Human skin is the largest organ, and it can transform multiple external stimuli into the biopotential signals by virtue of ions as information carriers. Ionic skins (i-skins) that can mimic human skin have been extensively explored; however, the limited sensing capacities as well as the need of an extra power supply significantly restrict their broad applications. Herein, we develop self-powered humanlike i-skins based on gradient polyelectrolyte membranes (GPMs) that can directly and accurately perceive multiple stimuli. Prepared by a hydrogel-assisted reaction-diffusion method, the GPMs exhibit gradient-distributed charged groups across polymer networks, enabling one to generate a thickness-dependent and thermoresponsive self-induced potential in a hydrated situation and in a humidity-sensitive self-induced potential in a dehydrated/dried situation, respectively. Consequently, the GPM-based i-skins can precisely detect pressure, temperature, and humidity in a self-powered manner. The coupling of mechano-electric and thermo-electric effects inherent in GPMs provides a general strategy for developing innovative self-powered ion-based perception systems.

Aim: The activation of extracellular signal-regulated kinase (ERK)1/2 protects against ischemic-reperfusion injury. Whether ERK1/2 mediates the cardioprotection of sevoflurane postconditioning is unknown. We tested whether sevoflurane postconditioning produces cardioprotection via an ERK1/2-dependent mechanism. Methods: In protocol 1, Langendorff-perfused Sprague-Dawley rat hearts (n=84, 12 per group), with the exception of the Sham group, were subjected to 30 min ischemia followed by 90 min reperfusion and were assigned to the untreated (control) group, followed by 4 cycles of ischemic postconditioning (25 s of each), 3% (v/v) sevoflurane postconditioning (for 5 min and 10 min of washout), and the PD98059 solvent DMSO (<0.2%), ERK1/2 inhibitor PD98059 (20 µmol/L), and Sevo+PD administration. Left ventricular hemodynamics and coronary flow at 30 min of equilibrium were recorded at 30, 60, and 90 min of reperfusion, respectively. Acute infarct size was measured by triphenyltetrazolium chloride staining. The configuration of mitochondria was observed by an electron microscope. Western blot analysis was used to determine the contents of cytosolic and mitochondrial cytochrome c at the end of reperfusion. In protocol 2, after 15 min of reperfusion, the expression of total and phosphorylated forms of ERK1/2 and its downstream target p70S6K was determined by Western blotting. Results: No differences in baseline hemodynamics were observed among the experimental groups (P>0.05). After reperfusion, compared with the control group, sevoflurane postconditioning and ischemic postconditioning significantly (P<0.05) improved functional recovery and largely (P<0.05) decreased myocardial infarct size (22.9%±4.6% and 21.2%±3.8%, vs 39.4%± 5.7%, both P<0.05). Sevoflurane-mediated protection was abolished by PD98059. Conclusion: Anesthetic postconditioning by sevoflurane effectively protects against reperfusion damage by activating ERK1/2 in vitro. Key wordssevoflurane; postconditioning; extracellular sig na l-regu l a ted prot ein k ina se ; p7 0 S6 k i n a se ; m i t o c h o n d r i a ; c y t o c h r o m e c ; ischemia-reperfusion 1 Project supported by the Open Project of the Health Department of Jiangsu Province, China (No WK2006 03). 6 C o rr e sp o nd e n c e t o P ro f C he n g -x ia n g YANG. P h n 86 -75 7-831 6-2 51 3.

The high mobility group protein A2 (HMGA2) has been demonstrated as an architectural transcription factor that is associated with pathogenesis of many malignant cancers; however, its role in prostate cancer cells remains largely unknown. To explore whether HMGA2 participates in the development and progression of prostate cancer, small interfering RNA (siRNA) targeted on human HMGA2 was transfected to suppress the HMGA2 expression in prostate cancer PC3 and DU145 cells, and then the cellular biology changes after decreased the expression of HMGA2 was examined. Our results showed that knockdown of HMGA2 markedly inhibited cell proliferation; this reduced cell proliferation was due to the promotion of cell apoptosis as the Bcl-xl was decreased, whereas Bax was up-regulated. In addition, we found that HMGA2 knockdown resulted in reduction of cell migration and invasion, as well as repressed the expression of matrix metalloproteinases (MMPs) and affected the occurrence of epithelial-mesenchymal transition (EMT) in both cell types. We further found that decreased HMGA2 expression inhibited the transforming growth factor-beta (TGF-beta)/Smad signalling pathway in cancer cells. In conclusion, our data indicated that HMGA2 was associated with apoptosis, migration and invasion of prostate cancer, which might be a promising therapeutic target for prostate cancer.

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