Microwave Speech Recognizer Empowered by a Programmable Metasurface.

Speech recognition becomes increasingly important in the modern society, especially for human-machine interactions, but its deployment is still severely thwarted by the struggle of machines to recognize voiced commands in challenging real-life settings: oftentimes, ambient noise drowns the acoustic sound signals, and walls, face masks or other obstacles hide the mouth motion from optical sensors. To address these formidable challenges, an experimental prototype of a microwave speech recognizer empowered by programmable metasurface is presented here that can remotely recognize human voice commands and speaker identities even in noisy environments and if the speaker's mouth is hidden behind a wall or face mask. The programmable metasurface is the pivotal hardware ingredient of the system because its large aperture and huge number of degrees of freedom allows the system to perform a complex sequence of sensing tasks, orchestrated by artificial-intelligence tools. Relying solely on microwave data, the system avoids visual privacy infringements. The developed microwave speech recognizer can enable privacy-respecting voice-commanded human-machine interactions is experimentally demonstrated in many important but to-date inaccessible application scenarios. The presented strategy will unlock new possibilities and have expectations for future smart homes, ambient-assisted health monitoring, as well as intelligent surveillance and security.

Intelligent indoor metasurface robotics.

Intelligent indoor robotics is expected to rapidly gain importance in crucial areas of our modern society such as at-home health care and factories. Yet, existing mobile robots are limited in their ability to perceive and respond to dynamically evolving complex indoor environments because of their inherently limited sensing and computing resources that are, moreover, traded off against their cruise time and payload. To address these formidable challenges, here we propose intelligent indoor metasurface robotics (I2MR), where all sensing and computing are relegated to a centralized robotic brain endowed with microwave perception; and I2MR's limbs (motorized vehicles, airborne drones, etc.) merely execute the wirelessly received instructions from the brain. The key aspect of our concept is the centralized use of a computation-enabled programmable metasurface that can flexibly mold microwave propagation in the indoor wireless environment, including a sensing and localization modality based on configurational diversity and a communication modality to establish a preferential high-capacity wireless link between the I2MR's brain and limbs. The metasurface-enhanced microwave perception is capable of realizing low-latency and high-resolution three-dimensional imaging of humans, even around corners and behind thick concrete walls, which is the basis for action decisions of the I2MR's brain. I2MR is thus endowed with real-time and full-context awareness of its operating indoor environment. We implement, experimentally, a proof-of-principle demonstration at ∼2.4 GHz, in which I2MR provides health-care assistance to a human inhabitant. The presented strategy opens a new avenue for the conception of smart and wirelessly networked indoor robotics.

Nodal regulates bladder cancer cell migration and invasion via the ALK/Smad signaling pathway.

BACKGROUND: Bladder cancer is the most common malignant tumor of the urinary tract. We aimed to explore the biological role and molecular mechanism of Nodal in bladder cancer. MATERIALS AND METHODS: The expression of Nodal in bladder cancer tissues and cells was determined by quantitative real-time polymerase chain reaction. The effect of silencing of Nodal on cell proliferation, clone formation, and migration and invasion was evaluated by MTT cell proliferation assay, colony formation, and transwell assays, respectively. Western blot analysis was employed to detect the expression of proliferation- and invasion-related proteins and proteins involved in ALK/Smad signaling. RESULTS: We found that the expression of Nodal was significantly increased in bladder cancer tissues and cell lines. Downregulation of Nodal effectively weakened cell proliferation, clone formation, and cell migration and invasion abilities. The protein expression levels of CDC6, E-cadherin, MMP-2, and MMP-9 were also altered by downregulation of Nodal. Knockdown of Nodal also blocked the expression of ALK4, ALK7, Smad2, and Smad4, which are involved in ALK/Smad signaling. Additionally, the ALK4/7 receptor blocker SB431542 reversed the promotive effects of Nodal overexpression on bladder cancer cell proliferation, migration, and invasion. CONCLUSION: Our study indicated that Nodal functions as an oncogene by regulating cell proliferation, migration, and invasion in bladder cancer via the ALK/Smad signaling pathway, thereby providing novel insights into its role in bladder cancer treatment.

[Effect of hydrogen sulfide on antiatherosclerosis in rats].

OBJECTIVE: To investigate the effect of hydrogen sulfide (H2S) on artherosclerosis (AS) and its mechanism in rats. METHODS: 125 healthy male SD rats of the weight (210 +/- 10) g were randomly divided into 5 groups: control group, AS model group, AS + low-dose NaHS (2.8 micromol/(kg x d)) group, AS+ middle-dose (14 micromol/(kg x d)) NaHS group, AS+ high-dose NaHS (28 micromol/(kg x d)) group. The atherosclerotic model was established by feeding high grease food and injecting large doses of VitD3. The rats were using NaHS by peritoneal injection for 12 weeks. 5 rats were executed in each group before the experiment and in the weeks of 3, 6, 9, 12 after the experiment, respeotively. The blood fat was analyzed by automatic biochemistry analysator. H2S content in serum was detected by the method of deproteinization. The pathological damage of vessels was observed and scored by HE stain. The expression of VEGF in the vessel tissue was detected by immunohistochemistry staining. RESULTS: Compared with the control group at contemporaneity, both serumal triglyceride (TG) and cholesterol (TC) increased significantly in the AS model group after rat feeded 3, 6, 9, 12 weeks, and scores of the artery pathological damage also increased obviously from the 6th week to the 12th week (P < 0.01), as well as artherosclerosis plaque appeared, displaying as lipid plaque in the positive part. The serumal H2S concentration decreased obviously, from (44.98 +/- 2.06) micromol/L of before feeding to (38.56 +/- 2.26), (32.96 +/- 2.38), (28.63 +/- 0.92), (23.55 +/- 0.92) nnol/L of after feeding 3, 6, 9, and 12 weeks, respectively, and lower than that of control at contemporaneity (44.72 +/- 0.85), (43.71 +/- 0.59), (41.96 +/- 0.97), (39.87 +/- 1.25) micromol/L, respectively ( P < 0.01), and VEGF expression of the vascular tissue also increased (P < 0.01). Compared with the AS model group, all of above indexes in rat of the low-dose of NaHS group did not appear any obvious change. The serumal H2S concentration in rat of the middle-dose NaHS began increase at the 6 week after rat feeded (36.13 +/- 0.3 vs. 32.96 +/- 2.38 micronol/L, P < 0.05), and continuously increased at the 9th and the 12th week (33.07 +/- 1.14 vs. 28.63 +/- 0.92 micromol/L, 30.16 +/- 0.2 vs. 23.55 +/- 0.92 micromol/L; P < 0.01, respectively). The serumal H2S concentration in high-dose NaHS groups, increased from the 3th to the 12th week (41.25 +/- 0.80, 38.71 +/- 0.46, 35.31 +/- 0.62, 33.38 +/- 0.78 micromol/L, respectively, P < 0.01). The rat serumal TC in both middle and high-dose NaHS groups, decreased from the 3th to the 12th week (P < 0.01), and TG began decrease from the 3th and the 6th week to the 12th week after rat feeded, respectively (P < 0.05, P < 0.01). Both of the pathological damage scores and the expression of VEGF decrease from the 6th week to the 12th week (P < 0.05). The correlation analysis showed that H2S in serum had a negative correlation with both pathological damage scores (r = -0.917, P < 0.01) and the expression of VEGF (r = -0. 885, P < 0.01). But it had no obvious correlation with serumal TG and TC. CONCLUSION: The formation and development of artherosclerosis has a close correlation with the depressing of endogenous H2S. Administration of exogenous H2S could raise the H2S concentration of serum in artherosclerosis, which might improve the damage of vessels and inhibit the expression of VEGF.