Effect of Interfacial Modification on the Low-Temperature Fatigue Properties of Polymer/MXene Flexible Pressure Sensors.

Maintaining an excellent force-electric response under cyclic bending at low temperatures is still challenging for resistive-type electrically conductive polymer composite-based pressure sensors. In this study, the effect of low temperature on the fatigue failure of flexible MXene/polymer pressure sensors was systematically investigated through the silane functionalization of MXene nanosheets embedded with different polymer matrixes. The results show that the MXene/polymer interfaces are the primary factors affecting the temperature-dependent bending fatigue of the Cu/MXene/polymer/Cu sensor. Using finite element analysis and theoretical calculations, we reveal that the MXene/polymer interfaces are affected by free volume changes and the molecular chain motion under different temperatures. At room temperature, the well-distributed free volume in the polydimethylsiloxane (PDMS) matrix permits local segmental mobility that promotes the affinity between the polymer and MXene. As the temperature decreases, the free volume in the matrix shrinks with less space left for molecular chains to slide relatively, weakening the polymer/MXene interfacial bonding strength. However, for PDMS/MXene sensors with the interface modified using the silane coupling agent KH550, the nanoconstrained structure formed by strong hydrogen bonds and covalent bonds at the PDMS/MXene interface can hinder the mobility of polymer chains, which greatly helps to dissipate the inter/intrachain friction. It thus alleviates the debonding energy dissipation during cyclic bending at subzero temperatures.

Introducing electrolysis to enhance anaerobic digestion resistance to acidification.

The phenomenon that the anaerobic system is inhibited by acid has always been a bottleneck hindering the application of anaerobic digestion (AD) technology. We tried to introduce electrolysis into AD to improve the acidification resistance, and eventually the productivity of the energy. In a batch fermentation device, the ability of electrochemical anaerobic digestion (EAD) to resist acidification was evaluated in current intensity, electrode potential, AC impedance, microbial community, pH value, and volatile fatty acids (VFAs). The results showed that the average concentration of VFAs in EAD was 32.9% lower than that in AD, the energy efficiency of EAD is 53.25% higher than AD, indicating that EAD has stronger anti-acidification ability and energy conversion efficiency than AD. When the EAD reaches a steady state, the current intensity fluctuates in the range of 7-12 mA, the electrode potential difference is maintained at 600 ± 5 mV, and the internal resistance decreases from 3333.3 ± 16Ω at startup to 68.9 ± 1.4Ω at the steady state, indicating that the EAD has stronger resistance to acidification may be due to the degradation of some VFAs on the electrode surface. Furthermore, the 16S rRNA sequencing analysis showed that the dominant electricity-producing bacteria on EAD anode surface were Clostridium, Hydrogenophaga and Trichloromonas, with a relative abundance of 40.32%, while the relative abundance of electrogenic bacteria in AD bulk solution and EAD bulk solution were about 1/2 and 1/4 that of EAD anode film, suggesting that the electricity-producing bacteria on the electrode surface play an important role in the degradation of VFAs.

Acupuncture for Quality of Life in Gastric Cancer Patients Undergoing Adjuvant Chemotherapy.

CONTEXT: Patients with gastric cancer experience health-related quality of life (HRQOL) decline during adjuvant chemotherapy following gastrectomy. OBJECTIVES: This pilot study aimed to evaluate the preliminary effect and feasibility of electro-acupuncture (EA) for HRQOL and symptom burden in these patients. METHODS: In this open-label, multicenter, parallel controlled trial, gastric cancer patients who planned to receive adjuvant chemotherapy were randomly assigned to receive high-dose EA (seven times each chemotherapy cycle for three cycles), low-dose EA (three times each chemotherapy cycle), or usual care only. The acupoints prescription consisted of bilateral ST36, PC6, SP4, and DU20, EX-HN3, and selected Back-shu points. Patients completed the Functional Assessment of Cancer Therapy-Gastric (FACT-Ga) weekly, and the Edmonton Symptom Assessment System (ESAS). The primary outcome was the difference among the groups on the gastric cancer subscale (GaCS) of the FACT-Ga. RESULTS: Of the 66 randomized patients, 58 were analyzed according to intention-to-treat principle, and 45 were in the per-protocol set (PPS). The average scores in PPS of GaCS were 52.12±9.71, 51.85±12.36, and 45.37±8.61 in high-dose EA, low-dose EA, and control groups, respectively. EA was significantly associated with improved average GaCS scores when compared with control group (51.98±10.91 vs. 45.37±8.61, P = 0.039). EA treatment also produced ESAS relief at the end of intervention (14.36 ± 12.28 vs. 23.91 ± 15.52, P = 0.027). Participants in EA groups had fewer grade ≥3 leukopenia (0% vs. 15.79%, P = 0.031) and neutropenia (2.56% vs. 26.31%, P = 0.012). CONCLUSION: EA showed promising effects in improving HRQOL, controlling symptom burden, and reducing toxicity during adjuvant chemotherapy in gastric cancer patients. Future adequately powered trials are feasible and needed to confirm the specific effect of EA.

MiR-146a functions as a potential tumor suppressor in retinoblastoma by negatively regulate neuro-oncological ventral antigen-1.

MicroRNAs (miRNAs) are dysregulated in many tumors and have been found to play crucial roles in cancer biology. Retinoblastoma is a rare tumor that develops rapidly from a malignant tumor of immature cells in the retina known as photoreceptor progenitors. Our study aimed to explore the role of miR-146a in the pathology of retinoblastoma. Potential target gene of miR-146a was predicted by Targetscan. Reverse transcription quantitative polymerase chain reaction (RT-PCR) showed that miR-146a was downregulated and ventral nerve tumor antigen 1 (Neuro - oncological ventral antigen 1, NOVA1) was upregulated in retinoblastoma. Luciferase assay confirmed that miR-146a directly target NOVA1. MiR-146a knockdown and overexpression experiments were performed and found that miR-146a could regulate the expression of NOVA1. The miR-146a knockdown and overexpression experiments were conducted to investigate the biological function of miR-146a. MiR-146a was found inhibited the viability, proliferation and invasion of retinoblastoma cell by MTT, EdU, and transwell assays. Flow cytometry was performed for the apoptosis analysis and miR-146a increased the apoptosis of retinoblastoma cell was found. Above phenomenon can be rescued by overexpression of NOVA1. In conclusion, these results suggest that miR-146a acts as a tumor suppressor and can act as a potential therapeutic target for retinoblastoma in the future.

PP2A inhibition by LB-100 protects retinal pigment epithelium cells from UV radiation via activation of AMPK signaling.

AMP-activated protein kinase (AMPK) signaling activation can inhibit Ultra-violet (UV) radiation (UVR)-induced retinal pigment epithelium (RPE) cell injuries. LB-100 is a novel inhibitor of protein phosphatase 2A (PP2A), the AMPKα1 phosphatase. Here, our results demonstrated that LB-100 significantly inhibited UVR-induced viability reduction, cell death and apoptosis in established ARPE-19 cells and primary murine RPE cells. LB-100 activated AMPK, nicotinamide adenine dinucleotide phosphate (NADPH) and Nrf2 (NF-E2-related factor 2) signalings, inhibiting UVR-induced oxidative injuries and DNA damage in RPE cells. Conversely, AMPK inhibition, by AMPKα1-shRNA, -CRISPR/Cas9 knockout or -T172A mutation, almost blocked LB-100-induced RPE cytoprotection against UVR. Importantly, CRISPR/Cas9-mediated PP2A knockout mimicked and nullified LB-100-induced anti-UVR activity in RPE cells. Collectively, these results show that PP2A inhibition by LB-100 protects RPE cells from UVR via activation of AMPK signaling.

Bending effect on the resistive switching behavior of a NiO/TiO2 p-n heterojunction.

Herein, NiO/TiO2 heterojunctions were fabricated by sol-gel spin coating on plastic substrates to investigate the effects of bending on resistive switching. The switching mechanism is well explained by the formation and rupture of oxygen-vacancy conducting filaments modulated by the p-n interface. Compared with that of the unbent film, the device ON/OFF ratio is slightly improved after 5000 bending repetitions. Finite element calculations indicate that the tensile stress of 0.79% can lead to the formation of channel cracks. Further charge transport analysis shows that the conducting filaments may cause an incomplete rupture because the bending-induced channel crack permeates through the p-n interface and reduces the local depletion-region width.

[Effect of Apollon siRNA combined with tetramethylpyrazine on proliferation and apoptosis of leukemia K562 cells].

OBJECTIVE: To investigate the effect of small interfering RNA (siRNA) silencing Apollon gene combined with tetramethylpyrazine (TMP) on the proliferation and apoptosis of human chronic myeloid leukemia cell line K562. METHODS: K562 cells were divided into blank control, negative control, and RNA interference (RNAi) group. For the RNAi group, the pGPHI-GFP-Neo-Apollon eukaryotic expression vector based on the best Apollon siRNA fragments screened out in previous experiments was constructed; the blank control group received no treatment, and the negative control group was transfected with negative plasmid vector. The mRNA and protein expression of Apollon was measured by RT-PCR and cell immunofluorescence, respectively. Additionally, TMP (320 µg/mL) was applied to set TMP, TMP+negative control, and TMP+RNAi groups. The cell viability and apoptosis rate were determined by MTT assay and flow cytometry, respectively. RESULTS: The constructed vector was stably expressed in K562 cells. The RNAi group had significantly lower mRNA and protein expression of Apollon than the blank control group and negative control (P<0.05). The RNAi group had significantly increased proliferation inhibition rate and apoptosis rate, as compared with the blank contorl group (P<0.05). The TMP+RNAi group had significantly increased proliferation inhibition rate and apoptosis rate, as compared with the RNAi, and TMP groups (P<0.05). CONCLUSIONS: Apollon siRNA can significantly inhibit the proliferation and promote the apoptosis of K562 cells, and the addition of TMP can further increase the proliferation inhibition rate and apoptosis rate, suggesting that siRNA technology combined with drugs has a significant potential value in the treatment of leukemia.

Conductance Switching and Photovoltaic Effect of Ru(II) Complex Molecular Junctions: Role of Complex Properties and the Metal/Molecule Interface.

The charge transport of Ru(II) complex molecular junctions, fabricated using a soft stamp-printing method, was investigated from 95 to 299 K under both dark and light conditions in order to explore the roles of the electrode/molecule interface and complex properties in the device performance. The junctions show asymmetric current-voltage characteristics with conductance switching and a photovoltaic effect at low temperature. The device performance depends greatly on the redox characteristics and built-in potential induced by electrode/molecule interface(s) and the molecular dipole. Our work may provide valuable information for the design of novel molecular electronics.

[Effect of astragalus injection on U937 leukemia cells proliferation and apoptosis and relevant molecular mechanisms].

OBJECTIVE: To study the effect of astragalus injection on U937 leukemia cells proliferation and apoptosis and relevant molecular mechanisms. METHODS: Leukemia cell line U937 cells were treated with different concentrations of astragalus (62.5, 125, 250, 500, 1 000 µg/mL). The U937 cells without astragalus treatment were used as the control group. The ability of cell proliferation was measured by MTT method. Flow cytometry was used to explore cell apoptosis. The cell morphology changes were observed under a fluorescent microscope by dyeing Hoechst33258. mRNA expression of c-myc and p27 in U937 cells which was exposed in 1 000 µg/mL astragalus after 0, 12, 24 and 48 hours was detected by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Various concentrations of astragalus injection inhibited U937 cell proliferation effectively compared with the control group (P<0.05). They also induced U937 cells apoptosis and the apoptosis rate reached to (63 ± 4)% in the 1 000 µg/mL astragalus treatment group. mRNA expression level of c-myc was gradually declined and p27 mRNA expression was gradually increased with astragalus treatment time (P<0.01). CONCLUSIONS: Astragalus injection may inhibit proliferation and induce apoptosis of leukemia cell line U937 in vitro. This contributes to down-regulation of c-myc expression and up-regulation of p27 expression.

[Expression of homeobox gene HOXA9 in childhood acute leukemia, and its clinical significance].

OBJECTIVE: To investigate the expression of homeobox gene HOXA9 in the bone marrow mononuclear cells of children with acute leukemia (AL) and its clinical significance. METHODS: Forty-six children with AL were divided into acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) groups. Fifteen children with idiopathic thrombocytopenic purpura were selected as a control group. The mRNA expression of HOXA9 was measured by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: HOXA9 expression was detected in 63% of the 52 bone marrow samples from 46 AL children. The positive HOXA9 expression rate in the AML group was significantly higher than in the ALL and control groups (86% vs 35% and 13%; P<0.05). The mRNA expression of HOXA9 in the AML group was significantly higher than in the ALL and control groups (P<0.05). Among the children with AML, those with M5 AML had the highest HOXA9 mRNA level, followed by children with M4 AML and children with M1 and/or M2 AML, but HOXA9 expression was not detected in children with M3 AML. The high-risk subgroup of AML children had relatively high levels of HOXA9 expression. In the children with AML, the initial treatment subgroup had significantly higher positive HOXA9 expression rate and HOXA9 mRNA levels than in the remission subgroup and control group (P<0.05), but there were no significant differences between the latter two groups (P>0.05). The non-remission subgroup had significantly higher HOXA9 expression than the remission subgroup and control group (P<0.05). CONCLUSIONS: High expression of HOXA9 is associated with the occurrence of AL, and its expression level is significantly higher in children with AML than in those with ALL. There is a positive correlation between the expression level of HOXA9 and the risk of childhood leukemia, and high expression of HOXA9 suggests poor prognosis. Therefore, HOXA9 can be used as one of the indices in the diagnosis, treatment and prognosis prediction of childhood AL.

[Effect of HOXA10 gene silenced by shRNA on proliferation and apoptosis of U937cell line].

OBJECTIVE: To investigate the effects of lentivirus-mediated RNA interference targeting HOXA10 gene on the proliferation, apoptosis and morphology of leukemic cell line U937. METHODS: Four different shRNA plasmids were designed and built to interfere with HOXA10 gene. The four interference plasmids were transfected into 293T cells with the HOXA10 over expression plasmid and then the RNAi efficiency of the four interference plasmids was determined by Western blot. The best one was chosen to transfect 293T cells with lentiviral helping plasmids to produce packaged lentivirus (lenti-shHOXA10). U937 cells were divided into interference group (lenti-shHOXA10), negative control group and untreated group. After infection with the packaged lentivirus, infection efficiency of lentivirus for U937 was detected by flow cytometry, and the expression of HOXA10 gene mRNA and protein was detected by real-time PCR and Western blot. Cell survival was determined by MTT assay. Apoptosis rate was detected by flow cytometry. RESULTS: Lentiviral-shRNA vector of HOXA10 gene was successfully constructed. Compared with the negative control and untreated groups, mRNA level of HOXA10 decreased by (92.3±1.3)%, protein levels decreased by 91.1%, and the inhibition rate of U937 cells [(43.9±0.7)%] increased in the interference group (P<0.05). Wright's staining showed that the ratio of karyon to cytoplasm was reduced and mitotic phase was rare in the interference group. Apoptosis rate in the interference group [(27.1±1.4)%] was significantly higher than in the negative [(19.4±1.9)%] and untreated groups [(5.5±1.3)%] (P<0.05). CONCLUSIONS: Lentivirus mediated RNAi can reduce the expression level of HOXA10, effectively inhibit proliferation and promote apoptosis of U937 cells. HOXA10 gene is expected to become a new target for the treatment of leukemia at gene level.

[Effects of bone marrow stromal cells and VLA-4 antibody on apoptosis of childhood leukemia cells].

OBJECTIVE: To study the protective effect of bone marrow stromal cells (BMSCs) upon childhood leukemia cells and the influence of VLA-4 antibody in vitro on leukemia cell apoptosis. METHODS: BMSCs from children with acute leukemia-were isolated by human lymphocyte separation medium. BMSCs (adherent) and leukemia cells (suspended) were cultured in vitro. This study included four groups: leukemia cells alone (control), leukemia cells+BMSCs, leukemia cells+BMSCs supernatant and leukemia cells+BMSCs+VLA-4 antibody. The apoptosis rate of leukemia cells in the four groups was determined by Annexin Ⅴ-FITC double-labeled flow cytometry. The expression of survivin and bcl-2 genes in leukemia cells was ascertained by RT-PCR. RESULTS: The apoptosis rate of leukemia cells in the leukemia cells+BMSCs and the leukemia cells+BMSCs supernatant groups was lower than that in the control group (P<0.05). Compared with the leukemia cells+BMSCs and the leukemia cells+BMSCs supernatant groups, the apoptosis rate of leukemia cells in the VLA-4 antibody group increased significantly (P<0.05). In the VLA-4 antibody group, the apoptosis rate of leukemia cells increased with prolonged culture time. There were significant differences in the apoptosis rate between 12 hrs and 24 hrs after VLA-4 antibody treatment (P<0.01). The expression of survivin and bcl-2 genes in leukemia cells from the VLA-4 antibody groups was reduced compared with that from the leukemia cells+BMSCs and the leukemia cells+BMSCs supernatant groups (P<0.05). CONCLUSIONS: BMSCs play protective roles on leukemia cells. VLA-4 antibody can block the adhesion between BMSCs and leukemia cells and promote leukemia cell apoptosis.

[Radiofrequency thermal ablation combined with arterial embolization for primary liver cancer].

OBJECTIVE: To explore the short-term effect of radiofrequency ablation (RFA) combined with arterial embolization in treating patients with primary liver cancer. METHODS: Thirty patients with primary liver cancer received the combined treatment and the pre- and post-operative alpha-fetoprotein (AFP) levels, imaging features, and liver function were investigated along with observation of the incidence of complications to evaluate the therapeutic effects. RESULTS: The post-operative AFP positivity and the tumor density were significantly reduced in these patients, and their one-year survival rate reached 96.7% with only minor complications observed. CONCLUSION: RFA combined with arterial embolization is effective for primary liver cancer.