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Sports fatigue of the lower limbs is one of the important factors affecting sports performance. How to improve the anti-fatigue ability of the lower limbs during endurance exercise is the focus of the research field of human sports biomechanics. This study systematically reviewed the relevant literature on transcranial direct current stimulation (tDCS) intervention on lower limb endurance performance, summarized the effect of tDCS on lower limb endurance performance, and analyzed the influencing factors and potential mechanisms. The results showed that: tDCS intervention has a significant effect on the endurance performance of the whole lower limbs, but there is no unified conclusion on the effect on the endurance performance of the knee joint. The researchers deem that tDCS can increase the excitability of the primary motor cortex and reduce the activation of the supplementary motor area and the premotor area to producing a lower rating of perceived exertion, but cannot affect the perception of exercise-induced pain, and stimulation protocols varied across studies, which may be partly responsible. This study can provide a theoretical basis for exploring the central mechanism of tDCS to improve endurance performance, formulating rehabilitation and sports training programsfor different groups of people, and developing new stimulation equipment to enhance the human body’s anti fatigue ability.
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A case of a 3-year-old child suffered with severe crush injury to the right forearm and right hand on June, 2017. A comprehensive treatment was conducted with limb salvage, free flap repair and the repair of nerve, vessel and tendon for functional reconstructions followed by rehabilitation therapies. The function and appearance of the injured limb and hand recovered well 3 years after surgery.
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To investigate the effects of thanatos-associated protein 11 (THAP11) on the proliferation and apoptosis of esophageal cancer cell and the underlying mechanism. Methods: Expression of THAP11 in human esophageal epithelial cells (Het-1A) and esophageal cancer cells (Eca109, TE-1, Ec 9706) were detected by Western blotting. Esophageal cancer TE-1 cells were divided into 3 groups: a normal control (NC) group, a negative control (LV-NC) group and a THAP11 (LV-THAP11) group. Then the cell proliferation were detected by MTT assay, cell apoptosis were detected by flow cytometry, caspase-3 and caspase-9 levels were detected by caspases kits. Ubiquitination of p53 was determined in esophageal cancer TE-1 cells. Results: Expression of THAP11 was reduced in esophageal cancer cells compared with human esophageal epithelial cells (P<0.05). After transfection with LV-THAP11 in TE-1 cells, cell viability was reduced (P<0.05), while apoptosis rate and caspase-3 and caspase-9 levels were increased (P<0.05), indicating that THAP11 inhibited growth of esophageal cancer cells. In addition, the THAP11 increased the levels of p53 (P<0.05) and inhibited the ubiquitination of p53 regulated by MDM2. Conclusion: THAP11 may inhibit the proliferation of esophageal cancer cells by inhibiting ubiquitination of p53.
Subject(s)
Humans , Apoptosis , Cell Line, Tumor , Cell Proliferation , Esophageal Neoplasms , Repressor Proteins , Metabolism , Tumor Suppressor Protein p53 , UbiquitinationABSTRACT
Objective To explore key gene and pathway of radioresistance in esophageal carcinoma and reveal its molecular mechanism of radioresistance. Methods The gene expression profiles of GSE61772 and GSE61620 were downloaded from the Gene Expression Omnibus (GEO). Differentially expressed genes ( DEGs ) were screened by GEO2R. Gene Ontology ( GO ) enrichment, Kyoto Encyclopedia of Genes and Genomes ( Kegg ) enrichment and protein-protein interaction ( PPI ) network construction were performed by DAVID and String softwares. RT-PCR was used to detect the differences in the expression of different genes in different radiosensitivity cells. Results A total of 49 differentially expression genes were screened. These genes were mainly involved in the regulation of multicellular biosynthesis, ion transport, DNA synthesis, metabolism, cell proliferation and so on. The major biological pathways included a Wnt signal pathway. 12 DEGs interacted with each other, and CHN2 may be a key node. The expression of CHN2 gene had no obvious difference between TE13R and TE13. Conclusions 49 differentially expressed genes, including CHN2, may be involved in radioresistance of esophageal carcinoma, and the Wnt signaling pathway may be an important pathway in this radioresistance.
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Objective To explore key gene and pathway of radioresistance in esophageal carcinoma and reveal its molecular mechanism of radioresistance. Methods The gene expression profiles of GSE61772 and GSE61620 were downloaded from the Gene Expression Omnibus (GEO). Differentially expressed genes ( DEGs ) were screened by GEO2R. Gene Ontology ( GO ) enrichment, Kyoto Encyclopedia of Genes and Genomes ( Kegg ) enrichment and protein-protein interaction ( PPI ) network construction were performed by DAVID and String softwares. RT-PCR was used to detect the differences in the expression of different genes in different radiosensitivity cells. Results A total of 49 differentially expression genes were screened. These genes were mainly involved in the regulation of multicellular biosynthesis, ion transport, DNA synthesis, metabolism, cell proliferation and so on. The major biological pathways included a Wnt signal pathway. 12 DEGs interacted with each other, and CHN2 may be a key node. The expression of CHN2 gene had no obvious difference between TE13R and TE13. Conclusions 49 differentially expressed genes, including CHN2, may be involved in radioresistance of esophageal carcinoma, and the Wnt signaling pathway may be an important pathway in this radioresistance.
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Aneurysmal bone cyst of mastoid bone is seldom, here one case was reported. The mastoid bone of the patient presented with a baloon-like swelling full of non-coagulated blood and serous-hemorrhagic fluid. CT scan demonstrated a large expansile destructive mass located in left mastoid bone region with the thin or absent cortical bone. The MRI demonstrated T2-weighted images and clear boudary from surrounding tissue. Pathologic reported that the mastoid bone was repalcement with lacunar divided by fibro-tissue, containing numerous hemosiderin, giant cells and inflammatory cells. A surgery was performed and the patient was cured.
Subject(s)
Humans , Bone Cysts, Aneurysmal , Diagnosis , Pathology , General Surgery , Magnetic Resonance Imaging , Mastoid , Pathology , Tomography, X-Ray ComputedABSTRACT
Objective To investigate the combination effect of curcumin and γ-ray irradiation on PANC-1 cells in vitro.Methods PANC-1 cells were exposed to γ-rays in the presence or absence of curcumin.MTT assay was performed to evaluate cell viability.The expression of P21 was evaluated with RT-PCR and Western blot.Cell cycle distribution and apoptosis were tested by flow cytometry.Results Compared with the γ-ray irradiation group,combination treatment of curcumin and irradiation decreased the cell viability (t =6.72,P ＜ 0.01) and increased the percentage of cells in S-phase (t =4.78,P ＜ 0.05),apoptosis rate (t =6.58,P ＜ 0.01),P21 protein and mRNA expression (t =5.72,5.63,P ＜ 0.01) in PANC-1 cells.Conclusions Curcumin increases the radiosensitivity of PANC-1 cells,which may have clinical implication on radiotherapy of pancreatic cancer.
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OBJECTIVE@#To detect the expression of Th17 nuclear factor RORC and cytokines IL-17A and IL-22 and neutrophil marker MPO and their correlations with CRSsNP.@*METHOD@#RT-PCR was used to detect mRNA expression of RORC, IL-17A and IL-22. Immunohistochemistry was used to assess the IL-17A positive cells in CRSsNP and control. ELISA was used to detect the expression of MPO.@*RESULT@#CRSsNP had higher mRNA expression of RORC, IL-17A and IL-22 and increased protein expression of MPO. The mRNA expression of RORC, IL-17A and IL-22 was positively correlated with each other but none of them was correlated with the expression of MPO in CRSsNP and control.@*CONCLUSION@#Both Th17 and neutrophils contribute to the pathogenesis of CRSsNP, however, the neutrophil infiltration may not be recruited by Th17 cytokines.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Chronic Disease , Interleukin-17 , Allergy and Immunology , Interleukins , Allergy and Immunology , Neutrophil Infiltration , Neutrophils , Allergy and Immunology , Nuclear Receptor Subfamily 1, Group F, Member 3 , Allergy and Immunology , Sinusitis , Allergy and Immunology , Th17 Cells , Allergy and ImmunologyABSTRACT
The effects of RNAi-mediated gene silencing of LRlG1 on proliferation and invasion of the human glioma cell line U251-MG and the possible mechanisms were explored in this study. The plasmids pGenesil2-LRIG1-shRNA1 and pGenesil2-LRIG1-shRNA2 were transfected into U251-MG glioma cells respectively by using Lipofectamine 2000 and the transfected cells in which the LRIG1 expression was stably suppressed were selected by G418. The cells transfected with negative shRNA served as control. The expression levels of LRIG1 mRNA and protein were measured by qRT-PCR and Western blotting, respectively. The cell cycle was analyzed by flow cytometry. The results showed that LRIG1 mRNA expression was reduced by 70% and 58% and LRIG1 protein expression by 58% and 26% in U251-MG cells transfected with pGenesil2-LRIG1-shRNAl and pGenesil2-LRIG1-shRNA2 relative to the negative shRNA-transfected U251-MG cells. The proliferative capacity of the LRIG1 specific siRNA-transfected cells was stronger than that of control cells. Cell cycle analysis showed that silencing LRIG1 significantly increased the percentage of S phase cells and the proliferation index (P<0.01). Moreover, silencing LRIG1 could promote the invasion of U251-MG cells (P<0.05). These findings suggested that LRIG1-targeting siRNA can exert a dramatically inhibitory effect on RNA transcription and protein expression of LRIG1, and LRIG1 down-regulation could promote the proliferation of U251-MG cells, arrest U251-MG cells in S phase, and enhance the invasion of U251-MG cells.
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BACKGROUND: Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) gene showed low expression in glioma cells. LRIG1 gene overexpression significantly enhanced LRIG1 mRNA and protein expression and inhibited its biological behavior. However, very few researchs are reported from the stand-point of inhibition of LRIG1 gene expression. OBJECTIVE: To construct specific RNA interference plasmids for LRIG1, establish stably transfected human glioma GL15 cell line, and observe its effect on expression of target gene LRIG1. METHODS: Designed and synthesized two shRNAs (named LRIG1-shRNA1 and LRIG1-shRNA2) specific for LRIG1 mRNA according to the GenBank, and one scrambled shRNA sequence as negative control, named pGenesil2-negative shRNA. The shRNA was inserted into pGenesil2 vector and sequenced. The recombinant vectors were transformed into E. coli. Picked up the positive clones and extracted the plasmids, which were transfected into GL15 cells by Metafectine. G418 was applied to select the stably transfected cell clones. Western Blotting was performed to examine the LRIG1 protein level.RESULTS AND CONCLUSION: The recombinant plasmids which contain shRNA were analyzed by restriction endonuclease digestion and DNA sequence, and it was proved that the fragment was inserted into the expected sites. Compared with the negative control group, the level of LRIG1 protein expression in pGenesil2-LRIG1-shRNA1(LRIG11) transfected cells and in pGenesil2-LRIG1-shRNA2(LRIG12) transfected cells was decreased by 47.9% (P 0.05). The results confirmed that RNAi expressing vector specific for LRIG1 gene (pGenesil2-LRIG1-shRNA1) was successfully constructed, and the stable cell clones transfected with the shRNA expression vector showed inhibition of the expression of LRIG1 in glioma cell line GL15.
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Objective To investigate the influence on the behavior of withdrawal and relapse after deep brain stimulation of bilateral nucleus accumbens in morphine-dependent rats. Methods The rats with a strong unconditioned preference were discarded in preconditioning test, the selected rats were distributed into five groups randomly. After operation,morphine hydrochloride was injected subcutaneously into SD rats for 12 days (once every day,initial 5 mg/kg,increasing by 5 mg/kg per time,stable in 20 mg/kg ). A modified electrical circuit was used to procedure the DBS,the parameter was 130 Hz,150 A,60 s,l h/d,14 d. CPP test was used to exam the effect of DBS. A minor morphine dose (3 mg/kg) was injected to induce the behavior of relapse, and CPP was tested again after 24 h. Two-way ANOVA was performed on the data with Bonferroni posttest. Result ①After CPP training,CPP score of group morphine, morphine + sham and morphine + DBS was ( 155. 87 ± 20. 45 ) s, (107.33 ± 18.10)s,(135.45 ±22.09)s,and had significant difference with group of control( ( -70.34 ± 15.40) s)(t = 9.45,P＜0.01; t = 6.94,P＜0.01;t = 8.04,P＜0.01).②After 7 days' DBS,the CPP score in group of morphine + DBS reduced significantly compared to group of morphine( t = 4.21, P＜0.01) and morphine + sham( t=1.10, P＜0.05).0n the 14th day,there was more pronounced reduction ( t = 5. 15, P＜0.01; t = 3.92, P＜ 0.01). ③ 24 hours after the minor morphine dose was injected,the CPP score in morphine + DBS didn't increase significantly, and had significant difference with group of morphine ( t = 4.04, P＜0.01) and morphine + sham ( t= 4. 13, P＜0.01). Conclusion DBS bilateral nucleus accumbens in morphine-dependent rats can interfere the behavior of morphine-induced CPP and relapse.
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This study examined the effects of over-expression of leucine-rich repeats and immunoglobulin-like domains 3 (LRIG3) on the cell cycle and survival of human glioma cell line U87 and U251 and explored the possible mechanisms. The LRIG3 gene was transduced into U87 and U251 cells respectively by using lentivirus and the transduced cells were selected by puromycin. The changes in LRIG3 mRNA and protein levels were measured by RT-PCR and Western blotting. The apoptosis rate was detected by Annexin V-FITC/PI double labeling and the cell cycle was flow cytometrically analyzed. Compared with control cells, LRIG3 mRNA expression in U251 and U87 cells transduced with pLVX-DsRed-LRIG3-Monomer-N1 were increased by 77.6% and 129.7%, and LRIG3 protein expression was raised by 141.3% and 322.7%, respectively. Cell cycle analysis showed that LRIG3 over-expression increased the percentage of cells at G(0)/G(1) phase (P<0.01). Over-expressed LRIG3 could significantly promote the apoptosis of U87 and U251 cells (P<0.05). These findings suggest that the over-expression of LRIG3 could arrest the cell cycle in G(0)/G(1) phase, and promote apoptosis of U87 and U251 cells.
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The Leucine-rich repeats and immunoglobulin-like domains-2 (LRIG2) gene expression in pituitary adenoma and its correlation with tumor invasiveness were studied. The expression of LRIG2 mRNA and protein in human pituitary adenoma obtained surgically was detected by RT-PCR (39 cases) and immunohistochemical staining (30 cases). It was found that LRIG2 was mostly localized at the nucleus of the pituitary adenoma cells. Its expression was significantly higher in the invasive cases than in the non-invasive cases. LRIG2 protein was positive in 14 cases out of 21 cases of invasive adenoma, but only 2 cases were positive in 9 cases of non-invasive adenoma. The positive expression rate of LRIG2 mRNA was 91.3% in invasive cases (total 23 cases) and 62.5% in non-invasive cases (total 16 cases), respectively. LRIG2 gene is overexpressed in invasive pituitary adenoma. It may play an important role in pituitary adenoma invasiveness and further studies are necessary to elucidate the mechanism under this phenomenon.
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Objective To determine the toxicity, maximal dose and clinical practicality of VM26 (teniposide) plus radiotherapy for postoperative brain neurospongioma. Methods Twenty patients were alloted in phase Ⅰ trial. The total dose was 60 Gy for the field radiotherapy (30 fractions of 2 Gy over six weeks). Teniposide at three dose levels (50 mg/m2, 75 mg/m2 and 100 mg/m2) was given intravenously once a week, totally five weeks. Dose escalation was based on each level, with a minimum of five patients in cohort if severe toxicity was not observed until the maximum tolerance dose(MTD). Results The predominant form of toxicity was hematologic toxicity. Four patients developed grade 3, 4 leucopenia when a second level of MTD (75 mg/m2) was given. Conclusion Combined radiotherapy and teniposide for postoperative brain neurospongioma is well tolerated. The dose of 50 mg/m2 for phase Ⅱ clinical trial was recommended.
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The effects of epidermal growth factor (EGF) on proliferation of G15 glioma cells and the possible mechanisms were investigated. GFAP and EGFR expression was detected by immunohistochemical method. After the cells were treated with EGF at different concentrations, cell count method was used to determine the proliferation of glioma cells, cell cycle and apoptosis were analyzed by flow cytometry (FCM), and laser scan confocal microscope (LSCM) was used to measure the cytoplasmic free calcium. The results showed that GFAP was diffusedly expressed in GL15 cells and EGFR was over-expressed. EGF at doses of < or =1 ng/mL could significantly stimulate cell proliferation, cells in phase G0/G1 decreased, and those in phase S increased. EGF at doses of 10 and 100 ng/ml could inhibit the cell proliferation significantly, and the apoptosis ratio in high dose of EGF group was higher than in control group. EGF could significantly induce a quick rise of intracellular free calcium, but the peak value of intracellular free calcium activated by high dose of EGF was higher than by low dose of EGF. It was suggested that EGF had a dual effect on gliomas: low dose of EGF could stimulate the cell proliferation of gliomas, but high dose of EGF could induce the cell apoptosis and inhibit the proliferation of gliomas, which might be contributed to the difference of intracellular free calcium.
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The effects of epidermal growth factor (EGF) on proliferation of G 15 glioma cells and the possible mechanisms were investigated. GFAP and EGFR expression was detected by immunohistochemical method. After the cells were treated with EGF at different concentrations, cell count method was used to determine the proliferation of glioma cells, cell cycle and apoptosis were analyzed by flow cytometry (FCM), and laser scan confocal microscope (LSCM) was used to measure the cytoplasmic free calcium. The results showed that GFAP was diffusedly expressed in GL15 cells and EGFR was over-expressed. EGF at doses of ≤ 1 ng/mL could significantly stimulate cell proliferation, cells in phase G0/G1 decreased, and those in phase S increased. EGF at doses of 10 and 100ng/ml could inhibit the cell proliferation significantly, and the apoptosis ratio in high dose of EGF group was higher than in control group. EGF could significantly induce a quick rise of intracellular free calcium, but the peak value of intracellular free calcium activated by high dose of EGF was higher than by low dose of EGF. It was suggested that EGF had a dual effect on gliomas: low dose of EGF could stimulate the cell proliferation of gliomas, but high dose of EGF could induce the cell apoptosis and inhibit the proliferation of gliomas, which might be contributed to the difference of intracellular free calcium.