Tunneling in graphene-topological insulator hybrid devices

Hybrid graphene-topological insulator (TI) devices were fabricated using a mechanical transfer method and studied via electronic transport. Devices consisting of bilayer graphene (BLG) under the TI Bi$_2$Se$_3$ exhibit differential conductance characteristics which appear to be dominated by tunneling, roughly reproducing the Bi$_2$Se$_3$ density of states. Similar results were obtained for BLG on top of Bi$_2$Se$_3$, with 10-fold greater conductance consistent with a larger contact area due to better surface conformity. The devices further show evidence of inelastic phonon-assisted tunneling processes involving both Bi$_2$Se$_3$ and graphene phonons. These processes favor phonons which compensate for momentum mismatch between the TI $\Gamma$ and graphene $K, K'$ points. Finally, the utility of these tunnel junctions is demonstrated on a density-tunable BLG device, where the charge-neutrality point is traced along the energy-density trajectory. This trajectory is used as a measure of the ground-state density of states

Surface defects reduce Carbon Nanotube toxicity in vitro

The cytotoxicity of two different types of Multi-walled Carbon Nanotubes (MWCNTs)in A549 lung epithelial cells and HepG2 hepatocytes was investigated. One MWCNT still contained iron that was used as a catalyst during production, while the other one had all iron removed in a post-production heat treatment resulting in significantly fewer surface defects. The WST-8 assay was applied to test cell viability. To check the integrity of the cell membrane, we performed the lactate dehydrogenases assay (LDH)and measured the cellular production of reactive oxygen species (ROS). Finally, to examine cell proliferation, we conducted a cell cycle analysis. The results showed a dose- and time-dependent decrease in cell viability for both MWCNTs in both cell types. Moreover, a dose- and time-dependent increase in LDH leakage was detected, thereby indicating a decreased membrane integrity. The production of ROS was significantly increased in the case of the heat-treated MWCNTs. The heat-treated MWCNTs showed significantly stronger adverse effects when compared to the non-treated MWCNTs. Additionally, the heat-treated MWCNTs induced a dose-dependent cell cycle arrest in A549 cells. Both MWCNTs induced a significant cytotoxicity, whereby the heat treatment, leading to a decrease in surface defects, further increased the indicated adverse effects. © 2019 The Author

Glyphosate and AMPA levels in human urine samples and their correlation with food consumption: results of the cross-sectional KarMeN study in Germany

Glyphosate (N-[phosphonomethyl]-glycine) is the most widely used herbicide worldwide. Due to health concerns about glyphosate exposure, its continued use is controversially discussed. Biomonitoring is an important tool in safety evaluation and this study aimed to determine exposure to glyphosate and its metabolite AMPA, in association with food consumption data, in participants of the cross-sectional KarMeN study (Germany). Glyphosate and AMPA levels were measured in 24-h urine samples from study participants (n = 301). For safety evaluation, the intake of glyphosate and AMPA was calculated based on urinary concentrations and checked against the EU acceptable daily intake (ADI) value for glyphosate. Urinary excretion of glyphosate and/or AMPA was correlated with food consumption data. 8.3% of the participants (n = 25) exhibited quantifiable concentrations (> 0.2 μg/L) of glyphosate and/or AMPA in their urine. In 66.5% of the samples, neither glyphosate (< 0.05 μg/L) nor AMPA (< 0.09 μg/L) was detected. The remaining subjects (n = 76) showed traces of glyphosate and/or AMPA. The calculated glyphosate and/or AMPA intake was far below the ADI of glyphosate. Significant, positive associations between urinary glyphosate excretion and consumption of pulses, or urinary AMPA excretion and mushroom intake were observed. Despite the widespread use of glyphosate, the exposure of the KarMeN population to glyphosate and AMPA was found to be very low. Based on the current risk assessment of glyphosate by EFSA, such exposure levels are not expected to pose any risk to human health. The detected associations with consuming certain foods are in line with reports on glyphosate and AMPA residues in food

The German National Reference Centre for Authentic Food (NRZ-Authent)☆

The present report describes the establishment, structure and objectives of the recently established German National Reference Center for Authentic Food (NRZ-Authent). The NRZ-Authent is completely integrated into the Max Rubner-Institut (MRI), the Federal Research Institute of Nutrition and Food in Germany. Various different departments of MRI have a long experience regarding the analysis of the quality of food in general and the testing of food authenticity in particular. Therefore, a close interaction between these food-related departments and the NRZ-Authent is a basic requirement for the successful work of this newly created centre. The addressees of the NRZ-Authent are the official food authorities and laboratories in the German states. In this context, the NRZ-Authent will establish a platform for providing quick access to updated, reliable and consistent technical data, research findings, new techniques and expertise necessary for the correct application of European Union legislation. The MRI has been working on the authenticity of edible oils for a number of years now, and some examples of this successful work are presented

Synthesis and in vitro characterization of the genotoxic, mutagenic and cell-transforming potential of nitrosylated heme

Data from epidemiological studies suggest that consumption of red and processed meat is a factor contributing to colorectal carcinogenesis. Red meat contains high amounts of heme, which in turn can be converted to its nitrosylated form, NO-heme, when adding nitrite-containing curing salt to meat. NO-heme might contribute to colorectal cancer formation by causing gene mutations and could thereby be responsible for the association of (processed) red meat consumption with intestinal cancer. Up to now, neither in vitro nor in vivo studies characterizing the mutagenic and cell transforming potential of NO-heme have been published due to the fact that the pure compound is not readily available. Therefore, in the present study, an already existing synthesis protocol was modified to yield, for the first time, purified NO-heme. Thereafter, newly synthesized NO-heme was chemically characterized and used in various in vitro approaches at dietary concentrations to determine whether it can lead to DNA damage and malignant cell transformation. While NO-heme led to a significant dose-dependent increase in the number of DNA strand breaks in the comet assay and was mutagenic in the HPRT assay, this compound tested negative in the Ames test and failed to induce malignant cell transformation in the BALB/c 3T3 cell transformation assay. Interestingly, the non-nitrosylated heme control showed similar effects, but was additionally able to induce malignant transformation in BALB/c 3T3 murine fibroblasts. Taken together, these results suggest that it is the heme molecule rather than the NO moiety which is involved in driving red meat-associated carcinogenesis. © 2020, The Author(s)

Electrostatic Coupling between Two Surfaces of a Topological Insulator Nanodevice

We report on electronic transport measurements of dual-gated nano-devices of the low-carrier density topological insulator Bi1.5Sb0.5Te1.7Se1.3. In all devices the upper and lower surface states are independently tunable to the Dirac point by the top and bottom gate electrodes. In thin devices, electric fields are found to penetrate through the bulk, indicating finite capacitive coupling between the surface states. A charging model allows us to use the penetrating electric field as a measurement of the inter-surface capacitance $C_{TI}$ and the surface state energy-density relationship $\mu$(n), which is found to be consistent with independent ARPES measurements. At high magnetic fields, increased field penetration through the surface states is observed, strongly suggestive of the opening of a surface state band gap due to broken time-reversal symmetry.Comment: 5 pages, 4 figures, accepted to Physical Review Letter

Mode of action-based risk assessment of genotoxic carcinogens

The risk assessment of chemical carcinogens is one major task in toxicology. Even though exposure has been mitigated effectively during the last decades, low levels of carcinogenic substances in food and at the workplace are still present and often not completely avoidable. The distinction between genotoxic and non-genotoxic carcinogens has traditionally been regarded as particularly relevant for risk assessment, with the assumption of the existence of no-effect concentrations (threshold levels) in case of the latter group. In contrast, genotoxic carcinogens, their metabolic precursors and DNA reactive metabolites are considered to represent risk factors at all concentrations since even one or a few DNA lesions may in principle result in mutations and, thus, increase tumour risk. Within the current document, an updated risk evaluation for genotoxic carcinogens is proposed, based on mechanistic knowledge regarding the substance (group) under investigation, and taking into account recent improvements in analytical techniques used to quantify DNA lesions and mutations as well as “omics” approaches. Furthermore, wherever possible and appropriate, special attention is given to the integration of background levels of the same or comparable DNA lesions. Within part A, fundamental considerations highlight the terms hazard and risk with respect to DNA reactivity of genotoxic agents, as compared to non-genotoxic agents. Also, current methodologies used in genetic toxicology as well as in dosimetry of exposure are described. Special focus is given on the elucidation of modes of action (MOA) and on the relation between DNA damage and cancer risk. Part B addresses specific examples of genotoxic carcinogens, including those humans are exposed to exogenously and endogenously, such as formaldehyde, acetaldehyde and the corresponding alcohols as well as some alkylating agents, ethylene oxide, and acrylamide, but also examples resulting from exogenous sources like aflatoxin B$_{1}$, allylalkoxybenzenes, 2-amino-3,8-dimethylimidazo[4,5-f] quinoxaline (MeIQx), benzo[a]pyrene and pyrrolizidine alkaloids. Additionally, special attention is given to some carcinogenic metal compounds, which are considered indirect genotoxins, by accelerating mutagenicity via interactions with the cellular response to DNA damage even at low exposure conditions. Part C finally encompasses conclusions and perspectives, suggesting a refined strategy for the assessment of the carcinogenic risk associated with an exposure to genotoxic compounds and addressing research needs

Predicting plankton net community production in the Atlantic Ocean

We present, test and implement two contrasting models to predict euphotic zone net community production (NCP), which are based on 14C primary production (PO14CP) to NCP relationships over two latitudinal (ca. 30°S–45°N) transects traversing highly productive and oligotrophic provinces of the Atlantic Ocean (NADR, CNRY, BENG, NAST-E, ETRA and SATL, Longhurst et al., 1995 [An estimation of global primary production in the ocean from satellite radiometer data. Journal of Plankton Research 17, 1245–1271]). The two models include similar ranges of PO14CP and community structure, but differ in the relative influence of allochthonous organic matter in the oligotrophic provinces. Both models were used to predict NCP from PO14CP measurements obtained during 11 local and three seasonal studies in the Atlantic, Pacific and Indian Oceans, and from satellite-derived estimates of PO14CP. Comparison of these NCP predictions with concurrent in situ measurements and geochemical estimates of NCP showed that geographic and annual patterns of NCP can only be predicted when the relative trophic importance of local vs. distant processes is similar in both modeled and predicted ecosystems. The system-dependent ability of our models to predict NCP seasonality suggests that trophic-level dynamics are stronger than differences in hydrodynamic regime, taxonomic composition and phytoplankton growth. The regional differences in the predictive power of both models confirm the existence of biogeographic differences in the scale of trophic dynamics, which impede the use of a single generalized equation to estimate global marine plankton NCP. This paper shows the potential of a systematic empirical approach to predict plankton NCP from local and satellite-derived P estimates

Modulation of Hepatic Amyloid Precursor Protein and Lipoprotein Receptor-Related Protein 1 by Chronic Alcohol Intake: Potential Link Between Liver Steatosis and Amyloid-β

Heavy alcohol consumption is a known risk factor for various forms of dementia and the development of Alzheimer’s disease (AD). In this work, we investigated how intragastric alcohol feeding may alter the liver-to-brain axis to induce and/or promote AD pathology. Four weeks of intragastric alcohol feeding to mice, which causes significant fatty liver (steatosis) and liver injury, caused no changes in AD pathology markers in the brain [amyloid precursor protein (APP), presenilin], except for a decrease in microglial cell number in the cortex of the brain. Interestingly, the decline in microglial numbers correlated with serum alanine transaminase (ALT) levels, suggesting a potential link between liver injury and microglial loss in the brain. Intragastric alcohol feeding significantly affected two hepatic proteins important in amyloid-beta (Aβ) processing by the liver: 1) alcohol feeding downregulated lipoprotein receptor-related protein 1 (LRP1, ∼46%), the major receptor in the liver that removes Aβ from blood and peripheral organs, and 2) alcohol significantly upregulated APP (∼2-fold), a potentially important source of Aβ in the periphery and brain. The decrease in hepatic LRP1 and increase in hepatic APP likely switches the liver from being a remover or low producer of Aβ to an important source of Aβ in the periphery, which can impact the brain. The downregulation of LRP1 and upregulation of APP in the liver was observed in the first week of intragastric alcohol feeding, and also occurred in other alcohol feeding models (NIAAA binge alcohol model and intragastric alcohol feeding to rats). Modulation of hepatic LRP1 and APP does not seem alcohol-specific, as ob/ob mice with significant steatosis also had declines in LRP1 and increases in APP expression in the liver. These findings suggest that liver steatosis rather than alcohol-induced liver injury is likely responsible for regulation of hepatic LRP1 and APP. Both obesity and alcohol intake have been linked to AD and our data suggests that liver steatosis associated with these two conditions modulates hepatic LRP1 and APP to disrupt Aβ processing by the liver to promote AD