Two-stage evolution of mantle peridotites from the Stalemate Fracture Zone, northwestern Pacific

This paper reports the results of a mineralogical study of 14 mantle peridotite samples dredged in 2009 from the eastern slope of the northwestern segment of the Stalemate Ridge in the northwestern Pacific during cruise SO201-KALMAR Leg 1b of the R/V Sonne. The sample collection included four serpentinized and silicified dunites and ten variably serpentinized lherzolites. The compositions of primary minerals (clinopyroxene, orthopyroxene, and spinel) change systematically from the lherzolites to dunites. Spinel from the lherzolites shows higher Mg# and lower Cr# values (0.65-0.68 and 0.26-0.33, respectively) compared with spinel from the dunites (Mg# = 0.56-0.64 and Cr# = 0.38-0.43). Clinopyroxene from the lherzolites is less magnesian (Mg# = 91.7-92.4) than clinopyroxene from dunite sample DR37-3 (Mg# = 93.7). Based on the obtained data, it was concluded that the lherzolites of the Stalemate Fracture Zone were derived by 10-12% near-fractional melting of a DMM-type depleted mantle reservoir beneath the Kula-Pacific spreading center. The dunites were produced by interaction of residual lherzolites with sodium- and titaniumrich melt and are probably fragments of a network of dunite channels in the shallow mantle. The moderately depleted composition of minerals clearly distinguishes the lherzolites from the strongly depleted peridotites of the East Pacific Rise and indicates the existence of slow-spreading mid-ocean ridges in the Pacific Ocean during the Cretaceous-Paleogene

Is Privacy Controllable?

One of the major views of privacy associates privacy with the control over information. This gives rise to the question how controllable privacy actually is. In this paper, we adapt certain formal methods of control theory and investigate the implications of a control theoretic analysis of privacy. We look at how control and feedback mechanisms have been studied in the privacy literature. Relying on the control theoretic framework, we develop a simplistic conceptual control model of privacy, formulate privacy controllability issues and suggest directions for possible research.Comment: The final publication will be available at Springer via http://dx.doi.org/ [in press

Geochemical and mineralogical indicators for aqueous processes in the Columbia Hills of Gusev crater, Mars

Water played a major role in the formation and alteration of rocks and soils in the Columbia Hills. The extent of alteration ranges from moderate to extensive. Five distinct rock compositional classes were identified; the order for degree of alteration is Watchtower = Clovis >Wishstone = Peace > Backstay. The rover’s wheels uncovered one unusual soil (Paso Robles) that is the most S-rich material encountered. Clovis class rocks have compositions similar to Gusev plains soil but with higher Mg, Cl, and Br and lower Ca and Zn; Watchtower and Wishstone classes have high Al, Ti, and P and low Cr and Ni; Peace has high Mg and S and low Al, Na, and K; Backstay basalts have high Na and K compared to plains Adirondack basalts; and Paso Robles soil has high S and P. Some rocks are corundum-normative, indicating that their primary compositions were changed by loss and/or gain of rock-forming elements. Clovis materials consist of magnetite, nanophase ferric-oxides (npOx), hematite, goethite, Ca-phosphates, Ca- and Mg-sulfates, pyroxene, and secondary aluminosilicates. Wishstone and Watchtower rocks consist of Fe-oxides/oxyhydroxides, ilmenite, Ca-phosphate, pyroxene, feldspar, Mg-sulfates, and secondary aluminosilicates. Peace consists of magnetite, npOx, Mg- and Ca-sulfates, pyroxene, olivine, feldspar, apatite, halides, and secondary aluminosilicates. Paso Robles consists of Fe3+-, Mg-, Ca-, and other sulfates, Ca-phosphates, hematite, halite, allophane, and amorphous silica. Columbia Hills outcrops and rocks may have formed by the aqueous alteration of basaltic rocks, volcaniclastic materials, and/or impact ejecta by solutions that were rich in acid-volatile elements

Neurotrophic actions of dopamine on the development of a serotonergic feeding circuit in Drosophila melanogaster

<p>Abstract</p> <p>Background</p> <p>In the fruit fly, <it>Drosophila melanogaster</it>, serotonin functions both as a neurotransmitter to regulate larval feeding, and in the development of the stomatogastric feeding circuit. There is an inverse relationship between neuronal serotonin levels during late embryogenesis and the complexity of the serotonergic fibers projecting from the larval brain to the foregut, which correlate with perturbations in feeding, the functional output of the circuit. Dopamine does not modulate larval feeding, and dopaminergic fibers do not innervate the larval foregut. Since dopamine can function in central nervous system development, separate from its role as a neurotransmitter, the role of neuronal dopamine was assessed on the development, and mature function, of the 5-HT larval feeding circuit.</p> <p>Results</p> <p>Both decreased and increased neuronal dopamine levels in late embryogenesis during development of this circuit result in depressed levels of larval feeding. Perturbations in neuronal dopamine during this developmental period also result in greater branch complexity of the serotonergic fibers innervating the gut, as well as increased size and number of the serotonin-containing vesicles along the neurite length. This neurotrophic action for dopamine is modulated by the D₂dopamine receptor expressed during late embryogenesis in central 5-HT neurons. Animals carrying transgenic RNAi constructs to knock down both dopamine and serotonin synthesis in the central nervous system display normal feeding and fiber architecture. However, disparate levels of neuronal dopamine and serotonin during development of the circuit result in abnormal gut fiber architecture and feeding behavior.</p> <p>Conclusions</p> <p>These results suggest that dopamine can exert a direct trophic influence on the development of a specific neural circuit, and that dopamine and serotonin may interact with each other to generate the neural architecture necessary for normal function of the circuit.</p

Methamphetamine Increases LPS-Mediated Expression of IL-8, TNF-α and IL-1β in Human Macrophages through Common Signaling Pathways

The use of methamphetamine (MA) has increased in recent years, and is a major health concern throughout the world. The use of MA has been associated with an increased risk of acquiring HIV-1, along with an increased probability of the acquisition of various sexually transmitted infections. In order to determine the potential effects of MA exposure in the context of an infectious agent, U937 macrophages were exposed to various combinations of MA and bacterial lipopolysaccharide (LPS). Treatment with MA alone caused significant increases in the levels of TNF-α, while treatment with both MA and LPS resulted in significant increases in TNF-α, IL-1β and the chemokine IL-8. The increases in cytokine or chemokine levels seen when cells were treated with both LPS and MA were generally greater than those increases observed when cells were treated with only LPS. Treatment with chemical inhibitors demonstrated that the signal transduction pathways including NF-kB, MAPK, and PI3-Akt were involved in mediating the increased inflammatory response. As discussed in the paper, these pathways appear to be utilized by both MA and LPS, in the induction of these inflammatory mediators. Since these pathways are involved in the induction of inflammation in response to other pathogens, this suggests that MA-exacerbated inflammation may be a common feature of infectious disease in MA abusers

Plasma Proteomic Profiling in HIV-1 Infected Methamphetamine Abusers

We wanted to determine whether methamphetamine use affects a subset of plasma proteins in HIV-infected persons. Plasma samples from two visits were identified for subjects from four groups: HIV+, ongoing, persistent METH use; HIV+, short-term METH abstinent; HIV+, long term METH abstinence; HIV negative, no history of METH use. Among 390 proteins identified, 28 showed significant changes in expression in the HIV+/persistent METH+ group over the two visits, which were not attributable to HIV itself. These proteins were involved in complement, coagulation pathways and oxidative stress. Continuous METH use is an unstable condition, altering levels of a number of plasma proteins

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

Methamphetamine (METH) is an illicit drug which is neurotoxic to the mammalian brain. Numerous studies have revealed significant decreases in dopamine and serotonin levels in the brains of animals exposed to moderate-to-large METH doses given within short intervals of time. In contrast, repeated injections of small nontoxic doses of the drug followed by a challenge with toxic METH doses afford significant protection against monoamine depletion. The present study was undertaken to test the possibility that repeated injections of the drug might be accompanied by transcriptional changes involved in rendering the nigrostriatal dopaminergic system refractory to METH toxicity. Our results confirm that METH preconditioning can provide significant protection against METH-induced striatal dopamine depletion. In addition, the presence and absence of METH preconditioning were associated with substantial differences in the identity of the genes whose expression was affected by a toxic METH challenge. Quantitative PCR confirmed METH-induced changes in genes of interest and identified additional genes that were differentially impacted by the toxic METH challenge in the presence of METH preconditioning. These genes include small heat shock 27 kD 27 protein 2 (HspB2), thyrotropin-releasing hormone (TRH), brain derived neurotrophic factor (BDNF), c-fos, and some encoding antioxidant proteins including CuZn superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx)-1, and heme oxygenase-1 (Hmox-1). These observations are consistent, in part, with the transcriptional alterations reported in models of lethal ischemic injuries which are preceded by ischemic or pharmacological preconditioning. Our findings suggest that multiple molecular pathways might work in tandem to protect the nigrostriatal dopaminergic pathway against the deleterious effects of the toxic psychostimulant. Further analysis of the molecular and cellular pathways regulated by these genes should help to provide some insight into the neuroadaptive potentials of the brain when repeatedly exposed to drugs of abuse

Differential effects of prenatal and postnatal expressions of mutant human DISC1 on neurobehavioral phenotypes in transgenic mice: evidence for neurodevelopmental origin of major psychiatric disorders

Strong genetic evidence implicates mutations and polymorphisms in the gene Disrupted-In-Schizophrenia-1 (DISC1) as risk factors for both schizophrenia and mood disorders. Recent studies have shown that DISC1 has important functions in both brain development and adult brain function. We have described earlier a transgenic mouse model of inducible expression of mutant human DISC1 (hDISC1) that acts in a dominant-negative manner to induce the marked neurobehavioral abnormalities. To gain insight into the roles of DISC1 at various stages of neurodevelopment, we examined the effects of mutant hDISC1 expressed during (1) only prenatal period, (2) only postnatal period, or (3) both periods. All periods of expression similarly led to decreased levels of cortical dopamine (DA) and fewer parvalbumin-positive neurons in the cortex. Combined prenatal and postnatal expression produced increased aggression and enhanced response to psychostimulants in male mice along with increased linear density of dendritic spines on neurons of the dentate gyrus of the hippocampus, and lower levels of endogenous DISC1 and LIS1. Prenatal expression only resulted in smaller brain volume, whereas selective postnatal expression gave rise to decreased social behavior in male mice and depression-like responses in female mice as well as enlarged lateral ventricles and decreased DA content in the hippocampus of female mice, and decreased level of endogenous DISC1. Our data show that mutant hDISC1 exerts differential effects on neurobehavioral phenotypes, depending on the stage of development at which the protein is expressed. The multiple and diverse abnormalities detected in mutant DISC1 mice are reminiscent of findings in major mental diseases