Journal: mBio

Article Title: Joint Transcriptional Control of Virulence and Resistance to Antibiotic and Environmental Stress in Acinetobacter baumannii

doi: 10.1128/mBio.01660-15

Figure Lengend Snippet: G. mellonella differentiates pathogenic and nonpathogenic Acinetobacter strains. (A) G. mellonella larvae were inoculated with 10 6 CFU of the strains indicated . Larvae were homogenized and bacteria were quantified immediately following infection ( t = 0) and after 4 h at 37°C ( t = 4). Data from a representative experiment are presented as the ratio of the number of CFU recovered at t = 4 to the number of CFU recovered at t = 0 (error bars, 1 standard deviation). (B) G. mellonella larvae were inoculated with 10 6 CFU of the strains indicated . Survival was monitored daily for 6 days. ****, P < 0.0001; ***, P < 0.001. ADP1, A. baylyi ADP1; 17978, A. baumannii ATCC 17978; AB5075, A. baumannii AB5075.

Article Snippet: For example, shows that Acinetobacter baylyi , a well-characterized, nonpathogenic Acinetobacter species, does not survive for 4 h within larvae, whereas the human-pathogenic isolates ATCC 17978 and AB5075 survive and grow within the larvae during the same time period.

Techniques: Bacteria, Infection, Standard Deviation

Journal: Redox Biology

Article Title: Metabolic adaptations in spontaneously immortalized PGC-1α knock-out mouse embryonic fibroblasts increase their oncogenic potential

doi: 10.1016/j.redox.2019.101396

Figure Lengend Snippet: PGC-1α KO iMEFs have a greater oncogenic potential than WT iMEFs. A) Matrigel plugs with embedded WT and KO iMEFs from injected in C56BL/6j mice. Top-left , H&E-stained sections. Top-center , immunofluorescence (IF) analysis of GFP + cells. Top-right , IF analysis of Ki67 + cells. Bottom panels , quantitative analysis of cell counts. B) Tumors dissected from NOD-SCID mice injected with WT and KO iMEFs. Left , full size tumors. Right , tumor volume. C) Histological analysis of primary tumors. Top-left , H&E staining. Bottom left , IHQ Ki67 staining. Right , quantitative analysis of Ki67 + cells. D) Ki67 staining shows the presence of hyper-proliferative nodules in KO but not in WT iMEFs tumors. Data are mean ± standard deviation. *, p < 0.05; **, p ≤ 0.01; ***, p ≤ 0.005.

Article Snippet: The following antibodies were used: β-catenin (Santa Cruz Biotechnology, sc-1496), GFP (Santa Cruz Biotechnology, sc-8334) and Ki67 (Thermo Scientific, RM-9106-S1).

Techniques: Injection, Staining, Immunofluorescence, Standard Deviation

Journal: International Journal of Medical Sciences

Article Title: Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagy via the mTOR/TFEB signaling pathway: Relevance to maladaptive cardiac hypertrophy

doi: 10.7150/ijms.88134

Figure Lengend Snippet: Beclin1-mediated autophagy was upregulated with cardiac hypertrophy in vivo and in vitro . (A) The expression of LC3, beclin1 and p62 in hypertrophic heart were determined by western blotting at indicated time point after TAC (Student t test, n =5-6, * P < 0.05 or ** P < 0.01 vs. sham. The expression of proteins in TAC mice was normalized to that of the sham mice in each time point, and β-actin served as a loading control). (B) Cardiomyocytes were challenged by ET-1 and the expression of LC3, beclin1 and p62 were examined by western blotting at indicated time point (one-way ANOVA, n =5-6, * P < 0.05 vs. 0h). (C) After infected with mRFP-GFP-LC3 adenoviral particles for 24h, the cells were challenged by ET-1. Fluorescent signals were captured with the confocal laser scanning microscopy at indicated time point and the number of autolysosomes and autophagosomes was determined by counting of red puncta or yellow puncta, respectively (one-way ANOVA, * P < 0.05 or ** P < 0.01 vs. 0h in yellow puncta. # P < 0.05, ## P < 0.01 vs. 0h in red puncta. Thirty randomly selected cells per experimental group were analyzed).

Article Snippet: Cell lysates were prepared in RIPA buffer and TFEB precipitates were generated from cardiomyocyte protein extracts with anti-TFEB antibody and protein A/G beads (Santa Cruz, CA, USA).

Techniques: In Vivo, In Vitro, Expressing, Western Blot, Control, Infection, Confocal Laser Scanning Microscopy

Journal: International Journal of Medical Sciences

Article Title: Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagy via the mTOR/TFEB signaling pathway: Relevance to maladaptive cardiac hypertrophy

doi: 10.7150/ijms.88134

Figure Lengend Snippet: Inhibition of Beclin1-mediated autophagy mitigated adverse cardiac remodeling and cardiac hypertrophy. (A) Ultrastructure analysis showing the autophagosomes (multimembrane vacuoles, arrow heads) and autolysosomes (electron dense structures, arrows) in the myocardium 8 weeks after TAC. (B) Representative cross-sectional images with H&E staining. (C) Representative cross-sectional images showing interstitial fibrosis with Masson staining. (D) Analysis results for cardiomyocyte cross-sectional area (one-way ANOVA, n =5, * P < 0.05 vs . sham, # P < 0.05 vs. TAC). (E) Analysis results for fibrosis (one-way ANOVA, n =5, * P < 0.05 vs. sham, # P < 0.05 vs. TAC). (F) mRNA level of β-MHC and BNP in hypertrophic heart were determined by real time RCR from mice in each experimental group (one-way ANOVA, n =5, * P < 0.05 vs. sham and # P < 0.05 vs. TAC, β-actin served as a loading control). (G) Neonatal cardiomyocytes pretreated with Beclin1 shRNA were subjected to ET-1 for 24h. Autolysosomes and autophagosomes were determined by use of a tandem mRFP-GFP-LC3 adenovirus in cardiomyocytes. The red puncta indicated autolysosomes and the yellow puncta indicated autophagosomes, respectively (one-way ANOVA, * P < 0.05 or # P < 0.05 vs. Control in yellow puncta or red puncta, respectively. $ P < 0.05 vs. ET in yellow puncta. △ P < 0.05 vs. ET in red puncta. Thirty randomly selected cells per experimental group were analyzed). (H) The cell size was assessed by Image J (one-way ANOVA, n =30, * P < 0.05 vs. control, # P < 0.05 vs. ET). (I) mRNA levels of β-MHC and BNP in cardiomyocytes were determined by real time RCR (one-way ANOVA, n =5, * P < 0.05 vs. control, # P < 0.05 vs. ET-1, β-actin served as a loading control).

Article Snippet: Cell lysates were prepared in RIPA buffer and TFEB precipitates were generated from cardiomyocyte protein extracts with anti-TFEB antibody and protein A/G beads (Santa Cruz, CA, USA).

Techniques: Inhibition, Staining, Control, shRNA

Journal: International Journal of Medical Sciences

Article Title: Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagy via the mTOR/TFEB signaling pathway: Relevance to maladaptive cardiac hypertrophy

doi: 10.7150/ijms.88134

Figure Lengend Snippet: DGKζ was decreased in response to the prohypertrophic stimuli in vivo and in vitro, and DGKζ deficiency linked to Beclin1-mediated autophagy during myocardial hypertrophy (A) Cardiac hypertrophy was induced by TAC in mice and the expression of DGKζ in the heart was determined by western blotting at indicated time point after surgery (Student t test, n =5, * P < 0.05 or ** P < 0.01 vs. sham. The expression of proteins in TAC mice was normalized to that of the sham mice in each time point, and β-actin served as a loading control). (B) The expression of DGKζ was determined by western blotting in ET-1-treated cardiomyocytes for indicated time point (one-way ANOVA, n =5, * P <0.05 or ** P <0.01 vs. 0h). (C) The level of DGKζ was successfully downregulated in cardiomyocytes by infecting lentiviral DGKζ shRNA. Lentiviral plasmid containing no targeted sequences or scramble sequences served as vector control and non-silencing control (one-way ANOVA, n =5, * P <0.05 vs. control). (D) The level of DAG was measured by ELISA kits in heart tissue 12 weeks after TAC and in cardiomyocytes after ET-1 treatment for 24h (one-way ANOVA, n =5). (E) Cardiomyocytes were challenged by ET-1 and the expression of LC3, beclin1 and p62 were examined by western blotting (one-way ANOVA, n =5-6, * P < 0.05 vs. control, # P < 0.05 vs. ET). (F) Autolysosomes and autophagosomes were determined by use of a tandem mRFP-GFP-LC3 adenovirus in cardiomyocytes. The red puncta indicated autolysosomes and the yellow puncta indicated autophagosomes, respectively (one-way ANOVA, ** P < 0.01 vs. control in yellow puncta. # P < 0.05 or ## P < 0.01 vs. control in red puncta. $ P < 0.05 vs. DGKζ shRNA+ET in yellow puncta. △ P < 0.05 vs. DGKζ shRNA+ET in red puncta. Thirty randomly selected cells per experimental group were analyzed). (G) The cell size was assessed by Image J (one-way ANOVA, n =30, ** P <0.01 vs. control, ## P <0.01 vs. ET). (H) mRNA level of β-MHC and BNP in cardiomyocytes were determined by real time RCR (one-way ANOVA, n =3, * P < 0.05 vs. control, # P < 0.05 vs. ET, $ P < 0.05 vs. DGKζ shRNA+ET, β-actin served as a loading control).

Article Snippet: Cell lysates were prepared in RIPA buffer and TFEB precipitates were generated from cardiomyocyte protein extracts with anti-TFEB antibody and protein A/G beads (Santa Cruz, CA, USA).

Techniques: In Vivo, In Vitro, Expressing, Western Blot, Control, shRNA, Plasmid Preparation, Enzyme-linked Immunosorbent Assay

Journal: International Journal of Medical Sciences

Article Title: Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagy via the mTOR/TFEB signaling pathway: Relevance to maladaptive cardiac hypertrophy

doi: 10.7150/ijms.88134

Figure Lengend Snippet: Deficiency of DGKζ promoted cardiac dysfunction by augmenting Beclin1-mediated autophagy. (A) Representative M-mode echocardiograms, transmitral flow and tissue doppler echocardiograms. (B) The analyzed results of LVAW and LVPW obtained from mice in each experimental group ((one-way ANOVA, n =6, * P <0.05 vs. TAC, # P <0.05 vs. DGKζ shRNA+TAC). (C) The analyzed results of EF and FS obtained from mice in each experimental group ((one-way ANOVA, n =6, * P <0.05 vs. TAC, # P <0.05 vs. DGKζ shRNA+TAC). (D) The analyzed results of E/A and e'/a' obtained from mice in each experimental group ((one-way ANOVA, n =6, * P <0.05 vs. TAC, # P <0.05 vs. DGKζ shRNA+TAC). (E) Representative cross-sectional images with H&E staining. (F) Representative cross-sectional images with masson staining. (G) Analysis results for cardiomyocyte cross-sectional area (one-way ANOVA, n =5, * P < 0.05 vs. TAC, # P <0.05 vs. DGKζ shRNA+TAC). (G) Analysis results for fibrosis (one-way ANOVA, n =5, * P < 0.05 vs. TAC, # P < 0.05 vs. DGKζ shRNA+TAC).

Article Snippet: Cell lysates were prepared in RIPA buffer and TFEB precipitates were generated from cardiomyocyte protein extracts with anti-TFEB antibody and protein A/G beads (Santa Cruz, CA, USA).

Techniques: shRNA, Staining

Journal: International Journal of Medical Sciences

Article Title: Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagy via the mTOR/TFEB signaling pathway: Relevance to maladaptive cardiac hypertrophy

doi: 10.7150/ijms.88134

Figure Lengend Snippet: AKT/mTOR dependent signaling is involved in the enhancement of cardiac autophagy by DGKζ deficiency Cardiomyocytes infected with lentivirus expressing DGKζ shRNA were subjected to ET-1 for 24h. The total protein expression and phosphorylated level of AKT, mTOR, AMPK, ULK1 and Beclin1 were examined by western blotting, respectively. (A) Representative blots depicting total and phosphorylated proteins. (B) The analyzed results of p-AKT/AKT level, p-mTOR/mTOR level, p-AMPK/AMPK level, p-ULK1/ULK1 level and p-Beclin1 level (one-way ANOVA, n =5, *P< 0.05 vs. control. # P< 0.05 or ## P< 0.01 vs. ET).

Article Snippet: Cell lysates were prepared in RIPA buffer and TFEB precipitates were generated from cardiomyocyte protein extracts with anti-TFEB antibody and protein A/G beads (Santa Cruz, CA, USA).

Techniques: Infection, Expressing, shRNA, Western Blot, Control

Journal: International Journal of Medical Sciences

Article Title: Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagy via the mTOR/TFEB signaling pathway: Relevance to maladaptive cardiac hypertrophy

doi: 10.7150/ijms.88134

Figure Lengend Snippet: Deficiency of DGKζ impaired the interaction of mTOR with TFEB and favored the nuclear translocation of TFEB. (A) Representative blot and the analyzed results of the nuclear TFEB level and cytoplasm TFEB levels in heart tissues after TAC (Student t test, n =7-8, * P < 0.05 or ** P < 0.01 vs. sham. The expression of proteins in TAC mice was normalized to that of the sham mice in each time point, and β-actin served as a loading control). (B) Representative blot and the analyzed results of the nuclear TFEB level and cytoplasm TFEB levels in ET-1-treated cardiomyocytes (one-way ANOVA, n =6, * P <0.05 vs. 0h). (C) Immunofluorescent staining showing the translocation of TFEB from cytoplasm to nucleus induced by ET-1. (D) The representative image of immunoprecipitation assay showing that mTOR interacted with TFEB in cardiomyocytes. Input was used as a positive control and IgG was used as a negative control. (E) Representative blot and the analyzed results of the nuclear TFEB level and cytoplasm TFEB levels in cardiomyocytes after DGKζ knockdown (one-way ANOVA, n =5-6, * P <0.05 vs. control, # P< 0.05 vs. ET). (F) Immunofluorescent staining showing the translocation of TFEB from cytoplasm to nucleus induced by ET-1 after DGKζ knockdown.

Article Snippet: Cell lysates were prepared in RIPA buffer and TFEB precipitates were generated from cardiomyocyte protein extracts with anti-TFEB antibody and protein A/G beads (Santa Cruz, CA, USA).

Techniques: Translocation Assay, Expressing, Control, Staining, Immunoprecipitation, Positive Control, Negative Control, Knockdown

Journal: International Journal of Medical Sciences

Article Title: Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagy via the mTOR/TFEB signaling pathway: Relevance to maladaptive cardiac hypertrophy

doi: 10.7150/ijms.88134

Figure Lengend Snippet: Genetic knockdown of TFEB abrogates Beclin1-mediated autophagy and ameliorate ET-1-induced myocardial hypertrophy. (A) Representative blot and the analyzed results of the expression of TFEB and Beclin1 in ET-1-treated cardiomyocytes (one-way ANOVA, n =5 , *P< 0.05 vs. scramble+ET, # P <0.05 vs. (scramble+DGKζ) shRNA+ET). (B) mRNA levels of Beclin1 in cardiomyocytes were determined by real time RCR (one-way ANOVA, n =3, * P < 0.05 vs. control, # P < 0.05 vs. ET, & P < 0.05 vs. DGKζ shRNA+ET, β-actin served as a loading control). (C) Schematic representation of conserved binding sequences identified in the promoter regions of Becn1 using JASPAR. (D) Occupancy of Becn1 promoter regions -1420 to -1290, 540 to -340, and -880 to -670 by TFEB, as determined by ChIP assay (one-way ANOVA, n =3, * P < 0.05 vs. control, # P <0.05 vs. ET, β-actin served as a loading control). (E) Luciferase activity in cardiomyocytes transfected with the Becn1 luciferase reporter constructs (one-way ANOVA, n =3, * P <0.05 vs. control, # P <0.05 vs. ET, & P <0.05 vs. DGKζ shRNA+ET). (F) Autolysosomes and autophagosomes were determined by use of a tandem mRFP-GFP-LC3 adenovirus in cardiomyocytes. The red puncta indicated autolysosomes and the yellow puncta indicated autophagosomes, respectively (Student t test, * P < 0.05 vs. ET in yellow puncta. ## P < 0.01 vs. ET in red puncta. Thirty randomly selected cells per experimental group were analyzed). (G) The cell size was assessed by Image J (one-way ANOVA, n =30, ** P < 0.01 vs. control, ## P < 0.01 vs. ET). (H) mRNA level of β-MHC and BNP in cardiomyocytes were determined by real time RCR (one-way ANOVA, n =3, * P < 0.05 vs. control, # P <0.05 vs. ET, & P <0.05 vs. DGKζ shRNA+ET, β-actin served as a loading control).

Article Snippet: Cell lysates were prepared in RIPA buffer and TFEB precipitates were generated from cardiomyocyte protein extracts with anti-TFEB antibody and protein A/G beads (Santa Cruz, CA, USA).

Techniques: Knockdown, Expressing, shRNA, Control, Binding Assay, Luciferase, Activity Assay, Transfection, Construct

Journal: The Journal of Neuroscience

Article Title: GABA A Receptor-Associated Protein Traffics GABA A Receptors to the Plasma Membrane in Neurons

doi: 10.1523/JNEUROSCI.3355-04.2004

Figure Lengend Snippet: Mutations in the γ2-binding domain of YFP-GABARAP disrupt the interaction of YFP-GABARAP with γ2 subunit and NSF in cultured hippocampal neurons. A, Adenovirus was used to direct expression of either wild-type YFP-GABARAP or mutated forms of GABARAP or V5-GABARAP in cultured hippocampal neurons. Western blot of homogenates from cultured neurons using antibody to GABARAP revealed the presence of a 42 kDa band corresponding to wild-type YFP-GABARAP (lane 1), P37A mutated YFP-GABARAP (lane 2), K38A mutated YFP-GABARAP (lane 3), K38A/R40A mutated YFP-GABARAP (lane 4), or V5-GABARAP (lane 6). Cells that did not receive any adenovirus (lane 5) did not have this 42 kDa band. B, Immunoprecipitation of YFP-GABARAP using anti-GFP antibody (or V5-GABARAP using V5 antibody) from neurons infected with wild-type or mutated forms of YFP-GABARAP. Western blot of YFP-GABARAP immunoprecipitate using anti-γ2 antibody shows that YFP-GABARAP (or V5-GABARAP) is capable of pulling down γ2 immunoreactivity. Mutations in the γ2-binding domain reduced the ability of YFP-GABARAP to pull down γ2 immunoreactivity. YFP-GABARAP was also able to pull down NSF immunoreactivity. Mutations in the γ2-binding domain also reduced the ability of YFP-GABARAP to pull down NSF immunoreactivity. C, Quantitation of the amount of immunoprecipitated γ2 or NSF by integration of the optical density of the autoradiograph bands from Western blots revealed that the P37A and K38A/R40A mutants were the most disrupted in there ability to pull down either γ2 or NSF immunoreactivity. Quantities of γ2 or NSF were normalized to the amount of GABARAP detected in each lane.

Article Snippet: Cells were spun down at 4°C, resuspended in antibody blocking buffer (PBS, 10% goat serum, 0.2% BSA, and 0.01% sodium azide), and blocked for 30 min on ice; cells were spun down again, resuspended in antibody incubation buffer (PBS, 2% goat serum, 0.2% BSA, and 0.01% sodium azide) containing mouse anti-GFP (1:500; Santa Cruz Biotechnology) antibody, and incubated on ice for 30 min.

Techniques: Binding Assay, Cell Culture, Expressing, Western Blot, Immunoprecipitation, Infection, Quantitation Assay, Autoradiography

Journal: Cell

Article Title: Nuclear Pores Promote Lethal Prostate Cancer by Increasing POM121-Driven E2F1, MYC, and AR Nuclear Import

doi: 10.1016/j.cell.2018.07.015

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Mouse monoclonal anti-karyopherin a2 (B-9) , Santa Cruz Biotechnology , SC-55538; RRID: AB_831493.

Techniques: Control, Electron Microscopy, Virus, Recombinant, Extraction, shRNA, Mutagenesis, Cloning, Negative Control, Plasmid Preparation, Binding Assay, Retroviral, Luciferase, Software

Journal: Applied Materials Today

Article Title: Liquid metal fillers enabled remote actuating and localizing reversible wrinkles on polymeric bilayer

doi: 10.1016/j.apmt.2022.101537

Figure Lengend Snippet: Fig. 2. (a) Schematic showing the fabrication of highly ordered wrinkled patterns on the PAN/PDMS bilayer, (b-c) the tunable diffraction grating phenomenon and optical microscopy imagery of (b) the highly ordered wrinkles on the PAN/PDMS bilayer enabled by prestretching of the PDMS substrate, and (c) the randomly aligned wrinkles on the PAN/PDMS bilayer enabled by non-prestretching of the PDMS substrate, (d) Plot of the light transmittance in the visible and near-infrared (NIR) region of the PDMS, the PAN/PDMS bilayer without wrinkles, the PAN/PDMS with wrinkles, and (e) Photos showing the tunable optical transparency of the PAN/PDMS bilayer enabled by the thermally triggered reversible wrinkles on the surface. Scale bar is 1 cm.

Article Snippet: Applied Materials Today 28 (2022) 101537 60 ◦C for 5 h using platinum-catalyzed PDMS silicone elastomer (Polydimethyl siloxane, Sylgard 184, Dow Corning) and cut into square shapes with dimensions 1.5 × 1.5 cm and 3 mm thickness.

Techniques: Microscopy

Journal: Applied Materials Today

Article Title: Liquid metal fillers enabled remote actuating and localizing reversible wrinkles on polymeric bilayer

doi: 10.1016/j.apmt.2022.101537

Figure Lengend Snippet: Fig. 3. (a) Schematic showing the procedure for fabricating the liquid metal dispersed PDMS substrates (LM–PDMS), (b) Surface temperature profiles of the LM–PDMS substrates as a function of IR exposure time and concentration of the liquid metal fillers in the PDMS substrates, (c) IR camera images showing the temperature on the bilayers surface as a function of concentration of the liquid metal fillers upon exposure to the IR for (5 and 540) s, (d) Optical microscopy images showing the regenerating wrinkles on (i)–(iii) the PAN/PDMS bilayer, and (iv)–(vi) the PAN/LM–PDMS (80 wt.% of liquid metal fillers) upon removing the IR light, (e) (i) Time required to erase the wrinkles upon applying the IR light, and (ii) Time required to regenerate the wrinkles upon removing IR light as a function of the liquid metal filler concentration. IR heat lamp was placed at a distance of 20 cm from the bilayer.

Article Snippet: Applied Materials Today 28 (2022) 101537 60 ◦C for 5 h using platinum-catalyzed PDMS silicone elastomer (Polydimethyl siloxane, Sylgard 184, Dow Corning) and cut into square shapes with dimensions 1.5 × 1.5 cm and 3 mm thickness.

Techniques: Concentration Assay, Microscopy

Journal: Applied Materials Today

Article Title: Liquid metal fillers enabled remote actuating and localizing reversible wrinkles on polymeric bilayer

doi: 10.1016/j.apmt.2022.101537

Figure Lengend Snippet: Fig. 4. Mechanical properties of the liquid metal dispersed PDMS substrates. (a) Plot of stress versus strain for the liquid metal dispersed PDMS substrates with various concentrations of liquid metal fillers, (b) Tensile modulus of the PDMS substrates as a function of the concentration of liquid metal fillers, and (c) Plot of elongation at break of the liquid metal dispersed PDMS substrates as a function of the concentration of the liquid metal fillers.

Article Snippet: Applied Materials Today 28 (2022) 101537 60 ◦C for 5 h using platinum-catalyzed PDMS silicone elastomer (Polydimethyl siloxane, Sylgard 184, Dow Corning) and cut into square shapes with dimensions 1.5 × 1.5 cm and 3 mm thickness.

Techniques: Concentration Assay

Journal: Applied Materials Today

Article Title: Liquid metal fillers enabled remote actuating and localizing reversible wrinkles on polymeric bilayer

doi: 10.1016/j.apmt.2022.101537

Figure Lengend Snippet: Fig. 5. The formation of the reversible wrinkles on the PAN/PDMS bilayer by electrically induced thermal trigger. (a) Schematic showing the fabrication process of the PDMS substrate patterned with the liquid metal wire; (b) (i) Photo of the PDMS substrate patterned with the liquid metal wire, (ii) IR image showing the surface temperature locally raised by applying Joule heating (a current of 1 A), and (iii) Profile of the surface temperature of the PAN/PDMS bilayer upon applying Joule heating through the liquid metal wire; and (c) Optical microscopy images showing the reversible wrinkles on the PAN/PDMS bilayer by applying Joule heating. The white area is the region patterned with the liquid metal wire, while the gray area is the non- patterned region. Scale bar is 1 cm.

Article Snippet: Applied Materials Today 28 (2022) 101537 60 ◦C for 5 h using platinum-catalyzed PDMS silicone elastomer (Polydimethyl siloxane, Sylgard 184, Dow Corning) and cut into square shapes with dimensions 1.5 × 1.5 cm and 3 mm thickness.

Techniques: Microscopy

Journal: Applied Materials Today

Article Title: Liquid metal fillers enabled remote actuating and localizing reversible wrinkles on polymeric bilayer

doi: 10.1016/j.apmt.2022.101537

Figure Lengend Snippet: Fig. 6. (a) Schematic showing the principle of the temperature-responsive switch, and (b) The resistance changes of the sensor upon repeatedly applying and removing the thermal trigger. (c) Manipulated intensity of LED enabled by the formation of reversible wrinkles on the PAN/ LM–PDMS bilayer, and (d) Activation of LED enabled by the formation of reversible wrinkles on the PAN/ LM–PDMS bilayer. Scale bar is 3 cm.

Article Snippet: Applied Materials Today 28 (2022) 101537 60 ◦C for 5 h using platinum-catalyzed PDMS silicone elastomer (Polydimethyl siloxane, Sylgard 184, Dow Corning) and cut into square shapes with dimensions 1.5 × 1.5 cm and 3 mm thickness.

Techniques: Activation Assay