A wireless controlled robotic insect with ultrafast untethered running speeds.

Running speed degradation of insect-scale (less than 5 cm) legged microrobots after carrying payloads has become a bottleneck for microrobots to achieve high untethered locomotion performance. In this work, we present a 2-cm legged microrobot (BHMbot, BeiHang Microrobot) with ultrafast untethered running speeds, which is facilitated by the complementary combination of bouncing length and bouncing frequency in the microrobot's running gait. The untethered BHMbot (2-cm-long, 1760 mg) can achieve a running speed of 17.5 BL s-1 and a turning centripetal acceleration of 65.4 BL s-2 at a Cost of Transport of 303.7 and a power consumption of 1.77 W. By controlling its two front legs independently, the BHMbot demonstrates various locomotion trajectories including circles, rectangles, letters and irregular paths across obstacles through a wireless control module. Such advancements enable the BHMbot to carry out application attempts including sound signal detection, locomotion inside a turbofan engine and transportation via a quadrotor.

Sirtuin 3 controls cardiac energetics and protects against oxidative stress in electromagnetic radiation-induced cardiomyopathy.

Electromagnetic radiation can cause injuries to both the structures and functions of the heart. No therapy is currently available to inhibit these untoward effects. Mitochondrial energetic damage and oxidative stress are drivers of electromagnetic radiation-induced cardiomyopathy (eRIC); however, the pathways that mediate these events are poorly defined. Sirtuin 3 (SIRT3) has been emerged as a key target for maintaining mitochondrial redox potential and metabolism, but its role in eRIC remains unknown. Here, Sirt3-KO mice and cardiac-specific SIRT3 transgenic mice were subjected to the investigation of eRIC. We found that Sirt3 protein expression level was down-regulated in eRIC mice model. Sirt3-KO markedly exaggerated decreases in cardiac energetics and increases in oxidative stress in microwave irradiation (MWI)-stressed mice. Conversely, cardiac-specific SIRT3 overexpression protected the hearts from these effects and rescued cardiac malfunction. Mechanistically, Sirt3 maintained AMP-activated protein kinase (AMPK) signaling pathway in MWI-stressed hearts in vivo. In conclusion, electromagnetic radiation repressed SIRT3 expression and disturbed cardiac energetics and redox homeostasis. The increased SIRT3 expression and AMPK activation in vivo prevented eRIC, indicating that SIRT3 will be a potential therapeutic target for curative interventions in eRIC.

Effect of Modified Wuzi Yanzong Pill () on Tip60-Mediated Apoptosis in Testis of Male Rats after Microwave Radiation.

OBJECTIVE: To investigate the effect of a modified Wuzi Yanzong Pill (, WZYZP) on the male rats' testis after microwave radiation, as well as its potential mechanism. METHODS: Forty-five male rats were randomly assigned to three groups: the control group, the radiation group, and the WZYZP group. The rats in the radiation group and WZYZP group were exposed to microwave radiation for 15 min once, while the rats in the control group were not exposed to any radiation. The rats in the WZYZP group were given a modified of WZYZP by gavage daily for 7 days. Apoptosis in the testis was evaluated using terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay. Histopathological alterations of the testis were observed by haematoxylin-eosin (HE) staining. Tat-interactive protein, 60kD (Tip60) and p53 expressions were determined by Western blotting. RESULTS: The apoptosis index (AI) in the radiation group was higher than that of the WZYZP group and control group on day 1 (D1), day 7 (D7) day 14 (D14) after radiation (P<0.05). The seminiferous tubules were of normal morphology in the control group. In the radiation group, the partial seminiferous tubules were collapsed, basement membranes of the seminiferous epithelia became detached. WZYZP could restore the morphological changes. There was no expression of Tip60 among the three groups on D7 and D14. The expression of p53 was higher in the radiation group than in the control group (P<0.05). WZYZP could down-regulate the rising p53 induced by radiation on D7 and D14 (P<0.05). CONCLUSION: A modified WZYZP may affect germ cells, and its protective effects may partly result from its ability to intervene in Tip60 mediated apoptosis.

Red Light Combined with Blue Light Irradiation Regulates Proliferation and Apoptosis in Skin Keratinocytes in Combination with Low Concentrations of Curcumin.

Curcumin is a widely known natural phytochemical from plant Curcuma longa. In recent years, curcumin has received increasing attention because of its capability to induce apoptosis and inhibit cell proliferation as well as its anti-inflammatory properties in different cancer cells. However, the therapeutic benefits of curcumin are severely hampered due to its particularly low absorption via trans-dermal or oral bioavailability. Phototherapy with visible light is gaining more and more support in dermatological therapy. Red light is part of the visible light spectrum, which is able to deeply penetrate the skin to about 6 mm, and directly affect the fibroblast of the skin dermis. Blue light is UV-free irradiation which is fit for treating chronic inflammation diseases. In this study, we show that curcumin at low concentrations (1.25-3.12 µM) has a strong anti-proliferative effect on TNF-α-induced psoriasis-like inflammation when applied in combination with light-emitting-diode devices. The treatment was especially effective when LED blue light at 405 nm was combined with red light at 630 or 660 nm, which markedly amplified the anti-proliferative and apoptosis-inducing effects of curcumin. The experimental results demonstrated that this treatment reduced the viability of human skin keratinocytes, decreased cell proliferation, induced apoptosis, inhibited NF-κB activity and activated caspase-8 and caspase-9 while preserving the cell membrane integrity. Moreover, the combined treatment also down-regulated the phosphorylation level of Akt and ERK. Taken together, our results indicated that the combination of curcumin with LED blue light united red light irradiation can attain a higher efficiency of regulating proliferation and apoptosis in skin keratinocytes.

Red light interferes in UVA-induced photoaging of human skin fibroblast cells.

The possible regulation mechanism of red light was determined to discover how to retard UVA-induced skin photoaging. Human skin fibroblasts were cultured and irradiated with different doses of UVA, thus creating a photoaging model. Fibroblasts were also exposed to a subtoxic dose of UVA combined with a red light-emitting diode (LED) for five continuous days. Three groups were examined: control, UVA and UVA plus red light. Cumulative exposure doses of UVA were 25 J cm(-2), and the total doses of red light were 0.18 J cm(-2). Various indicators were measured before and after irradiation, including cell morphology, viability, ß-galactosidase staining, apoptosis, cycle phase, the length of telomeres and the protein levels of photoaging-related genes. Red light irradiation retarded the cumulative low-dose UVA irradiation-induced skin photoaging, decreased the expression of senescence-associated ß-galactosidase, upregulated SIRT1 expression, decreased matrix metalloproteinase MMP-1 and the acetylation of p53 expression, reduced the horizon of cell apoptosis and enhanced cell viability. Furthermore, the telomeres in UVA-treated cells were shortened compared to those of cells in the red light groups. These results suggest that red light plays a key role in the antiphotoaging of human skin fibroblasts by acting on different signaling transduction pathways.