Facile fabrication of stretchable Ag nanowire/polyurethane electrodes using high intensity pulsed light

Silver nanowires (AgNWs) have emerged as a promising nanomaterial for next generation stretchable electronics. However, until now, the fabrication of AgNW-based components has been hampered by complex and time-consuming steps. Here, we introduce a facile, fast, and one-step methodology for the fabrication of highly conductive and stretchable AgNW/polyurethane (PU) composite electrodes based on a high-intensity pulsed light (HIPL) technique. HIPL simultaneously improved wire-wire junction conductivity and wire-substrate adhesion at room temperature and in air within 50 mu s, omitting the complex transfer-curing-implanting process. Owing to the localized deformation of PU at interfaces with AgNWs, embedding of the nanowires was rapidly carried out without substantial substrate damage. The resulting electrode retained a low sheet resistance (high electrical conductivity) of <10 Omega/sq even under 100% strain, or after 1,000 continuous stretching-relaxation cycles, with a peak strain of 60%. The fabricated electrode has found immediate application as a sensor for motion detection. Furthermore, based on our electrode, a light emitting diode (LED) driven by integrated stretchable AgNW conductors has been fabricated. In conclusion, our present fabrication approach is fast, simple, scalable, and cost-efficient, making it a good candidate for a future roll-to-roll process

The arrestin-domain containing protein AdcA is a response element to stress.

International audienceBACKGROUND: Cell behaviour is tightly determined by sensing and integration of extracellular changes through membrane detectors such as receptors and transporters and activation of downstream signalling cascades. Arrestin proteins act as scaffolds at the plasma membrane and along the endocytic pathway, where they regulate the activity and the fate of some of these detectors. Members of the arrestin clan are widely present from unicellular to metazoa, with roles in signal transduction and metabolism. As a soil amoeba, Dictyostelium is frequently confronted with environmental changes likely to compromise survival. Here, we investigated whether the recently described arrestin-related protein AdcA is part of the cell response to stresses. RESULTS: Our data provide evidence that AdcA responds to a variety of stresses including hyperosmolarity by a transient phosphorylation. Analysis in different mutant backgrounds revealed that AdcA phosphorylation involves pathways other than the DokA and cGMP-dependent osmostress pathways, respectively known to regulate PKA and STATc, key actors in the cellular response to conditions of hyperosmolarity. Interestingly, however, both AdcA and STATc are sensitive to changes in the F-actin polymerization status, suggesting a common primary sensor/trigger and linking the stress-sensitive kinase responsive for AdcA phosphorylation to the actin cytoskeleton. We also show that STATc-dependent transcriptional activity is involved for the timely dephosphorylation of AdcA in cells under stress. CONCLUSION: Under osmotic stress, AdcA undergoes a phosphorylation-dephosphorylation cycle involving a stress-sensitive kinase and the transcription regulator STATc. This transient post-transcriptional modification may allow a regulation of AdcA function possibly to optimize the cellular stress response

Photonics of fullerene-conducting polymer composites and multilayered structures: new results and prospects

SPIE's 1995 International Symposium on Optical Science, Engineering, and Instrumentation, 1995, San Diego, CA, United StatesKatsumi Yoshino, Kenji Yoshimoto, Kazuya Tada, Hishashi Araki, Tsuyoshi Kawai, Masanori Ozaki, and Anvar A. Zakhidov "Photonics of fullerene-conducting polymer composites and multilayered structures: new results and prospects", Proc. SPIE 2530, Fullerenes and Photonics II, (8 December 1995). DOI: https://doi.org/10.1117/12.22812

Identification of the protein kinases Pyk3 and Phg2 as regulators of the STATc-mediated response to hyperosmolarity

Cellular adaptation to changes in environmental osmolarity is crucial for cell survival. In Dictyostelium, STATc is a key regulator of the transcriptional response to hyperosmotic stress. Its phosphorylation and consequent activation is controlled by two signaling branches, one cGMP- and the other Ca(2+)-dependent, of which many signaling components have yet to be identified. The STATc stress signalling pathway feeds back on itself by upregulating the expression of STATc and STATc-regulated genes. Based on microarray studies we chose two tyrosine-kinase like proteins, Pyk3 and Phg2, as possible modulators of STATc phosphorylation and generated single and double knock-out mutants to them. Transcriptional regulation of STATc and STATc dependent genes was disturbed in pyk3(-), phg2(-), and pyk3(-)/phg2(-) cells. The absence of Pyk3 and/or Phg2 resulted in diminished or completely abolished increased transcription of STATc dependent genes in response to sorbitol, 8-Br-cGMP and the Ca(2+) liberator BHQ. Also, phospho-STATc levels were significantly reduced in pyk3(-) and phg2(-) cells and even further decreased in pyk3(-)/phg2(-) cells. The reduced phosphorylation was mirrored by a significant delay in nuclear translocation of GFP-STATc. The protein tyrosine phosphatase 3 (PTP3), which dephosphorylates and inhibits STATc, is inhibited by stress-induced phosphorylation on S448 and S747. Use of phosphoserine specific antibodies showed that Phg2 but not Pyk3 is involved in the phosphorylation of PTP3 on S747. In pull-down assays Phg2 and PTP3 interact directly, suggesting that Phg2 phosphorylates PTP3 on S747 in vivo. Phosphorylation of S448 was unchanged in phg2(-) cells. We show that Phg2 and an, as yet unknown, S448 protein kinase are responsible for PTP3 phosphorylation and hence its inhibition, and that Pyk3 is involved in the regulation of STATc by either directly or indirectly activating it. Our results add further complexities to the regulation of STATc, which presumably ensure its optimal activation in response to different environmental cues

Two <em>Dictyostelium</em> Tyrosine Kinase-Like kinases function in parallel, stress-induced STAT activation pathways

When Dictyostelium cells are hyperosmotically stressed, STATc is activated by tyrosine phosphorylation. Unusually, activation is regulated by serine phosphorylation and consequent inhibition of a tyrosine phosphatase: PTP3. The identity of the cognate tyrosine kinase is unknown, and we show that two tyrosine kinase–like (TKL) enzymes, Pyk2 and Pyk3, share this function; thus, for stress-induced STATc activation, single null mutants are only marginally impaired, but the double mutant is nonactivatable. When cells are stressed, Pyk2 and Pyk3 undergo increased autocatalytic tyrosine phosphorylation. The site(s) that are generated bind the SH2 domain of STATc, and then STATc becomes the target of further kinase action. The signaling pathways that activate Pyk2 and Pyk3 are only partially overlapping, and there may be a structural basis for this difference because Pyk3 contains both a TKL domain and a pseudokinase domain. The latter functions, like the JH2 domain of metazoan JAKs, as a negative regulator of the kinase domain. The fact that two differently regulated kinases catalyze the same phosphorylation event may facilitate specific targeting because under stress, Pyk3 and Pyk2 accumulate in different parts of the cell; Pyk3 moves from the cytosol to the cortex, whereas Pyk2 accumulates in cytosolic granules that colocalize with PTP3

Association of depressive symptomatology and dry-mouth feeling in relation to state of taking medicine in citizens from their 40s to 70s selected randomly from two cities in Hokkaido, Japan

Background: Troponin I (TnI) are highly specific to the myocardium, and measurement of the plasma TnI levels has been widely used to evaluate myocardial damage. This study was performed to ascertain the pathologic or perioperative variables that are significantly associated with the plasma cardiac TnI level. We also intended to provide reference range of TnI elevation after uncomplicated pediatric open heart surgery.Methods: One hundred fifty-one patients undergoing repair of atrial septal defects (ASDs) (n = 61), ventricular septal defects (VSDs) (n = 71), tetralogy of Fallot (TOF) (n = 14), or complete atrioventricular septal defects (CAVSDs) (n = 5) were included. The plasma TnI level was measured prior to surgery, on days 1 and 7 postoperatively. We analyzed the relationship between the TnI level and pathology, cardiopulmonary bypass, and other perioperative actors.Results: All patients underwent uncomplicated surgery and postoperative course. With all pathologies, the plasma TnI level peaked on postoperative day 1 and rapidly declined. The TnI level on postoperative day 1 was higher in VSD than ASD, and there was a further rise in TOF and CAVSD but no significant difference between them. The TnI level on postoperative day 1 was strongly correlated with the operative time, cardiopulmonary bypass time, and aortic cross-clamp (ACC) time. Multiple linear regression analysis showed that the operative time, ACC time, lowest rectal temperature, TOF lesion, and inotropic support period could influence the TnI level.Conclusions: Elevation of plasma TnI after pediatric open heart surgery for various congenital heart diseases is mainly associated with the condition of cardiopulmonary bypass (operative and ACC times) and is not affected with surgical procedures expect for ventricular muscle resection during repair of TOF. Level of TnI elevation confirmed in the study could provide reference range in uncomplicated open heart surgery for each four pathologies. (298 words

Association of depressive symptomatology and dry-mouth feeling in relation to state of taking medicine in citizens from their 40s to 70s selected randomly from two cities in Hokkaido, Japan

Background: Troponin I (TnI) are highly specific to the myocardium, and measurement of the plasma TnI levels has been widely used to evaluate myocardial damage. This study was performed to ascertain the pathologic or perioperative variables that are significantly associated with the plasma cardiac TnI level. We also intended to provide reference range of TnI elevation after uncomplicated pediatric open heart surgery.Methods: One hundred fifty-one patients undergoing repair of atrial septal defects (ASDs) (n = 61), ventricular septal defects (VSDs) (n = 71), tetralogy of Fallot (TOF) (n = 14), or complete atrioventricular septal defects (CAVSDs) (n = 5) were included. The plasma TnI level was measured prior to surgery, on days 1 and 7 postoperatively. We analyzed the relationship between the TnI level and pathology, cardiopulmonary bypass, and other perioperative actors.Results: All patients underwent uncomplicated surgery and postoperative course. With all pathologies, the plasma TnI level peaked on postoperative day 1 and rapidly declined. The TnI level on postoperative day 1 was higher in VSD than ASD, and there was a further rise in TOF and CAVSD but no significant difference between them. The TnI level on postoperative day 1 was strongly correlated with the operative time, cardiopulmonary bypass time, and aortic cross-clamp (ACC) time. Multiple linear regression analysis showed that the operative time, ACC time, lowest rectal temperature, TOF lesion, and inotropic support period could influence the TnI level.Conclusions: Elevation of plasma TnI after pediatric open heart surgery for various congenital heart diseases is mainly associated with the condition of cardiopulmonary bypass (operative and ACC times) and is not affected with surgical procedures expect for ventricular muscle resection during repair of TOF. Level of TnI elevation confirmed in the study could provide reference range in uncomplicated open heart surgery for each four pathologies. (298 words