A non-protein-coding RNA, UCA1, has been cloned from human bladder TCC cell line BLZ-211 by using 5 0 and 3 0 RACE. The UCA1 full-length cDNA was 1442 bp. RT-PCR analysis indicated that UCA1 is an embryonic development and bladder cancer-associated RNA. The proliferative, migrative, invasive, and drug resistance behaviors of human bladder TCC cell line BLS-211 were enhanced by exogenous UCA1 expression in vitro. Several potential target genes of UCA1 were identified through microarray analysis. Moreover, the expression of UCA1 also increased tumorigenic potential of BLS-211 cells in nude mice. Results from the present study suggested that UCA1 might play a pivotal role in bladder cancer progression and embryonic development.

Abstract-In this paper, we combine inertial sensing and sensor network technology to create a pedestrian dead reckoning system. The core of the system is a lightweight sensor-and-wireless-embedded device called NavMote that is carried by a pedestrian. The NavMote gathers information about pedestrian motion from an integrated magnetic compass and accelerometers. When the NavMote comes within range of a sensor network (composed of NetMotes), it downloads the compressed data to the network. The network relays the data via a RelayMote to an information center where the data are processed into an estimate of the pedestrian trajectory based on a dead reckoning algorithm. System details including the NavMote hardware/software, sensor network middleware services, and the dead reckoning algorithm are provided. In particular, simple but effective step detection and step length estimation methods are implemented in order to reduce computation, memory, and communication requirements on the Motes. Static and dynamic calibrations of the compass data are crucial to compensate the heading errors. The dead reckoning performance is further enhanced by wireless telemetry and map matching. Extensive testing results show that satisfactory tracking performance with relatively long operational time is achieved. The paper also serves as a brief survey on pedestrian navigation systems, sensors, and techniques.Index Terms-Dead reckoning, pedestrian navigation system, wireless sensor network.

Background: The Coronavirus Disease 2019 (COVID-19) has been demonstrated as the cause of pneumonia. Nevertheless, it has not been reported as the cause of acute myocarditis or fulminant myocarditis. Case Presentation: A 63-year-old male was admitted with pneumonia and cardiac symptoms. He was genetically confirmed as COVID-19 by testing sputum on the first day of admission. He also had an elevated troponin-I (Trop I) level and diffuse myocardial dyskinesia along with decreased left ventricular ejection fraction (LVEF) on echocardiography. The highest level of Interleukin 6 was 272.40pg/ml. Bedside chest radiograph had typical ground-glass changes of viral pneumonia. The laboratory test results of virus that can cause myocarditis are all negative. The patient conformed to the diagnostic criteria of Chinese expert consensus statement for fulminant myocarditis. After receiving antiviral therapy and mechanical life support, the Trop I reduced to 0.10 g/L, and Interleukin 6 was 7.63 pg/ml. Meanwhile the LVEF of the patient gradually recovered to 68%. Conclusion: COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure, and this is the first case of COVID-19 infection complicated with fulminant myocarditis. The mechanism of cardiac pathology caused by COVID-19 needs further study.

Together, our results revealed that urothelial carcinoma-associated 1 regulated the expression of GLS2 through interfering with miR-16, and repressed ROS formation in bladder cancer cells.

Background: Neuropathic pain is a type of chronic pain that results from dysfunctions of the somatosensory nerve system. This study was aimed to investigate the effect of mTOR/VEGF signaling pathway on neuropathic pain and the regulation mechanisms of miR-183 on AMPA Receptors through mTOR/VEGF signaling pathway. Methods: Chronic compress injury (CCI) model was constructed in the current study, we used paw withdrawal mechanic threshold (PWMT) and paw withdrawal thermal latency (PWTL) to observe mTOR and VEGF receptors. Dual luciferase analysis, western blot and qRT-PCR were also applied to complete this experiment. Results: It was observed that the inhibition of mTOR and VEGF receptors could significantly relieve neuropathic pain in the CCI model. Moreover mTOR was confirmed as the direct target of miR-183. Furthermore, miR-183 could modulate VEGF through regulating mTOR expressions. We also found the expressions of AMPA receptors (i.e. GluR1 and GluR2), located in the downstream of mTOR/VEGF signaling pathway, were significantly upregulated when miR-183 was downregulated or when the mTOR/VEGF signaling pathway was activated. Conclusion: The inhibition of mTOR or VEGF receptors can significantly relieve neuropathic pain, and the upregulation of miR-183 can suppress AMPA receptors by inhibiting mTOR/VEGF pathway.