Parylene C-coated PDMS-based microfluidic microbial fuel cells with low oxygen permeability

Yoon, Joon Yong,Ahn, Yoomin,Schrö,der, Uwe Elsevier 2018 Journal of Power Sources Vol.398 No.-

<P><B>Abstract</B></P> <P>Oxygen invasion is the main bottleneck in developing microscale microbial fuel cells as an efficient power source. This study reports for the first time the development of a polydimethylsiloxane -based co-laminar microbial fuel cell utilizing a parylene C coating to lower the oxygen permeability. In addition, the surface of the Au electrode is micropillar-structured to reduce the internal resistance of the microbial fuel cell. The performance of this novel microfluidic microbial fuel cell is investigated under various flow rates of electrolytes. The shear stress simulation shows that shear stress, induced by increasing flow rates, strongly impacts the biofilm electrode performance. To the best of our knowledge, the measured peak power density (71.89 ± 5.13 μW cm<SUP>−2</SUP>) and maximum current density (182.0 ± 4.82 μA cm<SUP>−2</SUP>) with the structured electrode are higher than those of any other reported polydimethylsiloxane-based microscale microbial fuel cells. The proposed microbial fuel cell appears to be a promising power supply that can be easily integrated with portable or implantable biomedical devices.</P> <P><B>Highlights</B></P> <P> <UL> <LI> A parylene C coating is proposed to reduce the oxygen permeability of a PDMS-based micro MFC. </LI> <LI> The power density and sustained time of the MFC were improved by coating PDMS with parylene C. </LI> <LI> The structured electrode shows better cell performance than a flat electrode. </LI> <LI> There is an optimal electrolyte flow rate that generates the best co-laminar MFC performance. </LI> <LI> The optimal flow rate depends on the biofilm, which is affected by the shear stress of the stream. </LI> </UL> </P>

The dialkyl resorcinol stemphol disrupts calcium homeostasis to trigger programmed immunogenic necrosis in cancer

Ji, Seungwon,Lee, Jin-Young,Schrö,r, Jan,Mazumder, Aloran,Jang, Dong Man,Chateauvieux, Sé,bastien,Schnekenburger, Michael,Hong, Che Ry,Christov, Christo,Kang, Hyoung Jin,Lee, Youngjo,Han, By Elsevier 2018 Cancer letters Vol.416 No.-

<P><B>Abstract</B></P> <P>Stemphol (STP) is a novel druggable phytotoxin triggering mixed apoptotic and non-apoptotic necrotic-like cell death in human acute myeloid leukemia (AML). Use of several chemical inhibitors highlighted that STP-induced non-canonical programmed cell death was Ca<SUP>2+</SUP>-dependent but independent of caspases, poly (ADP-ribose) polymerase-1, cathepsin, or calpains. Similar to thapsigargin, STP led to increased cytosolic Ca<SUP>2+</SUP> levels and computational docking confirmed binding of STP within the thapsigargin binding pocket of the sarco/endoplasmic reticulum (ER) Ca<SUP>2+</SUP>-ATPase (SERCA). Moreover, the inositol 1,4,5-trisphosphate receptor is implicated in STP-modulated cytosolic Ca<SUP>2+</SUP> accumulation leading to ER stress and mitochondrial swelling associated with collapsed cristae as observed by electron microscopy. Confocal fluorescent microscopy allowed identifying mitochondrial Ca<SUP>2+</SUP> overload as initiator of STP-induced cell death insensitive to necrostatin-1 or cycloheximide. Finally, we observed that STP-induced necrosis is dependent of mitochondrial permeability transition pore (mPTP) opening. Importantly, the translational immunogenic potential of STP was validated by HMGB1 release of STP-treated AML patient cells. STP reduced colony and <I>in vivo</I> tumor forming potential and impaired the development of AML patient-derived xenografts in zebrafish.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Stemphol induces cell death by disrupting calcium homeostasis. </LI> <LI> Stemphol induces necrosis by mediating mPTP opening. </LI> <LI> Stemphol triggers immunogenic cell death markers ER stress and HMGB1 release. </LI> <LI> Stemphol impairs development of leukemia patient-derived zebrafish xenografts. </LI> </UL> </P>

Physical properties of the HAT-P-23 and WASP-48 planetary systems from multi-colour photometry

Ciceri, S.,Mancini, L.,Southworth, J.,Bruni, I.,Nikolov, N.,D’Ago, G.,Schrö,der, T.,Bozza, V.,Tregloan-Reed, J.,Henning, Th. Springer-Verlag 2015 Astronomy and astrophysics Vol.577 No.-

<P>Context. Accurate and repeated photometric follow-up observations of planetary transit events are important to precisely characterize the physical properties of exoplanets. A good knowledge of the main characteristics of the exoplanets is fundamental in order to trace their origin and evolution. Multi-band photometric observations play an important role in this process. Aims. By using new photometric data, we computed precise estimates of the physical properties of two transiting planetary systems at equilibrium temperatures of ~2000 K. Methods. We present new broadband, multi-colour photometric observations obtained using three small class telescopes and the telescope-defocussing technique. In particular we obtained 11 and 10 light curves covering 8 and 7 transits of HAT-P-23 and WASP–48, respectively. For each of the two targets, one transit event was simultaneously observed through four optical filters. One transit of WASP-48b was monitored with two telescopes from the same observatory. The physical parameters of the systems were obtained by fitting the transit light curves with JKTEBOP and from published spectroscopic measurements. Results. We have revised the physical parameters of the two planetary systems, finding a smaller radius for both HAT-P-23?b and WASP–48?b, Rb = 1.224 ± 0.037 RJup and Rb = 1.396 ±0.051 RJup, respectively, than those measured in the discovery papers (Rb = 1.368 ± 0.090 RJup and Rb = 1.67 ±0.10 RJup). The density of the two planets are higher than those previously published (ρb ~ 1.1 and ~0.3 ρjup for HAT-P-23 and WASP–48, respectively) hence the two hot Jupiters are no longer located in a parameter space region of highly inflated planets. An analysis of the variation of the planet’s measured radius as a function of optical wavelength reveals flat transmission spectra within the experimental uncertainties. We also confirm the presence of the eclipsing contact binary NSVS–3071474 in the same field of view of WASP–48, for which we refine the value of the period to be 0.459?d.</P>

New liver cancer biomarkers: PI3K/AKT/mTOR pathway members and eukaryotic translation initiation factors

Golob-Schwarzl, Nicole,Krassnig, Stefanie,Toeglhofer, Anna M.,Park, Young Nyun,Gogg-Kamerer, Margit,Vierlinger, Klemens,Schrö,der, Fabian,Rhee, Hyungjn,Schicho, Rudolf,Fickert, Peter,Haybaeck, Joh Elsevier 2017 European journal of cancer Vol.83 No.-

<P><B>Abstract</B></P> <P>Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. The initiation of protein translation is an important rate-limiting step in eukaryotes and is crucial in many viral infections. Eukaryotic translation initiation factors (eIFs) are involved in the initiation step of protein translation and are linked to the phosphatidylinositol-3-kinases PI3K/AKT/mTOR pathway. Therefore we aimed to investigate a potential role of eIFs in HCC. We herein report on the immunohistochemical expression of the various eIF subunits in 235 cases of virus-related human HCC. Additionally, we used immunoblot analysis to investigate the expression of virus-related HCC and non-virus-related HCC in comparison to controls. Mammalian target of rapamycin (or mechanistic target of rapamycin as it is known now (mTOR) and activated mTOR were significantly increased in chronic hepatitis C (HCV)-associated HCC, in HCC without a viral background, in alcoholic liver disease and Wilson disease. pPTEN, phosphatase and tensin homologue (PTEN) and pAKT showed a significant increase in HBV- and HCV-associated HCC, chronic hepatitis B, HCC without a viral background, alcoholic steatohepatitis (ASH) and Wilson disease. Phosphorylated (p)-eIF2α, eIF2α, eiF3B, eIF3D, eIF3J, p-eIF4B, eIF4G and eIF6 were upregulated in HCV-associated HCC. eIF2α, p-eIF4B, eIF5 and various eIF3 subunits were significantly increased in chronic hepatitis B (HBV)-associated HCC. HCC without viral background displayed a significant increase for the eIF subunits p-2α, 3C, 3I, 4E and 4G. We noticed engraved differences in the expression pattern between chronic hepatitis B and C, HBV- and HCV-associated HCC and non-virus-related HCC.</P> <P><B>Highlights</B></P> <P> <UL> <LI> mTOR and activated mammalian target of rapamycin (mTOR) were significantly increased in liver cancer. </LI> <LI> Various eukaryotic translation initiation factor (eIF) subunits were increased in liver cancer. </LI> </UL> </P>

Strong Sensitivity of Pine Island Ice-Shelf Melting to Climatic Variability

Dutrieux, Pierre,De Rydt, Jan,Jenkins, Adrian,Holland, Paul R.,Ha, Ho Kyung,Lee, Sang Hoon,Steig, Eric J.,Ding, Qinghua,Abrahamsen, E. Povl,Schrö,der, Michael American Association for the Advancement of Scienc 2014 Science Vol.343 No.6167

<P><B>Cold Glacier Growth</B></P><P>Pine Island Glacier in Antarctica has thinned significantly during the last two decades and has provided a measurable contribution to sea-level rise as a result. Both glacier dynamics and climate are thought to be responsible for thinning, but exactly how they influence the glacier are incompletely known. <B>Dutrieux <I>et al.</I></B> (p. 174, published online 2 January) provide another layer of detail to our understanding of the process through observations of ocean temperatures in the surrounding waters. The thermocline adjacent in the sea adjacent to the glacier calving front (where ice is discharged) lowered by 250 meters in the austral summer of 2012. This change exposed the bottom of the ice shelf to colder surface waters rather than to the warmer, deeper layer, thereby reducing heat transfer from the ocean to the overlying ice and decreasing basal melting of the ice by more than 50% compared to 2010. Those 2012 ocean conditions were partly caused by a strong La Niña event, thus illustrating how important atmospheric variability is for regulating how the Antarctic Ice Sheet responds to climate change.</P>