Thermally Assisted Nonvolatile Memory in Monolayer MoS2 Transistors.

We demonstrate a novel form of thermally-assisted hysteresis in the transfer curves of monolayer MoS2 FETs, characterized by the appearance of a large gate-voltage window and distinct current levels that differ by a factor of ∼102. The hysteresis emerges for temperatures in excess of 400 K and, from studies in which the gate-voltage sweep parameters are varied, appears to be related to charge injection into the SiO2 gate dielectric. The thermally-assisted memory is strongly suppressed in equivalent measurements performed on bilayer transistors, suggesting that weak screening in the monolayer system plays a vital role in generating its strongly sensitive response to the charge-injection process. By exploiting the full features of the hysteretic transfer curves, programmable memory operation is demonstrated. The essential principles demonstrated here point the way to a new class of thermally assisted memories based on atomically thin two-dimensional semiconductors.

Probing weak localization in chemical vapor deposition graphene wide constriction using scanning gate microscopy.

Low-temperature scanning gate microscopy (LT-SGM) studies of graphene allow one to obtain important spatial information regarding coherent transport such as weak localization (WL) and universal conductance fluctuations. Although fascinating LT-SGM results on pristine graphene prepared by mechanical exfoliation have been reported in the literature, there appears to be a dearth of LT-SGM results on chemical vapor deposition (CVD)-grown graphene whose large scale and flexible substrate transferability make it an ideal candidate for coherent electronic applications. To this end, we have performed LT-SGM studies on CVD-grown graphene wide constriction (0.8 µm), which can be readily prepared by cost-effective optical lithography fully compatible with those in wafer foundry, in the WL regime. We find that the movable local gate can sensitively modulate the total conductance of the CVD graphene constriction possibly due to the intrinsic grain boundaries and merged domains, a great advantage for applications in coherent electronics. Moreover, such a conductance modulation by LT-SGM provides an additional, approximately magnetic-field-independent probe for studying coherent transport such as WL in graphene and spatial conductance variation.

Conduction Mechanisms in CVD-Grown Monolayer MoS2 Transistors: From Variable-Range Hopping to Velocity Saturation.

We fabricate transistors from chemical vapor deposition-grown monolayer MoS2 crystals and demonstrate excellent current saturation at large drain voltages (Vd). The low-field characteristics of these devices indicate that the electron mobility is likely limited by scattering from charged impurities. The current-voltage characteristics exhibit variable range hopping at low Vd and evidence of velocity saturation at higher Vd. This work confirms the excellent potential of MoS2 as a possible channel-replacement material and highlights the role of multiple transport phenomena in governing its transistor action.

A retrospective analysis of the risk factors for allergic reactions induced by the administration of oxaliplatin.

This study retrospectively investigated the clinical features and risk factors of allergic reactions induced by oxaliplatin administration. This study investigated the incidence of allergic reactions and analysed the background and laboratory data in patients with colorectal cancer treated with oxaliplatin-based chemotherapy at Kyushu Medical Center between April 2012 and September 2012. A total of 62 patients were included in this study. The number of patients in the allergic and non-allergic groups was 7 and 55 respectively. The incidence of allergic reactions was 11.3%. We compared the patients' characteristics and laboratory data between the two groups and found that the average dose of dexamethasone in the allergic group was significantly lower than that observed in the non-allergic group (P = 0.0111). Furthermore, the incidence of allergic reactions in the group that received prophylaxis of less than 12 mg of dexamethasone was significantly higher than that observed in the group that received more than 12 mg of dexamethasone (P = 0.0103). In conclusion, a lower dexamethasone dose is a possible risk factor for allergic reactions induced by the administration of oxaliplatin; however, given the retrospective design used in this study, further validation of this finding is warranted.

Antigen-reactive T cell clones restricted by mixed isotype A beta d/E alpha d class II molecules.

Mixed isotype A beta dE alpha d class II molecule-restricted antigen-reactive T cell clones were obtained from (BALB/c x B6E alpha d)F1 mice. These T cell clones responded to keyhole limpet hemocyanin in the presence of (BALB/c x B6E alpha d)F1 but not CBF1 APCs. Both anti-A beta d and anti-E alpha mAbs blocked the proliferative responses of these clones. The frequency of such mixed isotype A beta E alpha-restricted T cell clones in (BALB/c x B6E alpha d)F1 mice was estimated to be approximately 10% from our limiting dilution cloning. The existence of such mixed isotype class II molecule-restricted T cells would have important implications for the expansion of the T cell repertoire as well as the induction of autoimmunity.

Increased cardiovascular reactivity to agiotensin caused by renin.

After a short period of tachyphylaxis, there is a marked and sustained enhancement of pressor re sponses to renin and angiotensin during chronic administration of renin.

Neural cadherin: role in selective cell-cell adhesion.

Cadherins are a family of Ca2+-dependent intercellular adhesion molecules. Complementary DNAs encoding mouse neural cadherin (N-cadherin) were cloned, and the cell binding specificity of this molecule was examined. Mouse N-cadherin shows 92 percent similarity in amino acid sequence to the chicken homolog, while it shows 49 percent and 43 percent similarity to epithelial cadherin and to placental cadherin of the same species, respectively. In cell binding assays, mouse N-cadherin did not cross-react with other mouse cadherins, but it did cross-react with chicken N-cadherin. The results indicate that each cadherin type confers distinct adhesive specificities on different cells, and also that the specificity of N-cadherin is conserved between mammalian and avian cells.

Role of N-cadherin cell adhesion molecules in the histogenesis of neural retina.

We investigated the role of N-cadherin cell adhesion molecules in the histogenesis of the chicken neural retina. In the undifferentiated retina of early embryos, N-cadherin is almost evenly distributed. With differentiation, N-cadherin was gradually localized in particular cell layers. In the 8.5 to 10.5 day embryos, N-cadherin was most abundant in the optic nerve fiber layer, the plexiform layers and the outer limiting membrane. Thereafter, this molecule gradually diminished from most parts of the retina, except in the outer limiting membrane. When incubated with Fab fragments of a polyclonal antibody to N-cadherin, retinas of early embryos tended to dissociate and could not be maintained as a tissue mass. Retinas from older embryos were not dissociated by the Fab, but their morphogenesis was severely affected. We conclude that N-cadherin is essential for maintaining the overall structure of the undifferentiated retina, but during development, its role becomes restricted to maintaining more specific regions of the tissue. We also suggest that there might be additional, unidentified cadherin-like molecules in the retina.

[Usefulness of the thoracoscopic surgery under local anesthesia and irrigation for the patient with Bacillus cereus empyema; report of a case].

The case was 54-year-old male with some risks such as chronic heart failure, atrial fibrillation, and liver chirrhosis. He was admitted because of severe back pain and diagnosed as empyema by preoperative thoracentesis. By thoracoscopic procedures under local anesthesia, fibrinopurulent tissues were cleaned as much as possible and 3 of chest tubes were replaced. The final diagnosis was Bacillus cereus pyothorax by bacterial cultures of pleural effusion. Intrathoracic cavity was cleaned with physiological saline solution. The patient made favorable progress and recovered. Thoracoscopic surgery under local anesthesia with thoracic irrigation was so effective and safe methods to control the infection.

Combined transcriptome and proteome analysis as a powerful approach to study genes under glucose repression in Bacillus subtilis.

We used 2D protein gel electrophoresis and DNA microarray technologies to systematically analyze genes under glucose repression in B:acillus subtilis. In particular, we focused on genes expressed after the shift from glycolytic to gluconeogenic at the middle logarithmic phase of growth in a nutrient sporulation medium, which remained repressed by the addition of glucose. We also examined whether or not glucose repression of these genes was mediated by CcpA, the catabolite control protein of this bacterium. The wild-type and ccpA1 cells were grown with and without glucose, and their proteomes and transcriptomes were compared. 2D gel electrophoresis allowed us to identify 11 proteins, the synthesis of which was under glucose repression. Of these proteins, the synthesis of four (IolA, I, S and PckA) was under CcpA-independent control. Microarray analysis enabled us to detect 66 glucose-repressive genes, 22 of which (glmS, acoA, C, yisS, speD, gapB, pckA, yvdR, yxeF, iolA, B, C, D, E, F, G, H, I, J, R, S and yxbF ) were at least partially under CcpA-independent control. Furthermore, we found that CcpA and IolR, a repressor of the iol divergon, were involved in the glucose repression of the synthesis of inositol dehydrogenase encoded by iolG included in the above list. The CcpA-independent glucose repression of the iol genes appeared to be explained by inducer exclusion.

Controlled normothermia during ischemia is important for the induction of neuronal cell death after global ischemia in mouse.

A stable model of neuronal damage after ischemia is needed in mice to enable progression of transgenic strategies. We performed transient global ischemia induced by common carotid artery occlusions with and without maintaining normal rectal temperature (Trec) in order to determine the importance of body temperature control during ischemia. We measured brain temperature (Tb) during ischemia/reperfusion. Mice with normothermia (Trec within +/- 1 degrees C) had increased mortality and neuronal cell death in the CA1 region of hippocampus, which did not occur in hypothermic animals. If the Trec was kept within +/- 1 degrees C, the Tb decreased during ischemia. After reperfusion, Tb in the normothermia group developed hyperthermia, which reached > 40 degrees C and was > 2 degrees C higher than Trec. We suggest that tightly controlled normothermia and prevention of hypothermia (Trec) during ischemia are important factors in the development of a stable neuronal damage model in mice.

Multiple myeloma among atomic bomb survivors in Hiroshima and Nagasaki, 1950-76: relationship to radiation dose absorbed by marrow.

The relationship between atomic bomb exposure and the incidence of multiple myeloma has been examined in a fixed cohort of atomic bomb survivors and controls in the life-span study sample for Hiroshima and Nagasaki. From October 1950 to December 1976, 29 cases of multiple myeloma were confirmed in this sample. Our analysis shows that the standardized relative risk (RR) adjusted for city, sex, and age at the time of bombings (ATB) increased with marrow-absorbed radiation dose. The increased RR does not appear to differ between cities or sexes and is demonstrable only for those survivors whose age ATB was between 20 and 59 years. The estimated risk in these individuals is approximately 0.48 cases/million person-years/rad for bone marrow total dose. This excess risk did not become apparent in individuals receiving 50 rad or more in marrow total dose until 20 years or more after exposure.

Conductance fluctuations in high mobility monolayer graphene: Nonergodicity, lack of determinism and chaotic behavior.

We have fabricated a high mobility device, composed of a monolayer graphene flake sandwiched between two sheets of hexagonal boron nitride. Conductance fluctuations as functions of a back gate voltage and magnetic field were obtained to check for ergodicity. Non-linear dynamics concepts were used to study the nature of these fluctuations. The distribution of eigenvalues was estimated from the conductance fluctuations with Gaussian kernels and it indicates that the carrier motion is chaotic at low temperatures. We argue that a two-phase dynamical fluid model best describes the transport in this system and can be used to explain the violation of the so-called ergodic hypothesis found in graphene.

Effects of probes of membrane potential on metabolism in synaptosomes.

Effects of three probes for measuring membrane potential, tetraphenylphosphonium (TPP+), rhodamine 6G and 3,3'-dipropylthiocarbocyanine (diS-C3-(5)) on energy metabolism in synaptosomes were investigated. None of the three probes had any effect on lactate production in synaptosomes. TPP+ and rhodamine 6G did not inhibit the respiration of synaptosomes with pyruvate and succinate as exogenous substrate and were only weakly inhibitory with endogenous substrates. In contrast, diS-C3-(5) markedly inhibited the respiration of synaptosomes with glucose, pyruvate and endogenous substrates. All three probes reduced ATP content in synaptosomes and depolarized the membrane potential in synaptosomes with increasing concentrations of the probes. It is, therefore, preferable to estimate membrane potential with TPP+ or rhodamine 6G at their low concentrations where their effect on metabolism is negligible.

Enhancement of the uptake of 1-methyl-4-phenylpyridinium ion (MPP+) in mitochondria by tetraphenylboron.

The uptake of 1-methyl-4-phenylpyridinium (MPP+) by intact mitochondria was measured by an electrode sensitive to MPP+. The electrode was constructed with a polyvinyl chloride membrane that contained tetraphenylboron (TPB) as an ion-exchange. MPP+ was taken up by mitochondria in an energy-dependent process. TPB rapidly enhanced MPP+ uptake by mitochondria, and then induced release of MPP+ from mitochondria in medium containing glutamate and malate. No release of MPP+ from mitochondria after addition of TPB could be observed in medium containing succinate, the oxidation of which is not inhibited by MPP+. The release of MPP+ was caused by respiratory inhibition by MPP+ taken up in mitochondria. Since the release of MPP+ did not increased O2 uptake in mitochondria, the major part of MPP+ released from the matrix, where no respiratory enzyme inhibited by MPP+ exists. We concluded the following effect of TPB on MPP+ uptake from the results: (1) The increase of MPP+ concentration in matrix by addition of TPB increased the amount of bound to the inner membranes of mitochondria. (2) The increase of the amount of MPP+ in the inner membranes enhanced the respiratory inhibition. (3) The respiratory inhibition induced to release MPP+ from the matrix. The relation between MPP+ distribution in the membrane of mitochondria and the respiratory inhibition by MPP+ are discussed.

Effect of glucose and pyruvate metabolism on membrane potential in synaptosomes.

Fluorescence changes of rhodamine 6G in synaptosomal suspension, which are correlated to changes in membrane potential in synaptosomes, were measured in the presence of various monosaccharides and organic acids. Addition of D-glucose, D-mannose, pyruvate and L-lactate hyperpolarized the membrane potential, whereas D-fructose, L-glucose, D-galactose, citrate, succinate and L-glutamate were without effect on the membrane potential. Hyperpolarization induced by D-glucose was inhibited by cytochalasin B, phloretin, iodoacetate, F- and 2-deoxy-D-glucose, but not inhibited by oligomycin or phlorizin. On the other hand, hyperpolarization induced by pyruvate was inhibited by alpha-cyanocinnamate or phloretin, but not inhibited by cytochalasin B or F-. Elimination of Na+ in physiological saline depressed hyperpolarization of membrane potential induced by addition of D-glucose, L-lactate or pyruvate. These results suggest that the activity of (Na+ + K+)-ATPase in plasma membranes of synaptosomes is increased by ATP formed by glycolysis, and that the accumulated K+ in synaptosomes hyperpolarizes the membrane potential.

Mutation of an arginine biosynthesis gene causes reduced pathogenicity in Fusarium oxysporum f. sp. melonis.

Restriction enzyme-mediated integration (REMI) mutagenesis was used to tag genes required for pathogenicity of Fusarium oxysporum f. sp. melonis. Of the 1,129 REMI transformants tested, 13 showed reduced pathogenicity on susceptible melon cultivars. One of the mutants, FMMP95-1, was an arginine auxotroph. Structural analysis of the tagged site in FMMP95-1 identified a gene, designated ARG1, which possibly encodes argininosuccinate lyase, catalyzing the last step for arginine biosynthesis. Complementation of FMMP95-1 with the ARG1 gene caused a recovery in pathogenicity, indicating that arginine auxotrophic mutation causes reduced pathogenicity in this pathogen.

Studies on the activation and molecular weight of inactive renin in human plasma.

The mechanism of activation of inactive renin was studied in normal human plasma. The molecular weight of active renin and those of inactive renin before and after activation were analyzed by sephadex gel filtration. Active renin of human plasma had a molecular weight of 48,000 +/- 1000. Trypsin treatment and cold treatment activated inactive renin of a molecular weight of 54,000 +/- 1000. The inactive renin apparently did not change its molecular weight after activation. "Cryoactivation" of inactive renin was possible only when whole plasma was used. When the whole plasma was fractionated by gel filtration, cryoactivation was not observed in any of the fractions. Cryoactivation requires certain plasma factor(s) contained in some fractions. Plasma kallikrein is likely to be a major factor required for the cryoactivation of inactive renin, whereas some other factors may also participate in this mechanism.

Activation and reinactivation of inactive renin in normal human plasma.

Various facets of activation of inactive renin by acidification or cold exposure were investigated in normal human plasma. The acid activation obtained by titration was usually less than that by dialysis method, but varied from 41% to 122% of the latter. The acid phase of acid activation accounted for about 70% of the total activation achieved by the combined effects of the acid and alkaline phases on the average, and was not affected by any of the inhibitors for serine, thiol or carboxyl protease, whereas serine protease inhibitors suppressed the activation of both renin and plasma kallikrein in the alkaline phase of acid activation. A different mode of plasma kallikrein activation suggested some difference in the mechanism between the alkaline phase of acid activation and the cryoactivation. A part of cryoactivation of renin was independent of the action of plasma kallikrein. The renin activated by either acidification or cold exposure without concomitant activation of plasma kallikrein was reinactivated by the removal of pH and temperature, but recovered by repeating acidification or cold exposure. When active plasma kallikrein had been produced, it activated inactive renin irreversibly. It appears unlikely that irreversible activation of inactive renin is taking place in the normal circulation where practically no active plasma kallikrein is present.

Serum from patients with autoimmune diseases induces in vitro production of disease-associated antibodies by peripheral blood mononuclear cells from normal subjects.

Antibodies present in serum of patients with rheumatoid arthritis (RA), autoimmune thyroid diseases, and myasthenia gravis are preferentially cytotoxic to suppressor T lymphocytes from normal subjects induced by Concanavalin A. The aim of this study was to determine whether the lymphocytotoxic antibodies found in patients with these diseases also react with regulatory T cells to facilitate production of the autoantibodies responsible for each disease. Peripheral blood mononuclear cells (PBMC) from normal subjects were treated with serum from patients and complement. After washing, residual viable cells were cultured with pokeweed mitogen for 7 days. Immunoglobulin M rheumatoid factor and antihuman thyroglobulin antibody (anti-hTgAb) in the culture supernatants were measured by RIA. Anti-hTgAb was produced in culture supernatants of PBMC treated with serum samples from patients with autoimmune thyroid diseases, whereas serum samples from patients with RA, myasthemia gravis, or normal subjects did not stimulate production of detectable anti-hTgAb. In contrast, Immunoglobulin M rheumatoid factor was produced by normal PBMC treated only with serum from patients with RA. When normal T cells treated with serum were cultured with autologous untreated non-T cells in the presence of pokeweed mitogen, autoantibodies also were produced. Furthermore, the production of anti-hTgAb was suppressed by adding untreated T cells to the mixture of treated T cells and untreated non-T cells. These results suggest that lymphocytotoxic antibodies found in patients with autoimmune disorders may cause disease-associated suppressor T cell dysfunction.