cellular studies, the optimum concentration of 40 μg/mL aloin reduced apoptosis and reversed the loss of tight junctions by reducing the reactive oxygen species levels and changes in mitochondrial membrane potential after stretch injury. The mechanisms may be that aloin downregulates the phosphorylation of p38 mitogen-activated protein kinase, the activation of p65 nuclear factor-kappa B, and the ratios of B cell lymphoma (Bcl)-2-associated X protein/Bcl-2 and cleaved caspase-3/caspase-3. We conclude that aloin exhibits these protective effects on the BBB after TBI through its anti-oxidative stress and anti-apoptotic properties in mouse brain capillary endothelial cells. Aloin may thus be a promising therapeutic drug for TBI.
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<p><b>OBJECTIVE</b>To detect the expression level of miR-19a, one of the oncogenic miR-17-92 cluster, in multiple myeloma cell lines Lp-1 and U266 in vitro and to explore the effects of miR-19a on biological behavior, such as proliferation, migration and apoptosis of Lp-1 and U266 myeloma cells by transfection with miR-19a mimic through Lipofectamine2000.</p><p><b>METHODS</b>The reverse transcription-PCR was applied to detect the expression level of miR-19a in multiple myeloma cell lines Lp-1 and U266 in vitro. The CCK8 was used to assay the effect of miR-19a on the proliferation of Lp-1 and U266 cells in vitro, the transwell migration test was adopted to determine the effect of up-regulation of miR-19a on the migration of Lp-1 and U266 multiple myeloma cells in vitro. The flow cytometry was used to detect the effect of miR-19a on the apoptosis of Lp-1 and U266 cells in vitro.</p><p><b>RESULTS</b>The miR-19a expression was higher in Lp-1 and U266 multiple myeloma cells; compared with the transfected cells with a specific miR-19a NC, those samples transfected with miR-19a mimic displayed significantly higher expression of miR-19a (P<0.05), indicating a higher transfection efficiency; the miR-19a could promote the proliferation of Lp-1 and U266 multiple myeloma cells in vitro. MiR-19a could promote migration ability of Lp-1 and U266 multiple myeloma cell lines in vitro and could inhibit the apoptosis of Lp-1 and U266 cells.</p><p><b>CONCLUSION</b>miR-19a is overexpressed significantly in Lp-1 and U266 multiple myeloma cells, and promots the proliferation and invasion of the myeloma cells, but inhibits their apoptosis.</p>
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Humans , Apoptosis , Cell Line, Tumor , Cell Proliferation , Gene Expression Regulation, Neoplastic , MicroRNAs , Multiple MyelomaABSTRACT
Objective To investigate the therapeutic role and potential mechanisms of astaxanthin (ASX) pretreatment on cecal ligation and puncture (CLP)-induced sepsis in mice .Methods Sepsis was induced by CLP in male mice ,which were then randomly divided into saline control group ,sepsis model group (CLP group) ,and CLP+ASX group (mice received 60 mg/(kg · d) ASX dissolved in olive oil via oral gavage for 14 consecutive days before CLP operation) .① The mice were monitored to assess 72-hour survival rate .② Clinical scores of mice in the three groups were calculated 24 h after CLP to determine the severity of sepsis .Blood samples were collected at 24 h after CLP modeling to determine the serum ALT ,BUN ,TNF-α and IL-6 levels .The intestine ,lung ,liver and kidney tissues were collected to assess organ functions and pathological changes .Results The results showed that mice in CLP group had a significantly lower survival rate at 72 h than those in CLP+ASX group (P=0 .0202) .CLP+ASX sepsis group had a lower clinical score than CLP sepsis group(10 .78 ± 0 .79 vs .13 .67 ± 0 .44 ,P=0 .005) .The tissue histopathology and biochemical analysis revealed that ASX markedly alleviated histological examination damage in the intestines [villus height :(390 .67 ± 14 .58)μm vs .(326 .67 ± 10 .31)μm , P=0 .005] ,lung (lung wet/dry ratio :4.75±0.24 vs.5.05±0.22,P=0.0476),liver[ALT:(105.0±10.53)U/L vs.(174.8±9.289)U/L,P=0.0006] and kidney [BUN:(54 .50 ± 3 .57)mg/dL vs .(69 .17 ± 3 .33)mg/dL , P= 0 .0132] tissues in sepsis .Moreover , significant lower levels of TNF-α [(258 .06 ± 16 .21 )pg/mL vs . (538 .17 ± 30 .80 )pg/mL , P< 0 .0001 ] and IL-6 [(5 .90 ± 0 .80)ng/mL vs .(12 .56 ± 0 .55)ng/mL , P<0 .0001] were discovered in the CLP+ ASX sepsis group in contrast to the CLP sepsis group .Conclusion ASX can significantly lower the mortality of mice with CLP-induced sepsis by improving organ functions and inhibiting the release of inflammatory factors .
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Animal model is an animal material with human mimic performance established in biomedical scientific research. It can be used as experimental basis for studies of experimental hypothesis and clinical hypothesis. It can shorten the research time and observe the whole process of disease occurrence, development or prevention and treatment. Human biomedical research is largely limited by the biological complexity. In order to overcome this limitation, based on the immunosuppressive characteristics of a severely immunodeficient ( SCID) or recombinant activated gene ( Ragnul ) in mice, humanized mouse models of human diseases can be established and have been widely used to study the underlying principles of human immunobiology and complex pathological mechanisms of human diseases. This approach has become one of the important ways to promote the development of medical sciences, with practicality and foresight. In this paper, the application and research progress of humanized mouse models are reviewed.
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Animal model is an animal material with human mimic performance established in biomedical scientific research. It can be used as experimental basis for studies of experimental hypothesis and clinical hypothesis. It can shorten the research time and observe the whole process of disease occurrence, development or prevention and treatment. Human biomedical research is largely limited by the biological complexity. In order to overcome this limitation, based on the immunosuppressive characteristics of a severely immunodeficient ( SCID) or recombinant activated gene ( Ragnul ) in mice, humanized mouse models of human diseases can be established and have been widely used to study the underlying principles of human immunobiology and complex pathological mechanisms of human diseases. This approach has become one of the important ways to promote the development of medical sciences, with practicality and foresight. In this paper, the application and research progress of humanized mouse models are reviewed.
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Bacterial cellulose,as a new material,due to its unique nano-fiber mesh structure with good purity,physical and chemical properties such as mechanical strength and water holding capacity,biocompatibility and adaptability,has been widely used in medicine,food,paper,textile,acoustical materials and other industries.In medical field,especially,it has been rapidly developed in recent years.This review discusses the current bacterial cellulose and its performance optimization products which relates to the medical applications.
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<p><b>OBJECTIVE</b>To investigate the effects of occupational exposure to formaldehyde on the micronuclei frequencies in peripheral blood lymphocytes of workers.</p><p><b>METHODS</b>Two hundred thirty six plywood workers were divided into 3 exposure groups (low, middle and high) according to internal exposure biomarker (formaldehyde human serum albumin conjugate, FA-HSA), which was detected by ELISA. The concentrations of formaldehyde (FA) in air of two workshops were measure using the high performance liquid chromatography. Cytokinesis-block micronucleus (CBMN) test was used to detect the micronuclei frequencies of peripheral blood lymphocyte in 236 workers.</p><p><b>RESULTS</b>The average concentrations of FA in the low and high exposure workshops were 0.58 +/- 0.20 and 1.48 +/- 0.61 mg/m3, respectively, there was significant difference (P < 0.01). The average concentrations of serum FA-HAS of workers in two workshops were 69.22 +/- 15.37 and 136.29 +/- 89.49 pg/ml, respectively, there was significant difference (P < 0.01). The results of CBMN test showed that the micronucleus frequencies in low, middle and high exposure groups were 1.94 +/- 1.72, 2.10 +/- 1.92 and 2.10 +/- 1.70 per thousand, respectively, there were no significant differences between groups. However, the micronucleus frequencies in accumulative low, middle and high exposure groups were 1.36 +/- 1.36, 2.31 +/- 1.81 and 2.49 +/- 1.92 per thousand, respectively, there were significant differences between different accumulative exposure groups (P < 0.01). The results of correlation analysis indicated that there was a positive correlation between accumulative exposure levels and micronucleus frequencies (r(s) = 0.321, P < 0.01). The accumulative exposure doses may be a risk factor for high micronucleus frequencies in workers exposed to FA (P(trend) = 0.002).</p><p><b>CONCLUSION</b>FA-HSA levels can serve as an internal exposure biomarker for assessing the exposure level of workers exposed to FA. Accumulative formaldehyde exposure resulted in an increase of micronuclei frequencies of peripheral blood lymphocyte in plywood workers.</p>
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Adult , Humans , Asian People , Biomarkers , Blood , Formaldehyde , Blood , Lymphocytes , Cell Biology , Micronucleus Tests , Occupational Exposure , Respiratory Hypersensitivity , BloodABSTRACT
<p><b>BACKGROUND</b>Rosiglitazone is known as the most potent and specific peroxisome proliferators-activated receptor gamma (PPAR-gamma) ligand. It has potentially far-reaching effects on pathophysiological processes, from cancer to atherosclerosis and diabetes. However, it is not clear whether rosiglitazone affects the protein expression of transforming growth factor beta3 (TGF-beta3) and the cell proliferation in human uterine leiomyoma cells in vitro.</p><p><b>METHODS</b>Human uterine leiomyoma tissues were dissected and cultured. Cells were divided into 5 groups: one control group and other four groups with different concentrations of rosiglitazone (10(-7), 10(-8), 10(-9) and 10(-10) mol/L). Cells were cultured for 72 hours in serum-free Dulbecco's modified Eagle's medium. MTT reduction assay was used to detect the cell proliferation. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of PPAR-gamma and TGF-beta3. Immunofluorescence staining was used to detect the expressions of PPAR-gamma and TGF-beta3 proteins.</p><p><b>RESULTS</b>MTT reduction assay indicated that the treatment with rosiglitazone (from 10(-7) to 10(-9) mol/L) resulted in an inhibition of the cell growths after 72 hours (P < 0.01). RT-PCR analysis revealed that 10(-7) mol/L rosiglitazone significantly affected the gene expression at 72-hour: PPAR-gamma mRNA expression was up-regulated and TGF-beta3 mRNA was down-regulated and rosiglitazone at the concentration of 10(-7) mol/L affected these most effectively (P < 0.01). Immunofluorescence staining demonstrated that treatment with 10(-7) mol/L rosiglitazone resulted in the significant changes of PPAR-gamma and TGF-beta3 protein expressions compared with the other treatment groups and the control group at 72-hour (P < 0.01). All the effects of rosiglitazone on uterine leiomyoma cells were dose- and time-dependent in vitro.</p><p><b>CONCLUSIONS</b>The present study demonstrates that the PPAR-gamma activator, rosiglitazone, inhibits the cell proliferation partly through the regulations of PPAR-gamma and TGF-beta3 expressions. The cross-talk between the signal pathways of PPAR-gamma and TGF-beta3 may be involved in the process.</p>