Tropical mid-tropospheric CO_2 variability driven by the Madden–Julian oscillation

Carbon dioxide (CO_2) is the most important anthropogenic greenhouse gas in the present-day climate. Most of the community focuses on its long-term (decadal to centennial) behaviors that are relevant to climate change, but there are relatively few discussions of its higher-frequency forms of variability, and none regarding its subseasonal distribution. In this work, we report a large-scale intraseasonal variation in the Atmospheric Infrared Sounder CO_2 data in the global tropical region associated with the Madden–Julian oscillation (MJO). The peak-to-peak amplitude of the composite MJO modulation is ~1 ppmv, with a standard error of the composite mean < 0.1 ppmv. The correlation structure between CO2 and rainfall and vertical velocity indicate positive (negative) anomalies in CO_2 arise due to upward (downward) large-scale vertical motions in the lower troposphere associated with the MJO. These findings can help elucidate how faster processes can organize, transport, and mix CO_2 and provide a robustness test for coupled carbon–climate models

Vertical Moist Thermodynamic Structure and Spatial–Temporal Evolution of the MJO in AIRS Observations

The atmospheric moisture and temperature profiles from the Atmospheric Infrared Sounder (AIRS)/Advanced Microwave Sounding Unit on the NASA Aqua mission, in combination with the precipitation from the Tropical Rainfall Measuring Mission (TRMM), are employed to study the vertical moist thermodynamic structure and spatial–temporal evolution of the Madden–Julian oscillation (MJO). The AIRS data indicate that, in the Indian Ocean and western Pacific, the temperature anomaly exhibits a trimodal vertical structure: a warm (cold) anomaly in the free troposphere (800–250 hPa) and a cold (warm) anomaly near the tropopause (above 250 hPa) and in the lower troposphere (below 800 hPa) associated with enhanced (suppressed) convection. The AIRS moisture anomaly also shows markedly different vertical structures as a function of longitude and the strength of convection anomaly. Most significantly, the AIRS data demonstrate that, over the Indian Ocean and western Pacific, the enhanced (suppressed) convection is generally preceded in both time and space by a low-level warm and moist (cold and dry) anomaly and followed by a low-level cold and dry (warm and moist) anomaly. The MJO vertical moist thermodynamic structure from the AIRS data is in general agreement, particularly in the free troposphere, with previous studies based on global reanalysis and limited radiosonde data. However, major differences in the lower-troposphere moisture and temperature structure between the AIRS observations and the NCEP reanalysis are found over the Indian and Pacific Oceans, where there are very few conventional data to constrain the reanalysis. Specifically, the anomalous lower-troposphere temperature structure is much less well defined in NCEP than in AIRS for the western Pacific, and even has the opposite sign anomalies compared to AIRS relative to the wet/dry phase of the MJO in the Indian Ocean. Moreover, there are well-defined eastward-tilting variations of moisture with height in AIRS over the central and eastern Pacific that are less well defined, and in some cases absent, in NCEP. In addition, the correlation between MJO-related midtropospheric water vapor anomalies and TRMM precipitation anomalies is considerably more robust in AIRS than in NCEP, especially over the Indian Ocean. Overall, the AIRS results are quite consistent with those predicted by the frictional Kelvin–Rossby wave/conditional instability of the second kind (CISK) theory for the MJO

Vertical Moist Thermodynamic Structure of the Madden–Julian Oscillation in Atmospheric Infrared Sounder Retrievals: An Update and a Comparison to ECMWF Interim Re-Analysis

The large-scale vertical moist thermodynamic structure of the Madden–Julian oscillation (MJO) was documented using the first 2.5 yr (2002–05) of version 4 atmospheric specific humidity and temperature profiles from the Atmospheric Infrared Sounder (AIRS). In this study, this issue is further examined using currently available 7-yr version 5 AIRS data (2002–09) to test its dependence on the AIRS data record lengths, AIRS retrieval versions, and MJO event selection and compositing methods employed. The results indicate a strong consistency of the large-scale vertical moist thermodynamic structure of the MJO between different AIRS data record lengths (2.5 vs 7 yr), different AIRS retrieval versions (4 vs 5), and different MJO analysis methods [the extended empirical orthogonal function (EEOF) method vs the multivariate empirical orthogonal function (MEOF) method]. The large-scale vertical moist thermodynamic structures of the MJO between the AIRS retrievals and the ECMWF Interim Re-Analysis (ERA-Interim) products are also compared. The results indicate a much better agreement of the MJO vertical structure between AIRS and ERA-Interim than with the NCEP–NCAR reanalysis, although a significant difference exists in the magnitude of moisture anomalies between ERA-Interim and AIRS. This characterization of the vertical moist thermodynamic structure of the MJO by AIRS and ERA-Interim offers a useful observation-based metric for general circulation model diagnostics

Vertical Heating Structures Associated with the MJO as Characterized by TRMM Estimates, ECMWF Reanalyses, and Forecasts: A Case Study during 1998/99 Winter

The Madden–Julian oscillation (MJO) is a fundamental mode of the tropical atmosphere variability that exerts significant influence on global climate and weather systems. Current global circulation models, unfortunately, are incapable of robustly representing this form of variability. Meanwhile, a well-accepted and comprehensive theory for the MJO is still elusive. To help address this challenge, recent emphasis has been placed on characterizing the vertical structures of the MJO. In this study, the authors analyze vertical heating structures by utilizing recently updated heating estimates based on the Tropical Rainfall Measuring Mission (TRMM) from two different latent heating estimates and one radiative heating estimate. Heating structures from two different versions of the European Centre for Medium-Range Weather Forecasts (ECMWF) reanalyses/forecasts are also examined. Because of the limited period of available datasets at the time of this study, the authors focus on the winter season from October 1998 to March 1999. The results suggest that diabatic heating associated with the MJO convection in the ECMWF outputs exhibits much stronger amplitude and deeper structures than that in the TRMM estimates over the equatorial eastern Indian Ocean and western Pacific. Further analysis illustrates that this difference might be due to stronger convective and weaker stratiform components in the ECMWF estimates relative to the TRMM estimates, with the latter suggesting a comparable contribution by the stratiform and convective counterparts in contributing to the total rain rate. Based on the TRMM estimates, it is also illustrated that the stratiform fraction of total rain rate varies with the evolution of the MJO. Stratiform rain ratio over the Indian Ocean is found to be 5% above (below) average for the disturbed (suppressed) phase of the MJO. The results are discussed with respect to whether these heating estimates provide enough convergent information to have implications on theories of the MJO and whether they can help validate global weather and climate models

Tropical Atlantic Dust and Smoke Aerosol Variabilities Related to the Madden-Julian Oscillation in MODIS and MISR Observations

In this study, MODIS fine mode fraction and MISR non-spherical fraction are 2used to derive dust and smoke AOT components (tau(sub dust) and tau(sub smoke)) over the tropical Atlantic, and their variabilities related to the Madden-Julian Oscillation (MJO) are then investigated. Both MODIS and MISR show a very similar dust and smoke winter climatology. tau(sub dust) is found to be the dominant aerosol component over the tropical Atlantic while tau(sub smoke) is significantly smaller than tau(sub dust). The daily MODIS and MISR tau(sub dust) are overall highly correlated, with the correlation coefficients typically about 0.7 over the North Atlantic. The consistency between the MODIS and MISR dust and smoke aerosol climatology and daily variations give us confidence to use these two data sets to investigate their relative contributions to the total AOT variation associated with the MJO. However, unlike the MISR dust discrimination, which is based on particle shape retrievals, the smoke discrimination is less certain, based on assumed partitioning of maritime aerosol for both MISR and MODIS. The temporal evolution and spatial patterns of the tau(sub dust) anomalies associated with the MJO are consistent between MODIS and MISR. The tau(sub dust) anomalies are very similar to those of tau anomalies, and are of comparable magnitude. In contrast, the MJO-related tau(sub smoke) anomalies are rather small, and the tau(sub mar) anomalies are negligible. The consistency between the MODIS and MISR results suggests that dust aerosol is the dominant component on the intra-seasonal time scale over the tropical Atlantic Ocean

Northern Hemisphere mid-winter vortex-displacement and vortex-split stratospheric sudden warmings: Influence of the Madden-Julian Oscillation and Quasi-Biennial Oscillation

We investigate the connection between the equatorial Madden‐Julian Oscillation (MJO) and different types of the Northern Hemisphere mid‐winter major stratospheric sudden warmings (SSWs), i.e., vortex‐displacement and vortex‐split SSWs. The MJO‐SSW relationship for vortex‐split SSWs is stronger than that for vortex‐displacement SSWs, as a result of the stronger and more coherent eastward propagating MJOs before vortex‐split SSWs than those before vortex‐displacement SSWs. Composite analysis indicates that both the intensity and propagation features of MJO may influence the MJO‐related circulation pattern at high latitudes and the type of SSWs. A pronounced Quasi‐Biennial Oscillation (QBO) dependence is found for vortex‐displacement and vortex‐split SSWs, with vortex‐displacement (‐split) SSWs occurring preferentially in easterly (westerly) QBO phases. The lagged composites suggest that the MJO‐related anomalies in the Arctic are very likely initiated when the MJO‐related convection is active over the equatorial Indian Ocean (around the MJO phase 3). Further analysis suggests that the QBO may modulate the MJO‐related wave disturbances via its influence on the upper tropospheric subtropical jet. As a result, the MJO‐related circulation pattern in the Arctic tends to be wave number‐one/wave number‐two ~25–30 days following phase 3 (i.e., approximately phases 7–8, when the MJO‐related convection is active over the western Pacific) during easterly/westerly QBO phases, which resembles the circulation pattern associated with vortex‐displacement/vortex‐split SSWs

Estimating sampling biases and measurement uncertainties of AIRS/AMSU-A temperature and water vapor observations using MERRA reanalysis

We use MERRA (Modern Era Retrospective-Analysis for Research Applications) temperature and water vapor data to estimate the sampling biases of climatologies derived from the AIRS/AMSU-A (Atmospheric Infrared Sounder/Advanced Microwave Sounding Unit-A) suite of instruments. We separate the total sampling bias into temporal and instrumental components. The temporal component is caused by the AIRS/AMSU-A orbit and swath that are not able to sample all of time and space. The instrumental component is caused by scenes that prevent successful retrievals. The temporal sampling biases are generally smaller than the instrumental sampling biases except in regions with large diurnal variations, such as the boundary layer, where the temporal sampling biases of temperature can be ± 2 K and water vapor can be 10% wet. The instrumental sampling biases are the main contributor to the total sampling biases and are mainly caused by clouds. They are up to 2 K cold and > 30% dry over midlatitude storm tracks and tropical deep convective cloudy regions and up to 20% wet over stratus regions. However, other factors such as surface emissivity and temperature can also influence the instrumental sampling bias over deserts where the biases can be up to 1 K cold and 10% wet. Some instrumental sampling biases can vary seasonally and/or diurnally. We also estimate the combined measurement uncertainties of temperature and water vapor from AIRS/AMSU-A and MERRA by comparing similarly sampled climatologies from both data sets. The measurement differences are often larger than the sampling biases and have longitudinal variations

THE P2X7 RECEPTOR OF HUMAN LEUKOCYTES

Lymphocytes from normal subjects and patients with B-chronic lymphocytic leukemia (B-CLL) show functional responses to extracellular ATP characteristic of the P2X7 receptor. These responses include opening of a cation selective channel/pore which allows entry of the fluorescent dye, ethidium+ and activation of a membrane metalloprotease which sheds the adhesion molecule L-selectin. In this thesis, the surface expression of P2X7 receptors was measured in normal leucocytes, platelets and B-CLL lymphocytes and compared with their functional responses. Monocytes showed 4-5 fold greater expression of P2X7 than B-, T- and NK- lymphocytes, while P2X7 expression on neutrophils and platelets was weak. All cell types demonstrated abundant intracellular expression of this receptor. All 12 subjects with B-CLL expressed surface P2X7 at about the same level as for B-lymphocytes from normal subjects. P2X7 function, measured by ATP-induced uptake of ethidium, correlated closely with surface expression of this receptor in normal and B-CLL lymphocytes and monocytes. However, the ATP-induced uptake of ethidium into the malignant B-lymphocytes in 3 patients was low or absent. The lack of P2X7 function in these B-lymphocytes was confirmed by the failure of ATP to induce Ba2+ uptake into their lymphocytes. This lack of function of the P2X7 receptor resulted in a failure of ATP-induced shedding of L-selectin, an adhesion molecule which directs the recirculation of lymphocytes from blood into the lymph node. To study a possible genetic basis of non-functional P2X7 receptor, we sequenced DNA coding for the carboxyl terminal tail of P2X7. In 33 of 130 normal subjects a heterozygous nucleotide substitution (1513A--C) was found while 3 subject carried the homozygous substitution which codes for glutamic acid to alanine at amino acid position 496. Surface expression of P2X7 on lymphocytes was not affected by this 496Glu--Ala polymorphism demonstrated both by confocal microscopy and immunofluorescent staining. Monocytes and lymphocytes from the 496Glu--Ala homozygote subject expressed non-functional receptor while heterozygotes showed P2X7 function which was half that of wild type P2X7. Results of transfection experiments showed the mutant P2X7 receptor was non-functional when expressed at low receptor density but regained function at a high receptor density. This density-dependence of mutant P2X7 function was also seen on differentiation of fresh monocytes to macrophages with interferon-gamma which upregulated mutant P2X7 and partially restored its function. P2X7-mediated apoptosis of lymphocytes was impaired in homozygous mutant P2X7 compared with wild type. The data suggest that the glutamic acid at position 496 is required for optimal assembly of the P2X7 receptor. Apart from the 496Glu--Ala polymorphism, three other single nucleotide polymorphisms, 155His--Tyr, 348Ala--Thr and 568Ile--Asn were also found in the P2X7 receptor. The site directed mutant cDNA were generated for all 3 polymorphisms and transfected into HEK293 cells to study the impact of these polymorphisms on P2X7 function. Results suggested that Ile568 is important for P2X7 protein trafficking to cell surface. Further study of these two loss-of-function polymorphisms (496Glu--Ala and 568Ile--Asn) may help better understanding of the functional domains in the P2X7 receptor and its role in CLL, lymphoma and infectious diseases. Conclusions: 1.P2X7 receptor is expressed in human leukocytes, including lymphocytes, natural killer cells as well as monocytes, on both surface and intracellular locations. 2.Both the expression and function of P2X7 are highly variable between in human individuals. Non-functional P2X7 receptors are found in some subjects, including both normal subjects and CLL patients, and are often associated with defects in ATP-induced cytotoxicity and L-selectin shedding. 3.Two single nucleotide polymorphisms (SNPs), 496Glu--Ala and 568Ile--Asn, are found at low frequency in the human population and lead to the loss-of-function of P2X7. Both permeabllity function and the downstream effects mediated by P2X7 are affected by these two SNPs. The mechanisms for the loss-of-function differs between the two polymorphisms

TWO PATHWAYS OF SHEDDING OF L-SELECTIN AND CD23 FROM HUMAN B-LYMPHOCYTES

Lymphocytes from patients with B-chronic lymphocytic leukemia (B-CLL) express large numbers of P2X7 receptors for extracellular adenosine triphosphate (ATP). Activation of P2X7 receptors induces multiple downstream effects, of which the best documented is the opening of an ionic channel that is selective for divalent cations. Another effect of ATP is to induce the shedding of L-selectin (CD62L), a molecule which is involved in the adhesive interactions of lymphocytes on endothelial cells. High levels of soluble L-selectin and CD23 are found in the serum of patients with B-CLL, although the mechanisms involved in their production are poorly characterized. Because extracellular ATP causes shedding of L-selectin, we studied the effect of ATP on shedding of CD23, an adhesion molecule expressed on the surface of B-CLL lymphocytes. ATP induced the shedding of CD23 at an initial rate of 12% of that for L-selectin, while the EC50 of ATP (35 uM) and BzATP (10 uM) was identical for shedding of both molecules. Inactivation of the P2X7 receptor by pre-incubation with OxATP, an irreversible inhibitor of P2X7 purinoceptor, abolished ATP-induced shedding of both molecules. Moreover, KN-62, the most potent inhibitor for the P2X7 receptor inhibited ATP-induced shedding of both CD23 and L-selectin with the same IC50 (12 nM). Ro 31-9790, a membrane permeant zinc chelator which inhibits the phorbol-ester stimulated shedding of L-selectin also inhibited shedding of CD23 from B-CLL lymphocytes, but the IC50 was different for the two shed molecules (25 versus 1 ug/ml respectively). Although L-selectin was completely shed by incubation of cells with phorbol-ester no CD23 was lost under these conditions. Also, Ca2+ inhibits ATP-induced CD23 shedding but not L-selectin shedding. Since soluble CD23 and L-selectin are found in the serum of normal subjects and B-CLL patients, the expression of these two adhesion molecules on lymphocytes before and after transendothelial migration was studied in an in vitro model of this process. In normal and B-CLL subjects, 71±5% of L-selectin from both T and B cells and 90% of CD23 from B cells was lost following transmigration, while the expression of a range of other adhesion molecules such as VLA-4, ICAM-1, LFA-1 and CD44 was unchanged. Lymphocytes incubated with OxATP retained their capacity for transendothelial migration and showed the same loss of L-selectin as control leukaemic lymphocytes. Ro 31-9790, which can protect ATP-induced both L-selectin and CD23 shedding, had no effect on inhibiting L-selectin and CD23 lost during transmigration. These data show the presence of a second pathway for the downregulation of L-selectin and CD23 from the lymphocyte surface. Data in vivo from 'knock-out' mice show that L-selectin is essential for the emigration of lymphocytes through high endothelial venules into lymph nodes. The migration of normal and B-CLL lymphocytes across confluent human umbilical vein endothelial monolayers was studied in an in vitro model of this process. Lymphocytes treated with ATP or BzATP showed 56±25% or 67±16% loss of L-selectin on the surface and 36±24% or 64±19% decrease of transmigration, respectively, while OxATP, which does not alter the L-selectin level, had no effect on lymphocyte transmigration. Further experiments examined this correlation between L-selectin expression and lymphocyte transendothelial migration in this model system. A quantitative assay for cell surface L-selectin showed that expression of L-selectin was lower on B-CLL lymphocytes (8,880±5,700 molecules/cell) than on normal lymphocytes (29,500±7,500 molecules/cell, p less than 0.001). Also the rate of transmigration of B-CLL lymphocytes (1.5±0.9 migrated cells/HUVEC) was lower than normal peripheral lymphocytes (2.4±0.9 migrated cells/HUVEC, p=0.04). Incubation of lymphocytes in complete medium for 24 hrs increased the expression of L-selectin on B-CLL lymphocytes by 1.5 to 2 fold while the normal lymphocyte L-selectin remained at the initial level. This upregulation of B-CLL L-selectin correlated with a 2 fold increased rate of transendothelial migration. A correlation was found between L-selectin expression on lymphocytes and their ability for transendothelial migration (r^2=0.6). This study shows that the adhesion molecules L-selectin and CD23 can be lost from lymphocytes by two different physiological pathways. One is by P2X7 receptor activation by extracellular ATP while the second is activated by transendothelial migration of these cells. A second finding is that B-CLL lymphocytes have lower level of L-selectin expression and an impaired ability for transendothelial migration compared with normal peripheral blood lymphocytes. Do these results explain the high serum levels of soluble L-selectin and CD23 observed in B-CLL? Although B-CLL lymphocytes do not recirculate as rapidly as normal peripheral blood lymphocytes, the greatly increased number of leukaemic cells in B-CLL ensures that much more soluble L-selectin and CD23 is generated during the recirculation of these cells through the body

THE P2X7 RECEPTOR OF HUMAN LEUKOCYTES

Lymphocytes from normal subjects and patients with B-chronic lymphocytic leukemia (B-CLL) show functional responses to extracellular ATP characteristic of the P2X7 receptor. These responses include opening of a cation selective channel/pore which allows entry of the fluorescent dye, ethidium+ and activation of a membrane metalloprotease which sheds the adhesion molecule L-selectin. In this thesis, the surface expression of P2X7 receptors was measured in normal leucocytes, platelets and B-CLL lymphocytes and compared with their functional responses. Monocytes showed 4-5 fold greater expression of P2X7 than B-, T- and NK- lymphocytes, while P2X7 expression on neutrophils and platelets was weak. All cell types demonstrated abundant intracellular expression of this receptor. All 12 subjects with B-CLL expressed surface P2X7 at about the same level as for B-lymphocytes from normal subjects. P2X7 function, measured by ATP-induced uptake of ethidium, correlated closely with surface expression of this receptor in normal and B-CLL lymphocytes and monocytes. However, the ATP-induced uptake of ethidium into the malignant B-lymphocytes in 3 patients was low or absent. The lack of P2X7 function in these B-lymphocytes was confirmed by the failure of ATP to induce Ba2+ uptake into their lymphocytes. This lack of function of the P2X7 receptor resulted in a failure of ATP-induced shedding of L-selectin, an adhesion molecule which directs the recirculation of lymphocytes from blood into the lymph node. To study a possible genetic basis of non-functional P2X7 receptor, we sequenced DNA coding for the carboxyl terminal tail of P2X7. In 33 of 130 normal subjects a heterozygous nucleotide substitution (1513A--C) was found while 3 subject carried the homozygous substitution which codes for glutamic acid to alanine at amino acid position 496. Surface expression of P2X7 on lymphocytes was not affected by this 496Glu--Ala polymorphism demonstrated both by confocal microscopy and immunofluorescent staining. Monocytes and lymphocytes from the 496Glu--Ala homozygote subject expressed non-functional receptor while heterozygotes showed P2X7 function which was half that of wild type P2X7. Results of transfection experiments showed the mutant P2X7 receptor was non-functional when expressed at low receptor density but regained function at a high receptor density. This density-dependence of mutant P2X7 function was also seen on differentiation of fresh monocytes to macrophages with interferon-gamma which upregulated mutant P2X7 and partially restored its function. P2X7-mediated apoptosis of lymphocytes was impaired in homozygous mutant P2X7 compared with wild type. The data suggest that the glutamic acid at position 496 is required for optimal assembly of the P2X7 receptor. Apart from the 496Glu--Ala polymorphism, three other single nucleotide polymorphisms, 155His--Tyr, 348Ala--Thr and 568Ile--Asn were also found in the P2X7 receptor. The site directed mutant cDNA were generated for all 3 polymorphisms and transfected into HEK293 cells to study the impact of these polymorphisms on P2X7 function. Results suggested that Ile568 is important for P2X7 protein trafficking to cell surface. Further study of these two loss-of-function polymorphisms (496Glu--Ala and 568Ile--Asn) may help better understanding of the functional domains in the P2X7 receptor and its role in CLL, lymphoma and infectious diseases. Conclusions: 1.P2X7 receptor is expressed in human leukocytes, including lymphocytes, natural killer cells as well as monocytes, on both surface and intracellular locations. 2.Both the expression and function of P2X7 are highly variable between in human individuals. Non-functional P2X7 receptors are found in some subjects, including both normal subjects and CLL patients, and are often associated with defects in ATP-induced cytotoxicity and L-selectin shedding. 3.Two single nucleotide polymorphisms (SNPs), 496Glu--Ala and 568Ile--Asn, are found at low frequency in the human population and lead to the loss-of-function of P2X7. Both permeabllity function and the downstream effects mediated by P2X7 are affected by these two SNPs. The mechanisms for the loss-of-function differs between the two polymorphisms