Eiszeitliche Ablagerungen in Hochlagen des Süntels (Süd-Hannover) und seinen Karstschlotten

Aus dem Karstgebiet des Riesenberges im Süntel werden hochgelegene kies- und steinführende Ablagerungen verschiedenen Alters beschrieben. Außer kiesführenden Höhlensedimenten präglazialen Alters treten kiesführende Ablagerungen auf, die eiszeitlich entstanden sind. Während die Kies- und Steinanteile der präglazialen Ablagerungen aus lokalen (Kalkstein des Malm) und z. T. ortsfremden Komponenten (Sandstein des Wealden) bestehen, enthalten die jüngeren Ablagerungen zusätzlich Kiesanteile aus nordisch-skandinavischen Gesteinen sowie resedimentierten Weserkies. Die eiszeitlichen Ablagerungen wurden im Kammbereich sowie in Karsthöhlen abgelagert.Gravel deposits positioned in high altitude areas of Süntel Mountains are described from the carst area of Riesenberg. Not only cave gravel of pre-glacial age, but also those of glacial age occur. While the pre-glacial deposits comprise local, but xenotopic components, the younger ones display also material of northern derivation as well as reworked gravels from the Weser-River. The sediments were deposited both in caves and at summit region of the Süntel Mountains. Conditions of deposition and age relation to the glaciations are discussed

Investigation of emitter homogeneity on laser doped emitters

The selective emitter formation by laser doping is a well known process to increase the efficiency of silicon solar cells [1], [2]. For the characterization of laser doped emitters, SIMS (Secondary Ion Mass Spectroscopy) and ECV (Electrochemical Capacitance Voltage Measurement) techniques are used to analyze the emitter profile [3]. It is very difficult to get acceptable result by SIMS on a textured surface, so only ECV can be used. It has been shown, that a charge carrier depth profile can be measured on a homogeneous emitter only by ECV. The use of laser doping results in a non-homogeneous emitter. We have shown that the emitter depth is not just a function of the pulse power, but in addition of the surface structure of the wafer. The texture seems responsible for a strong variability in the doping profile. It has been shown, that the ECV measurement is not applicable to characterize the emitter depth on laser doped areas, because of the microscopic inhomogeneities in the emitter on the macroscopic measurement area. The real emitter profiles are to complex to be characterized by SIMS or ECV. We have shown that the variation in the emitter profile is resulting from the texture in the laser-doped regions

Investigation of emitter homogeneity on laser doped emitters

The selective emitter formation by laser doping is a well known process to increase the efficiency of silicon solar cells [1], [2]. For the characterization of laser doped emitters, SIMS (Secondary Ion Mass Spectroscopy) and ECV (Electrochemical Capacitance Voltage Measurement) techniques are used to analyze the emitter profile [3]. It is very difficult to get acceptable result by SIMS on a textured surface, so only ECV can be used. It has been shown, that a charge carrier depth profile can be measured on a homogeneous emitter only by ECV. The use of laser doping results in a non-homogeneous emitter. We have shown that the emitter depth is not just a function of the pulse power, but in addition of the surface structure of the wafer. The texture seems responsible for a strong variability in the doping profile. It has been shown, that the ECV measurement is not applicable to characterize the emitter depth on laser doped areas, because of the microscopic inhomogeneities in the emitter on the macroscopic measurement area. The real emitter profiles are to complex to be characterized by SIMS or ECV. We have shown that the variation in the emitter profile is resulting from the texture in the laser-doped regions

GABA transporter function, oligomerization state, and anchoring: correlates with subcellularly resolved FRET

The mouse γ-aminobutyric acid (GABA) transporter mGAT1 was expressed in neuroblastoma 2a cells. 19 mGAT1 designs incorporating fluorescent proteins were functionally characterized by [^3H]GABA uptake in assays that responded to several experimental variables, including the mutations and pharmacological manipulation of the cytoskeleton. Oligomerization and subsequent trafficking of mGAT1 were studied in several subcellular regions of live cells using localized fluorescence, acceptor photobleach Förster resonance energy transfer (FRET), and pixel-by-pixel analysis of normalized FRET (NFRET) images. Nine constructs were functionally indistinguishable from wild-type mGAT1 and provided information about normal mGAT1 assembly and trafficking. The remainder had compromised [^3H]GABA uptake due to observable oligomerization and/or trafficking deficits; the data help to determine regions of mGAT1 sequence involved in these processes. Acceptor photobleach FRET detected mGAT1 oligomerization, but richer information was obtained from analyzing the distribution of all-pixel NFRET amplitudes. We also analyzed such distributions restricted to cellular subregions. Distributions were fit to either two or three Gaussian components. Two of the components, present for all mGAT1 constructs that oligomerized, may represent dimers and high-order oligomers (probably tetramers), respectively. Only wild-type functioning constructs displayed three components; the additional component apparently had the highest mean NFRET amplitude. Near the cell periphery, wild-type functioning constructs displayed the highest NFRET. In this subregion, the highest NFRET component represented ~30% of all pixels, similar to the percentage of mGAT1 from the acutely recycling pool resident in the plasma membrane in the basal state. Blocking the mGAT1 C terminus postsynaptic density 95/discs large/zona occludens 1 (PDZ)-interacting domain abolished the highest amplitude component from the NFRET distributions. Disrupting the actin cytoskeleton in cells expressing wild-type functioning transporters moved the highest amplitude component from the cell periphery to perinuclear regions. Thus, pixel-by-pixel NFRET analysis resolved three distinct forms of GAT1: dimers, high-order oligomers, and transporters associated via PDZ-mediated interactions with the actin cytoskeleton and/or with the exocyst

Migration of cytotoxic lymphocytes in cell cycle permits local MHC I–dependent control of division at sites of viral infection

Virus-specific cytotoxic CD8+ T cells are in cell cycle as they transit from lymphoid tissues to sites of infection

The Regenerative Capacity of the Zebrafish Caudal Fin Is Not Affected by Repeated Amputations

Background: The zebrafish has the capacity to regenerate many tissues and organs. The caudal fin is one of the most convenient tissues to approach experimentally due to its accessibility, simple structure and fast regeneration. In this work we investigate how the regenerative capacity is affected by recurrent fin amputations and by experimental manipulations that block regeneration. Methodology/Principal Findings: We show that consecutive repeated amputations of zebrafish caudal fin do not reduce its regeneration capacity and do not compromise any of the successive regeneration steps: wound healing, blastema formation and regenerative outgrowth. Interfering with Wnt/ß-catenin signalling using heat-shock-mediated overexpression of Dickkopf1 completely blocks fin regeneration. Notably, if these fins were re-amputated at the non-inhibitory temperature, the regenerated caudal fin reached the original length, even after several rounds of consecutive Wnt/ß-catenin signalling inhibition and re-amputation. Conclusions/Significance: We show that the caudal fin has an almost unlimited capacity to regenerate. Even after inhibition of regeneration caused by the loss of Wnt/ß-catenin signalling, a new amputation resets the regeneration capacity within the caudal fin, suggesting that blastema formation does not depend on a pool of stem/progenitor cells that require Wnt/ßcateni

Nicotinic acid adenine dinucleotide phosphate-mediated calcium signalling in effector T cells regulates autoimmunity of the central nervous system

Nicotinic acid adenine dinucleotide phosphate represents a newly identified second messenger in T cells involved in antigen receptor-mediated calcium signalling. Its function in vivo is, however, unknown due to the lack of biocompatible inhibitors. Using a recently developed inhibitor, we explored the role of nicotinic acid adenine dinucleotide phosphate in autoreactive effector T cells during experimental autoimmune encephalomyelitis, the animal model for multiple sclerosis. We provide in vitro and in vivo evidence that calcium signalling controlled by nicotinic acid adenine dinucleotide phosphate is relevant for the pathogenic potential of autoimmune effector T cells. Live two photon imaging and molecular analyses revealed that nicotinic acid adenine dinucleotide phosphate signalling regulates T cell motility and re-activation upon arrival in the nervous tissues. Treatment with the nicotinic acid adenine dinucleotide phosphate inhibitor significantly reduced both the number of stable arrests of effector T cells and their invasive capacity. The levels of pro-inflammatory cytokines interferon-gamma and interleukin-17 were strongly diminished. Consecutively, the clinical symptoms of experimental autoimmune encephalomyelitis were ameliorated. In vitro, antigen-triggered T cell proliferation and cytokine production were evenly suppressed. These inhibitory effects were reversible: after wash-out of the nicotinic acid adenine dinucleotide phosphate antagonist, the effector T cells fully regained their functions. The nicotinic acid derivative BZ194 induced this transient state of non-responsiveness specifically in post-activated effector T cells. Naïve and long-lived memory T cells, which express lower levels of the putative nicotinic acid adenine dinucleotide phosphate receptor, type 1 ryanodine receptor, were not targeted. T cell priming and recall responses in vivo were not reduced. These data indicate that the nicotinic acid adenine dinucleotide phosphate/calcium signalling pathway is essential for the recruitment and the activation of autoaggressive effector T cells within their target organ. Interference with this signalling pathway suppresses the formation of autoimmune inflammatory lesions and thus might qualify as a novel strategy for the treatment of T cell mediated autoimmune diseases

Modelling the regulation of telomere length: the effects of telomerase and G-quadruplex stabilising drugs

Telomeres are guanine-rich sequences at the end of chromosomes which shorten during each replication event and trigger cell cycle arrest and/or controlled death (apoptosis) when reaching a threshold length. The enzyme telomerase replenishes the ends of telomeres and thus prolongs the life span of cells, but also causes cellular immortalisation in human cancer. G-quadruplex (G4) stabilising drugs are a potential anticancer treatment which work by changing the molecular structure of telomeres to inhibit the activity of telomerase. We investigate the dynamics of telomere length in different conformational states, namely t-loops, G-quadruplex structures and those being elongated by telomerase. By formulating deterministic differential equation models we study the effects of various levels of both telomerase and concentrations of a G4-stabilising drug on the distribution of telomere lengths, and analyse how these effects evolve over large numbers of cell generations. As well as calculating numerical solutions, we use quasicontinuum methods to approximate the behaviour of the system over time, and predict the shape of the telomere length distribution. We find those telomerase and G4-concentrations where telomere length maintenance is successfully regulated. Excessively high levels of telomerase lead to continuous telomere lengthening, whereas large concentrations of the drug lead to progressive telomere erosion. Furthermore, our models predict a positively skewed distribution of telomere lengths, that is, telomeres accumulate over lengths shorter than the mean telomere length at equilibrium. Our model results for telomere length distributions of telomerase-positive cells in drug-free assays are in good agreement with the limited amount of experimental data available

Knocking at the brain’s door: intravital two-photon imaging of autoreactive T cell interactions with CNS structures

Since the first applications of two-photon microscopy in immunology 10 years ago, the number of studies using this advanced technology has increased dramatically. The two-photon microscope allows long-term visualization of cell motility in the living tissue with minimal phototoxicity. Using this technique, we examined brain autoantigen-specific T cell behavior in experimental autoimmune encephalitomyelitis, the animal model of human multiple sclerosis. Even before disease symptoms appear, the autoreactive T cells arrive at their target organ. There they crawl along the intraluminal surface of central nervous system (CNS) blood vessels before they extravasate. In the perivascular environment, the T cells meet phagocytes that present autoantigens. This contact activates the T cells to penetrate deep into the CNS parenchyma, where the infiltrated T cells again can find antigen, be further activated, and produce cytokines, resulting in massive immune cell recruitment and clinical disease