On the climate response of the low-latitude Pacific Ocean to changes in the global freshwater cycle

Under global warming, the predicted intensification of the global freshwater cycle will modify the net freshwater flux at the ocean surface. Since the freshwater flux maintains ocean salinity structures, changes to the density-driven ocean circulation are likely. A modified ocean circulation could further alter the climate, potentially allowing rapid changes, as seen in the past. The relevant feedback mechanisms and timescales are poorly understood in detail, however, especially at low latitudes where the effects of salinity are relatively subtle. In an attempt to resolve some of these outstanding issues, we present an investigation of the climate response of the low-latitude Pacific region to changes in freshwater forcing. Initiated from the present-day thermohaline structure, a control run of a coupled ocean-atmosphere general circulation model is compared with a perturbation run in which the net freshwater flux is prescribed to be zero over the ocean. Such an extreme experiment helps to elucidate the general adjustment mechanisms and their timescales. The atmospheric greenhouse gas concentrations are held constant, and we restrict our attention to the adjustment of the upper 1,000 m of the Pacific Ocean between 40°N and 40°S, over 100 years. In the perturbation run, changes to the surface buoyancy, near-surface vertical mixing and mixed-layer depth are established within 1 year. Subsequently, relative to the control run, the surface of the low-latitude Pacific Ocean in the perturbation run warms by an average of 0.6°C, and the interior cools by up to 1.1°C, after a few decades. This vertical re-arrangement of the ocean heat content is shown to be achieved by a gradual shutdown of the heat flux due to isopycnal (i.e. along surfaces of constant density) mixing, the vertical component of which is downwards at low latitudes. This heat transfer depends crucially upon the existence of density-compensating temperature and salinity gradients on isopycnal surfaces. The timescale of the thermal changes in the perturbation run is therefore set by the timescale for the decay of isopycnal salinity gradients in response to the eliminated freshwater forcing, which we demonstrate to be around 10-20 years. Such isopycnal heat flux changes may play a role in the response of the low-latitude climate to a future accelerated freshwater cycle. Specifically, the mechanism appears to represent a weak negative sea surface temperature feedback, which we speculate might partially shield from view the anthropogenically-forced global warming signal at low latitudes. Furthermore, since the surface freshwater flux is shown to play a role in determining the ocean's thermal structure, it follows that evaporation and/or precipitation biases in general circulation models are likely to cause sea surface temperature biases.

A new feedback on climate change from the hydrological cycle

An intensification of the hydrological cycle is a likely consequence of global warming. But changes in the hydrological cycle could affect sea-surface temperature by modifying diffusive ocean heat transports. We investigate this mechanism by studying a coupled general circulation model sensitivity experiment in which the hydrological cycle is artificially amplified. We find that the amplified hydrological cycle depresses sea-surface temperature by enhancing ocean heat uptake in low latitudes. We estimate that a 10% increase in the hydrological cycle will contribute a basin-scale sea-surface temperature decrease of around 0.1°C away from high latitudes, with larger decreases locally. We conclude that an intensified hydrological cycle is likely to contribute a weak negative feedback to anthropogenic climate change.

Life cycle of the QBO-modulated 11-year solar cycle signals in the Northern Hemispheric winter

This paper provides some insights on the quasi-biennial oscillation (QBO) modulated 11-year solar cycle (11-yr SC) signals in Northern Hemisphere (NH) winter temperature and zonal wind. Daily ERA-40 Reanalysis and ECMWF Operational data for the period of 1958-2006 were used to examine the seasonal evolution of the QBO-solar cycle relationship at various pressure levels up to the stratopause. The results show that the solar signals in the NH winter extratropics are indeed QBO-phase dependent, moving poleward and downward as winter progresses with a faster descent rate under westerly QBO than under easterly QBO. In the stratosphere, the signals are highly significant in late January to early March and have a life span of 30-50 days. Under westerly QBO, the stratospheric solar signals clearly lead and connect to those in the troposphere in late March and early April where they have a life span of 10 days. As the structure changes considerably from the upper stratosphere to the lower troposphere, the exact month when the maximum solar signals occur depends largely on the altitude chosen. For the low-latitude stratosphere, our analysis supports a vertical double-peaked structure of positive signature of the 11-yr SC in temperature, and demonstrates that this structure is further modulated by the QBO. These solar signals have a longer life span (3-4 months) in comparison to those in the extratropics. The solar signals in the lower stratosphere are stronger in early winter but weaker in late winter, while the reverse holds in the upper stratosphere.

Carbon dioxide induced stomatal closure increases radiative forcing of climate via a rapid reduction in low cloud

We performed an ensemble of twelve five-year experiments using a coupled climate-carbon-cycle model with scenarios of prescribed atmospheric carbon dioxide concentration; CO2 was instantaneously doubled or quadrupled at the start of the experiments. Within these five years, climate feedback is not significantly influenced by the effects of climate change on the carbon system. However, rapid changes take place, within much less than a year, due to the physiological effect of CO2 on plant stomatal conductance, leading to adjustment in the shortwave cloud radiative effect over land, due to a reduction in low cloud cover. This causes a 10% enhancement to the radiative forcing due to CO2, which leads to an increase in the equilibrium warming of 0.4 and 0.7 K for doubling and quadrupling. The implications for calibration of energy-balance models are discussed.

Diurnal cycle of land surface temperature in a desert encroachment zone as observed from satellites

Climate variability in the African Soudano-Sahel savanna zone has attracted much attention because of the persistence of anomalously low rainfall. Past efforts to monitor the climate of this region have focused on rainfall and vegetation conditions, while land surface temperature (LST) has received less attention. Remote sensing of LST is feasible and possible at global scale. Most remotely sensed estimates of LST are based on the National Oceanic and Atmospheric Administration (NOAA) Advanced Very High Resolution Radiometer (AVHRR) that are limited in their ability to capture the full diurnal cycle. Although more frequent observations are available from past geostationary satellites, their spatial resolution is coarser than that of polar orbiting satellites. In this study, the improved capabilities of the Spinning Enhanced Visible and Infrared Imager (SEVIRI) on the METEOSAT Second Generation (MSG) instrument are used to remotely sense the LST in the African Soudano-Sahel savanna zone at a resolution of 3 km and 15 minutes. In support of the Radiative Atmospheric Divergence using the ARM Mobile Facility (AMF), GERB and AMMA Stations (RADAGAST) project, African Monsoon Multidisciplinary Analyses (AMMA) project and the Department of Energy's Atmospheric Radiation Measurement (ARM) program, the ARM Mobile Facility was deployed during 2006 in this climatically sensitive region, thereby providing a unique opportunity to evaluate remotely sensed algorithms for deriving LST.

Galactic cosmic ray hazard in the unusual extended solar minimum between solar cycle 23 and 24

Galactic cosmic rays (GCRs) are extremely difficult to shield against and pose one of the most severe long-term hazards for human exploration of space. The recent solar minimum between solar cycles 23 and 24 shows a prolonged period of reduced solar activity and low interplanetary magnetic field strengths. As a result, the modulation of GCRs is very weak, and the fluxes of GCRs are near their highest levels in the last 25 years in the fall of 2009. Here we explore the dose rates of GCRs in the current prolonged solar minimum and make predictions for the Lunar Reconnaissance Orbiter (LRO) Cosmic Ray Telescope for the Effects of Radiation (CRaTER), which is now measuring GCRs in the lunar environment. Our results confirm the weak modulation of GCRs leading to the largest dose rates seen in the last 25 years over a prolonged period of little solar activity.

Variation in pituitary expression of mRNAs encoding the putative inhibin co-receptor (betaglycan) and type-I and type-II activin receptors during the chicken ovulatory cycle

Secretion of LH and FSH from the anterior pituitary is regulated primarily by hypothalamic GnRH and ovarian steroid hormones. More recent evidence indicates regulatory roles for certain members of the transforming growth factor beta (TGF beta) superfamily including inhibin and activin. The aim of this study was to identify expression of mRNAs encoding key receptors and ligands of the inhibin/activin system in the hen pituitary gland and to monitor their expression throughout the 24-25-h ovulatory cycle. Hens maintained on long days (16 h light/8 h dark) were killed 20, 12, 6 and 2 h before predicted ovulation of a midsequence egg (n = 8 per group). Anterior pituitary glands were removed, RNA extracted and cDNA synthesized. Plasma concentrations of LH, FSH, progesterone and inhibin A were measured. Real-time quantitative PCR was used to quantify pituitary expression of mRNAs encoding betaglycan, activin receptor (ActR) subtypes (type I, IIA), GnRH receptor (GnP,H-R), LH beta subunit, FSH beta subunit and GAPDH. Levels of mRNA for inhibin/activin beta A and beta B subunits, inhibin alpha subunit, follistatin and ActRIIB mRNA in pituitary were undetectable by quantitative PCR (< 2 amol/reaction). Significant changes in expression (P < 0.05) of ActRIIA and betaglycan mRNA were found, both peaking 6 h before ovulation just prior to the preovulatory LH surge and reaching a nadir 2 h before ovulation, just after the LH surge. There were no significant changes in expression of ActRI mRNA throughout the cycle although values were correlated with mRNA levels for both ActRIIA (r=0.77; P < 0.001) and betaglycan (r=0.45; P < 0.01). Expression of GnRH-R mRNA was lowest 20 h before ovulation and highest (P < 0.05) 6 h before ovulation; values were weakly correlated with betaglycan (r=0.33; P=0.06) and ActRIIA (r=0.34; P=0.06) mRNA levels. Expression of mRNAs encoding LH beta and FSH beta subunit were both lowest (P < 0.05) after the LH surge, 2 h before ovulation. These results are consistent with an endocrine, but not a local intrapituitary, role of inhibin-related proteins in modulating gonadotroph function during the ovulatory cycle of the hen, potentially through interaction with betaglycan and ActRIIA. In contrast to mammals, intrapituitary expression of inhibin/activin subunits and follistatin appears to be extremely low or absent in the domestic fowl.

Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit vascular smooth muscle cell proliferation via differential effects on the cell cycle

Abnormal vascular smooth muscle cell (VSMC) proliferation plays an important role in the pathogenesis of both atherosclerosis and restenosis. Recent studies suggest that high-dose salicylates, in addition to inhibiting cyclooxygenase activity, exert an antiproliferative effect on VSMC growth both in-vitro and in-vivo. However, whether all non-steroidal anti-inflammatory drugs (NSAIDs) exert similar anti proliferative effects on VSMCs, and do so via a common mechanism of action, remains to be shown. In this study, we demonstrate that the NSAIDs aspirin, sodium salicylate, diclofenac, ibuprofen, indometacin and sulindac induce a dose-dependent inhibition of proliferation in rat A10 VSMCs in the absence of significant cytotoxicity. Flow cytometric analyses showed that exposure of A10 cells to diclofenac, indometacin, ibuprofen and sulindac, in the presence of the mitotic inhibitor, nocodazole, led to a significant G0/G1 arrest. In contrast, the salicylates failed to induce a significant G1 arrest since flow cytometry profiles were not significantly different from control cells. Cyclin A levels were elevated, and hyperphosphorylated p107 was present at significant levels, in salicylate-treated A10 cells, consistent with a post-G1/S block, whereas cyclin A levels were low, and hypophosphorylated p107 was the dominant form, in cells treated with other NSAIDs consistent with a G1 arrest. The ubiquitously expressed cyclin-dependent kinase (CDK) inhibitors, p21 and p27, were increased in all NSAID-treated cells. Our results suggest that diclofenac, indometacin, ibuprofen and sulindac inhibit VSMC proliferation by arresting the cell cycle in the G1 phase, whereas the growth inhibitory effect of salicylates probably affects the late S and/or G2/M phases. Irrespective of mechanism, our results suggest that NSAIDs might be of benefit in the treatment of certain vasculoproliferative disorders.

Damage rate is a predictor of fatigue life and creep strain rate in fatigue of tensile human cortical bone samples

We present results on the growth of damage in 29 fatigue tests of human femoral cortical bone from four individuals, aged 53–79. In these tests we examine the interdependency of stress, cycles to failure, rate of creep strain, and rate of modulus loss. The behavior of creep rates has been reported recently for the same donors as an effect of stress and cycles (Cotton, J. R., Zioupos, P., Winwood, K., and Taylor, M., 2003, "Analysis of Creep Strain During Tensile Fatigue of Cortical Bone," J. Biomech. 36, pp. 943–949). In the present paper we first examine how the evolution of damage (drop in modulus per cycle) is associated with the stress level or the "normalized stress" level (stress divided by specimen modulus), and results show the rate of modulus loss fits better as a function of normalized stress. However, we find here that even better correlations can be established between either the cycles to failure or creep rates versus rates of damage than any of these three measures versus normalized stress. The data indicate that damage rates can be excellent predictors of fatigue life and creep strain rates in tensile fatigue of human cortical bone for use in practical problems and computer simulations.

Analysis of creep strain during tensile fatigue of cortical bone

During fatigue tests of cortical bone specimens, at the unload portion of the cycle (zero stress) non-zero strains occur and progressively accumulate as the test progresses. This non-zero strain is hypothesised to be mostly, if not entirely, describable as creep. This work examines the rate of accumulation of this strain and quantifies its stress dependency. A published relationship determined from creep tests of cortical bone (Journal of Biomechanics 21 (1988) 623) is combined with knowledge of the stress history during fatigue testing to derive an expression for the amount of creep strain in fatigue tests. Fatigue tests on 31 bone samples from four individuals showed strong correlations between creep strain rate and both stress and “normalised stress” (σ/E) during tensile fatigue testing (0–T). Combined results were good (r2=0.78) and differences between the various individuals, in particular, vanished when effects were examined against normalised stress values. Constants of the regression showed equivalence to constants derived in creep tests. The universality of the results, with respect to four different individuals of both sexes, shows great promise for use in computational models of fatigue in bone structures.

Apolipoprotein E genotype and alpha-tocopherol modulate amyloid precursor protein metabolism and cell cycle regulation

Apolipoprotein E4 (apoE4) genotype is associated with an increased risk for Alzheimer's disease (AD). This is thought to be in part attributable to an impact of apoE genotype on the processing of the transmembrane amyloid precursor protein (APP) thereby contributing to amyloid beta peptide formation in apoE4 carriers, which is a primary patho-physiological feature of AD. As apoE and alphato-copherol (alpha-toc) have been shown to modulate membrane bilayer properties and hippocampal gene expression, we studied the effect of apoE genotype on APP metabolism and cell cycle regulation in response to dietary a-toc. ApoE3 and apoE4 transgenic mice were fed a diet low (VE) or high (+VE) in vitamin E (3 and 235 mg alpha-toe/kg diet, respectively) for 12 weeks. Cholesterol levels and membrane fluidity were not different in synaptosomal plasma membranes isolated from brains of apoE3 and apoE4 mice (-VE and +VE). Non-amyloidogenic alpha-secretase mRNA concentration and activity were significantly higher in brains of apoE3 relative to apoE4 mice irrespective of the dietary a-toe supply, while amyloidogenic beta-secretase and gamma-secretase remained unchanged. Relative mRNA concentration of cell cycle related proteins were modulated differentially by dietary a-toc supplementation in apoE3 and apoE4 mice, suggesting genotype-dependent signalling effects on cell cycle regulation.

Variation in pituitary expression of mRNAs encoding the putative inhibin co-receptor (betaglycan) and type-I and type-II activin receptors during the chicken ovulatory cycle

Secretion of LH and FSH from the anterior pituitary is regulated primarily by hypothalamic GnRH and ovarian steroid hormones. More recent evidence indicates regulatory roles for certain members of the transforming growth factor beta (TGF beta) superfamily including inhibin and activin. The aim of this study was to identify expression of mRNAs encoding key receptors and ligands of the inhibin/activin system in the hen pituitary gland and to monitor their expression throughout the 24-25-h ovulatory cycle. Hens maintained on long days (16 h light/8 h dark) were killed 20, 12, 6 and 2 h before predicted ovulation of a midsequence egg (n = 8 per group). Anterior pituitary glands were removed, RNA extracted and cDNA synthesized. Plasma concentrations of LH, FSH, progesterone and inhibin A were measured. Real-time quantitative PCR was used to quantify pituitary expression of mRNAs encoding betaglycan, activin receptor (ActR) subtypes (type I, IIA), GnRH receptor (GnP,H-R), LH beta subunit, FSH beta subunit and GAPDH. Levels of mRNA for inhibin/activin beta A and beta B subunits, inhibin alpha subunit, follistatin and ActRIIB mRNA in pituitary were undetectable by quantitative PCR (< 2 amol/reaction). Significant changes in expression (P < 0.05) of ActRIIA and betaglycan mRNA were found, both peaking 6 h before ovulation just prior to the preovulatory LH surge and reaching a nadir 2 h before ovulation, just after the LH surge. There were no significant changes in expression of ActRI mRNA throughout the cycle although values were correlated with mRNA levels for both ActRIIA (r=0.77; P < 0.001) and betaglycan (r=0.45; P < 0.01). Expression of GnRH-R mRNA was lowest 20 h before ovulation and highest (P < 0.05) 6 h before ovulation; values were weakly correlated with betaglycan (r=0.33; P=0.06) and ActRIIA (r=0.34; P=0.06) mRNA levels. Expression of mRNAs encoding LH beta and FSH beta subunit were both lowest (P < 0.05) after the LH surge, 2 h before ovulation. These results are consistent with an endocrine, but not a local intrapituitary, role of inhibin-related proteins in modulating gonadotroph function during the ovulatory cycle of the hen, potentially through interaction with betaglycan and ActRIIA. In contrast to mammals, intrapituitary expression of inhibin/activin subunits and follistatin appears to be extremely low or absent in the domestic fowl.

Assays for enhanced activity of low efficacy partial agonists at the D-2 dopamine receptor

Background and purpose: Low efficacy partial agonists at the D-2 dopamine receptor may be useful for treating schizophrenia. In this report we describe a method for assessing the efficacy of these compounds based on stimulation of [S-35]GTP gamma S binding. Experimental approach: Agonist efficacy was assessed from [S-35]GTP gamma S binding to membranes of CHO cells expressing D2 dopamine receptors in buffers with and without Na+. Effects of Na+ on receptor/G protein coupling were assessed using agonist/[H-3] spiperone competition binding assays. Key results: When [S-35]GTP gamma S binding assays were performed in buffers containing Na+, some agonists (aripiprazole, AJ-76, UH-232) exhibited very low efficacy whereas other agonists exhibited measurable efficacy. When Na+ was substituted by N-methyl D-glucamine, the efficacy of all agonists increased (relative to that of dopamine) but particularly for aripiprazole, aplindore, AJ-76, (-)-3-PPP and UH-232. In ligand binding assays, substitution of Na+ by N-methyl D-glucamine increased receptor/G protein coupling for some agonists -. aplindore, dopamine and (-)-3-PPP-but for aripiprazole, AJ-76 and UH-232 there was little effect on receptor/G protein coupling. Conclusions and implications: Substitution of Na+ by NMDG increases sensitivity in [S-35] GTPgS binding assays so that very low efficacy agonists were detected clearly. For some agonists the effect seems to be mediated via enhanced receptor/G protein coupling whereas for others the effect is mediated at another point in the G protein activation cycle. AJ-76, aripiprazole and UH-232 seem particularly sensitive to this change in assay conditions. This work provides a new method to discover these very low efficacy agonists.

Nox2 regulates endothelial cell cycle arrest and apoptosis via p21 (cip1) and p53

Endothelial cells (EC) express constitutively two major isofonns (Nox2 and Nox4) of the catalytic subunit of NADPH oxidase, which is a major source of endothelial reactive oxygen species. However, the individual roles of these Noxes in endothelial function remain unclear. We have investigated the role of Nox2 in nutrient deprivation-induced cell cycle arrest and apoptosis. In proliferating human dermal microvascular EC, Nox2 mRNA expression was low relative to Nox4 (Nox2:Nox4 similar to 1:13), but was upregulated 24 It after starvation and increased to 8 +/- 3.5-fold at 36 h of starvation. Accompanying the upregulation of Nox2, there was a 2.28 +/- 0.18-fold increase in O-2(-); production, a dramatic induction of p21(cip1) and p53, cell cycle arrest, and the onset of apoptosis (all p < 0.05). All these changes were inhibited significantly by in vitro deletion of Nox2 expression and in coronary microvascular EC isolated from Nox2 knockout mice. In Nox2 knockout cells, although there was a 3.8 +/- 0.5fold increase in Nox4 mRNA expression after 36 h of starvation (p < 0.01), neither production nor the p21(cip1) or p53 expression was increased significantly and only 0.46% of cells were apoptotic. In conclusion, Nox2-derived O-2(-), through the modulation of p21(cip1) and p53 expression, participates in endothelial cell cycle regulation and apoptosis. (c) 2007 Elsevier Inc. All rights reserved.

The advection of high-resolution tracers by low-resolution winds

The usefulness of any simulation of atmospheric tracers using low-resolution winds relies on both the dominance of large spatial scales in the strain and time dependence that results in a cascade in tracer scales. Here, a quantitative study on the accuracy of such tracer studies is made using the contour advection technique. It is shown that, although contour stretching rates are very insensitive to the spatial truncation of the wind field, the displacement errors in filament position are sensitive. A knowledge of displacement characteristics is essential if Lagrangian simulations are to be used for the inference of airmass origin. A quantitative lower estimate is obtained for the tracer scale factor (TSF): the ratio of the smallest resolved scale in the advecting wind field to the smallest “trustworthy” scale in the tracer field. For a baroclinic wave life cycle the TSF = 6.1 ± 0.3 while for the Northern Hemisphere wintertime lower stratosphere the TSF = 5.5 ± 0.5, when using the most stringent definition of the trustworthy scale. The similarity in the TSF for the two flows is striking and an explanation is discussed in terms of the activity of potential vorticity (PV) filaments. Uncertainty in contour initialization is investigated for the stratospheric case. The effect of smoothing initial contours is to introduce a spinup time, after which wind field truncation errors take over from initialization errors (2–3 days). It is also shown that false detail from the proliferation of finescale filaments limits the useful lifetime of such contour advection simulations to 3σ−1 days, where σ is the filament thinning rate, unless filaments narrower than the trustworthy scale are removed by contour surgery. In addition, PV analysis error and diabatic effects are so strong that only PV filaments wider than 50 km are at all believable, even for very high-resolution winds. The minimum wind field resolution required to accurately simulate filaments down to the erosion scale in the stratosphere (given an initial contour) is estimated and the implications for the modeling of atmospheric chemistry are briefly discussed.