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Proof-of-principle is demonstrated for a method of measuring the oxygen diffusion properties of thin polymer films based on quenching of the delayed upconverted [S.sub.2] fluorescence of Zn(II) meso-tetraphenylporphine (ZnTPP). Empirical oxygen diffusion coefficients and permeability coefficients for poly(vinyl alcohol) (PVA) have been computed using Stern-Volmer kinetics in the steady-state regime and a nonlinear gas solubility model in the time domain. Simplified dual-mode theory has been used to calculate crude theoretical oxygen permeability coefficients to compare with the experimental values. It is confirmed that oxygen permeability in the PVA matrix is controlled largely by the characteristics of the polymer matrix, particularly its water content and distribution. Key words: oxygen diffusion, triplet-triplet annihilation, upconverted fluorescence, Stern-Volmer kinetics, nonlinear gas solubility model, dual-mode theory. On presente une demonstration du principe de preuve pour une methode de mesure des proprieetes de diffusion de l'oxygene a partir de films minces de polymere ; elle est baseee sur le pieegeage de la fluorescence [S.sub.2] retardeee et non convertie du sel de zinc(II) de la meso-tetraphenylporphyne (ZnTPP). On a calcule les coefficients empiriques de diffusion de l'oxygene et les coefficients de permeabilite de l'alcool polyvinylique en faisant appel a la cinetique de Stern-Volmer dans le regime d'etat stationnaire et un modele de solubilite gazeuse non lineaire dans le domaine du temps. On a fait appel a la theorie simplifieee du double mode pour calculer les coefficients bruts de permeabilite theorique de l'oxygene afin de les comparer aux valeurs expeerimentales. Il est confirmee que la permeabilite; de l'oxygene dans la matrice d'alcool polyvinylique est controleee principalement par les caracteeristiques de la matrice de polymere, en particulier par son contenu en au et sa distribution. Mots-cles: diffusion de l'oxygene, annihilation triplet-triplet, fluorescence non convertie, cinetique de Stern-Volmer, modele de solubilitee gazeuse non lineeaire, theorie du double mode. [Traduit par la Redaction], Introduction The transport properties of gas molecules through polymer media has been an area of long-standing interest from both fundamental and applied perspectives. (1-3) In addition to the fundamental interest [...]

The Hakon Mosby Mud Volcano is a highly active methane seep hosting different chemosynthetic communities such as thiotrophic bacterial mats and siboglinid tubeworm assemblages. This study focuses on in situ measurements of methane fluxes to and from these different habitats, in comparison to benthic methane and oxygen consumption rates. By quantifying in situ oxygen, methane, and sulfide fluxes in different habitats, a spatial budget covering areas of 10-1000-m diameter was established. The range of dissolved methane efflux (770-2 mmol [m.sup.-2] [d.sup.-1]) from the center to the outer rim was associated with a decrease in temperature gradients from 46[degrees]C [m.sup.-1] to < 1[degrees]C [m.sup.-1], indicating that spatial variations in fluid flow control the distribution of benthic habitats and activities. Accordingly, total oxygen uptake (TOU) varied between the different habitats by one order of magnitude from 15 mmol [m.sup.-2] [d.sup.-1] to 161 mmol [m.sup.-2] [d.sup.-1]. High fluid flow rates appeared to suppress benthic activities by limiting the availability of electron acceptors. Accordingly, the highest TOU was associated with the lowest fluid flow and methane efflux. This was most likely due to the aerobic oxidation of methane, which may be more relevant as a sink for methane as previously considered in submarine ecosystems. doi: 10.4319/lo.2010.55.6.2366

Tissue oxygen levels are tightly regulated in all organs. This poses a challenge for the kidney, as its function requires blood flow, and thus, oxygen delivery to greatly exceed its metabolic requirements. Because superoxide production in the kidney is dependent on oxygen availability, tissue hyperoxia could drive oxidative stress. In the mammalian renal cortex, this problem may have been solved, in part, through a structural antioxidant defense mechanism. That is, arteries and veins are closely associated in a countercurrent arrangement, facilitating diffusional arterial-to-venous (AV) oxygen shunting. Because of this mechanism, a proportion of the oxygen delivered in the renal artery never reaches kidney tissue but instead diffuses to the closely associated renal veins, thus limiting oxygen transport to tissue. In the nonmammalian kidney, arteries and veins are not arranged in an intimate countercurrent fashion as in mammals; thus AV oxygen shunting is likely less important in regulation of kidney oxygenation in these species. Instead, the kidney's blood supply is predominately of venous origin. This likely has a similar impact on tissue oxygenation as AV oxygen shunting, of limiting delivery of oxygen to renal tissue. Thus, we hypothesize the evolution of structural antioxidant mechanisms that are anatomically divergent but functionally homologous in the mammalian and nonmammalian kidney. hyperoxia; hypoxia; kidney circulation; oxidative stress; portal system doi: 10.1152/ajpregu.00364.2010.

We used a mathematical model of [O.sub.2] transport and the urine concentrating mechanism of the outer medulla of the rat kidney to study the effects of blood pH and medullary blood flow on [O.sub.2] availability and [Na.sup.+] reabsorption. The model predicts that in vivo paracellular [Na.sup.+] fluxes across medullary thick ascending limbs (toTALs) are small relative to transcellular [Na.sup.+] fluxes and that paracellular fluxes favor [Na.sup.+] reabsorption from the lumen along most of the mTAL segments. In addition, model results suggest that blood pH has a significant impact on [O.sub.2] transport and Nat reabsorption owing to the Bohr effect, according to which a lower pH reduces the binding affinity of hemoglobin for [O.sub.2]. Thus our model predicts that the presumed greater acidity of blood in the interbundle regions, where mTALs are located, relative to that in the vascular bundles, facilitates the delivery of [O.sub.2] to support the high metabolic requirements of the mTALs and raises the concentrating capability of the outer medulla. Model results also suggest that increases in vascular and tubular flow rates result in disproportional, smaller increases in active [O.sub.2] consumption and mTAL active [Na.sup.+] transport, despite the higher delivery of [O.sub.2] and [Na.sup.+]. That is, at a sufficiently high medullary [O.sub.2] supply, [O.sub.2] demand in the outer medulla does not adjust precisely to changes in [O.sub.2] delivery. mathematical model; thick ascending limb; [T.sub.Na]/[Qo.sub.2] ratio; paracellular; transcellular doi: 10.1152/ajprenal.00572.2009.

Bacteria coordinate expression of virulence determinants in response to localized microenvironments in their hosts. Here we show that Shigella flexneri, which causes dysentery, encounters varying oxygen concentrations in the gastrointestinal tract, which govern activity of its type three secretion system (T3SS). The T3SS is essential for cell invasion and virulence (1). In anaerobic environments (for example, the gastrointestinal tract lumen), Shigella is primed for invasion and expresses extended T3SS needles while reducing Ipa (invasion plasmid antigen) effector secretion. This is mediated by FNR (fumarate and nitrate reduction), a regulator of anaerobic metabolism that represses transcription of spa32 and spa33, virulence genes that regulate secretion through the T3SS. We demonstrate there is a zone of relative oxygenation adjacent to the gastrointestinal tract mucosa, caused by diffusion from the capillary network at the tips of villi. This would reverse the anaerobic block of Ipa secretion, allowing T3SS activation at its precise site of action, enhancing invasion and virulence., Shigella virulence depends on its ability to enter epithelial cells by delivering Ipa effectors via its T3SS (which acts as a molecular syringe) into the host cell cytoplasm (1). Secretion [...]

We examined the mechanisms that maintain stable renal tissue [Po.sub.2] during moderate renal ischemia, when changes in renal oxygen delivery ([??]o.sub.2]) and consumption ([[??]o.sub.2]) are mismatched. When renal artery pressure (RAP) was reduced progressively from 80 to 40 mmHg, [[??]o.sub.2] (-38 [+ or -] 7%) was reduced more than [Do.sub.2] (-26 [+ or -] 4%). Electrical stimulation of the renal nerves (RNS) reduced [Do.sub.2] (-49 [+ or -] 4% at 2 Hz) more than [[??]o.sub.2] (-30 [+ or -] 7% at 2 Hz). Renal arterial infusion of angiotensin II reduced [Do.sub.2] (-38 [+ or -] 3%) but not [[??]o.sub.2] (+ 10 [+ or -] 10%). Despite mismatched changes in [[??]o.sub.2] and [[??]o.sub.2], renal tissue [Po.sub.2] remained remarkably stable at [greater than or equal to] 40 mmHg RAP, during RNS at [less than or equal to] 2 Hz, and during angiotensin II infusion. The ratio of sodium reabsorption to [[??]o.sub.2] was reduced by all three ischemic stimuli. None of the stimuli significantly altered the gradients in P[co.sub.2] or pH across the kidney. Fractional oxygen extraction increased and renal venous Po2 fell during 2-Hz RNS and angiotensin II infusion, but not when RAP was reduced to 40 mmHg. Thus reduced renal [[??]o.sub.2] can help. prevent tissue hypoxia during mild renal ischemia, but when renal [[??]o.sub.2] is reduced less than [[??]o.sub.2], other mechanisms prevent a fall in renal [Po.sub.2]. These mechanisms do not include increased efficiency of renal oxygen utilization for sodium reahsorption or reduced washout of carbon dioxide from the kidney, leading to increased oxygen extraction. However, increased oxygen extraction could be driven by altered countercurrent exchange of carbon dioxide and/or oxygen between renal arteries and veins. angiotensin II; carbon dioxide; hypoxia; hypotension; oxygen; sympathetic nervous system doi: 10.1152/ajprenal.00647.2009

The effect of low blood flow at onset of moderate-intensity exercise on the rate of rise in muscle oxygen uptake was examined. Seven male subjects performed a 3.5-min one-legged knee-extensor exercise bout (24 [+ or -] 1 W, mean [+ or -] SD) without (Con) and with (double blockade; DB) arterial infusion of inhibitors of nitric oxide synthase (NG-monomethyl-L-arginine) and cyclooxygenase (indomethacin) to inhibit the synthesis of nitric oxide and prostanoids, respectively. Leg blood flow and leg oxygen delivery throughout exercise was 25-50% lower (P < 0.05) in DB compared with Con. Leg oxygen extraction (arteriovenous O2 difference) was higher (P < 0.05) in DB than in Con (5 s: 127 [+ or -] 3 vs. 56 [+ or -] 4 ml/1), and leg oxygen uptake was not different between Con and DB during exercise. The difference between leg oxygen delivery and leg oxygen uptake was smaller (P < 0.05) during exercise in DB than in Con (5 s: 59 [+ or -] 12 vs. 262 [+ or -] 39 ml/min). The present data demonstrate that muscle blood flow and oxygen delivery can be markedly reduced without affecting muscle oxygen uptake in the initial phase of moderate-intensity exercise, suggesting that blood flow does not limit muscle oxygen uptake at the onset of exercise. Additionally, prostanoids and/or nitric oxide appear to play important roles in elevating skeletal muscle blood flow in the initial phase of exercise. oxygen delivery; oxygen extraction; nitric oxide; prostanoids doi:10.1152/ajpregu.00730.2009

The increase in [O.sub.2] tension after birth is a major factor stimulating ductus arteriosus (DA) constriction and closure. Here we studied the role of the mitochondrial electron transport chain (ETC) as sensor, [H.sub.2][O.sub.2] as mediator, and voltage-gated potassium ([K.sub.v]) channels and Rho kinase as effectors of [O.sub.2]-induced contraction in the chicken DA during fetal development. Switching from 0% to 21% [O.sub.2] contracted the pulmonary side of the mature DA (mature pDA) but had no effect in immature pDA and relaxed the aortic side of the mature DA (mature aDA). This contraction of the pDA was attenuated by inhibitors of the mitochondrial ETC and by the [H.sub.2][O.sub.2] scavenger polyethylene glycol (PEG)-catalase. Moreover, [O.sub.2] increased reactive oxygen species (ROS) production, measured with the fluorescent probes dihydroethidium and 2',7'-dichlorofluorescein, only in mature pDA. The [H.sub.2][O.sub.2] analog t-butyl-hydroperoxide mimicked the responses to 02 in the three vessels. In contrast to immature pDA cells, mature pDA cells exhibited high-amplitude [O.sub.2]-sensitive potassium currents. The Kv channel blocker 4-aminopyridine prevented the current inhibition elicited by [O.sub.2]. The L-type [Ca.sup.2+] ([Ca.sub.L]) channel blocker nifedipine and the Rho kinase inhibitors Y-27632 and hydroxyfasudil induced a similar relaxation when mature pDA were stimulated with [O.sub.2] or [H.sub.2][O.sub.2]. Moreover, the sensitivity to these drugs increased with maturation. Our results indicate the presence of a common mechanism for [O.sub.2] sensing/signaling in mammalian and nonmammalian DA and favor the idea that, rather than a single mechanism, a parallel maturation of the sensor and effectors is critical for [O.sub.2] sensitivity appearance during development. oxygen sensing; potassium channels; hydrogen peroxide doi:10.1152/ajplung.00092.2009.

Chronic exposure to hypoxia is associated with muscle atrophy (i.e., a reduction in muscle fiber cross-sectional area), reduced oxidative capacity, and capillary growth. It is controversial whether these changes are muscle and fiber type specific. We hypothesized that different regions of the same muscle would also respond differently to chronic hypoxia. To investigate this, we compared the deep (oxidative) and superficial (glycolytic) region of the plantaris muscle of eight male rats exposed to 4 wk of hypobaric hypoxia (410 mmHg, [Po.sub.2]:11.5 kPa) with those of nine normoxic rats. Hematocrit was higher in chronic hypoxic than control rats (59% vs. 50%, P < 0.001). Using histochemistry, we observed 10% fiber atrophy (P < 0.05) in both regions of the muscle but no shift in the fiber type composition and myoglobin concentration of the fibers. In hypoxic rats, succinate dehydrogenase (SDH) activity was elevated in fibers of each type in the superficial region (25%, P < 0.05) but not in the deep region, whereas in the deep region but not the superficial region the number of capillaries supplying a fiber was elevated (14%, P < 0.05). Model calculations showed that the region-specific alterations in fiber size, SDH activity, and capillary supply to a fiber prevented the occurrence of anoxic areas in the deep region but not in the superficial region. Inclusion of reported acclimatization-induced increases in mean capillary oxygen pressure attenuated the development of anoxic tissue areas in the superficial region of the muscle. We conclude that the determinants of tissue oxygenation show region-specific adaptations, resulting in a marked differential effect on tissue [Po.sub.2]. tissue oxygenation; capillarization; oxidative capacity

Convective oxygen transport by microvessels depends on several parameters, including red blood cell flux and oxygen saturation. We demonstrate the use of intravital microscopy techniques to measure hemoglobin saturations, red blood cell fluxes and velocities, and microvessel cross-sectional areas in regions of microvascular networks containing multiple vessels. With these methods, data can be obtained at high spatial and temporal resolution and correlations between oxygen transport and hemodynamic parameters can be assessed. In vivo data are presented for a mouse mammary adenocarcinoma grown in a dorsal skinfold window chamber model. OCIS codes: 180.0180, 170.2655, 170.3880.

Conventional pulse oximetry has limited accuracy in measuring blood oxygen saturation in low-saturation and -perfusion scenarios. This limits the application of pulse oximetry in patients suffering from peripheral vascular afflictions. We present a novel pulse oximetry system that proposes solutions to these low-saturation and -perfusion scenarios by inducing an artificial pulse in the detected photoplethysmograph (PPG). A novel arteriovenous hypothesis was formulated to extract arterial and venous saturation data from the artificial PPG using arterial-to-venous compliance ratios. Sensor wavelengths were selected to provide high- and low-saturation accuracy, followed by an in vitro sensor calibration procedure. System performance was validated by means of an in vivo procedure. In vivo results indicate good accuracy for high saturation, with limited accuracy in low-saturation scenarios. The arteriovenous hypothesis was validated, indicating that venous saturation can be extracted from the artificial PPG. The results indicate that the proposed system might be able to accurately monitor arterial and venous saturation in low- or no-perfusion scenarios. It is recommended that further studies into the system's performance are conducted. Index Terms--In vitro calibration, low perfusion, low saturation, photon diffusion theory, pulse oximetry, venous saturation.

The pseudogap region of the phase diagram is an important unsolved puzzle in the field of high-transition-temperature (high-[T.sub.c]) superconductivity, characterized by anomalous physical properties (1,2). There are open questions about [...]

Myoglobin is a globular protein involved in oxygen storage and transport. No consensus yet exists on the atomic level mechanism by which oxygen and other small nonpolar ligands move between the myoglobin's buried heme, which is the ligand binding site, and surrounding solvent. This study uses room temperature molecular dynamics simulations to provide a complete atomic level picture of ligand migration in myoglobin. Multiple trajectories--providing a cumulative total of 7/[micro]s of simulation--are analyzed. Our simulation results are consistent with and tie together previous experimental findings. Specifically, we characterize: (i) Explicit full trajectories in which the CO ligand shuttles between the internal binding site and the solvent and (ii) pattern and structural origins of transient voids available for ligand migration. The computations are performed both in sperm whale myoglobin wild-type and in sperm whale V68F myoglobin mutant, which is experimentally known to slow ligand-binding kinetics. On the basis of these independent, but mutually consistent ligand migration and transient void computations, we find that there are two discrete dynamical pathways for ligand migration in myoglobin. Trajectory hops between these pathways are limited to two bottleneck regions. Ligand enters and exits the protein matrix in common identifiable portals on the protein surface. The pathways are located in the 'softer' regions of the protein matrix and go between its helices and in its loop regions. Localized structural fluctuations are the primary physical origin of the simulated CO migration pathways inside the protein. proteins | molecular dynamics | kinetics | structure-function relationships

The majority of mitochondrial proteins are encoded by nuclear genes and synthesized in the cytosol as preproteins containing a mitochondria import sequence. Preproteins traverse the outer mitochondrial membrane in an unfolded state and then translocate through the inner membrane into the matrix via import machinery that includes mitochondrial heat shock protein 70 (mtHSP70). Neonatal rat cardiac myocytes (NCM) infected with an adenoviral vector expressing mtHSP70 or an empty control ([Adv.sup.-]) for 48 h were submitted to 8 h of simulated ischemia (hypoxia) followed by 16 h of reperfusion (reoxygenation). Infection with mtHSP70 virus yielded an increase in mtHSP70 protein in NCM mitochondria compared with [Adv.sup.-] (P < 0.05). Cell viability after simulated ischemia/reperfusion (I/R) was decreased in both [Adv.sup.-] and mtHSP70 groups, relative to control (P < 0.05), but mtHSP70-infected NCM had enhanced viability after I/R relative to Adv-infected NCM (P < 0.05). Simulated I/R caused an increase in reactive oxygen species generation and lipid peroxidation in Adv-infected NCM (P < 0.05, for both) that was not observed in mtHSP70-infected NCM. Mitochondrial complex III and IV activities were greater in mtHSP70-infected NCM after simulated I/R compared with [Adv.sup.-] (P < 0.05 for both). After simulated I/R, ATP content increased in mtHSP70-infected NCM, compared with [Adv.sup.-] (P < 0.05). Apoptotic markers were decreased in mtHSP70-infected NCM compared with [Adv.sup.-] after simulated I/R (P < 0.05). These results indicate that overexpression of mtHSP70 protects the mitochondria against damage from simulated I/R that may be due to a decrease in reactive oxygen species leading to preservation of mitochondrial complex function activities and ATP formation. ischemia; reperfusion; free radical scavenger

We sought to describe cerebrovascular responses to incremental exercise and test the hypothesis that changes in cerebral oxygenation influence maximal performance. Eleven men cycled in three conditions: 1) sea level (SL); 2) acute hypoxia [AH; hypobaric chamber, inspired [Po.sub.2] ([Pi.sub.o.sub.2]) 86 Torr]; and 3) chronic hypoxia [CH; 4,300 m, [Pi.sub.o.sub.2], 86 Torr]. At maximal work rate ([W.sub.max]), fraction of inspired oxygen ([Fi.sub.o.sub.2]) was surreptitiously increased to 0.60, while subjects were encouraged to continue pedaling. Changes in cerebral (frontal lobe) ([C.sub.ox]) and muscle (vastus lateralis) oxygenation ([M.sub.ox]) (near infrared spectroscopy), middle cerebral artery blood flow velocity (MCA [V.sub.mean]; transcranial Doppler), and end-tidal [Pco.sub.2] ([Pet.sub.co.sub.2]) were analyzed across % [W.sub.max] (significance at P < 0.05). At SL, [Pet.sub.co.sub.2], MCA [V.sub.mean], and [C.sub.ox] fell as work rate rose from 75 to 100% [W.sub.max]. During AH, [Pet.sub.co.sub.2] and MCA [V.sub.mean], declined from 50 to 100% [W.sub.max], while [C.sub.ox] fell from rest. With CH, [Pet.sub.co.sub.2] and [C.sub.ox] dropped throughout exercise, while MCA [V.sub.mean] fell only from 75 to 100% [W.sub.max]. [M.sub.ox] fell from rest to 75% [W.sub.max] at SL and AH and throughout exercise in CH. The magnitude of fall in [C.sub.ox], but not [M.sub.ox], was different between conditions (CH > AH > SL). [Fi.sub.o.sub.2] 0.60 at [W.sub.max] did not prolong exercise at SL, yet allowed subjects to continue for 96 [+ or -] 61 s in AH and 162 [+ or -] 90 s in CH. During [Fi.sub.o.sub.2] 0.60, [C.sub.ox] rose and [M.sub.ox] remained constant as work rate increased. Thus cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia ([Pi.sub.o.sub.2] 86 Torr), since its reversal was associated with improved performance. altitude; near infrared spectroscopy; cerebral blood flow; fatigue; muscle oxygenation

The interaction of chemical vapor deposition (CVD) diamond films with atomic oxygen (AO) produce by radio frequency (rf) oxygen plasma is analyzed. The diamond surface is not completely regenerated after annealing and in situ exposure to thermally activated hydrogen, because of the irreversible deterioration of the surface by AO.

In some animals, the oxygen transport capacity of blood decreases when pH is lowered, yielding oxygen binding curves with Hill-coefficients smaller than unity. This so-called Root effect is observed in several fishes and is important for creating large oxygen partial pressures locally, for example in the swim bladder. While there is general agreement on the physiological advantages of this effect, its molecular basis remains ambiguous. Various studies show that isoforms of hemoglobins usually are present in the hemolymph, when the Root effect is observed. Here, we show that in such a case the mixture of these isoforms can exhibit apparent negative cooperativity, although each component taken separately can be described by the MWC model. In other cases, isolated isoforms exhibit true negative cooperativity. The well established MWC model describes many cooperative phenomena of enzymes and respiratory proteins but is not capable of describing negative cooperativity. In order to model negative cooperativity within a single molecular species a decoupling model might be employed, as pointed out previously. However, simulations show that it is not mandatory to have species with negative cooperativity, in order to obtain the binding curves typically seen for whole blood. These two aspects of the Root effect will be discussed on the basis of data from the literature.

This review summarizes recent highlights of our joint work on the structure, evolution, and function of a family of highly complex proteins, the hemocyanins. They are blue-pigmented oxygen carriers, occurring freely dissolved in the hemolymph of many arthropods and molluscs. They are copper type-3 proteins and bind one dioxygen molecule between two copper atoms in a side-on coordination. They possess between 6 and 160 oxygen-binding sites, and some of them display the highest molecular cooperativity observed in nature. The functional properties of hemocyanins can be convincingly described by either the Monod-Wyman-Changeux (MWC) model or its hierarchical extension, the Nested MWC model; the latter takes into account the structural hierarchies in the oligomeric architecture. Recently, we applied these models to interpret the influence of allosteric effectors in detailed terms. Effectors shift the allosteric equilibria but have no influence on the oxygen affinities characterizing the various conformational states. We have shown that hemocyanins from species living at different environmental temperatures have a cooperativity optimum at the typical temperature of their natural habitat. Besides being oxygen carriers, some hemocyanins function as a phenoloxidase (tyrosinase/catecholoxidase) which, however, requires activation. Chelicerates such as spiders and scorpions lack a specific phenoloxidase, and in these animals activated hemocyanin might catalyse melanin synthesis in vivo. We propose a similar activation mechanism for arthropod hemocyanins, molluscan hemocyanins and tyrosinases: amino acid(s) that sterically block the access of phenolic compounds to the active site have to be removed. The catalysis mechanism itself can now be explained on the basis of the recently published crystal structure of a tyrosinase. In a series of recent publications, we presented the complete gene and primary structure of various hemocyanins from different molluscan classes. From these data, we deduced that the molluscan hemocyanin molecule evolved ca. 740 million years ago, prior to the separation of the extant molluscan classes. Our recent advances in the 3D cryo-electron microscopy of hemocyanins also allow considerable insight into the oligomeric architecture of these proteins of high molecular mass. In the case of molluscan hemocyanin, the structure of the wall and collar of the basic decamers is now rapidly becoming known in greater detail. In the case of arthropod hemocyanin, a 10-[Angstrom] structure and molecular model of the Limulus 8 x 6mer shows the amino acids at the various interfaces between the eight hexamers, and reveals histidine-rich residue clusters that might be involved in transferring the conformational signals establishing cooperative oxygen binding.

High altitude decreases birth weight, but this effect is diminished in long vs. short-resident, high-altitude populations. We asked whether women from long vs. short-resident, high-altitude populations had higher arterial oxygenation levels by comparing 42 Andean and 26 European residents of La Paz, Bolivia (3,600 m), serially during pregnancy (weeks 20, 30, and 36) and again 4 mo postpartum. Pregnancy raised hypoxic ventilatory sensitivity threefold, resting ventilation ([V.sub.E]), and arterial [O.sub.2] saturation ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCI..]) in both groups. Ancestry, as identified using 81 genetic markers, correlated with respiratory pattern, such that greater Andean ancestry was associated with higher respiratory frequency and lower tidal volume. Pregnancy increased total blood and plasma volume ~40% in both groups without changing red blood cell mass relative to body weight; hence, hemoglobin fell. The hemoglobin decline was compensated for by the rise in [V.sub.E] and [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.] with the result that arterial [O.sub.2] content ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.]) was maintained near nonpregnant levels in both groups. Birth weights were similar for all Andean and European babies, but after adjusting for variation in gestational age, maternal height and parity, Andeans weighed 209 g more than Europeans. Babies with heavier birth weights and greater ponderal indices were born to Andean women with higher [V.sub.E] during pregnancy. We concluded that while maternal [V.sub.E] and arterial oxygenation were important, some factor other than higher [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.] was responsible for protecting Andeans from altitude-associated reductions in fetal growth. hypoxia; ventilation; ventilatory control; infant birth weight; fetal growth; genetics of birth weight: human adaptation; respiratory pattern

Multigenerational (Andean) compared with shorter-term (European) high-altitude residents exhibit less hypoxia-associated reductions in birth weight. Because differences in arterial [O.sub.2] content are not responsible, we asked whether greater pregnancy-associated increases in uterine artery (UA) blood flow and [O.sub.2] delivery were involved. Serial studies were conducted in 42 Andean and 26 European residents of La Paz, Bolivia (3600 m) at weeks 20, 30, 36 of pregnancy and 4 mo postpartum using Doppler ultrasound. There were no differences postpartum but Andean vs. European women had greater UA diameter (0.65 [+ or -] 0.01 vs. 0.56 [+ or -] 0.01 cm), cross-sectional area (33.1 [+ or -] 0.97 vs. 24.7 [+ or -] 1.18 [mm.sup.2]), and blood flow at week 36 (743 [+ or -] 87 vs. 474 [+ or -] 36 ml/min) (all P < 0.05) and thus 1.6-fold greater uteroplacental [O.sub.2] delivery near term (126.82 [+ or -] 18.47 vs. 80.33 [+ or -] 8.69 ml [O.sub.2]*ml [blood.sup.-1]*[min.sup.-1], P < 0.05). Andeans had greater common iliac (CI) flow and lower external iliac relative to CI flow (0.52 [+ or -] 0.11 vs. 0.95 [+ or -] 0.14, P < 0.05) than Europeans at week 36. After adjusting for gestational age, maternal height, and parity, Andean babies weighed 209 g more than the Europeans. Greater UA cross-sectional area at week 30 related positively to birth weight in Andeans (r = +0.39) but negatively in Europeans (r = -0.37) (both P < 0.01). We concluded that a greater pregnancy-associated increase in UA diameter raised UA blood flow and uteroplacental [O.sub.2] delivery in the Andeans and contributed to their ability to maintain normal fetal growth under conditions of high-altitude hypoxia. These data implicate the involvement of genetic factors in protecting multigenerational populations from hypoxia-associated reductions in fetal growth, but future studies are required for confirmation and identification of the specific genes involved. birth weight; genetic adaptation; hypoxia; small-for-gestational age; uteroplacental vascular resistance

Several pulmonary and neurological conditions, both in the newborn and adult, result in hypercapnia. This leads to disturbances in normal pH homeostasis. Most mammalian cells maintain tight control of intracellular pH ([pH.sub.i]) using a group of transmembrane proteins that specialize in acid-base transport. These acid-base transporters are important in adjusting [pH.sub.i] during acidosis arising from hypoventilation. We hypothesized that exposure to chronic hypercapnia induces changes in the expression of acid-base transporters. Neonatal and adult CD-1 mice were exposed to either 8% or 12% C[O.sub.2] for 2 wk. We used Western blot analysis of membrane protein fractions from heart, kidney, and various brain regions to study the response of specific acid-base transporters to C[O.sub.2]. Chronic C[O.sub.2] increased the expression of the sodium hydrogen exchanger 1 (NHE1) and electroneutral sodium bicarbonate cotransporter (NBCn1) in the cerebral cortex, heart, and kidney of neonatal but not adult mice. C[O.sub.2] increased the expression of electrogenic NBC (NBCe1) in the neonatal but not the adult mouse heart and kidney. Hypercapnia decreased the expression of anion exchanger 3 (AE3) in both the neonatal and adult brain but increased AE3 expression in the neonatal heart. We conclude that: 1) chronic hypercapnia increases the expression of the acid extruders NHE1, NBCe1 and NBCn1 and decreases the expression of the acid loader AE3, possibly improving the capacity of the cell to maintain [pH.sub.i] in the face of acidosis; and 2) the heterogeneous response of tissues to hypercapnia depends on the level of C[O.sub.2] and development. anion exchanger; sodium bicarbonate cotransporter; sodium hydrogen exchanger; acidosis; hypercapnia

Tissue [Po.sub.2] (t[Po.sub.2]) reflects the balance between local [O.sub.2] supply and demand and, thus, could be a useful monitoring modality. However, the consistency and amplitude of the t[Po.sub.2] response in different organs during different cardiorespiratory insults is unknown. Therefore, we investigated the effects of endotoxemia, hemorrhage, and hypoxemia on t[Po.sub.2] measured in deep and peripheral organ beds. We compared arterial pressure, blood gas and lactate levels, descending aortic and renal blood flow, and t[Po.sub.2] in skeletal muscle, bladder epithelium, liver, and renal cortex during 1) LPS infusion (10 mg/kg), 2) sequential removal of 10% of circulating blood volume, and 3) reductions in inspired 02 concentration in an anesthetized Wistar rat model with values measured in sham-operated animals. Different patterns were seen in each of the shock states, with condition-specific variations in the degree of acidemia, lactatemia, and tissue [O.sub.2] responses between organs. Endotoxemia resulted in a rise in bladder t[Po.sub.2] and an early fall in liver t[Po.sub.2] but no significant change in muscle and renal cortical t[Po.sub.2]. Progressive hemorrhage, however, produced proportional declines in liver, muscle, and bladder t[Po.sub.2], but renal conical t[Po.sub.2] was maintained until profound blood loss had occurred. By contrast, progressive hypoxemia resulted in proportional decreases in t[Po.sub.2] in all organ beds. This study highlights the heterogeneity of responses in different organ beds during different shock states that are likely related to local changes in [O.sub.2] supply and utilization. Whole body monitoring is not generally reflective of these changes. tissue oxygen tension; hemodynamics; rat; endotoxemia; hemorrhage; hypoxemia doi:10.1152/ajpheart.00052.2006

It has been proposed by Saltin (J Exp Biol 115: 345-354, 1985) that oxygen delivery by blood is limiting for maximal work and oxygen consumption in humans during whole body exercise but not during single-muscle exercise. To test this prediction quantitatively, we developed a static (steady-state) computer model of oxygen transport to and within human skeletal muscle during single-muscle (quadriceps) exercise and whole body (cycling) exercise. The main system fluxes, namely cardiac output and oxygen consumption by muscle, are described as a function of the 'primary' parameter: work rate. The model is broadly validated by comparison of computer simulations with various experimental data. In silico studies show that, when all other parameters and system properties are kept constant, an increase in the working muscle mass from 2.5 kg (single quadriceps) to 15 kg (two legs) causes, at some critical work intensity, a drop in oxygen concentration in muscle cells to (very near) zero, and therefore oxygen supply by blood limits maximal oxygen consumption and oxidative ATP production. Therefore, the maximal oxygen consumption per muscle mass is significantly higher during single-muscle exercise than during whole body exercise. The effect is brought about by a distribution of a limited amount of oxygen transported by blood in a greater working muscle mass during whole body exercise. oxygen transport; oxygen consumption; muscle exercise doi:10.1152/ajpheart.01371.2006

Controversy over the oxygen isotope composition of seawater began in the 1950's, since which time there has been no agreement over whether the oxygen isotope composition of the oceans has changed over time. Resolving this uncertainty would allow the [[delta].sup.18]O values of demonstrably well preserved marine authigenic precipitates to be used to reconstruct surface climate trends back to early Archean times and would help towards a more quantitative description of Earth's global water cycle on geological time scales. Isotopic studies of marine carbonate and silica reveal a trend of increasing [[delta].sup.18]O values with decreasing age since the Archean. This trend has been interpreted by some to reflect a progressive increase in seawater [[delta].sup.18]O through time; however, it is generally accepted on the basis of ophiolite studies and theoretical considerations that seawater [[delta].sup.18]O cannot change significantly because of the buffering effects of ocean crust alteration at mid-ocean ridges. As a result many alternative interpretations have been proposed, including meteoric alteration; warmer paleoclimates; higher seawater pH; salinity stratification and biased sampling. Here we review these interpretations in the light of an updated compilation of marine carbonate [[delta].sup.18]O from around the world, coveting the Phanerozoic and Precambrian rock records. Recent models of the geological water cycle demonstrate how long-term trends in chemical weathering and hydrothermal circulation can indeed influence the O-isotope composition of the global ocean to the extent necessary to explain the carbonate [[delta].sup.18]O trend, with residual variation attributed to climatic fluctuations and post-depositional alteration. We present the further development of an existing model of the geological water cycle. In the model, seawater [[delta].sup.18]O increased from about -13.3[per thousand] to -0.3[per thousand] over a period of 3.4 Ga, with average surface temperatures fluctuating between 10[degrees]C to 33[degrees]C, which is consistent with known biological constraints. Similar temperature variations are also obtained, although with higher starting seawater [[delta].sup.18]O composition, when more conservative approaches are used that take into account the systematic effects of diagenetic alteration on mean calcite [[delta].sup.18]O values. In contrast to much published opinion, the average [[delta].sup.18]O value of ocean crust in the model remained relatively unchanged throughout all model runs. Invariable ophiolite [[delta].sup.18]O values can, therefore, not be used as a definitive argument against changing seawater [[delta].sup.18]O. The most likely explanation for the long-term trend in seawater [[delta].sup.18]O invokes two stepwise increases in the ratio of high- to low-temperature fluid/rock interactions. An initial increase may have occurred close to the Archean-Proterozoic boundary, but a possibly more significant increase took place near the Proterozoic-Phanerozoic boundary. Possible explanations for extremely low seawater [[delta].sup.18]O during the Archean include higher continental weathering rates caused by a combination of higher atmospheric pC[O.sub.2] (necessarily combined with high C[O.sub.2] outgassing rates), a greater abundance of relatively easily weathered volcanic rocks in greenstone belts and partial emergence of spreading ridges. The second increase may have been caused by the suppression of low-temperature overprinting of ocean crust alteration by the formation of a thick sediment cover on ridge flanks due to the emergence of shelly plankton at the beginning of the Phanerozoic. Postulated increases in spreading ridge depths since the Archean would also have enhanced the efficiency of vertical heat flux and changed the depth at which hydrothermal fluids boil, both of which would favour high- over low-temperature interactions with time. Keywords: marine carbonates; [[delta].sup.18]O record; seawater [[delta].sup.18]O; paleotemperature; diagenesis; box modelling

Barrier dysfunction, involving the endothelium or epithelium, is implicated in the pathophysiology of many disease states, including acute and ventilator-associated lung injury. Evidence from cell culture, in vivo and clinical studies, has identified myosin light chain kinase as a drug discovery target for such diseases. Here, we measured disease-relevant end points to test the hypothesis that inhibition of myosin light chain kinase is a potential therapeutic target for treatment of barrier dysfunction resulting from acute lung injury. We used a combined gene knockout and chemical biology approach with an in vivo intact lung injury model. We showed that inhibition of myosin light chain kinase protects lung function, preserves oxygenation, prevents acidosis, and enhances survival after endotoxin exposure with subsequent mechanical ventilation. This protective effect provided by the small molecule inhibitor of myosin light chain kinase is present when the inhibitor is administered during a clinically relevant injury paradigm after endotoxin exposure. Treatment with inhibitor confers additional protection against acute lung injury to that provided by a standard protective mode of ventilation. These results support the hypothesis that myosin light chain kinase is a potential therapeutic target for acute lung injury and provide clinical end points of arterial blood gases and pulmonary compliance that facilitate the direct extrapolation of these studies to measures used in critical care medicine. endothelium; acute respiratory distress syndrome; protein kinase; oxygenation doi:10.1152/ajplung.00380.2006.

Portal branch ligation (PBL) may prevent liver failure after extended hepatic resection. However, clinical studies indicate that tumors within the ligated lobe develop accelerated growth. Although it is well known that tumor growth depends on the host's microvascularization, there is no information about how PBL affects the hepatic microcirculation. Our aims were to determine hepatic artery response, liver microcirculation, tissue oxygenation, and cell proliferation after PBL. Therefore, we used intravital multifluorescence microscopy, laser-Doppler flowmetry, immunohistochemistry, and biochemical techniques to examine microcirculatory responses, microvascular remodeling, and cellular consequences after left lateral PBL in BALB/c mice. During the first 7 days, PBL induced a reduction of left hilar blood flow by ~50%. This resulted in 80% sinusoidal perfusion failure, significant parenchymal hypoxia, and liver atrophy. After 14 days, however, left hilar blood flow was found to be restored. However, remodeling of the microvasculature included a rarefaction of the sinusoidal network, however, without substantial perfusion failure, compensated by a hepatic arterial buffer response and significant sinusoidal dilatation. This resulted in normalization of tissue oxygenation, indicating arterialization of the ligated lobe. Interestingly, late microvascular remodeling was associated with increased endothelial nitric oxide synthase expression, significant hepatocelhilar proliferation, and weight gain of the ligated lobe. Thus PBL induces only an initial microcirculatory failure with liver atrophy, followed by a hepatic arterial buffer response, microvascular remodeling, normoxygenation, and hepatocellular proliferation. This may explain the accelerated tumor progression occasionally observed in patients after PBL. liver; microcirculation doi: 10.1152/ajpgi.00503.2006

Dissociation of oxygen from the heme domain of the bacterial oxygen sensor protein FixL constitutes the first step in hypoxia-induced signaling. In the present study, the photodissociation of the heme-[O.sub.2] bond was used to synchronize this event, and time-resolved resonance Raman (T[R.sup.3]) spectroscopy with subpicosecond rime resolution was implemented to characterize the heme configuration of the primary photoproduct. T[R.sup.3] measurements on heme-oxycomplexes are highly challenging and have not yet been reported. Whereas in all other known six-coordinated heme protein complexes with diatomic ligands, including the oxymyoglobin reported here, heme iron out-of-plane motion (doming) occurs faster than 1 ps after iron-ligand bond breaking; surprisingly, no sizeable doming is observed in the oxycomplex of the Bradyrhizobium japonicum FixL sensor domain (FixLH). This assessment is deduced from the absence of the iron-histidine band around 217 [cm.sup.-1] as early as 0.5 ps. We suggest that efficient ultrafast oxygen rebinding to the heme occurs on the femtosecond time scale, thus hindering heme doming. Comparing WT oxy-FixLH, mutant proteins FixLH-R220H and FixLH-R220Q, the respective carbonmonoxy-complexes, and oxymyoglobin, we show that a hydrogen bond of the terminal oxygen atom with the residue in position 220 is responsible for the observed behavior; in WT FixL this residue is arginine, crucially implicated in signal transmission. We propose that the rigid [O.sub.2] configuration imposed by this residue, in combination with the hydrophobic and constrained properties of the distai cavity, keep dissociated oxygen in place. These results uncover the origin of the 'oxygen cage' properties of this oxygen sensor protein. heme protein | molecular dynamics | ultrafast spectroscopy | vibrational spectroscopy

Kidney proximal tubules develop a severe but highly reversible energetic deficit due to nonesterified fatty acid (NEFA)-induced dissipation of mitochondrial membrane potential ([DELTA][PSI]m) during reoxygenation after severe hypoxia. To assess the mechanism for this behavior, we have compared the efficacies of different NEFA for inducing mitochondrial deenergization in permeabilized tubules measured using safranin O uptake and studied the modification of NEFA-induced deenergization by inhibitors of the ADP/ATP carrier and glutamate using both normoxic tubules treated with exogenous NEFA and tubules deenergized during hypoxia-reoxygenation (H/R). Among the long-chain NEFA that accumulate during H/R of isolated tubules and ischemia-reperfusion of the kidney in vivo, oleate, linoleate, and arachidonate had strong effects to dissipate [DELTA][[PSI].sub.m] that were slightly greater than palmitate, while stearate was inactive at concentrations reached in the cells. This behavior correlates well with the protonophoric effects of each NEFA. Inhibition of the ADP/ATP carrier with either carboxyatractyloside or bongkrekic acid or addition of glutamate to compete for the aspartate/ glutamate carrier improved [DELTA][[PSI].sub.m] in the presence of exogenous oleate and after H/R. Effects on the two carders were additive and restored safranin O uptake to as much as 80% of normal under both conditions. The data strongly support NEFA cycling across the inner mitochondrial membrane using anion carriers as the main mechanism for NEFA-induced deenergization in this system and provide the first evidence for a contribution of this process to pathophysiological events that impact importantly on energetics of intact cells. acute renal failure; kidney; membrane potential; mitochondria doi:10.1152/ajprenal.00476.2006.

Mathematical simulations of oxygen delivery to tissue from capillaries that take into account the particulate nature of blood flow predict the existence of oxygen tension (P[O.sub.2]) gradients between erythrocytes (RBCs). As RBCs and plasma alternately pass an observation point, these gradients are manifested as rapid fluctuations in P[O.sub.2], also known as erythrocyte-associated transients (EATs). The impact of hemodilution on EATs and oxygen delivery at the capillary level of the microcirculation has yet to be elucidated. Therefore, in the present study, phosphorescence quenching microscopy was used to measure EATs and P[O.sub.2] in capillaries of the rat spinotrapezius muscle at the following systemic hematocrits ([Hct.sub.sys]): normal (39%) and after moderate (HES 1; 27%) or severe (HES2; 15%) isovolemic hemodilution using a 6% hetastarch solution. A 532-nm laser, generating 10-[micro]s pulses concentrated onto a 0.9-[micro]m spot, was used to obtain plasma P[O.sub.2] values 100 times/s at points along surface capillaries of the muscle. Mean capillary P[O.sub.2] (PC[O.sub.2]; means [+ or -] SE) significantly decreased between conditions (normal: 56 [+ or -] 2 mmHg, n = 45; HESI: 47 [+ or -] 2 mmHg, n = 62; HES2: 27 [+ or -] 2 mmHg, n = 52, where n = capillary number). In addition, the magnitude of P[O.sub.2] transients ([DELTA]P[O.sub.2]) significantly decreased with hemodilution (normal: 19 [+ or -] 1 mmHg, n = 45; HES1: 11 [+ or -] 1 mmHg, n = 62; HES2: 6 [+ or -] 1 mmHg, n = 52). Results suggest that the decrease in [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.] and [DELTA]P[O.sub.2] with hemodilution is primarily dependent on [Hct.sub.sys] and subsequent microvascular compensations. microcirculation; oxygen transport; erythrocytes; oxygen tension gradients; phosphorescence quenching microscopy doi:10.1152/ajpheart.00915.2006.

To further explore the limitations to maximal [O.sub.2] consumption (V[O.sub.2 max]) in exercise-trained skeletal muscle, six cyclists performed graded knee-extensor exercise to maximum work rate (W[R.sub.max]) in hypoxia (12% [O.sub.2]), hyperoxia (100% [O.sub.2]), and hyperoxia + femoral arterial infusion of adenosine (ADO) at 80% W[R.sub.max]. Arterial and venous blood sampling and thermodilution blood flow measurements allowed the determination of muscle [O.sub.2] delivery and [O.sub.2] consumption. At W[R.sub.max], [O.sub.2] delivery rose progressively from hypoxia (1.0 [+ or -] 0.04 l/min) to hyperoxia (1.20 [+ or -] 0.09 l/min) and hyperoxia + ADO (1.33 [+ or -] 0.05 l/min). Leg V[O.sub.2] max varied with [O.sub.2] availability (0.81 [+ or -] 0.05 and 0.97 [+ or -] 0.07 l/min in hypoxia and hyperoxia, respectively) but did not improve with ADO-mediated vasodilation (0.80 [+ or -] 0.09 l/min in hyperoxia + ADO). Although a vasodilatory reserve in the maximally working quadriceps muscle group may have been evidenced by increased leg vascular conductance after ADO infusion beyond that observed in hyperoxia (increased blood flow but no change in blood pressure), we recognize the possibility that the ADO infusion may have provoked vasodilation in nonexercising tissue of this limb. Together, these findings imply that maximally exercising skeletal muscle may maintain some vasodilatory capacity, but the lack of improvement in leg V[O.sub.2max] with significantly increased [O.sub.2] delivery (hyperoxia + ADO), with a degree of uncertainty as to the site of this dilation, suggests an ADO-induced mismatch between [O.sub.2] consumption and blood flow in the exercising limb. exercise; blood flow; vasodilatory reserve doi: 10.1152/ajpheart.01396.2006.

The oxygen-iodine lasers discharge singlet oxygen that produces large quantities of atomic oxygen. The study conducted calculates the rate constant for quenching Ozone that is generated during the discharge.

The fundamental study of blood flow past a circular cylinder filled with an oxygen source is investigated as a building block for an artificial lung. The Casson constitutive equation is used to describe the shear-thinning and yield stress properties of blood. The presence of hemoglobin is also considered. Far from the cylinder, a pulsatile blood flow in the x direction is prescribed, represented by a time periodic (sinusoidal) component superimposed on a steady velocity. The dimensionless parameters of interest for the characterization of the flow and transport are the steady Reynolds number (Re), Womersley parameter ([alpha]), pulsation amplitude (A), and the Schmidt number (Sc). The Hill equation is used to describe the saturation curve of hemoglobin with oxygen. Two different feed-gas mixtures were considered: pure [O.sub.2] and air. The flow and concentration fields were computed for Re=5, 10, and 40, 0 [less than or equal to] A [less than or equal to] 0.75, [alpha] = 0.25, 0.4, and Schmidt number, Sc = 1000. The Casson fluid properties result in reduced recirculations (when present) downstream of the cylinder as compared to a Newtonian fluid. These vortices oscillate in size and strength as A and [alpha] are varied. Hemoglobin enhances mass transport and is especially important for an air feed which is dominated by oxyhemoglobin dispersion near the cylinder For a pure [O.sub.2] feed, oxygen transport in the plasma dominates near the cylinder. Maximum oxygen transport is achieved by operating near steady flow (small A) for both feed-gas mixtures. The time averaged Sherwood number, [??], is found to be largely influenced by the steady Reynolds number, increasing as Re increases and decreasing with A. Little change is observed with varying [alpha] for the ranges investigated. The effect of pulsatility on [??] is greater at larger Re. Increasing Re aids transport, but yields a higher cylinder drag force and shear stresses on the cylinder surface which are potentially undesirable. [DOI: 10.1115/1.2485961]

The oxygen isotope composition of fossil fish teeth, a paleo-upper ocean temperature proxy exceptionally resistant to diagenetic alteration, provides new insight on the evolution of the low- to middle-latitude thermal gradient between the middle Cretaceous climatic optimum and the cooler latest Cretaceous period. The new middle Cretaceous low to middle latitude thermal gradient agrees with that previously inferred from planktonic foraminifera [[delta][sup.18]]O recovered from Deep Sea Drilling Project and Ocean Drilling Program drilling sites, although the isotopic temperatures derived from [[delta][sup.18]]O of fish teeth are uniformly higher by ~3-4 [degrees]C. In contrast, our new latest Cretaceous thermal gradient is markedly steeper than those previously published for this period. Fish tooth [delta][sup.18]O data demonstrate that low- to middle-latitude thermal gradients of the middle Cretaceous climatic optimum and of the cooler latest Cretaceous are similar to the modern one, despite a cooling of 7 [degrees]C between the two periods. Our new results imply that no drastic changes in meridional heat transport are required to explain the Late Cretaceous climate. Based on climate models, such a cooling without any change in the low to middle latitude thermal gradient supports an atmospheric C[O.sub.2] decrease as the primary driver of the climatic evolution recorded during the Late Cretaceous. Keywords: Cretaceous, climate, oxygen isotopes, apatite.

Since the first discovery of extraordinary oxygen isotope compositions in carbonaceous meteorites by Clayton et al. [Clayton, R.N., Grossman, L., Mayeda, T.K., 1973. Science 182, 485-488], numerous studies have been done to explain the unusual mass-independent isotope fractionation, but the problem is still unresolved to this day. Clayton's latest interpretation [Clayton, R.N., 2002. Nature 415,860-861] sheds new light on the problem, and possible hypotheses now seem to be fairly well defined. A key issue is to resolve whether the oxygen isotopes in the Solar System represented by the Sun (solar oxygen) are the same as oxygen isotopes in planetary objects such as bulk meteorites, Mars, Earth, and Moon, or whether the solar oxygen is more similar to the lightest oxygen isotopes observed in CAIs (Calcium Aluminum-rich Inclusions) in primitive meteorites. Here, we examined the problem using oxygen isotope analytical data of about 400 bulk meteorite samples of various classes or types (data compiled by K. Lodders). We used in our discussion exclusively the parameter A 170, a direct measure of the degree of mass-independent isotope fractionation of oxygen isotopes. When [DELTA][.sup.17]O is arranged according to a characteristic size of their host planetary object, it shows a systematic trend: (1) [DELTA][sup.17]O values scatter around zero; (2) the scatter from the mean ([DELTA][.sup.17]O : 0) decreases with increasing representative size of the respective host planetary object. This systematic trend is easily understood on the basis of a hierarchical scenario of planetary formation, that is, larger planetary objects have formed by progressive accretion of planetesimals by random sampling over a wide spectrum of proto-solar materials. If this progressive random sampling of planetesimals were the essential process of planetary formation, the isotopic composition of planetary oxygen should approach that of the solar oxygen. To test this random sampling hypothesis, we applied a multiscale, multistep bootstrap statistical method [Shimodaira, H., 2004. Ann. Statist. 32, 2616-2641] to the meteorite oxygen isotope data, and deduced a [sigma]-N relation, where is the standard deviation of [DELTA][sup.17]O, and N is the representative size of a host planetary object. If we assign 200 and 500 km as a representative sizes of the chondrite and achondrite parent bodies, the observed a of AlTo agree well with the values predicted by the [sigma]-N relation. A common mean value of [DELTA][sup.17]O = 0 for all planetary objects also agrees with the progressive random sampling process. Therefore, we conclude that the solar oxygen is the same as planetary oxygen, but differs from CAI oxygen. The conclusion implies that a massive enrichment in [sup.17]O and [sup.18]O resulting from CO self-shielding, a current influential interpretation of CAI-O, did not occur. Keywords: Accretion; Planetary formation; Planetesimals; Solar nebula

The effect of oxygen incorporation on microstructure and media performance in CoCrPt-Si[O.sub.2] films with various oxygen contents (OC) from 3 to 10 at% at different CoCrPt-Si[O.sub.2] film thicknesses ([t.sub.MAG]) from 2 to 27 nm is investigated. Nonuniform microstructure with less grain isolation close to Ru and more grain isolation at the top region is clearly seen. Higher density of stacking faults is found at the top region. A higher OC is needed to reduce the thickness of the initial layer with less grain isolation. The increase in coercivity and saturation magnetization with increasing OC is due to the formation of lower Cr and higher Pt-containing core grains caused by the preferred oxidation of Cr. These excess Pt atoms mostly align along the c-axis direction. The magnetocrystalline anisotropy constant enhanced by the excess Pt improves thermal stability factor but it is sensitive to temperature. Crystallographic c-axis orientation and magnetic anisotropy dispersion deteriorate with increasing OC but are independent of [t.sub.MAG]. Index Terms--CoCrPt-oxide granular media, grain isolation, media recording performance, microstructure, oxygen incorporation, perpendicular magnetic recording.

The destruction wrought by North Atlantic hurricanes in 2004 and 2005 dramatically emphasizes the need for better understanding of tropical cyclone activity apart from the records provided by meteorological data and historical documentation. We present a 220-year record of oxygen isotope values of [alpha]-cellulose in longleaf pine tree rings that preserves anomalously low isotope values in the latewood portion of the ring in years corresponding with known 19th and 20th century landfalling/near-coastal tropical storms and hurricanes. Our results suggest the potential for a tree-ring oxygen isotope proxy record of tropical cyclone occurrence extending back many centuries based on remnant pine wood from protected areas in the southeastern U.S. hurricanes | isotope proxy | stable isotopes | tree ring

Changes in sea surface temperature (SST) during the Paleocene-Eocene Thermal Maximum (PETM) have been estimated primarily from oxygen isotope and Mg/Ca records generated from deep-sea cores. Here we present a record of sea surface temperature change across the Paleocene-Eocene boundary for a nearshore, shallow marine section located on the eastern margin of North America. The SST record, as inferred from [TEX.sub.86] data, indicates a minimum of 8 [degrees]C of warming, with peak temperatures in excess of 33 [degrees]C. Similar SSTs are estimated from planktonic foraminifer oxygen isotope records, although the excursion is slightly larger. The slight offset in the oxygen isotope record may reflect on seasonally higher runoff and lower salinity. Keywords: Paleocene, Eocene, isotopes, greenhouse.

Water treatment with ozone has been utilized, but a higher oxidation technology is required to decompose persistent substances such as dioxin. In this paper, water treatment by a direct O radical injection method with dc-driven atmospheric microplasma and fast oxygen gas flow was examined. O radicals and OH radicals are able to realize stronger oxidation processes than those of the ozone method. The effect of water treatment by radical injection was observed by measurement of the acetic-acid (C[H.sub.3]COOH) decomposition. This was examined while varying the discharge current and oxygen gas flow rates. The acetic acid was successfully decomposed by a direct radical flow into the solution; meanwhile, no decomposition was observed with ozone injection. A clear correlation was found between the decomposition rate and the gas-flow velocity estimated by the gas-flow rates. This result indicates that the rapid radical injection is crucial at the gas-liquid interface because a key radical, which is thought to be O, has a very short lifetime in atmospheric oxygen. Index Terms--Advanced oxidation process (AOP), atmospheric plasma, O radical, oxygen gas flow, water treatment.