Description and chemical composition of manganese deposits during the deep-sea expedition of the streamer Valdivia in 1898-1899

This monograph forms the fourth part of the tenth volume of the scientific results of the voyage of the German exploring ship Valdivia in the Atlantic and Indian Oceans, made during the years 1898-1899. These volumes are published under the editorship of Prof. Chun, the zoologist of Leipzig, who was leader of the expedition ; and Prof. E. Philippi with the cooperation of Sir John Murray. The nature of the materials brought up at various points during the voyage is well illustrated by a series of plates, similar to those accompanying the Challenger volumes. Among the concretions from the Agulhas Bank were found phosphatic nodules containing 33 per cent, of calcium carbonate, 28 of calcium phosphate, 14.6 of calcium sulphate, and 4.8 of magnesium carbonate, with some ferric oxide, alumina, and silica. These nodules were dredged at a depth of 155 metres. Off the coast of Namibia, a large quantity of manganese nodules were also dredged. Their chemical analysis performed at the Mineralogical Institute of the University Jena show similar composition as the nodules recovered by the "Challenger" at station 253 in the Pacific Ocean.

Geochemistry at DSDP Site 76-533

Bulk X-ray mineralogy of 47 hemipelagic mud and clay samples from the Blake Outer Ridge has revealed that the sediments contain low magnesian calcite, calcian dolomite, ferroan dolomite, and magnesian siderite. Dolomite and siderite are authigenic and occur as rhombohedrons scattered through the sediments, whereas calcite is mostly biogenic. Pliocene dolomitic lenses are made up of interlocking polyhedral grains of ferroan dolomite. The contents of authigenic dolomite and siderite are 3 to 8% in carbonate sediments and 70 to 89% in dolomitic lenses. Dolomite occurs largely in the cores above 192 m sub-bottom depth, whereas siderite occurs in the cores below 87 m. The distribution and occurrence of dolomite and siderite have determined the diagenetic zonation of carbonates as Zone I (dolomitic zone, top-90 m), Zone II (transition zone, 90-180 m), and Zone III (sideritic zone, 180 m-bottom). Measurements of major and minor elements in the untreated total sediment samples and the insoluble residues after digestion in acid-reducing solution have revealed that the soluble fraction concentrates carbonates and ferromanganese associations (Ca, Mg, Sr, Fe, and Mn). Typical "hydrogenous elements" (Co, Cu, Ni, and V) are more concentrated in the insoluble residues rather than in the soluble fraction; the concentrations of these four elements are low and comparable to modern offshore mud, probably because the Site 533 sediments were deposited at a high rate of sedimentation. The contents of Fe2O3 and MnO are somewhat high for rapidly accumulated mud, particularly in the Pliocene sediments (8.09 and 0.26%, respectively, on a Carbonate-free basis). The high Fe and Mn contents are mainly due to the high contribution of the leacheable nonlithogenous fraction; leacheable Fe and Mn originate in the ferromanganese oxide accumulated on the seafloor. Only a small amount of ferric oxide was converted to iron sulfide in the surficial part of Zone I. Most ferromanganese oxide was reduced and precipitated as ferroan dolomite and magnesian siderite in Zones II and III under high alkalinity and high pH conditions in the organic-matter-rich sediments. Fe2+ and Mn2+ in the deeper sediments beneath Zone III possibly migrated upward and concentrated as siderite in Zone III, hence resulting in high contents of Fe and Mn in the Pliocene sediments. Analysis of carbonate zonation on the Blake Outer Ridge has revealed that the zonation is subparallel to the bedding plane rather than to the present seafloor. The sediments at Site 103 on the flank region of the Ridge are lacking Zone I and most of Zone II, probably the result of erosion of the most of the Pleistocene and Pliocene sediments by the enhanced bottom currents during the Pleistocene.

Design construction and testing of a heat loop for study of fouling and its interrelationship to corrosion in heat exchanger tubes

A heat loop suitable for the study of thermal fouling and its relationship to corrosion processes was designed, constructed and tested. The design adopted was an improvement over those used by such investigators as Hopkins and the Heat Transfer Research Institute in that very low levels of fouling could be detected accurately, the heat transfer surface could be readily removed for examination and the chemistry of the environment could be carefully monitored and controlled. In addition, an indirect method of electrical heating of the heat transfer surface was employed to eliminate magnetic and electric effects which result when direct resistance heating is employed to a test section. The testing of the loop was done using a 316 stainless steel test section and a suspension of ferric oxide and water in an attempt to duplicate the results obtained by Hopkins. Two types of thermal ·fouling resistance versus time curves were obtained . (i) Asymptotic type fouling curve, similar to the fouling behaviour described by Kern and Seaton and other investigators, was the most frequent type of fouling curve obtained. Thermal fouling occurred at a steadily decreasing rate before reaching a final asymptotic value. (ii) If an asymptotically fouled tube was cooled with rapid cir- ·culation for periods up to eight hours at zero heat flux, and heating restarted, fouling recommenced at a high linear rate. The fouling results obtained were observed to be similar and 1n agreement with the fouling behaviour reported previously by Hopkins and it was possible to duplicate quite closely the previous results . This supports the contention of Hopkins that the fouling results obtained were due to a crevice corrosion process and not an artifact of that heat loop which might have caused electrical and magnetic effects influencing the fouling. The effects of Reynolds number and heat flux on the asymptotic fouling resistance have been determined. A single experiment to study the effect of oxygen concentration has been carried out. The ferric oxide concentration for most of the fouling trials was standardized at 2400 ppM and the range of Reynolds number and heat flux for the study was 11000-29500 and 89-121 KW/M², respectively.

Arsenic Geochemitry in Warm Spring Ponds: New Field and Experimental Results

Silver Bow Creek (SBC) flows into the Warm Springs Ponds Operable Unit (WSPOU), where various containment cells are used to precipitate copper and other metals (e.g., Cd, Cu, Mn, Pb, Zn). Lime is added seasonally to increase the pH and assist in removal of metals from the water column. Although the WSPOU is effective at removing copper and other cationic trace metals, concentrations of dissolved arsenic exiting the facility are often above the site specific standard, 20 20 ug/L, during low-flow periods each summer and fall. This thesis is a continuation of arsenic geochemistry studies by Montana Tech in the WSPOU. Field work focused on Pond 3, the largest and first in the series of treatment ponds. Shallow groundwater was sampled from 8 PVC piezometers located near the south end of Pond 3. Three sediment pore-water diffusion samplers (“peepers”) were also deployed at the south end of Pond 3 to examine vertical gradients in chemistry in the top 25 cm of the pond sediment. In general, the pH and Eh values of the shallow groundwater and sediment pore-water were less than in the pond water. Concentrations of arsenic were generally higher in subsurface water, and tended to pass through a maximum (up to 530 g/L) about 10 cm below the sediment-water interface. In the peeper cells, there was a strong positive correlation between dissolved As and dissolved Fe, and an inverse correlation with sulfate. Therefore, the zone of arsenic release corresponds to a zone of bacterial Fe and sulfate reduction in the shallow, organic-rich sediment. Redox speciation of arsenic shows that arsenate (As(V)) is dominant in the pond, and arsenite (As(III)) is dominant in the subsurface water. A series of laboratory experiments with pH adjustment were completed using SBC water collected near the inlet to the WSPOU as well as water and shallow sediment collected from Pond 3. Water ± sediment mesocosms were set up in 1-L Nalgene bottles (closed system) or a 20-L aquarium (open system), both with continuous stirring. The pH of the mesocosm was adjusted by addition of NaOH or HNO3 acid. The closed system provided better pH control since the water was not in contact with the atmosphere, which prevented exchange of carbon dioxide. In both the closed and open systems, dissolved arsenic concentrations either decreased or stayed roughly the same with increase in pH to values > 11. Therefore, the release of dissolved As into the treatment ponds in low-flow periods is not due to changes in pH alone. All of these results support the hypothesis that the arsenic release in WSPOU is linked to microbial reduction of ferric oxide minerals in the organic-rich sediment. Upwards diffusion of dissolved As from the sediment pore-water into the pond water is the most likely explanation for the increase in As concentration of the WSPOU in low-flow periods.

Peroxisome proliferator-activated receptor-gamma ligand, 15-deoxy-Delta A(12,14)-prostaglandin J(2), reduces neutrophil migration via a nitric oxide pathway

Ligands for peroxisome proliferator-activated receptor gamma (PPAR-gamma), such as 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) have been implicated as a new class of anti-inflammatory compounds with possible clinical applications. Based on this concept, this investigation was designed to determine the effect of 15d-PGJ(2)-mediated activation of PPAR-gamma ligand on neutrophil migration after an inflammatory stimulus and clarify the underlying molecular mechanisms using a mouse model of peritonitis. Our results demonstrated that 15d-PGJ(2) administration decreases leukocyte rolling and adhesion to the inflammated mesenteric tissues by a mechanism dependent on NO. Specifically, pharmacological inhibitors of NO synthase remarkably abrogated the 15d-PGJ(2)-mediated suppression of neutrophil migration to the inflammatory site. Moreover, inducible NOS(-/-) mice were not susceptible to 15d-PGJ(2)-mediated suppression of neutrophil migration to the inflammatory sites when compared with their wild type. In addition, 15d-PGJ(2)-mediated suppression of neutrophil migration appeared to be independent of the production of cytokines and chemokines, since their production were not significantly affected in the carrageenan-injected peritoneal cavities. Finally, up-regulation of carrageenan-triggered ICAM-I expression in the mesenteric microcirculation vessels was abrogated by pretreatment of wild-type mice with 15d-PGJ(2), whereas 15d-PGJ(2) inhibited F-actin rearrangement process in neutrophils. Taken together these findings demonstrated that 15d-PGJ(2) suppresses inflammation-initiated neutrophil migration in a mechanism dependent on NO production in mesenteric tissues.

A study of the vacuum gamma-radiolysis of two aromatic polyimide fluoropolymers containing phenylphosphine oxide

The vacuum gamma -radiolysis of two fluorinated polyimides containing phenylphosphine oxide units, TOR-RC and TOR-RC ODPA, have been studied at 77 K and 300 K. The phenyl phosphine oxide units provide protection of the polymers towards oxidation by oxygen atoms and the bulky fluoromethyl groups reduce the colouration of the polymers by limiting donor-acceptor complex formation through the aromatic units. At 77 K the radicals formed were identified to be a mixture of neutral radicals (60%) and anion radicals. At 300 K only neutral radicals were found. The G-values for radical formation were found to be 0.50 and 0.42 at 77 K and 0.051 and 0.052 at 300 K for TOR-RC and TOR-RC ODPA, respectively. Little change was observed in the visible spectra of the polyimides following vacuum radiolysis at 300 K up to a dose of 3.3 MGy, and the polymers were shown to undergo net cross linking with a gel dose of 0.45 MGy.

A study of the oxidation of two aromatic polyimide fluoropolymers containing phenylphosphine oxide by a water plasma and gamma-radiolysis in air

The oxidation of two fluorinated polyimides containing phenylphosphine oxide units, TOR-RC and TOR-RC ODPA, have been studied at 300 K for treatment by a water plasma and gamma -radiolysis in air. The changes in the O 1s/C 1s ratios obtained from x-ray photoelectron spectroscopy (XPS) analysis showed that for exposure to the water plasma the ratio increases at short exposure times and then levels to a constant value. Evidence for the formation of phosphate species was also obtained from the XPS analyses. Similar observations were made for gamma -radiolysis of the polymers in air. The polymers containing phenylphosphine oxide were found to be more resistant to oxidation in the water plasma than Kapton(R). Radiolysis of the polymers in air to high doses were also accompanied by a red shift in the visible absorption spectra.

The behaviour of phenylphosphine oxide containing polyimides in a water plasma following gamma-radiolysis

The surface oxidation of two polyimides containing fluorinated phenylphosphine oxide units, TOR-RC and TOR-RC ODPA, have been studied by (XPS) spectroscopy following gamma -radiolysis under vacuum or in air and subsequent treatment in a water plasma. The changes in the O 1s/C 1s ratios obtained from (XPS) analysis showed that on exposure to the water plasma the ratio increases and then levels to a constant value which is similar to that found for exposure to the plasma without prior gamma -radiation treatment. Evidence for the formation of phosphate species was also obtained from the (XPS) analyses. (C) 2001 Elsevier Science Ltd. All rights reserved.

gamma-alumina nanofibers prepared from aluminum hydrate with poly(ethylene oxide) surfactant

Introducing poly(ethylene oxide) surfactant to aluminum hydrate colloids can effectively direct the crystal growth of boehmite and the crystal morphology of final gamma-alumina crystallites. Fibrous crystallites of gamma-alumina about 3-4 nm thick and 30-60 nm long are obtained. They stack randomly, resulting in a structure with a low contact area between the fibers but with a very large porosity. Such a structure exhibits strong resistance to sintering when heated to high temperatures. A sample retains a BET surface area of 68 m(2)/g, after being heated to 1473 K. The surfactant molecules form micelles that interact with the colloid particles of aluminum hydroxide through hydrogen bonding. This interaction is not sufficient to change the intrinsic crystal structure of boehmite, but induces profound changes in the morphology of boehmite crystallites and their growth. The surfactant-induced fiber formation (SIFF) process has distinct features from templated synthesis but shows similarities in some respects to biomineralization processes in which inorganic crystals with complex morphological shapes can be formed in biological systems. SIFF offers an effective approach to create new nanostructures of inorganic oxide from aqueous media.

Role of iron in the nitric oxide-mediated fungicidal mechanism of IFN-gamma-activated murine macrophages against Paracoccidioides brasiliensis conidia

Iron is an essential growth element of virtually all microorganisms and its restriction is one of the mechanisms used by macrophages to control microbial multiplication. Paracoccidioides brasiliensis, the agent of paracoccidioidomycosis, an important systemic mycosis in Latin America, is inhibited in its conidia-to-yeast conversion in the absence of iron. We studied the participation of iron in the nitric oxide (NO)-mediated fungicidal mechanism against conidia. Peritoneal murine macrophages activated with 50U/mL of IFN-gamma or treated with 35 µM Deferoxamine (DEX) and infected with P. brasiliensis conidia, were co-cultured and incubated for 96 h in the presence of different concentrations of holotransferrin (HOLO) and FeS0(4). The supernatants were withdrawn in order to assess NO2 production by the Griess method. The monolayers were fixed, stained and observed microscopically. The percentage of the conidia-to-yeast transition was estimated by counting 200 intracellular propagules. IFN-gamma-activated or DEX-treated Mthetas presented marked inhibition of the conidia-to-yeast conversion (19 and 56%, respectively) in comparison with non-activated or untreated Mthetas (80%). IFN-gamma-activated macrophages produced high NO levels in comparison with the controls. Additionally, when the activated or treated-macrophages were supplemented with iron donors (HOLO or FeSO4), the inhibitory action was reversed, although NO production remained intact. These results suggest that the NO-mediated fungicidal mechanism exerted by IFN-gamma-activated macrophages against P. brasiliensis conidia, is dependent of an iron interaction.

Induction of macrophage nitric oxide production by interferon-gamma and tumor necrosis factor-alpha is enhanced by interleukin-10.

Interleukin-10 (IL-10) has been reported to inhibit nitric oxide (NO) synthesis and microbicidal activity of interferon-gamma (IFN-gamma)-stimulated macrophages (M phi) by preventing the secretion of tumor necrosis factor-alpha (TNF-alpha) which serves as an autocrine activating signal. We have examined the effects of recombinant IL-10 on the capacity of IFN-gamma together with exogenous TNF-alpha to induce NO synthesis by bone marrow-derived M phi. Under these conditions and in contrast to its reported deactivating potential, IL-10 strongly enhanced NO synthesis measured as nitrite (NO2-) release (half maximal stimulation at approximately 10 U/ml). IL-10 further increased NO2- production by M phi stimulated in the presence of optimal concentrations of prostaglandin E2, a positive modulator of M phi activation by IFN-gamma/TNF-alpha. Increased steady state levels of NO synthase mRNA were observed in 4-h IFN-gamma/TNF-alpha cultures and enhanced NO2(-)-release was evident 24 h but not 48 h after stimulation. These results suggest that the effects of IL-10 on M phi function are more complex than previously recognized.

Neurodegeneration and Increased Production of Nitrotyrosine, Nitric Oxide Synthase, IFN-gamma and S100 beta Protein in the Spinal Cord of IL-12p40-Deficient Mice Infected with Trypanosoma cruzi

Background/Aim: Chagas` disease is caused by Trypanosoma cruzi and occurs in most Latin American countries. The protozoan may colonize the central nervous system (CNS) of immune-compromised human hosts, thus causing neuronal disorders. Systemic control of the intracellular forms of the parasite greatly depends on the establishment of a TH1 response and subsequent nitric oxide (NO) release. At the CNS, it is known that low concentrations of NO promote neuronal survival and growth, while high concentrations exert toxic effects and neuron death. Accounting for NO production by astrocytes is the glia-derived factor S100 beta, which is overproduced in some neurodegenerative diseases. In the current work, we studied the expression of NO, interferon (IFN)-gamma and S100 beta in the spinal cord tissue of IL-12p40KO mice infected with T. cruzi, a model of neurodegenerative process. Methods: IL-12p40KO and wild-type (WT) female mice infected with T. cruzi Sylvio X10/4 (10(5) trypomastigotes, intraperitoneally) were euthanized when IL-12p40KO individuals presented limb paralysis. Spinal cord sections were submitted to immunohistochemical procedures for localization of neurofilament, laminin, nitrotyrosine, NO synthases (NOS), IFN-gamma and S100 beta. The total number of neurons was estimated by stereological analysis and the area and intensity of immunoreactivities were assessed by microdensitometric/morphometric image analysis. Results: No lesion was found in the spinal cord sections of WT mice, while morphological disarrangements, many inflammatory foci, enlarged vessels, amastigote nests and dying neurons were seen at various levels of IL-12p40KO spinal cord. Compared to WT mice, IL-12p40KO mice presented a decrement on total number of neurons (46.4%, p<0.05) and showed increased values of immunoreactive area for nitrotyrosine (239%, p<0.01) and NOS (544%, p<0.001). Moreover, the intensity of nitrotyrosine (16%, p<0.01), NOS (38%, p<0.05) and S100 beta (21%, p<0.001) immunoreactivities were also augmented. No IFN-gamma labeled cells were seen in WT spinal cord tissue, contrary to IL-12p40KO tissue that displayed inflammatory infiltrating cells and also some parenchymal cells positively labeled.Conclusion: We suggest that overproduction of NO may account for neuronal death at the spinal cord of T. cruzi-infected IL-12p40KO mice and that IFN-gamma and S100 beta may contribute to NOS activation in the absence of IL-12. Copyright (C) 2009 S. Karger AG, Basel

Inhibition of interferon-gamma-induced nitric oxide production in endotoxin-activated macrophages by cytolethal distending toxin

Introduction: Cytolethal distending toxin (CDT) is a DNA-targeting agent produced by certain pathogenic gram-negative bacteria such as the periodontopathogenic organism Aggregatibacter actinomycetemcomitans. CDT targets lymphocytes and other cells causing cell cycle arrest and apoptosis, impairing the host immune response and contributing to the persistence of infections caused by this microorganism. In this study we explored the effects of CDT on the innate immune response, by investigating how it affects production of nitric oxide (NO) by macrophages. Methods: Murine peritoneal macrophages were stimulated with Escherichia coli sonicates and NO production was measured in the presence or not of active CDT. Results: We observed that CDT promptly and significantly inhibited NO production by inducible nitric oxide synthase (iNOS) in a dose-dependent manner. This inhibition is directed towards interferon-gamma-dependent pathways and is not mediated by either interleukin-4 or interleukin-10. Conclusion: This mechanism may constitute an important aspect of the immunosuppression mediated by CDT and may have potential clinical implications in A. actinomycetemcomitans infections.

Nitric oxide contributes to LPS/IFN-gamma-induced macrophage apoptosis via JNK and BCL-2 family regulation

Lipopolysaccharide (LPS) and interferon-gamma (IFN) activate macrophages and produce nitric oxide (NO) by initiating the expression of inducible Nitric Oxide Synthase (iNOS). Prolonged LPS/IFN-activation results in the death of macrophage-like RAW 264.7 cells and wild-type murine macrophages. This study was implemented to determine how NO contributes to LPS/IFN-induced macrophage death. The iNOS-specific inhibitor L-NIL protected RAW 264.7 cells from LPS/IFN-activated death, supporting a role for NO in the death of LPS/IFN-activated macrophages. A role for iNOS in cell death was confirmed in iNOS-/- macrophages which were resistant to LPS/IFN-induced death. Cell death was accompanied by nuclear condensation, caspase 3 activation, and PARP cleavage, all of which are hallmarks of apoptosis. The involvement of NO in modulating the stress-activated protein kinase (SAPK)/c-jun N-terminal kinase (JNK) signal transduction pathway was examined as a possible mechanism of LPS/IFN-mediated apoptosis. Western analysis demonstrated that NO modifies the phosphorylation profile of JNK and promotes activation of JNK in the mitochondria in RAW 264.7 cells. Inhibition of JNK with sIRNA significantly reduced cell death in RAW 264.7 cells, indicating the participation of the JNK pathway in LPS/IFN-mediated death. JNK has been demonstrated to induce mitochondrial-mediated apoptosis through modulation of Bcl-2 family members. Therefore, the effect of NO on the balance between pro- and anti-apoptotic Bcl-2 family members was examined. In RAW 264.7 cells, Bim was upregulated and phosphorylated by LPS/IFN independently of NO. However, co-immunoprecipitation studies demonstrated that NO promotes the association of Bax with the BimL splice variant. Examination of Bax phosphorylation by metabolic labeling demonstrated that Bax is basally phosphorylated and becomes dephosphorylated upon LPS/IFN treatment. L-NIL inhibited the dephosphorylation of Bax, indicating that Bax dephosphorylation is NO-dependent. NO also mediated LPS/IFN-induced downregulation of Mcl-1, an anti-apoptotic Bcl-2 family member, as demonstrated by Western blotting for Mcl-1 protein expression. Thus, NO contributes to macrophage apoptosis via a JNK-mediated mechanism involving interaction between Bax and Bim, dephosphorylation of Bax, and downregulation of Mcl-1. ^

Nitric oxide inhibits hypothalamic luteinizing hormone-releasing hormone release by releasing gamma-aminobutyric acid.

Nitric oxide synthase (NOS)-containing neurons, termed NOergic neurons, occur in various regions of the hypothalamus, including the median eminence-arcuate region, which plays an important role in controlling the release of luteinzing hormone-releasing hormone (LHRH). We examined the effect of NO on release of gamma-aminobutyric acid (GABA) from medial basal hypothalamic (MBH) explants incubated in vitro. Sodium nitroprusside (NP) (300 microM), a spontaneous releaser of NO, doubled the release of GABA. This release was significantly reduced by incubation of the tissue with hemoglobin, a scavenger of NO, whereas hemoglobin alone had no effect on the basal release of GABA. Elevation of the potassium concentration (40 mM) in the medium increased GABA release 15-fold; this release was further augmented by NP. Hemoglobin blocked the increase in GABA release induced by NP but had no effect on potassium-induced release, suggesting that the latter is not related to NO. As in the case of hemoglobin, NG-monomethyl-L-arginine (NMMA), a competitive inhibitor of NOS, had no effect on basal release of GABA, which indicates again that NO is not significant to basal GABA release. However, NMMA markedly inhibited the release of GABA induced by high potassium, which indicates that NO plays a role in potassium-induced release of GABA. In conditions in which the release of GABA was substantially augmented, there was a reduction in GABA tissue stores as well, suggesting that synthesis of GABA in these conditions did not keep up with release of the amine. Although NO released GABA, there was no effect of the released GABA on NO production, for incubation of MBH explants with GABA had no effect on NO release as measured by [14C]citrulline production. To determine whether GABA had any effect on the release of LHRH from these MBH explants, GABA was incubated with the tissue and the effect on LHRH release was determined. GABA (10(-5) or 10(-6) M) induced a 70% decrease in the release of LHRH, indicating that in the male rat GABA inhibits the release of this hypothalamic peptide. This inhibition in LHRH release induced by GABA was blocked by NMMA (300 microM), which indicates that GABA converts the stimulatory effect of NO on LHRH release into an inhibitory one, presumably via GABA receptors, which activate chloride channels that hyperpolarize the cell. Previous results have indicated that norepinephrine stimulates release of NO from the NOergic neurons, which then stimulates the release of LHRH. The current results indicate that the NO released also induces release of GABA, which then inhibits further LHRH release. Thus, in vivo the norepinephrinergic-driven pulses of LHRH release may be terminated by GABA released from GABAergic neurons via NO.