development-validation-chromium-getters-for-solid-oxide-fuel-cell

Development and Validation of Chromium Getters for Solid Oxide Fuel Cell Power Systems

Degradation of cathode in solid oxide fuel cells (SOFC) remains a major concern for the long-term performance stability and operational reliability. The ...

stereological-estimation-cholinergic-fiber-length-nucleus-basalis

Stereological Estimation of Cholinergic Fiber Length in the Nucleus Basalis of Meynert of the Mouse Brain

The length of cholinergic or other neuronal axons in various brain regions are often correlated with the specific function of the region. Stereology is a ...

University of Connecticut

Kansas City Veterans Affairs Medical Center

Obstructive sleep apnea (OSA) leads to cognitive impairment in about 25% patients, though it remains elusive what makes one more susceptible than the other to be cognitively impaired. G protein-coupled receptor kinase-5 (GRK5) deficiency is recently found to render subjects more susceptible to cognitive impairment triggered by over-expression of Swedish mutant ß-amyloid precursor protein. This study is to determine whether GRK5 deficiency also renders subjects more susceptible to the OSA-triggered cognitive impairment. Both wild type (WT) and GRK5 knockout (KO) mice were placed in conditions absence and presence of intermittent hypoxia (IH) with 8%/21% O2 90-s cycle for 8h a day for a month, and then followed by behavioral assessments with battery of tasks. We found that the selected IH condition only induced marginally abnormal behavior (slightly elevated anxiety with most others unchanged) in the WT mice but it caused significantly more behavioral deficits in the KO mice, ranging from elevated anxiety, impaired balancing coordination, and impaired short-term spatial memory. These results suggest that GRK5 deficiency indeed makes the mice more susceptible to wide range of behavioral impairments, including cognitive impairments. 

GRK5 deficiency leads to susceptibility to intermittent hypoxia-induced cognitive impairment.

In this study, octamethylcyclotetrasiloxane (D4) was removed by using a novel modified solid adsorbent of mesoporous silica. The adsorbent was synthesized using inverse micelles with some modifications in the synthesis process (temperature of gelation) and in the post treatment conditions (calcination temperature and heating rate) with a concomitant improvement of D4 uptake. This is the first report on regulating the textural properties of the mesoporous silica material UCT-14 to develop an active silica adsorbent. These adjustments resulted in an increase of the silica surface area from 391 to 798 m(2)·g(-1), which leads to a high capacity (686 mg·g(-1)) of D4-capture for the silica synthesized at 80 °C, calcined at 450 °C with the heating rate of 100 °C·min(-1) (Si-Syn80). This adsorbent showed comparable adsorption performance with the widely used commercial silica gel under dry and humid condition. Recyclability tests on the commercial silica gel and mesoporous silica synthesized at 120 °C and calcined at 450 °C with a heating rate of 100 °C·min(-1) (called Si-Syn120 or Si-450 or Si-100 °C·min(-1)) indicated that the Si-Syn120 (capacity drop 10%) is more efficient than silica gel (capacity drop 15%) after three cycles. Although, the presence of moisture (25%) in the nitrogen gas stream led to capacity reduction in both Si-Syn120 and commercial silica gel, the modified UCT-14 shows slightly better resistance to humid condition.

Modified Mesoporous Silica for Efficient Siloxane Capture.

Why certain diseases primarily affect one specific neuronal subtype rather than another is a puzzle whose solution underlies the development of specific therapies. Selective basal forebrain cholinergic (BFC) neurodegeneration participates in cognitive impairment in Alzheimer's disease (AD), yet the underlying mechanism remains elusive. Here, we report the first recapitulation of the selective BFC neuronal loss that is typical of human AD in a mouse model termed GAP. We created GAP mice by crossing Tg2576 mice that over-express the Swedish mutant human β-amyloid precursor protein gene with G protein-coupled receptor kinase-5 (GRK5) knockout mice. This doubly defective mouse displayed significant BFC neuronal loss at 18 months of age, which was not observed in either of the singly defective parent strains or in the wild type. Along with other supporting evidence, we propose that GRK5 deficiency selectively renders BFC neurons more vulnerable to degeneration.

GRK5 Deficiency Leads to Selective Basal Forebrain Cholinergic Neuronal Vulnerability.

Contractile behavior of cardiomyocytes relies on directed signal propagation through the electroconductive networks that exist within the native myocardium. Due to their unique electrical properties, electroactive materials, such as graphene, have recently emerged as promising candidate materials for cardiac tissue engineering applications. In this work, the potential of three-dimensional (3D) nanofibrous graphene and poly(caprolactone) (PCL + G) composite scaffold for cardiac tissue engineering has been explored for the first time. The addition of graphene into PCL led to an increased volume conductivity of scaffolds with an even distribution of graphene particles throughout the matrix. Graphene particles provided local conductive sites within the PCL matrix, which enabled application of external electrical stimulation throughout the scaffold using a custom point stimulation device. When mouse embryonic stem cell derived cardiomyocytes (mES-CM) were seeded on PCL + G scaffolds, cells adhered well, contracted spontaneously, and exhibited classical cardiomyocyte phenotype confirming the biocompatibility of electroactive PCL + G scaffolds. Further functional characterization demonstrated that graphene especially affected Ca handling properties of mES-CM compared to that of cardiomyocytes cultured in 2D culture, highlighting the potential of PCL + G for in vitro cardiac tissue engineering. © 2018 Wiley Periodicals, Inc. J. Biomed. Mater. Res. Part A: 106A: 2923-2933, 2018.

Electroactive graphene composite scaffolds for cardiac tissue engineering.

Solid oxide electrochemical systems, such as solid oxide fuel cells (SOFC), solid oxide electrolysis cells (SOEC), and oxygen transport membranes (OTM) enable clean and reliable production of energy or fuel for a range of applications, including, but not limited to, residential, commercial, industrial, and grid-support. These systems utilize solid-state ceramic oxides which offer enhanced stability, fuel flexibility, and high energy conversion efficiency throughout operation. However, the nature of system conditions, such as high temperatures, complex redox atmosphere, and presence of volatile reactive species become taxing on solid oxide materials and limit their viability during long-term operation. Ongoing research efforts to identify the material corrosion and degradation phenomena, as well as discover possible mitigation techniques to extend material efficiency and longevity, is the current focus of the research and industrial community. In this review, degradation processes in select solid oxide electrochemical systems, system components, and comprising materials will be discussed. Overall degradation phenomena are presented and certain degradation mechanisms are discussed. State-of-the-art technologies to mitigate or minimize the above-mentioned degradation processes are presented.

ArticleTotal : 2	Year
Publication title Cited by 3	2019
Publication title	2020

Article	Year
GRK5 deficiency leads to susceptibility to intermittent hypoxia-induced cognitive impairment. Behavioural brain research\| PubMed ID: 26778781	2016
Modified Mesoporous Silica for Efficient Siloxane Capture. Langmuir : the ACS journal of surfaces and colloids\| PubMed ID: 26890152	2016
GRK5 Deficiency Leads to Selective Basal Forebrain Cholinergic Neuronal Vulnerability. Scientific reports\| PubMed ID: 27193825	2016
Electroactive graphene composite scaffolds for cardiac tissue engineering. Journal of biomedical materials research. Part A\| PubMed ID: 30325093	2018
Solid Oxide Electrochemical Systems: Material Degradation Processes and Novel Mitigation Approaches. Materials (Basel, Switzerland)\| PubMed ID: 30400173	2018

Prabhakar Singh

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