New Porous Carbon Materials as Gas Diffusion Layer for Polymer Electrolyte Fuel Cells

New porous carbon materials are proposed in which washi, the Japanese paper as well as cotton and other cellulose materials are carbonized by new method, retaining their original fibrous structures. Porous carbon sheets thus fabricated are used as gas diffusion layer in fuel cells. Fuel cell testing is conducted and the optimum conditions of fabrication are investigated. Low cost and superior characteristics of new carbon structure are demonstrated based on morphological study and fuel cell polarization data

Comparison of Diagnostic Yield and Safety of Serial Pancreatic Juice Aspiration Cytologic Examination (SPACE) with Different Indications

We assessed whether there are differences in the diagnostic yield and safety of serial pancreatic juice aspiration cytologic examination (SPACE) among different indications. We retrospectively analyzed 226 patients who underwent SPACE. They were classified into group A (patients with pancreatic masses, including advanced adenocarcinoma, sclerosing pancreatitis, or autoimmune pancreatitis), group B (suspicious pancreatic carcinoma patients without obvious pancreatic masses, including small pancreatic carcinoma, carcinoma in situ, or benign pancreatic duct stenosis), and group C (intraductal papillary mucinous neoplasm, IPMN). There were 41, 66, and 119 patients, with malignancy diagnosed in 29, 14, and 22 patients, in groups A, B, and C, respectively. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were 69%, 100%, 100%, 57%, and 78% in group A; 79%, 98%, 92%, 94%, and 94% in group B; and 27%, 87%, 32%, 84%, and 76% in group C, respectively. PEP was observed in three (7.3%), three (4.5%), and fifteen (13%) patients in group A, B, and C, respectively (p = 0.20). SPACE is useful and safe in patients with suspicious small pancreatic carcinoma. However, it has limited efficacy and might not be recommended in patients with IPMN because of the high frequency of PEP

Prefoldin Protects Neuronal Cells from Polyglutamine Toxicity by Preventing Aggregation Formation

Huntington disease is caused by cell death after the expansion of polyglutamine (polyQ) tracts longer than similar to 40 repeats encoded by exon 1 of the huntingtin (HTT) gene. Prefoldin is a molecular chaperone composed of six subunits, PFD1-6, and prevents misfolding of newly synthesized nascent polypeptides. In this study, we found that knockdown of PFD2 and PFD5 disrupted prefoldin formation in HTT-expressing cells, resulting in accumulation of aggregates of a pathogenic form of HTT and in induction of cell death. Dead cells, however, did not contain inclusions of HTT, and analysis by a fluorescence correlation spectroscopy indicated that knockdown of PFD2 and PFD5 also increased the size of soluble oligomers of pathogenic HTT in cells. In vitro single molecule observation demonstrated that prefoldin suppressed HTT aggregation at the small oligomer (dimer to tetramer) stage. These results indicate that prefoldin inhibits elongation of large oligomers of pathogenic Htt, thereby inhibiting subsequent inclusion formation, and suggest that soluble oligomers of polyQ-expanded HTT are more toxic than are inclusion to cells

Synaptic vesicle glycoprotein 2A (SV2A) regulates kindling epileptogenesis via GABAergic neurotransmission

Synaptic vesicle glycoprotein 2A (SV2A) is a prototype synaptic vesicle protein regulating action potential-dependent neurotransmitters release. SV2A also serves as a specific binding site for certain antiepileptics and is implicated in the treatment of epilepsy. Here, to elucidate the role of SV2A in modulating epileptogenesis, we generated a novel rat model (Sv2aL[174Q]rat) carrying a Sv2a-targeted missense mutation (L174Q) and analyzed its susceptibilities to kindling development. Although animals homozygous for the Sv2a[L174Q] mutation exhibited normal appearance and development, they are susceptible to pentylenetetrazole (PTZ) seizures. In addition, development of kindling associated with repeated PTZ treatments or focal stimulation of the amygdala was markedly facilitated by the Sv2a[L174Q]mutation. Neurochemical studies revealed that the Sv2a[L174Q] mutation specifically reduced depolarization-induced GABA, but not glutamate, release in the hippocampus without affecting basal release or the SV2A expression level in GABAergic neurons. In addition, the Sv2a[L174Q] mutation selectively reduced the synaptotagmin1 (Syt1) level among the exocytosis-related proteins examined. The present results demonstrate that dysfunction of SV2A due to the Sv2a[L174Q] mutation impairs the synaptic GABA release by reducing the Syt1 level and facilitates the kindling development, illustrating the crucial role of SV2A-GABA system in modulating kindling epileptogenesis

A Missense Mutation of the Gene Encoding Synaptic Vesicle Glycoprotein 2A (SV2A) Confers Seizure Susceptibility by Disrupting Amygdalar Synaptic GABA Release

Synaptic vesicle glycoprotein 2A (SV2A) is specifically expressed in the membranes of synaptic vesicles and modulates action potential-dependent neurotransmitter release. To explore the role of SV2A in the pathogenesis of epileptic disorders, we recently generated a novel rat model (Sv2a[L174Q] rat) carrying a missense mutation of the Sv2a gene and showed that the Sv2a[L174Q] rats were hypersensitive to kindling development (Tokudome et al., 2016). Here, we further conducted behavioral and neurochemical studies to clarify the pathophysiological mechanisms underlying the seizure vulnerability in Sv2a[L174Q] rats. Sv2a[L174Q] rats were highly susceptible to pentylenetetrazole (PTZ)-induced seizures, yielding a significantly higher seizure scores and seizure incidence than the control animals. Brain mapping analysis of Fos expression, a biological marker of neural excitation, revealed that the seizure threshold level of PTZ region-specifically elevated Fos expression in the amygdala in Sv2a[L174Q] rats. In vivo microdialysis study showed that the Sv2a[L174Q] mutation preferentially reduced high K+(depolarization)-evoked GABA release, but not glutamate release, in the amygdala. In addition, specific control of GABA release by SV2A was supported by its predominant expression in GABAergic neurons, which were co-stained with antibodies against SV2A and glutamate decarboxylase 1. The present results suggest that dysfunction of SV2A by the missense mutation elevates seizure susceptibility in rats by preferentially disrupting synaptic GABA release in the amygdala, illustrating the crucial role of amygdalar SV2A-GABAergic system in epileptogenesis

Size Distribution of Linear and Helical Polymers in Actin Solution Analyzed by Photon Counting Histogram

Actin is a ubiquitous protein that is a major component of the cytoskeleton, playing an important role in muscle contraction and cell motility. At steady state, actin monomers and filaments (F-actin) coexist, and actin subunits continuously attach and detach at the filament ends. However, the size distribution of actin oligomers in F-actin solution has never been clarified. In this study, we investigated the size distribution of actin oligomers using photon-counting histograms. For this purpose, actin was labeled with a fluorescent dye, and the emitted photons were detected by confocal optics (the detection volume was of femtoliter (fL) order). Photon-counting histograms were analyzed to obtain the number distribution of actin oligomers in the detection area from their brightness, assuming that the brightness of an oligomer was proportional to the number of protomers. We found that the major populations at physiological ionic strength were 1–5mers. For data analysis, we successfully applied the theory of linear and helical aggregations of macromolecules. The model postulates three states of actin, i.e., monomers, linear polymers, and helical polymers. Here we obtained three parameters: the equilibrium constants for polymerization of linear polymers, K(l) = (5.2 ± 1.1) × 10(6) M(−1), and helical polymers, K(h) = (1.6 ± 0.5) × 10(7) M(−1); and the ratio of helical to linear trimers, γ = (3.6 ± 2.3) × 10(−2). The excess free energy of transforming a linear trimer to a helical trimer, which is assumed to be a nucleus for helical polymers, was calculated to be 2.0 kcal/mol. These analyses demonstrate that the oligomeric phase at steady state is predominantly composed of linear 1–5mers, and the transition from linear to helical polymers occurs on the level of 5–7mers

In situ observations of ions and magnetic field around Phobos: the mass spectrum analyzer (MSA) for the Martian Moons eXploration (MMX) mission

International audienceThe mass spectrum analyzer (MSA) will perform in situ observations of ions and magnetic fields around Phobos as part of the Martian Moons eXploration (MMX) mission to investigate the origin of the Martian moons and physical processes in the Martian environment. MSA consists of an ion energy mass spectrometer and two magnetometers which will measure velocity distribution functions and mass/charge distributions of low-energy ions and magnetic field vectors, respectively. For the MMX scientific objectives, MSA will observe solar wind ions, those scattered at the Phobos surface, water-related ions generated in the predicted Martian gas torus, secondary ions sputtered from Phobos, and escaping ions from the Martian atmosphere, while monitoring the surrounding magnetic field. MSA will be developed from previous instruments for space plasma missions such as Kaguya, Arase, and BepiColombo/Mio to contribute to the MMX scientific objectives