ABSTRACT
In this paper, a photonic-assisted system for simultaneous and unambiguous measurement of the Doppler frequency shift (DFS) and angle-of-arrival (AOA) using a dual-parallel dual-drive Mach-Zehnder modulator (DP-DDMZM) is proposed and investigated. The echo signals received by two receiving antennas are applied to the radio frequency ports of one sub-DDMZM of the DP-DDMZM. The bias port of the sub-DDMZM is fed by a binary electrical signal that is used to construct two different mapping curves on the relationship between the phase difference and the power of the output intermediate frequency (IF) signal. Therefore, unambiguous AOA measurement with extended range can be realized. The transmitted signal is input into the other sub-DDMZM to implement single-sideband modulation, which is then frequency shifted based on serrodyne modulation. Both the value and direction of DFS can be derived intuitively from the frequency of the output IF signal. Simulation results show that the measurement error of unambiguous DFS measurement is no more than ±0.008H z in the range of -100k H z to 100 kHz, and the measurement error of unambiguous AOA is less than ±0.2∘ in the range of -70.8∘ to 70.8°. Moreover, since the scheme does not involve the construction of multi-channels or use of any filter or polarization dependent device, the system has concise structure, high accuracy, large operating bandwidth, and strong robustness, and can be considered as a very promising solution for actual applications.
ABSTRACT
BACKGROUND: Upregulation of lncRNA BBOX1 antisense RNA 1 (BBOX1-AS1) has been examined in various tumors. However, its role in nasopharyngeal carcinoma (NPC) remains poorly understood. METHODS: RT-qPCR was performed to measure the expression of BBOX1-AS1, KPNA2, and miR-3940-3p. In vitro assays were performed to determine the alteration of cell phenotypes in NPC cells upon transfection or co-transfection with sh-BBOX1-AS1, sh-KPNA2, or miR-3940-3p inhibitor. The BBOX1-AS1-miR-3940-3p and miR-3940-3p-KPNA2 interplay was verified via luciferase reporter and RNA pull-down assays. RESULTS: High BBOX1-AS1 levels were detected in the nasopharyngeal carcinoma tissues. BBOX1-AS1 silencing considerably suppressed the proliferative, migratory, and invasive abilities of NPC cells in vitro. Interestingly, BBOX1-AS1 could specifically bind to miR-3940-3 and abrogate the inhibition of KPNA2 induced by miR-3940-3. Additionally, analysis of tissue samples showed that miR-3940-3 was inversely correlated with BBOX1-AS1 and KPNA2. CONCLUSION: Our findings revealed that the BBOX1-AS1/miR-3940-3/KPNA2 axis is pro-oncogenic in NPC progression, uncovering novel insights into targeted therapy for this disorder.
ABSTRACT
@#[Abstract] Objective: To explore the anti-tumor activity of oncolytic adenovirus co-expressing lymphocyte activation gene 3 (LAG-3) antibody (aLAG) against glioblastoma. Methods: aLAG sequence was inserted into the skeleton of oncolytic adenovirus Ad3 to obtain recombinant oncolytic adenovirus (Ad3-aLAG). The expression of aLAG in infected gliblastoma GL261 cells was detected by WB. The cytotoxicity of recombinant oncolytic adenovirus against glioblastoma was detected by MTT method. The tumor inhibitory activity of recombinant oncolytic adenovirus against glioblastoma in vivo was evaluated with mice subcutaneous xenograft model. Tumor infiltrating T cells were detected by immunohistochemical staining, and the levels of cytokines TNF-α and IFN-γ secreted by tumor infiltrating T cells were detected by Flow cytometry. Results: The recombinant oncolytic adenovirus was successfully constructed, which could effectively express aLAG and kill GL261 cells in vitro (all P<0.01). Experimental results of mice subcutaneous xenograft model showed that the tumor inhibition ability of recombinant oncolytic adenovirus Ad3-aLAG was stronger than that of Ad3 oncolytic adenovirus (P<0.01), and Ad3-aLAG could effectively enhance the infiltration of CD3+ T cells in tumor tissue (P<0.01) and enhance the IFN-γ secretion ability of infiltrating T cells (P<0.01). Conclusion: Ad3-aLAG recombinant oncolytic adenovirus can significantly inhibit the growth of glioblastoma cells in vivo and in vitro, and enhance the anti-tumor immune response in vivo, which is promising to provide a new scheme for the treatment of glioblastoma.
ABSTRACT
@#[Abstract] Objective: To explore the effect of exosome-derived miR-181a on angiogenesis and tumor progression in gliomas. Methods: 83 cases of glioma tissues and 13 cases of peritumoral tissues resected in the Second Affiliated Hospital of Hainan Medical University from August 2017 to December 2019, glioma cells U87, A172, U251, LN229, U373 and microglial cell line HM, were selected to detect the expression of miR-181a in tumor tissues and cells by qPCR method. Glioma U373 cells with miR-181a over-expression or knockdown were constructed, and exosomes were isolated and identified. The effects of exsome-derived miR-181a on angiogenesis of HUVEC cells were investigated by tubule formation and chicken chorioallantoic membrane assay in vitro. Nude mice bearing U373 cell transplanted xenograft was constructed to observe the effect of exsome-derived miR-181a on angiogenesis and tumor growth in vivo. Results: The expression of miR-181a in glioma tissues and cells was significantly higher than that in normal tissues and normal glial HM cells (all P<0.01). The exsome-derived miR-181a could significantly promote the tubule formation of HUVEC cells (P<0.01) and the angiogenesis of chicken chorioallantoic membrane (all P<0.01). In vivo experiments showed that the growth of xenografts was promoted (P<0.05) and the amount of angiogenesis in the tumor tissues was increased in the nude mice after being transfused with exsome-derived miR-181a (P<0.01). Conclusion: miR-181a plays an important role in promoting angiogenesis of gliomas and may be a potential target for diagnosis and treatment of gliomas.
ABSTRACT
BACKGROUND: lncRNA MIR17HG was upregulated in glioma, and participated in promoting proliferation, migration and invasion of glioma. However, the role of MIR17HG polymorphisms in the occurrence and prognosis of glioma is still unclear. METHODS: In the study, 592 glioma patients and 502 control subjects were recruited. Agena MassARRAY platform was used to detect the genotype of MIR17HG polymorphisms. Logistic regression analysis was used to evaluate the relationship between MIR17HG single nucleotide polymorphisms (SNPs) and glioma risk by odds ratio (OR) and 95% confidence intervals (CIs). Kaplan-Meier curves, Cox hazards models were performed for assessing the role of these SNPs in glioma prognosis by hazard ratios (HR) and 95% CIs. RESULTS: We found that rs7318578 (OR = 2.25, p = 3.18 × 10- 5) was significantly associated with glioma susceptibility in the overall participants. In the subgroup with age < 40 years, rs17735387 (OR = 1.53, p = 9.05 × 10- 3) and rs7336610 (OR = 1.35, p = 0.016) were related to the higher glioma susceptibility. More importantly, rs17735387 (HR = 0.82, log-rank p = 0.026) were associated with the longer survival of glioma patients. The GA genotype of rs17735387 had a better overall survival (HR = 0.75, log-rank p = 0.013) and progression free survival (HR = 0.73, log-rank p = 0.032) in patients with I-II glioma. We also found that rs72640334 was related to the poor prognosis (HR = 1.49, Log-rank p = 0.035) in female patients. In the subgroup of patients with age ≥ 40 years, rs17735387 was associated with a better prognosis (HR = 0.036, Log-rank p = 0.002). CONCLUSION: Our study firstly reported that MIR17HG rs7318578 was a risk factor for glioma susceptibility and rs17735387 was associated with the longer survival of glioma among Chinese Han population, which might help to enhance the understanding of MIR17HG gene in gliomagenesis. In subsequent studies, we will continue to collect samples and follow up to further validate our findings and further explore the function of these MIR17HG SNPs in glioma in a larger sample size.
Subject(s)
Brain Neoplasms/genetics , Glioma/genetics , RNA, Long Noncoding/genetics , Adult , Asian People/genetics , Disease Susceptibility , Female , Genetic Predisposition to Disease , Humans , Male , Polymorphism, Single Nucleotide , Prognosis , Risk FactorsABSTRACT
OBJECTIVE: To investigate the treatment efficacy of tympanostomy microtube placement surgery for middle ear atelectasis. METHODS: A retrospective analysis was conducted on 26 patients (28 ears) with middle ear atelectasis, who complained fullness or pressure in the ears.Otoscope showed tympanic membrane invagination, scattered or disappeared cone of light, tympanic membrane was pale and dull. The pure tone audiometry air-bone gap >10 dB. Acoustic immittance showed tympanic negative pressure. All the ears had atelectasis of I-III grade. Patients were performed tympanic membrane microtube placement under local anesthesia, and were followed up for 6-12 months. RESULTS: Twenty-five ears recovered from the fullness after operation, in which, 23 ears reverted from type "C" to type "A" in acoustic immittance tests and the pure-tone average (PTA) of hearing thresholds were decreasing from 5 to 20 dB, while 2 ears relapse after removal of the microtube. Three ears with middle ear atelectasis of III grade were ineffectiveness. All the 26 cases had no complications including middle ear infection, tympanosclerosis, and permanent perforation after removal of the microtubes. CONCLUSIONS: The placement of tympanostomy microtube can be used to treat middle ear atelectasis, especially to the patients with middle ear atelectasis of I-II grade as it is effective on elimination of middle ear negative pressure and remission of fullness.