Linear optics implementation of general two-photon projective measurement

We will present a method of implementation of general projective measurement of two-photon polarization state with the use of linear optics elements only. The scheme presented succeeds with a probability of at least 1/16. For some specific measurements, (e.g. parity measurement) this probability reaches 1/4.Comment: 8 page

Dynamics of Action Potential Initiation in the GABAergic Thalamic Reticular Nucleus In Vivo

Understanding the neural mechanisms of action potential generation is critical to establish the way neural circuits generate and coordinate activity. Accordingly, we investigated the dynamics of action potential initiation in the GABAergic thalamic reticular nucleus (TRN) using in vivo intracellular recordings in cats in order to preserve anatomically-intact axo-dendritic distributions and naturally-occurring spatiotemporal patterns of synaptic activity in this structure that regulates the thalamic relay to neocortex. We found a wide operational range of voltage thresholds for action potentials, mostly due to intrinsic voltage-gated conductances and not synaptic activity driven by network oscillations. Varying levels of synchronous synaptic inputs produced fast rates of membrane potential depolarization preceding the action potential onset that were associated with lower thresholds and increased excitability, consistent with TRN neurons performing as coincidence detectors. On the other hand the presence of action potentials preceding any given spike was associated with more depolarized thresholds. The phase-plane trajectory of the action potential showed somato-dendritic propagation, but no obvious axon initial segment component, prominent in other neuronal classes and allegedly responsible for the high onset speed. Overall, our results suggest that TRN neurons could flexibly integrate synaptic inputs to discharge action potentials over wide voltage ranges, and perform as coincidence detectors and temporal integrators, supported by a dynamic action potential threshold

Emerging pharmacotherapy for cancer patients with cognitive dysfunction

Advances in the diagnosis and multi-modality treatment of cancer have increased survival rates for many cancer types leading to an increasing load of long-term sequelae of therapy, including that of cognitive dysfunction. The cytotoxic nature of chemotherapeutic agents may also reduce neurogenesis, a key component of the physiology of memory and cognition, with ramifications for the patient's mood and other cognition disorders. Similarly radiotherapy employed as a therapeutic or prophylactic tool in the treatment of primary or metastatic disease may significantly affect cognition. A number of emerging pharmacotherapies are under investigation for the treatment of cognitive dysfunction experienced by cancer patients. Recent data from clinical trials is reviewed involving the stimulants modafinil and methylphenidate, mood stabiliser lithium, anti-Alzheimer's drugs memantine and donepezil, as well as other agents which are currently being explored within dementia, animal, and cell culture models to evaluate their use in treating cognitive dysfunction

Listeria pathogenesis and molecular virulence determinants

The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research

The concealed granite massif of Eichigt−Schönbrunn (Vogtland, Germany): Petrography, mineralogy, geochemistry and age of the Eichigt apical intrusion

The Eichigt granite is one of two apical intrusions forming the concealed massif of Eichigt−Schönbrunn in the Erzgebirge−Vogtland metallogenic province of Germany. It represents a peraluminuous, medium-grained, Si-rich biotite monzo- to syenogranite of aluminuous A-type affinity and post-collisional (-orogenic) tectonic setting, which belongs to the group of medium-F, low-P Variscan granites of the Erzgebirge. Mineralogically and geochemically, the Eichigt granite shows the closest affinity to the Gottesberg subvolcanic microgranite/rhyolite complex some 25 km north-east of the massif. The granites contain phenocrysts of quartz and K-feldspar and sporadically accessory topaz and andalusite. A special feature is the presence of accessory primary fergusonite-(Y) and secondary synchysite-(Ce). Minor amounts of quartz, K-feldspar, and siderophyllite likely represent antecrysts, i.e., crystallized from a lesser silicic forerunner magma. These observations attest to the operation of magma mingling during the formation of the Eichigt granite. Calculation of Th−U−total Pb uraninite ages proves that the Eichigt and Schönbrunn granites are coeval and emplaced at about 306 ± 3 Ma (2σ), i.e., were formed during the same magmatic episode as the northwesterly Henneberg granite in Thuringia und the microgranite/rhyolith suite at Gottesberg and the Seiffen granite in the Erzgebirge−Vogtland. Geochemical data and mineralogical features do not lend support a genetical relation between the Eichigt−Schönbrunn granites and the spatially associated Sn-polymetallic veins