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

Ultrafast YBCO photodetector based on the kinetic-inductive process

We make use of the nonequilibrium kinetic-inductive effect in epitaxial YBa2Cu3O7-x (YBCO) thin films to demonstrate an ultrafast, high-sensitivity, broadband photodetector, The photoresponse of a 5-mum-wide, 10-mum-long, 100-nm-thick YBCO microbridge embedded in a 20-mum-wide coplanar strip transmission line was measured using a >1-THz, submillivolt-sensitivity electro-optic sampling system. We performed a comprehensive study of the optical power and wavelength dependency on the YBCO photodetector response. The quantum coherence Rothwarf-Taylor model together with the hot-electron relaxation effect were used to explain the measured data and to extract the number of generated quasiparticles for each absorbed photon, revealing the intrinsic quantum yield of our device to be similar to 450, The amplitude, response time, and the intrinsic gain of the YBCO photoresponses were observed to be spectrally flat over the tested range of 390 nm to 810 nm

Current transport in ramp-type junctions with engineered interface

The transport properties of "interface-engineered" edge-type YBa2Cu3O7 Josephson junctions are investigated in detail. We have investigated the dependence of the current-voltage characteristics on external magnetic field, temperature, and microwave irradiation and compare them to the resistively shunted junction model. The temperature dependence of the critical current and the normal resistance allows us to draw conclusions to the transport of quasiparticles and Cooper pairs in the investigated "interface-engineered" junctions. We have studied the properties of junctions for which La doped YBa2Cu3O7 is used for the superconducting electrodes. We will propose a model for the undoped and the La doped case which takes into account a barrier which consists of a series connection of a normal conducting layer and an insulator, containing superconducting microconstrictions. (C) 2001 American Institute of Physics