A Comparative Note on the Bangla Particle to and the German Particle doch

The Bangla discourse particle –to and the German discourse particle doch share a number of syntactic and semantic properties. Their phonetic similarity suggests a remote historical relation. While the latter part will only be mentioned and must remain for the specialists in Indo-European reconstruction, the present short study will highlight points of convergence between the two languages with respect to these particles along a series of concrete tests. The convergence appears to be more than accidental

Организация дежурной смены личного состава караула пожарной охраны

В статье освещается вопросы распорядка дня дежурных суток личного состава пожарно-спасательных подразделений и формирований Юргинского пожарно-спасательного гарнизона

Blockade but not overexpression of the junctional adhesion molecule C influences virus-induced type 1 diabetes in mice

Type 1 diabetes (T1D) results from the autoimmune destruction of insulin-producing beta-cells in the pancreas. Recruitment of inflammatory cells is prerequisite to beta-cell-injury. The junctional adhesion molecule (JAM) family proteins JAM-B and JAM–C are involved in polarized leukocyte transendothelial migration and are expressed by vascular endothelial cells of peripheral tissue and high endothelial venules in lympoid organs. Blocking of JAM-C efficiently attenuated cerulean-induced pancreatitis, rheumatoid arthritis or inflammation induced by ischemia and reperfusion in mice. In order to investigate the influence of JAM-C on trafficking and transmigration of antigen-specific, autoaggressive T-cells, we used transgenic mice that express a protein of the lymphocytic choriomeningitis virus (LCMV) as a target autoantigen in the β-cells of the islets of Langerhans under the rat insulin promoter (RIP). Such RIP-LCMV mice turn diabetic after infection with LCMV. We found that upon LCMV-infection JAM-C protein was upregulated around the islets in RIP-LCMV mice. JAM-C expression correlated with islet infiltration and functional beta-cell impairment. Blockade with a neutralizing anti-JAM-C antibody reduced the T1D incidence. However, JAM-C overexpression on endothelial cells did not accelerate diabetes in the RIP-LCMV model. In summary, our data suggest that JAM-C might be involved in the final steps of trafficking and transmigration of antigen-specific autoaggressive T-cells to the islets of Langerhans

Licensing Question-Sensitive Discourse Particles: Evidence from Grammaticality Judgments, Self-Paced Reading and EEG Studies

Contribution to Linguistic Evidence 202

Breaking tolerance to the natural human liver autoantigen cytochrome P450 2D6 by virus infection

Autoimmune liver diseases, such as autoimmune hepatitis (AIH) and primary biliary cirrhosis, often have severe consequences for the patient. Because of a lack of appropriate animal models, not much is known about their potential viral etiology. Infection by liver-tropic viruses is one possibility for the breakdown of self-tolerance. Therefore, we infected mice with adenovirus Ad5 expressing human cytochrome P450 2D6 (Ad-2D6). Ad-2D6–infected mice developed persistent autoimmune liver disease, apparent by cellular infiltration, hepatic fibrosis, “fused” liver lobules, and necrosis. Similar to type 2 AIH patients, Ad-2D6–infected mice generated type 1 liver kidney microsomal–like antibodies recognizing the immunodominant epitope WDPAQPPRD of cytochrome P450 2D6 (CYP2D6). Interestingly, Ad-2D6–infected wild-type FVB/N mice displayed exacerbated liver damage when compared with transgenic mice expressing the identical human CYP2D6 protein in the liver, indicating the presence of a stronger immunological tolerance in CYP2D6 mice. We demonstrate for the first time that infection with a virus expressing a natural human autoantigen breaks tolerance, resulting in a chronic form of severe, autoimmune liver damage. Our novel model system should be instrumental for studying mechanisms involved in the initiation, propagation, and precipitation of virus-induced autoimmune liver diseases

MMX - development of a rover locomotion system for Phobos

The MMX mission (Martian Moons eXploration) is a robotic sample return mission of the JAXA (Japan Aerospace Exploration Agency), CNES (Centre National d'Etudes Spatiales ) and DLR (German Aerospace Center) for launch in 2024. The mission aims to answer the question on the origin of Phobos and Deimos which will also help to understand the material transport in the earliest period of our solar system and the most important question how was the water brought on Earth. Besides the MMX mothership (JAXA) which is responsible for sampling and sample return to Earth a small rover which is built by CNES and DLR shall land on Phobos for in-situ measurements similar to MASCOT (Mobile Asteroid Surface Scout) on Ryugu. The MMX rover is a four wheel driven autonomous system with a size of 41 cm x 37 cm x 30 cm and a weight of approx. 25 kg. Multiple science instruments and cameras are integrated in the rover body. The rover body is basically a rectangular box, attached at the sides are four legs with one wheel per leg. When the rover is detached from the mothership, the legs are folded together at the side of the rover body. When the rover has landed passively (no parachute, braking rockets) on Phobos, the legs are autonomously controlled to bring the rover in an upright orientation. One Phobos day lasts 7 earth hours, which gives for the total mission time of 3 earth months, the number of about 300 extreme temperature cycles. These cycles and the wide span of surface temperature between day and night are main design drivers for the rover. This paper gives a short overview on the MMX mission, the MMX rover and a detailed view on the development of the MMX rover locomotion subsystem