A new species of Luperus from the Canary Islands (Col. Chrysomelidae)

Up to now Luperits 'wollastoni Paiva seems the only representative of the genus to be known from the Canary Islands. Rather recently, however, I happened to find, in the island of La Palma, a second species which will be described below under the name of L. bispiniger sp. nov. Of L. wollastoni I also found some specimens. Moreover I have had access, by the courtesy of Dr. Walter Hackman, to a series brought together in three of the islands by the late Prof. Hitkan Lindberg and now in the collections of the Zoological Museum of the University in Helsingfors. And so I am able also to complete the old diagnosis.Peer reviewe

Impurity Effects on the A_1-A_2 Splitting of Superfluid 3He in Aerogel

When liquid 3He is impregnated into silica aerogel a solid-like layer of 3He atoms coats the silica structure. The surface 3He is in fast exchange with the liquid on NMR timescales. The exchange coupling of liquid 3He quasiparticles with the localized 3He spins modifies the scattering of 3He quasiparticles by the aerogel structure. In a magnetic field the polarization of the solid spins gives rise to a splitting of the scattering cross-section of for `up' vs. `down' spin quasiparticles, relative to the polarization of the solid 3He. We discuss this effect, as well as the effects of non-magnetic scattering, in the context of a possible splitting of the superfluid transition for $\uparrow\uparrow$ vs. $\downarrow\downarrow$ Cooper pairs for superfluid 3He in aerogel, analogous to the A_1-A_2 splitting in bulk 3He. Comparison with the existing measurements of T_c for B< 5 kG, which show no evidence of an A_1-A_2 splitting, suggests a liquid-solid exchange coupling of order J = 0.1 mK. Measurements at higher fields, B > 20 kG, should saturate the polarization of the solid 3He and reveal the A_1-A_2 splitting.Comment: 7 pages, 3 figure

A High Efficiency PSOFC/ATS-Gas Turbine Power System

A study is described in which the conceptual design of a hybrid power system integrating a pressurized Siemens Westinghouse solid oxide fuel cell generator and the Mercury{trademark} 50 gas turbine was developed. The Mercury{trademark} 50 was designed by Solar Turbines as part of the US. Department of Energy Advanced Turbine Systems program. The focus of the study was to develop the hybrid power system concept that principally would exhibit an attractively-low cost of electricity (COE). The inherently-high efficiency of the hybrid cycle contributes directly to achieving this objective, and by employing the efficient, power-intensive Mercury{trademark} 50, with its relatively-low installed cost, the higher-cost SOFC generator can be optimally sized such that the minimum-COE objective is achieved. The system cycle is described, major system components are specified, the system installed cost and COE are estimated, and the physical arrangement of the major system components is discussed. Estimates of system power output, efficiency, and emissions at the system design point are also presented. In addition, two bottoming cycle options are described, and estimates of their effects on overall-system performance, cost, and COE are provided

Role of mitochondrial raft-like microdomains in the regulation of cell apoptosis

Lipid rafts are envisaged as lateral assemblies of specific lipids and proteins that dissociate and associate rapidly and form functional clusters in cell membranes. These structural platforms are not confined to the plasma membrane; indeed lipid microdomains are similarly formed at subcellular organelles, which include endoplasmic reticulum, Golgi and mitochondria, named raft-like microdomains. In addition, some components of raft-like microdomains are present within ER-mitochondria associated membranes. This review is focused on the role of mitochondrial raft-like microdomains in the regulation of cell apoptosis, since these microdomains may represent preferential sites where key reactions take place, regulating mitochondria hyperpolarization, fission-associated changes, megapore formation and release of apoptogenic factors. These structural platforms appear to modulate cytoplasmic pathways switching cell fate towards cell survival or death. Main insights on this issue derive from some pathological conditions in which alterations of microdomains structure or function can lead to severe alterations of cell activity and life span. In the light of the role played by raft-like microdomains to integrate apoptotic signals and in regulating mitochondrial dynamics, it is conceivable that these membrane structures may play a role in the mitochondrial alterations observed in some of the most common human neurodegenerative diseases, such as Amyotrophic lateral sclerosis, Huntington's chorea and prion-related diseases. These findings introduce an additional task for identifying new molecular target(s) of pharmacological agents in these pathologies

Modeling mitochondrial dysfunctions in the brain: from mice to men

The biologist Lewis Thomas once wrote: “my mitochondria comprise a very large proportion of me. I cannot do the calculation, but I suppose there is almost as much of them in sheer dry bulk as there is the rest of me”. As humans, or indeed as any mammal, bird, or insect, we contain a specific molecular makeup that is driven by vast numbers of these miniscule powerhouses residing in most of our cells (mature red blood cells notwithstanding), quietly replicating, living independent lives and containing their own DNA. Everything we do, from running a marathon to breathing, is driven by these small batteries, and yet there is evidence that these molecular energy sources were originally bacteria, possibly parasitic, incorporated into our cells through symbiosis. Dysfunctions in these organelles can lead to debilitating, and sometimes fatal, diseases of almost all the bodies’ major organs. Mitochondrial dysfunction has been implicated in a wide variety of human disorders either as a primary cause or as a secondary consequence. To better understand the role of mitochondrial dysfunction in human disease, a multitude of pharmacologically induced and genetically manipulated animal models have been developed showing to a greater or lesser extent the clinical symptoms observed in patients with known and unknown causes of the disease. This review will focus on diseases of the brain and spinal cord in which mitochondrial dysfunction has been proven or is suspected and on animal models that are currently used to study the etiology, pathogenesis and treatment of these diseases

Major histocompatibility complex class I molecules protect motor neurons from astrocyte-induced toxicity in amyotrophic lateral sclerosis

Astrocytes isolated from individuals with amyotrophic lateral sclerosis (ALS) are toxic to motor neurons (MNs) and play a non–cell autonomous role in disease pathogenesis. The mechanisms underlying the susceptibility of MNs to cell death remain unclear. Here we report that astrocytes derived from either mice bearing mutations in genes associated with ALS or human subjects with ALS reduce the expression of major histocompatibility complex class I (MHCI) molecules on MNs; reduced MHCI expression makes these MNs susceptible to astrocyte-induced cell death. Increasing MHCI expression on MNs increases survival and motor performance in a mouse model of ALS and protects MNs against astrocyte toxicity. Overexpression of a single MHCI molecule, HLA-F, protects human MNs from ALS astrocyte–mediated toxicity, whereas knockdown of its receptor, the killer cell immunoglobulin-like receptor KIR3DL2, on human astrocytes results in enhanced MN death. Thus, our data indicate that, in ALS, loss of MHCI expression on MNs renders them more vulnerable to astrocyte-mediated toxicity