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Organic-inorganic hybrid thermoelectric (TE) materials have attracted tremendous interest for harvesting waste heat energy. Due to their mechanical flexibility, inorganic-organic hybrid TE materials are considered to be promising candidates for flexible energy harvesting devices. In this work, enhanced TE properties of Tellurium (Te) nanowires (NWs)- poly (3-hexylthiophene-2, 5-diyl) (P3HT) hybrid materials are reported by improving the charge transport at interfacial layer mediated via controlled oxidation. A power factor of ≈9.8 µW (mK2)-1 is obtained at room temperature for oxidized P3HT-TeNWs hybrid materials, which increases to ≈64.8 µW (mK2)-1 upon control of TeNWs oxidation. This value is sevenfold higher compared to P3HT-TeNWs-based hybrid materials reported in the literature. MD simulation reveals that oxidation-free TeNWs demonstrate better templating for P3HT polymer compared to oxidized TeNWs. The Kang-Snyder model is used to study the charge transport in these hybrid materials. A large σE0 value is obtained which is related to better templating of P3HT on oxygen-free TeNWs. This work provides evidence that oxidation control of TeNWs is critical for better interface-driven charge transport, which enhances the thermoelectric properties of TeNWs-P3HT hybrid materials. This work provides a new avenue to improve the thermoelectric properties of a new class of hybrid thermoelectric materials.
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Personalized cancer vaccines based on neoantigens have become an important research direction in cancer immunotherapy. However, their therapeutic effects are limited by the efficiency of antigen uptake and presentation by antigen presenting cells. Here, the low-toxicity cholesterol-modified antimicrobial peptide (AMP) DP7 (DP7-C), which has dual functions as a carrier and an immune adjuvant, improved the dendritic cell (DC)-based vaccine efficacy. As a delivery carrier, DP7-C can efficiently delivery various antigen peptides into 75-95% of DCs via caveolin- and clathrin-dependent pathways. As an immune adjuvant, DP7-C can induce DC maturation and proinflammatory cytokine release via the TLR2-MyD88-NF-κB pathway and effectively increase antigen presentation efficiency. In addition, DP7-C enhanced the efficacy of DC-based individualized cancer immunotherapy and achieved excellent antitumor effects on mouse tumor models using the OVA antigen peptides and LL2-neoantigens. Excitingly, after DP7-C stimulation, the antigen uptake efficiency of monocytes-derived DCs (MoDCs) in patients with advanced lung cancer increased from 14-40% to 88-98%, the presentation efficiency increased from approximately 15% to approximately 65%, and the proportion of mature MoDCs increased from approximately 20% to approximately 60%. These findings suggest that our approach may be a potentially alternative strategy to produce cancer vaccines designed for individual patients.
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Vacunas contra el Cáncer , Neoplasias , Animales , Colesterol , Células Dendríticas , Humanos , Inmunoterapia , Ratones , Neoplasias/terapiaRESUMEN
Objective:To investigate the relationship between the dose of preoperative neoadjuvant radiotherapy and the pathologic complete response (pCR) rate in patients with locally advanced squamous cell esophageal cancer (ESCC).Methods:Clinical data of 116 patients with ESCC who received neoadjuvant chemoradiotherapy followed by esophagectomy in our cancer center from July 2017 to December 2019 were retrospectively analyzed. The radiation doses were divided into 2 ranges based on Grays (Gy) received: 40-45 Gy and 45 Gy or more.Results:The overall pCR rate was 38. 8%(45/116). pCR was observed in 35 out of 80(44%) patients treated with 40-45 Gy and 10 of 36(28%) patients treated with 45 Gy or more. The pCR rate did not significantly differ between two groups [(40-45 Gy) vs.( ≥ 45 Gy), P=0.105)]. Conclusions:Preoperative neoadjuvant radiotherapy with a higher dose (≥ 45 Gy) fails to increase the pCR rate in patients with locally advanced ESCC. Prospective randomized trials are required to determine the optimal dose of preoperative adjuvant radiotherapy.
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Objective To investigate if down regulation of MTDH could inhibit proliferation and induce apoptosis in breast cancer SK-BR-3 cells.Methods RNA interference was employed to reduce MTDH expression in human breast cancer SK-BR-3 cells.Western blot assay was applied to measure the down regulation of MTDH.MTT assay was performed to assess the proliferation of SK-BR-3 cell.Flow cytometry was employed to detect cell cycle and apoptosis.Western blot assay was applied to detect the molecular alterations that was associated with cell proliferation,cell cycle and apoptosis.Results MTDH down regulation significantly inhibited cell proliferation.48 hours and 72 hours after trasnfection,the absorbance value(A value)in blank control,negative control and treatment group was (2.0 ± 0.1) vs (1.9 ± 0.3) vs (0.9 ± 0.1) (P =0.02) and (2.7 ± 0.2) vs (2.5 ± 0.4) vs (1.3 ± 0.2) (P =0.008).MTDH down regulation resulted in accumulation of the G0/G1 phase cells and reduction of S and G2/M phase cells.Moreover,MTDH down regulation significantly induced cell apoptosis.The cell apoptosis rate in blank control,negative control and trial group was (1.3 ± 0.2) %,(1.4 ± 0.3) % and (19.6 ± 2.7) % (P =0.012).MTDH down regulation resulted in a decreased expression of cyclinD1 and Bcl-2,an increased expression of P21 and the activation of caspase-3.Conclusions Reduced MTDH expression in SKBR-3 cells can inhibit proliferation and induce apoptosis,which may be associated with decreased expression of cyclinD1 and Bcl-2,an increased expression of P21 and the activation of caspase-3.
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Objective To investigate the effect of genistein on the expression of Bax and Bcl-2 protein in PC12 cells transfected with mutant APP695 Type.Methods PC12 cells were transfected with pIRES2-EGFP plasmid or pIRES2-EGFP/APP695MT expression plasmid,and then divided into normal control group,Unladen group,APP695 transfected group,GST treatment group(5 μmol/L,15 μmol/L).The Bax and Bcl-2 protein expression in PC12 cells was measured by Immunocytochemistry SABC and Western-blot.Results Immunocyto-chemistry SABC showed that:compared with the normal control group,the expression of bax protein in APP695 transfected group was strongly increased((78.02 ± 1.26) %,P<0.01)) and the expression of bcl-2 protein was very weak oppositely ((15.40 ± 0.72) %,P<0.01)).Compared with APP695 transfected group,the expression of bax protein in cells of 15umol/L GST treatment group was significantly decreased((22.35 ± 0.49) %,P<0.01))and the expression of bcl-2 protein in these cells was strongly increased ((68.11 ± 0.24) %,P <0.01)).Western-Blot showed that:compared with the normal control group,the expression of bax protein in APP695 transfected group was markedly increased and the expression of Bcl-2 protein was significantly decreased.Compared with the APP695 transfected group,the expression of Bax protein was markedly decreased and the expression of Bcl-2 protein was significantly increased in the cells of the GST treatment groups.Conclusion GST can reduce the expression of bax protein and the increased expression of Bcl-2 protein has protective effect on PC12 cells transfected with APP696MT.
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ObjectiveTo investigate the effect of Genistein (GST) on cell cycle and apoptosis in PC12 cells transfected App695MT gene.MethodsPC12 cells were transfected with pIRES2-EGFP plasmid or pIRES2-EGFP/APP695MT expression plasmid,and then were divided into control vectortransfected group,APP695 transfected group and GST treatment group.Flow cytometry was applied to detect cell cycle and apoptosis,laser confocal microscope was used to observe morphological changes of cell apoptosis.ResultsCompared with control vectortransfected group,PC12 cells in APP695 transfected group increased significantly in G0 and G1 phase,and less into S phase,cell proliferation index was decreased significantly( (55.6 ±0.57)%,P<0.0l ),apoptosis rate was increased significantly( (77.10 ± 12.53)%,P<0.01 ).Emitted red fluorescence increased significantly when cell death,cell body swelling,organelle disintegration,nuclear condensation or fragmentation.Compared with APP695 transfected group,PC12 cells in GST( 15μ mol/L) treatment group,decreased significantly in G0 and G1 phase,and more into S phase,cell proliferation index was increased significantly ( ( 61.57 ± 0.47 ) %,P < 0.01 ),apoptosis rate was decreased significantly ( (46.00 ± 8.43 ) %,P < 0.01 ).Cell death was significantly reduced red fluorescence,emitted green fluorescence was significantly enhanced,compared with APP695 transfected group cell morphology improved.ConclusionGST can improve APP695MT gene caused cell cycle arrest,promote cell to S phase transition,reduce apoptosis rate in PC12 cells,and have a protective effect on transfected cells.
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Cytokine-induced killer cells (CIK) is the fourth largest cancer treatment after surgery,chemotherapy and radiotherapy,and it is the development direction of cancer treatment.It is a new type of immune cell,and it is named after natural killer cell samples T lymphocytes as it express CD3 and CD56.Currently,CIK treatment has a broader range of clinical applications,and it has achieved the better clinical efficacy in the blood system cancer and solid tumors,The CIK adoptive immunotherapy is considered to be a new hope for the anticancer treatment.
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BACKGROUND: Signal transducer and activator of transcription 3 (STAT3) protein is widely expressed in cells and tissues of different type and. It is the important component of signal transduction and transcription chain that participates in the regulation of various physiological functions of cells like proliferation and differentiation. However, there is no literature reported regarding if there is STAT3 expression and whether it participates in embryo liver development both at home and abroad.OBJECTIVE: To explore the effects and mechanism of STAT3 signal transduction route on development of embryo liver by. Studying the expression of STAT3 protein during embryo liver development in mice.DESIGN: Randomized controlled study based on STAT3 protein.SETTING: Department of histology and embryology in a military medical university of Chinese PLA.MATERIALS: The study was completed in the Department of Histology and Embryology, Third Military Medical University of Chinese PLA during January to June 2004. Kunming mice were provided by Animal Centre of Third Military Medical University of Chinese PLA. Ten male mice and 20 female mice with body mass during 25 to 30 grams were randomly chosen.METHODS: Serial frozen sections of mouse embryo was performed in the 13.5 days ( n = 8), 14.5 days ( n = 9) and 15.5 days ( n = 7) after mating respectively. One of the every 2 slices was used as negative control by replacing first antibody of STAT3 with 0. 01 mol/L PBS. Immunochemical technique and immunofluorescence method were used to display the expression of STAT3 protein in embryo liver development in mice.MAIN OUTCOME MEASURES: Expression of STAT3 protein in serial frozen sections of mouse embryo.RESULTS: There was strong expression of STAT3 protein in liver cells in E13.5 days mouse embryo while the expression was decreased in E14.5 days and E15.5 days mouse embryos.CONCLUSION: STAT3 protein has participated in the development of embryo liver. The expression of STAT3 in liver development can be used to explain the mechanism of liver regeneration and provide experimental data for organ repair.