Approaches to Mitigate Metal Catalyst Deactivation in Solid Oxide Fuel Cell (SofC) Fuel Electrodes

While Ni/YSZ cermets have been used successfully in SOFCs, they also have several limitations, thus motivating the use of highly conductive ceramics to replace the Ni components in SOFC anodes. Ceramic electrodes are promising for use in SOFC anodes because they are expected to be less susceptible to sintering and coking, be redox stable, and be more tolerant of impurities like sulfur. In this thesis, for catalytic studies, the infiltration procedure has been used to form composites which have greatly simplified the search for the best ceramics for anode applications. In the development of ceramic fuel electrodes for SOFC, high performance can only be achieved when a transition metal catalyst is added. Because of the high operating temperatures, deactivation of the metal catalyst by sintering and/or coking is a severe problem. In this thesis, two approaches aimed at mitigating metal catalyst deactivation which was achieved by: 1) designing a catalyst that is resistant to coking and sintering and 2) developing a new method for catalyst deposition, will be presented. The first approach involved synthesizing a self-regenerating, smart catalyst, in which Co, Cu, or Ni were inserted into the B-site of a perovskite oxide under oxidizing conditions and then brought back to the surface under reducing conditions. This restores lost surface area of sintered metal particles through an oxidation/reduction cycle. Results will be shown for each of the metals, as well as for Cu-Co mixed metal systems, which are found to exhibit good tolerance to carbon deposition and interesting catalytic properties. The second strategy involves depositing novel Pd@CeO2 core-shell nanostructure catalysts onto a substrate surface which had been chemically modified to anchor the nanoparticles. The catalyst deposited onto the chemically modified, hydrophobic surface is shown to be uniform and well dispersed, and exhibit excellent thermal stability to temperatures as high as 1373 K. Similar metal catalyst deposition method was also employed to access their suitability for use in SOFC anodes

Penatalaksanaan Fisioterapi pada Kasus Post Orif Fracture Femur Condylus Lateral Sinistra dengan Modalitas Infra Red Radiation (IRR) dan Terapi Latihan di Klinik Rajawali Cirebon Tahun 2021

Fraktur adalah rupturnya kontinuitas struktur dari tulang atau kartilago dengan atau tanpa disertai subluksasi fragmen. Jika kulit diatasnya masih utuh, disebut fraktur tertutup sedangkan jika tembus ke area luar kulit disebut fraktur terbuka. Sedangkan fraktur femur sendiri adalah terputusnya kontinuitas tulang femur yang bisa terjadi akibat trauma langsung seperti kecelakaan lalu lintas dan jatuh dari ketinggian. Tujuan penulisan ini untuk mengetahui penatalaksanaan fisioterapi menggunakan modalitas Infra Red Radiation dan Terapi Latihan pada Post ORIF Fracture Femur Condylus Sinistra. Penyusunan Karya Tulis Ilmiah ini menggunakan metode studi kasus dengan cara tindakan fisioterapi pada pasien An. B umur 15 tahun di Klinik Rajawali sebanyak 4 kali terapi. Evaluasi tindakan fisioterapi berupa pemeriksaan nyeri dengan Visual Analogue Scale, pemeriksaan kekuatan otot dengan Manual Muscle Testing, pemeriksaan lingkup gerak sendi dengan Goneometer, pemeriksaan atrofi otot dengan Midline, pemeriksaan kemampuan aktivitas fungsional dengan Knee Injury and Osteoathritis Outcomr Score (KOOS). Setelah dilakukan 4 kali terapi terdapat hasil adanya penurunan nyeri tekan T1 = 1 menjadi T4 = 0, nyeri gerak T1 = 2 menjadi T4 = 1. Peningkatan kekuatan otot flexor pada T1 = 3 menjadi T4 = 5, otot extensor pada T1 = 3 menjadi T4 = 4. Peningkatan LGS pada T1 = extensi - flexi S: 10 – 10 – 85 menjadi T4 = extensi – flexi S: 5 – 5 – 100. Peningkatan atrofi otot pada lingkar otot paha pada T1= 22cm menjadi T4 = 27cm , lingkar otot betis pada T1 = 32cm menjadi T4 = 36cm . Dan peningkatan kemampuan aktivitas fungsional pada T1 = 17 menjadi T4 =54. Pasien An. B dengan diagnosis Post ORIF Fracture Femur Condylus Sinistra setelah diberikan program fisioterapi dengan modalitas Infra Red Radiation dan Terapi Latihan selama 4 kali terapi dengan hasil meningkatnya aktivitas fungsional, berkurangnya nyeri, meningkatnya kekuatan otot dan lingkup gerak sendi serta meningkatnya tonus otot. Pasien disarankan untuk melakukan terapi secara rutin dan melakukan latihan-latihan yang telah diberikan oleh fisioterapis serta rutin untuk meminum susu atau vitamin untuk tulang

Polarization-Induced Hysteresis in CuCo-Doped Rare Earth Vanadates SOFC Anodes

The physical and electrochemical properties of strontium substituted cerium vandates in which a portion of the cerium cations have been substituted with transition metals (Ce0.8Sr0.1Cu0.05TM0.05VO4−0.5x, TM = Ni or Co) were investigated and their suitability for use in solid oxide fuel cell (SOFC) anodes was assessed. Upon reduction at elevated temperature, Cu and Co or Cu and Ni were exsolved from the electronically conductive Ce1−xSrxVO4 lattice to produce Cu-Ni and Cu-Co catalytic nanoparticles. The Ce0.8Sr0.1Cu0.05Co0.05VO3 appears to have high activity and relatively high hydrocarbon tolerance, suggesting that intimate contact between the exsolved Cu and Co and that the majority of the Co nanoparticles must be at least partially coated with the Cu. The electrochemical performance when used in anodes operating on hydrogen has been characterized, and the results demonstrate the exsolution of both metals from the host lattice; but observed dynamic changes in the structure of the resulting metal nanoparticles as a function of SOFC operating conditions complicate their use in SOFC anodes

MICU1 Controls Both the Threshold and Cooperative Activation of the Mitochondrial Ca(2+) Uniporter.

Mitochondrial Ca(2+) uptake via the uniporter is central to cell metabolism, signaling, and survival. Recent studies identified MCU as the uniporter\u27s likely pore and MICU1, an EF-hand protein, as its critical regulator. How this complex decodes dynamic cytoplasmic [Ca(2+)] ([Ca(2+)]c) signals, to tune out small [Ca(2+)]c increases yet permit pulse transmission, remains unknown. We report that loss of MICU1 in mouse liver and cultured cells causes mitochondrial Ca(2+) accumulation during small [Ca(2+)]c elevations but an attenuated response to agonist-induced [Ca(2+)]c pulses. The latter reflects loss of positive cooperativity, likely via the EF-hands. MICU1 faces the intermembrane space and responds to [Ca(2+)]c changes. Prolonged MICU1 loss leads to an adaptive increase in matrix Ca(2+) binding, yet cells show impaired oxidative metabolism and sensitization to Ca(2+) overload. Collectively, the data indicate that MICU1 senses the [Ca(2+)]c to establish the uniporter\u27s threshold and gain, thereby allowing mitochondria to properly decode different inputs

Phosphorus poisoning during wet oxidation of methane over Pd@CeO2/graphite model catalysts

10siThe influence of phosphorus and water on methane catalytic combustion was studied over Pd@CeO2 model catalysts supported on graphite, designed to be suitable for X-ray Photoelectron Spectroscopy/Synchrotron Radiation Photoelectron Spectroscopy (XPS/SRPES) analysis. In the absence of P, the catalyst was active for the methane oxidation reaction, although introduction of 15% H2O to the reaction mixture did cause reversible deactivation. In the presence of P, both thermal and chemical aging treatments resulted in partial loss of activity due to morphological transformation of the catalyst, as revealed by Scanning Electron Microscopy (SEM) and Atomic Force Microscopy (AFM) analysis. At 600 °C the combined presence of PO43− and water vapor caused a rapid, irreversible deactivation of the catalyst. XPS/SRPES analysis, combined with operando X-ray Absorption Near Edge Structure (XANES) and AFM measurements, indicated that water induces severe aggregation of CeO2 nanoparticles, exposure of CePO4 on the outer layer of the aggregates and incorporation of the catalytic-active Pd nanoparticles into the bulk. This demonstrates a temperature-activated process for P-poisoning of oxidation catalysts in which water vapor plays a crucial role.partially_openembargoed_20171009Monai, Matteo; Montini, Tiziano; Melchionna, Michele; Duchoň, Tomáš; Kúš, Peter; Tsud, Nataliya; Prince, Kevin C.; Matolin, Vladimir; Gorte, Raymond J.; Fornasiero, PaoloMonai, Matteo; Montini, Tiziano; Melchionna, Michele; Duchoň, Tomáš; Kúš, Peter; Tsud, Nataliya; Prince, Kevin C.; Matolin, Vladimir; Gorte, Raymond J.; Fornasiero, Paol

CNTF Mediates Neurotrophic Factor Secretion and Fluid Absorption in Human Retinal Pigment Epithelium

Ciliary neurotrophic factor (CNTF) protects photoreceptors and regulates their phototransduction machinery, but little is known about CNTF's effects on retinal pigment epithelial (RPE) physiology. Therefore, we determined the expression and localization of CNTF receptors and the physiological consequence of their activation in primary cultures of human fetal RPE (hfRPE). Cultured hfRPE express CNTF, CT1, and OsM and their receptors, including CNTFRα, LIFRβ, gp130, and OsMRβ, all localized mainly at the apical membrane. Exogenous CNTF, CT1, or OsM induces STAT3 phosphorylation, and OsM also induces the phosphorylation of ERK1/2 (p44/42 MAP kinase). CNTF increases RPE survivability, but not rates of phagocytosis. CNTF increases secretion of NT3 to the apical bath and decreases that of VEGF, IL8, and TGFβ2. It also significantly increases fluid absorption (JV) across intact monolayers of hfRPE by activating CFTR chloride channels at the basolateral membrane. CNTF induces profound changes in RPE cell biology, biochemistry, and physiology, including the increase in cell survival, polarized secretion of cytokines/neurotrophic factors, and the increase in steady-state fluid absorption mediated by JAK/STAT3 signaling. In vivo, these changes, taken together, could serve to regulate the microenvironment around the distal retinal/RPE/Bruch's membrane complex and provide protection against neurodegenerative disease

Metabolic acid transport in human retinal pigment epithelium

At the back of our eyes, photoreceptors capture light and convert it into electrical signals that we perceive in our brain as vision. Photoreceptor function is energy expensive, even more so than many other processes in the body. Furthermore, photoreceptor metabolism increases in the dark and releases more metabolic by-products (CO2, lactic acid, and H2O) into the photoreceptor extracellular space (SRS). The retinal pigment epithelium (RPE) maintains photoreceptor health by transporting these metabolic acids from the SRS to the choroidal blood supply. By using native and cultured fetal human RPE, we show that the apical membrane is significantly more permeable to CO2 than the basolateral membrane. This feature traps CO 2 in the cell and drives carbonic anhydrase (CA)-mediated hydration of CO2 into HCO3-, which is subsequently transported out of the basolateral membrane by a Na+-linked HCO3- co-transporter (NBC). This process increases net steady-state fluid absorption, thus maintaining retinal adhesion to the RPE. Oxidative metabolism generates significantly more ATP than glycolysis, but photoreceptors derive ≈ 50% of their total ATP consumed from glycolysis due to the low oxygen level at the photoreceptor inner segment. Furthermore, lactic acid production and release into the SRS almost doubles in the dark. We show that the RPE transports lactic acid from the SRS via a proton-linked monocarboxylate transporter (MCT1), and this process activates pHi-regulatory mechanisms at the RPE apical membrane: Na+/H+ exchanger (NHE) and Na+-linked HCO3- transporters (NBC1 & NBC3). These mechanisms also facilitate MCT1-mediated lactic acid transport by preventing buildup of a proton-gradient across the RPE apical membrane. We show that an increase in SRS CO2 or lactic acid level causes RPE cell swelling. The RPE alleviates swell-induced osmotic stress by activating apical membrane K+-channel (Kir 7.1) and basolateral membrane Cl--channel (ClC-2), which drives KCl (and fluid) out of the cell to decrease cell volume. In this study, we identified the cellular mechanisms in RPE that prevent acidosis and fluid accumulation in the SRS caused by increased photoreceptor metabolism in the dark. These homeostatic processes maintain the close anatomical relationship between photoreceptors and RPE, thus protecting photoreceptor health and preserving visual function