Design and Research of All-Terrain Wheel-Legged Robot.

Aiming at the crossing problem of complex terrain, to further improve the ability of obstacles crossing, this paper designs and develops an all-terrain wheel-legged hybrid robot (WLHR) with strong adaptability to the environment. According to the operation requirements in different road conditions, the robot adopts a wheel and leg compound structure, which can realize the transformation of wheel movement and leg movement to adjust its motion state. The straight and turning process of the robot is analyzed theoretically, the kinematics model is established and solved, and obstacle crossing analysis is carried out by establishing the mathematical model of front wheel obstacle crossing when the robot meets obstacles. To verify the analysis results, ADAMS software is used to simulate and analyze the process of robot running on the complex road surface and obstacles-crossing. Finally, a theoretical prototype is made to verify its feasibility. Theoretical analysis and experimental results show that the designed WLHR is feasible and has the stability of the wheeled mechanism and the higher obstacle crossing ability of the legged mechanism so that the robot can adapt to a variety of complex road conditions.

Obstacle Avoidance of Multi-Sensor Intelligent Robot Based on Road Sign Detection.

The existing ultrasonic obstacle avoidance robot only uses an ultrasonic sensor in the process of obstacle avoidance, which can only be avoided according to the fixed obstacle avoidance route. Obstacle avoidance cannot follow additional information. At the same time, existing robots rarely involve the obstacle avoidance strategy of avoiding pits. In this study, on the basis of ultrasonic sensor obstacle avoidance, visual information is added so the robot in the process of obstacle avoidance can refer to the direction indicated by road signs to avoid obstacles, at the same time, the study added an infrared ranging sensor, so the robot can avoid potholes. Aiming at this situation, this paper proposes an intelligent obstacle avoidance design of an autonomous mobile robot based on a multi-sensor in a multi-obstruction environment. A CascadeClassifier is used to train positive and negative samples for road signs with similar color and shape. A multi-sensor information fusion is used for path planning and the obstacle avoidance logic of the intelligent robot is designed to realize autonomous obstacle avoidance. The infrared sensor is used to obtain the environmental information of the ground depression on the wheel path, the ultrasonic sensor is used to obtain the distance information of the surrounding obstacles and road signs, and the information of the road signs obtained by the camera is processed by the computer and transmitted to the main controller. The environment information obtained is processed by the microprocessor and the control command is output to the execution unit. The feasibility of the design is verified by analyzing the distance acquired by the ultrasonic sensor, infrared distance measuring sensors, and the model obtained by training the sample of the road sign, as well as by experiments in the complex environment constructed manually.

LncRNA MALAT1 Aggravates the Progression of Non-Small Cell Lung Cancer by Stimulating the Expression of COMMD8 via Targeting miR-613.

BACKGROUND: Non-small cell lung cancer (NSCLC) is a common malignant tumor in humans. Long non-coding RNA (lncRNA) involved in cancer progression has been reported frequently. The objective of this study was to investigate the role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and explore a novel mechanism in NSCLC development. MATERIALS AND METHODS: The expression of MALAT1, copper metabolism MURR1 domain-containing 8 (COMMD8) and microRNA-613 (miR-613) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of COMMD8, Cyclin D1, Ki67, B cell lymphoma/leukemia-2 (Bcl-2), Bcl-2 associated X protein (Bax), lactate dehydrogenase A (LDHA), CD63 and CD81 were determined by Western blot. Cell proliferation, the number of colonies and cell apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation and flow cytometry assays, respectively. Glycolysis was distinguished based on glucose consumption, lactate production and LDHA activity. The role of MALAT1 in vivo was verified by animal experiments. The relationship between miR-613 and MALAT1 or COMMD8 was predicted by the bioinformatics tool starbase and verified by dual-luciferase reporter assay. The exosomes were isolated using the corresponding kit and identified by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). RESULTS: MALAT1 and COMMD8 were aberrantly upregulated in NSCLC tissues and cells. MALAT1 or COMMD8 knockdown blocked cell proliferation, colony formation and glycolysis but accelerated cell apoptosis in vitro. Besides, MALAT1 knockdown reduced tumor growth in vivo. We found that miR-613 was a target of MALAT1, and miR-613 could bind to the 3' untranslated region (3'UTR) of COMMD8. MALAT1 regulated the expression of COMMD8 by absorbing miR-613. Moreover, the extracellular MALAT1 was transmitted by wrapping into exosomes. CONCLUSION: MALAT1 promoted malignant activities of NSCLC cells through targeting miR-613/COMMD8 axis, and exosome-mediated transfer of NSCLC might be a novel approach for NSCLC treatment.

Overexpression of CTHRC1 in human melanoma promotes tumorigenesis targeted by miRNA155.

Most of human malignant melanoma is metastatic and invasive, which has poor therapeutic response and poor prognosis as well as high incidence worldwide. CTHRC1 was overexpressed in metastatic primary melanomas. The relationship between CTHRC1 and miRNA in affecting the melanoma has not been studied. This study was aimed to explore the function of CTHRC1 in human melanoma and finding its regulator miRNA. CTHRC1 and miR155 expression in cancer tissues and paracancer tissues was examined. The cell proliferation, cell cycle, cell migration and cell invasion was evaluated in M21 cell transfected with CTHRC1 siRNA or miR155. The mRNA expression of miR155 in cancer tissues was lower than that in paracancer tissues. The mRNA expression of CTHRC1 in the cancer tissues was higher than that in corresponding paracancer tissues. The mRNA expression of CTHRC1 in the M21 cells was decreased by treated with miR155 mimic. CTHRC1 promoted the cell proliferation, cell cycle process, cell migration and invasion capacity and prevented the cell from apoptosis. miR155 inhibited the cell proliferation, cell migration and cell invasion, arrested the cell cycle process at G1 phase and enhanced the cell apoptosis. The luciferases reporter assay showed that miR155 bound to the 3'-UTR of CTHRC1 and regulated the expression of CTHRC1, further influenced the functions of CTHRC1 in human melanoma development. The study contributed to unearthing a novel potential predictor and therapeutic targets of human melanoma. CTHRC1 was a potential independent predictor and therapeutic target for human melanoma.

Haptoglobin protein and mRNA expression in psoriasis and its clinical significance.

The present study aimed to explore the association between haptoglobin protein and mRNA expression and psoriasis. A total of 138 patients with psoriasis that were undergoing therapy at Linyi People's Hospital (Linyi, China) between January 2011 and January 2015 were enrolled in the present study. The mRNA expression levels of haptoglobin were detected by in situ hybridization; immunohistochemistry was used to detect haptoglobin protein expression; and double­labeling immunofluorescence was used to count Langerhans cells; western blotting was also conducted to determine protein expression. A receiver operating characteristic (ROC) curve was generated to assess the diagnostic value of haptoglobin for psoriasis. Compared with the normal and negative control (NC) groups, the mRNA expression levels of haptoglobin were markedly increased in the experimental group (P<0.05). Haptoglobin protein expression was also markedly increased in the experimental group compared with in the normal and NC groups (P<0.05). Conversely, there was no significant difference in haptoglobin expression between the NC group and the normal group (P>0.05). The critical value of haptoglobin mRNA in the diagnosis of psoriasis was 2.93, and sensitivity and specificity were 91.3 and 73.6%, respectively. The area under the ROC curve was 0.883 [95% confidence interval (CI)=0.837­0.929]. The critical value of haptoglobin protein in the diagnosis of psoriasis was 0.995, and sensitivity and specificity were 76.1 and 99.9%, respectively. The area under the ROC curve was 0.926 (95% CI=0.837­0.929). The present study demonstrated that the mRNA and protein expression levels of haptoglobin were increased in patients with psoriasis. Haptoglobin mRNA and protein expression were closely associated with the occurrence of psoriasis; therefore, haptoglobin may be considered a promising novel clinical indicator for the diagnosis of psoriasis.

Adenovirus siMDM2 and NDRG2 Gene Therapy Inhibits Cell Proliferation and Induces Apoptosis of Squamous Cell Carcinoma.

Squamous cell carcinoma (SCC) is one of the most common skin cancers. In the present study, we explored the effects of depletion of murine double minute gene 2 (MDM2) together with overexpression of N-myc downstream-regulated gene 2 (NDRG2) on cutaneous SCC. In order to achieve high efficiency of gene knockdown and overexpression in SCC-13 cells, recombinant adenovirus carrying siMDM2 and NDRG2 expression construct was produced. We found Ad-siMDM2, Ad-NDRG2, and Ad-siMDM2-NDRG2 infections inhibit the growth of SCC-13 cells in vitro, and Ad-siMDM2-NDRG2 infection has the highest inhibitory effect. Subcutaneous injections of Ad-siMDM2, Ad-NDRG2, and Ad-siMDM2-NDRG2 into SCC-13 xenograft nude mice resulted in the reduction of tumor volume. Moreover, we found that apoptosis protein caspase 3 was up-regulated in the Ad-siMDM2-, Ad-NDRG2-, and Ad-siMDM2-NDRG2-treated groups. Our data indicate that the adenovirus-mediated MDM2 silencing and NDRG2 overexpression can synergistically inhibit local cancer cell proliferation, induce apoptosis, and further prevent metastases of SCC. Our study provides a promising method that can be further developed as a new therapeutic approach against SCC.