Hochfrequenzverhalten gekoppelter und ungekoppelter Josephson-Kontakte auf der Basis von Hochtemperatur-Supraleitern

The behaviour of HTS Josephson junctions have been investigated experimentally and theoretically with the aim to THz-applications. In the first part the behaviour of intrinsic Josephson junction stacks are measured and the possibility of phase locking is discussed by the theoretical analysis of two different shunt technologies depending on the parameter spread of the junction (up to 15%) and the shunt parameters. In the second part the mixing properties, especially noise, conversion efficiency and saturation behaviour, of HTS bicrystal Josephson junctions as wave guide mixers for 115 and 345 GHz have been investigated. The lowest noise temperatures have been obtained when the E-plane and the backshort tuner generate a resonant coupling to the Josephson junction. At 20 K operating temperature a lowest DSB mixer noise temperature of about 1000 K and a mixer conversion efficiency of ?0.8 dB was obtained with a 345 GHz mixer

Physcomitrium patens PpRIC, an ancestral CRIB-domain ROP effector, inhibits auxin-induced differentiation of apical initial cells

RHO guanosine triphosphatases are important eukaryotic regulators of cell differentiation and behavior. Plant ROP (RHO of plant) family members activate specific, incompletely characterized downstream signaling. The structurally simple land plant Physcomitrium patens is missing homologs of key animal and flowering plant RHO effectors but contains a single CRIB (CDC42/RAC interactive binding)-domain -contain-ing RIC (ROP-interacting CRIB-containing) protein (PpRIC). Protonemal P. patens filaments elongate based on regular division and PpROP-dependent tip growth of apical initial cells, which upon stimulation by the hor-mone auxin differentiate caulonemal characteristics. PpRIC interacts with active PpROP1, co-localizes with this protein at the plasma membrane at the tip of apical initial cells, and accumulates in the nucleus. Remark-ably, PpRIC is not required for tip growth but is targeted to the nucleus to block caulonema differentiation downstream of auxin-controlled gene expression. These observations establish functions of PpRIC in medi-ating crosstalk between ROP and auxin signaling, which contributes to the maintenance of apical initial cell identity

Manifestation of Resonance-Related Chaos in Coupled Josephson Junctions

Chaotic features of systems of coupled Josephson junctions are studied. Manifestation of chaos in the temporal dependence of the electric charge, related to a parametric resonance, is demonstrated through the calculation of the maximal Lyapunov exponent, phase-charge and charge-charge Lissajous diagrams and correlation functions. The number of junctions in the stack strongly influences the fine structure in the current voltage characteristics and a strong proximity effect results from the nonperiodic boundary conditions. The observed resonance-related chaos exhibits intermittency over a range of conditions and parameters. General features of the system are analyzed by means of a linearized equation and the criteria for a breakpoint region with no chaos are obtained. Such criteria could clarify recent experimental observations of variations in the power output from intrinsic Josephson junctions in high temperature superconductors.Comment: 13 pages, 16 figure

Pathogenesis of Scleroderma

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65784/1/j.1365-4362.1984.tb05678.x.pd

Neuronal Deletion of Caspase 8 Protects against Brain Injury in Mouse Models of Controlled Cortical Impact and Kainic Acid-Induced Excitotoxicity

system. mice demonstrated superior survival, reduced seizure severity, less apoptosis, and reduced caspase 3 processing. Uninjured aged knockout mice showed improved learning and memory, implicating a possible role for caspase 8 in cognitive decline with aging.Neuron-specific deletion of caspase 8 reduces brain damage and improves post-traumatic functional outcomes, suggesting an important role for this caspase in pathophysiology of acute brain trauma

Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation

Background: The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary injury factor that can drive ongoing neuronal injury. Despite this, treatments that have targeted aspects of the inflammatory pathway have not shown significant efficacy in clinical trials. Main body: We suggest that this may be because classical inflammation only represents part of the story, with activation of neurogenic inflammation potentially one of the key initiating inflammatory events following TBI. Indeed, evidence suggests that the transient receptor potential cation channels (TRP channels), TRPV1 and TRPA1, are polymodal receptors that are activated by a variety of stimuli associated with TBI, including mechanical shear stress, leading to the release of neuropeptides such as substance P (SP). SP augments many aspects of the classical inflammatory response via activation of microglia and astrocytes, degranulation of mast cells, and promoting leukocyte migration. Furthermore, SP may initiate the earliest changes seen in blood-brain barrier (BBB) permeability, namely the increased transcellular transport of plasma proteins via activation of caveolae. This is in line with reports that alterations in transcellular transport are seen first following TBI, prior to decreases in expression of tight-junction proteins such as claudin-5 and occludin. Indeed, the receptor for SP, the tachykinin NK1 receptor, is found in caveolae and its activation following TBI may allow influx of albumin and other plasma proteins which directly augment the inflammatory response by activating astrocytes and microglia. Conclusions: As such, the neurogenic inflammatory response can exacerbate classical inflammation via a positive feedback loop, with classical inflammatory mediators such as bradykinin and prostaglandins then further stimulating TRP receptors. Accordingly, complete inhibition of neuroinflammation following TBI may require the inhibition of both classical and neurogenic inflammatory pathways.Frances Corrigan, Kimberley A. Mander, Anna V. Leonard and Robert Vin