bluuebunny/crossref_metadata_2025 huggingface dataset:
Alterations of protein turnover underlying disuse atrophy in human skeletal muscle
Authors: Phillips S. M. , Glover E. I. , Rennie M. J.
Published: July 2009

Unloading-induced atrophy is a relatively uncomplicated form of muscle loss, dependent almost solely on the loss of mechanical input, whereas in disease states associated with inflammation (cancer cachexia, AIDS, burns, sepsis, and uremia), there is a procatabolic hormonal and cytokine environment. It is therefore predictable that muscle loss mainly due to disuse alone would be governed by mechanisms somewhat differently from those in inflammatory states. We suggest that in vivo measurements made in human subjects using arterial-venous balance, tracer dilution, and tracer incorporation are dynamic and thus robust by comparison with static measurements of mRNA abundance and protein expression and/or phosphorylation in human muscle. In addition, measurements made with cultured cells or in animal models, all of which have often been used to infer alterations of protein turnover, appear to be different from results obtained in immobilized human muscle in vivo. In vivo measurements of human muscle protein turnover in disuse show that the primary variable that changes facilitating the loss of muscle mass is protein synthesis, which is reduced in both the postabsorptive and postprandial states; muscle proteolysis itself appears not to be elevated. The depressed postprandial protein synthetic response (a phenomenon we term “anabolic resistance”) may even be accompanied by a diminished suppression of proteolysis. We therefore propose that most of the loss of muscle mass during disuse atrophy can be accounted for by a depression in the rate of protein synthesis. Thus the normal diurnal fasted-to-fed cycle of protein balance is disrupted and, by default, proteolysis becomes dominant but is not enhanced.
Mechanism of increased inspiratory rib elevation in ascites
Authors: Leduc Dimitri , De Troyer André
Published: July 2009

The detrimental effect of ascites on the lung-expanding action of the diaphragm is partly compensated for by an increase in the inspiratory elevation of the ribs, but the mechanism of this increase is uncertain. To identify this mechanism, the effect of ascites on the response of rib 4 to isolated phrenic nerve stimulation was first assessed in four dogs with bilateral pneumothoraces. Stimulation did not produce any axial displacement of the rib ( Xr) in the control condition and caused a cranial rib displacement in the presence of ascites. This displacement, however, was small. In a second experiment, the effects of ascites on the pleural pressure swing (ΔPpl), intercostal activity, and Xr during spontaneous inspiration were measured in eight animals. As the volume of ascites increased from 0 to 200 ml/kg body wt, Xr increased from 3.5 ± 0.5 to 7.5 ± 0.9 mm ( P < 0.001), ΔPpl decreased from −6.4 ± 0.4 to −3.6 ± 0.3 cmH20 ( P < 0.001), and parasternal intercostal activity increased 61 ± 19% ( P < 0.001). The role of the decrease in ΔPpl in causing the increase in Xr was then separated from that of the increase in intercostal muscle force using the relation between Xr and ΔPpl during passive lung inflation. The loss in ΔPpl accounted for two-thirds of the increase in Xr. These observations indicate that 1) the increased inspiratory elevation of the ribs in ascites is not the result of the increase in the rib cage-expanding action of the diaphragm and 2) it is due mostly to the decrease in ΔPpl and partly to the increase in the force exerted by the parasternal intercostals on the ribs. These observations also suggest, however, that the rib cage expansion caused by ascites makes the parasternal intercostals less effective in pulling the ribs cranially.
Impact of protein and carbohydrate supplementation on plasma volume expansion and thermoregulatory adaptation by aerobic training in older men
Authors: Okazaki Kazunobu , Ichinose Takashi , Mitono Hiroyuki , Chen Mian , Masuki Shizue , Endoh Hiroshi , Hayase Hideki , Doi Tatsuya , Nose Hiroshi
Published: July 2009

We examined whether protein-carbohydrate (CHO) supplementation immediately after exercise each day during aerobic training facilitated plasma volume (PV) expansion and thermoregulatory and cardiovascular adaptations in older men. Fourteen moderately active older men [68 ± 5 (SD) yr] were divided into two groups so as to have no significant differences in anthropometric measures, PV, and peak oxygen consumption rate (V̇o2peak). Each group was provided with a mixture of protein and CHO (3.2 kcal, 0.18 g protein/kg body wt, Pro-CHO, n = 7) or a non-protein and low-calorie placebo (0.5 kcal, 0 g protein/kg body wt, CNT, n = 7) immediately after cycling exercise (60–75% V̇o2peak, 60 min/day, 3 days/wk) each day for 8 wk at ∼19°C ambient temperature (Ta) and ∼43% relative humidity (RH). Before and after training, we measured PV, cardiac stroke volume (SV), and esophageal temperature (Tes) during 20-min exercise at 60% of pretraining V̇o2peak at 30°C Ta and 50% RH. Moreover, we determined the sensitivity of the chest sweat rate (ΔSR/ΔTes) and forearm vascular conductance (ΔFVC/ΔTes) in response to increased Tes during exercise. After training, PV increased by ∼6% in Pro-CHO ( P < 0.001), with an ∼10% increase in SV during exercise ( P < 0.001), but not in CNT ( P > 0.07). ΔFVC/ΔTes increased by 80% and ΔSR/ΔTes by 18% in Pro-CHO (both P < 0.01) but not in CNT ( P > 0.07). Moreover, we found a significant interactive effect of group × training on PV, SV, and ΔFVC/ΔTes (all P < 0.02) but with no significant effect of group ( P > 0.4), suggesting that the supplement enhanced these responses to aerobic training. Thus postexercise protein-CHO supplementation during training caused PV expansion and facilitated thermoregulatory and cardiovascular adaptations, possibly providing a new training regimen for older men.
Adaptations to high-intensity intermittent exercise in rodents
Authors: Bexfield Nathan A. , Parcell Allen C. , Nelson W. Bradley , Foote Kristopher M. , Mack Gary W.
Published: July 2009

In humans, exercise-induced plasma volume (PV) expansion is typically associated with an increase in plasma albumin content, due in part to an increase in hepatic albumin synthesis. We tested the ability of a 12-day high-intensity intermittent exercise protocol to induce an increase in PV in rodents. Since albumin synthesis is transcriptionally regulated, we tested the hypothesis that exercise training would induce an increase in hepatic albumin gene expression. Fifty adult male Sprague-Dawley rats weighing between 245 and 350 g were randomly assigned to one of five groups: cage control (CC), sham exercise (sham), continuous moderate-intensity exercise training (MI), high-intensity intermittent exercise training (HI), or a single day of HI training (1-HI). Twenty-four hours after the last training session, rats were anesthetized. PV was determined, and the liver was removed, flash frozen, and stored for later analysis. Citrate synthase (CS) activity of the red quadriceps muscle, a marker of aerobic adaptation, increased with training (MI and HI) and in response to 1-HI ( P < 0.05). We did not see a significant exercise-induced PV expansion as PV averaged 23.6 ± 2.7 ml/kg body wt in the CC group and 26.6 ± 1.3 ml/kg body wt in the HI group ( P > 0.05). However, hepatic albumin mRNA expression, as determined by real-time PCR, increased 2.9 ± 0.4- and 4.1 ± 0.4-fold after MI and HI, respectively, compared with CC. A single bout of HI (1-HI) did not alter hepatic albumin mRNA expression. These data demonstrate an increase in both CS activity and hepatic albumin gene expression with 12 days of aerobic exercise training in the rodent with a rapid (within 24 h) adaptation in the skeletal muscle to high-intensity intermittent exercise.
Fibrillar Collagen Inhibits Cholesterol Biosynthesis in Human Aortic Smooth Muscle Cells
Authors: Ferri Nicola , Roncalli Elisa , Arnaboldi Lorenzo , Fenu Simone , Andrukhova Olena , Aharinejad Seyedhossein , Camera Marina , Tremoli Elena , Corsini Alberto
Published: July 2009

Objective—

Integrin-mediated cell adhesion to type I fibrillar collagen regulates gene and protein expression, whereas little is known of its effect on lipid metabolism. In the present study, we examined the effect of type I fibrillar collagen on cholesterol biosynthesis in human aortic smooth muscle cells (SMCs).

Methods and Results—

SMCs were cultured on either fibrillar or monomer collagen for 48 hours and [
14
C]-acetate incorporation into cholesterol was evaluated. Fibrillar collagen reduced by 72.9±2.6% cholesterol biosynthesis without affecting cellular cholesterol levels. Fibrillar collagen also reduced 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA) promoter activity (−72.6±7.3%), mRNA (−58.7±6.4%), protein levels (−35.5±8.5%), and enzyme activity (−37.7±2.2%). Intracellular levels of the active form of sterol regulatory element binding proteins (SREBP) 1a was decreased by 60.7±21.7% in SMCs cultured on fibrillar collagen, whereas SREBP2 was not significantly affected (+12.1±7.1%). The overexpression of the active form of SREBP1a rescued the downregulation of fibrillar collagen on HMG-CoA reductase levels. Blocking antibody to α2 integrin partially reversed the downregulation of HMG-CoA reductase mRNA expression. Finally, fibrillar collagen led to an intracellular accumulation of unprenylated Ras.

Conclusions—

Our study demonstrated that α2β1 integrin interaction with fibrillar collagen affected the expression of HMG-CoA reductase, which led to the inhibition of cholesterol biosynthesis in human SMCs.
Hemorrhage and Large Lipid-Rich Necrotic Cores Are Independently Associated With Thin or Ruptured Fibrous Caps
Authors: Ota Hideki , Yu Wei , Underhill Hunter R. , Oikawa Minako , Dong Li , Zhao Xihai , Polissar Nayak L. , Neradilek Blazej , Gao Tianli , Zhang Zhuo , Yan Zixu , Guo Miao , Zhang Zhaoqi , Hatsukami Thomas S. , Yuan Chun
Published: July 2009

Objective—

Histological studies suggest associations between hemorrhage and large lipid-rich/necrotic cores with thin or ruptured fibrous caps in advanced atherosclerosis. We investigated these associations in carotid arteries with mild to severe stenosis by in vivo 3T MRI.

Methods and Results—

Seventy-seven patients with ≥50% carotid stenosis in at least one side by duplex ultrasound underwent bilateral multi-contrast carotid MRI scans. Measurements for wall and lipid-rich/necrotic core sizes, presence of hemorrhage, and fibrous cap status (classified as intact thick, intact thin or ruptured) were recorded. Arteries with poor image quality, occlusion, or no detectable lipid-rich/necrotic core were excluded. For the 798 MRI slices included, multivariate ordinal regression analysis demonstrated larger %lipid-rich/necrotic core (odds ratio for 10% increase, 1.49;
P
=0.02) and presence of hemorrhage (odds ratio, 5.91;
P
<0.001) were independently associated with a worse (intact thin or ruptured) stage of fibrous cap status. For artery-based multivariate analysis, a larger maximum %lipid-rich/necrotic core and presence of hemorrhage independently associated with worse fibrous cap status (
P
<0.001, for both). No hemorrhage was detected in arteries with thick fibrous caps.

Conclusion—

Hemorrhage and larger %lipid-rich/necrotic core were independently associated with a thin or ruptured fibrous cap status at an early to advanced stage of carotid atherosclerosis.
Obesity Promotes Inflammation in Periaortic Adipose Tissue and Angiotensin II-Induced Abdominal Aortic Aneurysm Formation
Authors: Police Sara B. , Thatcher Sean E. , Charnigo Richard , Daugherty Alan , Cassis Lisa A.
Published: July 2009

Objective—

Obesity promotes macrophage infiltration into adipose tissue and is associated with increases in several cardiovascular diseases. Infusion of angiotensin II (AngII) to mice induces formation of abdominal aortic aneurysms (AAAs) with profound medial and adventitial macrophage infiltration. We sought to determine whether obesity promotes macrophage infiltration and proinflammatory cytokines in periaortic adipose tissue surrounding abdominal aortas and increases AngII-induced AAAs.

Methods and Results—

Hypertrophied white adipocytes surrounded abdominal aortas, whereas brown adipocytes surrounded thoracic aortas of obese mice. mRNA abundance of macrophage proinflammatory chemokines and their receptors were elevated with obesity to a greater extent in abdominal compared to thoracic periaortic adipose tissue. Periaortic adipose tissue explants surrounding abdominal aortas of obese mice released greater concentrations of MCP-1 and promoted more macrophage migration than explants from thoracic aortas. Male C57BL/6 mice were fed a high-fat (HF) diet for 1, 2, or 4 months and then infused with AngII (1000 ng/kg/min) for 28 days. AAA incidence increased progressively with the duration of HF feeding (18%, 36%,and 60%, respectively). Similarly, AngII-infused
ob/ob
mice exhibited increased AAAs compared to lean controls (76% compared to 32%, respectively,
P
<0.05). Infusion of AngII to obese mice promoted further macrophage infiltration into periaortic and visceral adipose tissue, and obese mice exhibiting AAAs had greater macrophage content in visceral adipose tissue than mice not developing AAAs.

Conclusions—

Increased macrophage accumulation in periaortic adipose tissue surrounding abdominal aortas of AngII-infused obese mice is associated with enhanced AAA formation.
Prevalence of Sarcomere Protein Gene Mutations in Preadolescent Children With Hypertrophic Cardiomyopathy
Authors: Kaski Juan Pablo , Syrris Petros , Esteban Maria Teresa Tome , Jenkins Sharon , Pantazis Antonios , Deanfield John E. , McKenna William J. , Elliott Perry M.
Published: July 2009

Background—

Hypertrophic cardiomyopathy (HCM) in infants and children is thought to be commonly associated with metabolic disorders and malformation syndromes. Familial disease caused by mutations in cardiac sarcomere protein genes, which accounts for most cases in adolescents and adults, is believed to be a very rare cause of HCM.

Methods and Results—

Seventy-nine consecutive patients diagnosed with HCM aged 13 years or younger underwent detailed clinical and genetic evaluation. The protein-coding sequences of 9 sarcomere protein genes (
MYH7
,
MYBPC3
,
TNNI3
,
TNNT2
,
TPM1
,
MYL2
,
MYL3
,
ACTC
, and
TNNC1
), the genes encoding desmin (
DES
), and the γ-2 subunit of AMP kinase (
PRKAG2
) were screened for mutations. A family history of HCM was present in 48 patients (60.8%). Forty-seven mutations (15 novel) were identified in 42 (53.2%) patients (5 patients had 2 mutations). The genes most commonly implicated were
MYH7
(48.9%) and
MYBPC3
(36.2%); mutations in
TNNT2
,
ACTC
,
MYL3
, and
TNNI3
accounted for <5% of cases each. A total of 16.7% patients with sarcomeric mutations were diagnosed before 1 year of age. There were no differences in clinical and echocardiographic features between those children with sarcomere protein gene mutations and those without or between patients with 2 mutations and those with 1 or no mutations.

Conclusions—

This study shows that familial disease is common among infants and children with HCM and that, in most cases, disease is caused by mutations in cardiac sarcomere protein genes. The major implication is that all first-degree relatives of any child diagnosed with HCM should be offered screening. Furthermore, the finding that one sixth of patients with sarcomeric disease were diagnosed in infancy suggests that current views on pathogenesis and natural history of familial HCM may have to be revised.
CaMKII Negatively Regulates Calcineurin–NFAT Signaling in Cardiac Myocytes
Authors: MacDonnell Scott M. , Weisser-Thomas Jutta , Kubo Hajime , Hanscome Marie , Liu Qinghang , Jaleel Naser , Berretta Remus , Chen Xiongwen , Brown Joan H. , Sabri Abdel-Karim , Molkentin Jeffery D. , Houser Steven R.
Published: July 2009

Rationale:

Pathological cardiac myocyte hypertrophy is thought to be induced by the persistent increases in intracellular Ca
2+
needed to maintain cardiac function when systolic wall stress is increased. Hypertrophic Ca
2+
binds to calmodulin (CaM) and activates the phosphatase calcineurin (Cn) and CaM kinase (CaMK)II. Cn dephosphorylates cytoplasmic NFAT (nuclear factor of activated T cells), inducing its translocation to the nucleus where it activates antiapoptotic and hypertrophic target genes. Cytoplasmic CaMKII regulates Ca
2+
handling proteins but whether or not it is directly involved in hypertrophic and survival signaling is not known.

Objective:

This study explored the hypothesis that cytoplasmic CaMKII reduces NFAT nuclear translocation by inhibiting the phosphatase activity of Cn.

Methods and Results:

Green fluorescent protein–tagged NFATc3 was used to determine the cellular location of NFAT in cultured neonatal rat ventricular myocytes (NRVMs) and adult feline ventricular myocytes. Constitutively active (CaMKII-CA) or dominant negative (CaMKII-DN) mutants of cytoplasmic targeted CaMKII
δc
were used to activate and inhibit cytoplasmic CaMKII activity. In NRVM CaMKII-DN (48.5±3%,
P
<0.01 versus control) increased, whereas CaMKII-CA decreased (5.9±1%,
P
<0.01 versus control) NFAT nuclear translocation (Control: 12.3±1%). Cn inhibitors were used to show that these effects were caused by modulation of Cn activity. Increasing Ca
2+
increased Cn-dependent NFAT translocation (to 71.7±7%,
P
<0.01) and CaMKII-CA reduced this effect (to 17.6±4%). CaMKII-CA increased TUNEL and caspase-3 activity (
P
<0.05). CaMKII directly phosphorylated Cn at Ser197 in CaMKII-CA infected NRVMs and in hypertrophied feline hearts.

Conclusion:

These data show that activation of cytoplasmic CaMKII inhibits NFAT nuclear translocation by phosphorylation and subsequent inhibition of Cn.
Differential Macrophage Polarization in Male and Female BALB/c Mice Infected With Coxsackievirus B3 Defines Susceptibility to Viral Myocarditis
Authors: Li Kang , Xu Wei , Guo Qiang , Jiang Zhenggang , Wang Ping , Yue Yan , Xiong Sidong
Published: July 2009

Rational:

Myocardial infiltrating macrophages play an important role in the pathogenesis of viral myocarditis in male BALB/c mice following coxsackievirus B3 (CVB3) infection. Interestingly, comparable macrophage numbers were observed in the myocardium of female mice during acute myocarditis.

Objective:

Given CVB3 infection causes severe myocarditis in male but not female mice, we postulated that macrophages infiltrating the myocardium of female mice may display distinct functional properties that contribute to differential susceptibility to CVB3 myocarditis.

Methods and Results:

Here, we found that myocardial infiltrating macrophages from CVB3-infected male mice expressed high levels of classically activated macrophages (M1) markers, including inducible nitric oxide synthase, interleukin-12, tumor necrosis factor-α, and CD16/32, whereas those of females showed enhanced expression of arginase 1, interleukin-10, macrophage mannose receptor (MMR) and macrophage galactose type C-type lectin (MGL) that were associated with alternatively activated macrophage (M2) phenotype. Moreover, distinct myocardial-derived cytokines were found to play a critical role in differential macrophage polarization between sexes after CVB3 infection. Adoptive transfer of ex vivo programmed M1 macrophages, as expectedly, significantly increased myocarditis in both male and female mice. Strikingly, transfer of M2 macrophages into susceptible male mice remarkably alleviated myocardial inflammation by modulating local cytokine profile and promoting peripheral regulatory T cell (Treg) differentiation.

Conclusions:

Taken together, this study may facilitate the understanding of the mechanism underlying gender bias in susceptibility to CVB3 myocarditis and the development of therapeutic strategies based on macrophage polarization for inflammatory heart disease.
Nitric Oxide Increases Cardiac
I
K1
by Nitrosylation of Cysteine 76 of Kir2.1 Channels
Authors: Gómez Ricardo , Caballero Ricardo , Barana Adriana , Amorós Irene , Calvo Enrique , López Juan Antonio , Klein Helene , Vaquero Miguel , Osuna Lourdes , Atienza Felipe , Almendral Jesús , Pinto Ángel , Tamargo Juan , Delpón Eva
Published: July 2009

Rationale:

The cardiac inwardly rectifying K
+
current (
I
K1
) plays a critical role in modulating excitability by setting the resting membrane potential and shaping phase 3 of the cardiac action potential.

Objective:

This study aims to analyze the effects of nitric oxide (NO) on human atrial
I
K1
and on Kir2.1 channels, the major isoform of inwardly rectifying channels present in the human heart.

Methods and Results:

Currents were recorded in enzymatically isolated myocytes and in transiently transfected CHO cells, respectively. NO at myocardial physiological concentrations (25 to 500 nmol/L) increased inward and outward
I
K1
and
I
Kir2.1
. These effects were accompanied by hyperpolarization of the resting membrane potential and a shortening of the duration of phase 3 of the human atrial action potential. The
I
Kir2.1
increase was attributable to an increase in the open probability of the channel. Site-directed mutagenesis analysis demonstrated that NO effects were mediated by the selective
S
-nitrosylation of Kir2.1 Cys76 residue. Single ion monitoring experiments performed by liquid chromatography/tandem mass spectrometry suggested that the primary sequence that surrounds Cys76 determines its selective
S
-nitrosylation. Chronic atrial fibrillation, which produces a decrease in NO bioavailability, decreased the
S
-nitrosylation of Kir2.1 channels in human atrial samples as demonstrated by a biotin-switch assay, followed by Western blot.

Conclusions:

The results demonstrated that, under physiological conditions, NO regulates human cardiac
I
K1
through a redox-related process.
Hydrogen Sulfide Mediates Cardioprotection Through Nrf2 Signaling
Authors: Calvert John W. , Jha Saurabh , Gundewar Susheel , Elrod John W. , Ramachandran Arun , Pattillo Christopher B. , Kevil Christopher G. , Lefer David J.
Published: July 2009

Rationale:

The recent emergence of hydrogen sulfide (H
2
S) as a potent cardioprotective signaling molecule necessitates the elucidation of its cytoprotective mechanisms.

Objective:

The present study evaluated potential mechanisms of H
2
S-mediated cardioprotection using an in vivo model of pharmacological preconditioning.

Methods and Results:

H
2
S (100 μg/kg) or vehicle was administered to mice via an intravenous injection 24 hours before myocardial ischemia. Treated and untreated mice were then subjected to 45 minutes of myocardial ischemia followed by reperfusion for up to 24 hours, during which time the extent of myocardial infarction was evaluated, circulating troponin I levels were measured, and the degree of oxidative stress was evaluated. In separate studies, myocardial tissue was collected from treated and untreated mice during the early (30 minutes and 2 hours) and late (24 hours) preconditioning periods to evaluate potential cellular targets of H
2
S. Initial studies revealed that H
2
S provided profound protection against ischemic injury as evidenced by significant decreases in infarct size, circulating troponin I levels, and oxidative stress. During the early preconditioning period, H
2
S increased the nuclear localization of Nrf2, a transcription factor that regulates the gene expression of a number of antioxidants and increased the phosphorylation of protein kinase Cε and STAT-3. During the late preconditioning period, H
2
S increased the expression of antioxidants (heme oxygenase-1 and thioredoxin 1), increased the expression of heat shock protein 90, heat shock protein 70, Bcl-2, Bcl-xL, and cyclooxygenase-2 and also inactivated the proapoptogen Bad.

Conclusions:

These results reveal that the cardioprotective effects of H
2
S are mediated in large part by a combination of antioxidant and antiapoptotic signaling.
Adipocyte Fatty Acid–Binding Protein Suppresses Cardiomyocyte Contraction
Authors: Lamounier-Zepter Valéria , Look Christiane , Alvarez Julio , Christ Torsten , Ravens Ursula , Schunck Wolf-Hagen , Ehrhart-Bornstein Monika , Bornstein Stefan R. , Morano Ingo
Published: July 2009

Rationale:

Adipocyte fatty acid–binding protein (FABP4) is a member of the intracellular lipid-binding protein family and is predominantly expressed in adipose tissue. Emerging evidence suggests that FABP4 plays a role in some aspects of the metabolic syndrome including the development of type 2 diabetes and atherosclerosis. We have recently reported that secretory products from human adipocytes directly and acutely depressed cardiac contractile function.

Objective:

The purpose of this study was to identify this adipocyte-derived cardiodepressant factor.

Methods and Results:

Through mass spectrometry and immunoblotting, we have identified this cardiodepressant factor as FABP4. FABP4 represents 1.8% to 8.1% of total protein secreted by adipocytes in extracellular medium. FABP4 acutely depressed shortening amplitude as well as intracellular systolic peak Ca
2+
in a dose-dependent manner in isolated rat cardiomyocytes. Heart-specific FABP isoform (FABP3) revealed a similar cardiodepressant effect. The N-terminal amino acids 1 to 20 of FABP4 could be identified as the most effective cardiodepressive domain. We could exclude any effect of FABP4 on action potential duration and L-type Ca
2+
current, suggesting a reduced excitation-contraction gain caused by FABP4 as the main inhibitory mechanism.

Conclusion:

We conclude that the release of FABP4 from adipocytes may be involved in the development of cardiac contractile dysfunction of obese subjects.
Migraine and Biomarkers of Endothelial Activation in Young Women
Authors: Tietjen Gretchen E. , Herial Nabeel A. , White Leah , Utley Christine , Kosmyna Janet M. , Khuder Sadik A.
Published: July 2009

Background and Purpose—

There is mounting evidence of endothelial activation and dysfunction in migraine. Our objectives were to determine in a population of premenopausal women whether endothelial activation markers are associated with migraine.

Methods—

Women (18 to 50 years) with and without migraine and free from cardiovascular disease were evaluated with tests of coagulation (von Willebrand factor activity, prothrombin fragment), fibrinolysis (tissue-type plasminogen activator antigen), inflammation (high-sensitivity C-reactive protein), and oxidative stress (homocysteine, total nitrate/nitrite concentrations, thiobarbituric acid–reactive substances).

Results—

Sixty-one participants had migraine with aura (MA), 64 had migraine without aura (MO), and 50 were controls. Compared with controls, women with migraine had higher adjusted odds ratios for elevated von Willebrand factor activity of 6.51 (95% CI, 1.94 to 21.83) in those with MA and of 4.59 (95% CI, 1.37 to 15.38) in those with MO, elevated high-sensitivity C-reactive protein of 7.99 (95% CI, 2.32 to 27.61) in those with MA and of 2.63 (95% CI, 0.73 to 9.45) in those with MO, and for lower nitrate/nitrite levels of 6.60 (95% CI, 2.06 to 21.16) in those with MA and of 3.03 (95% CI, 0.90 to 10.15) in those with MO. Within the migraine group, von Willebrand factor activity was correlated with tissue-type plasminogen activator antigen (
P
=0.035) and nitrate/nitrite (
P
=0.024). There was a trend with high-sensitivity C-reactive protein (
P
=0.09).

Conclusions—

In premenopausal women with migraine, particularly in those with MA, there is evidence of increased endothelial activation, a component of endothelial dysfunction.
National Institutes of Health Stroke Scale Score Is Poorly Predictive of Proximal Occlusion in Acute Cerebral Ischemia
Authors: Maas Matthew B. , Furie Karen L. , Lev Michael H. , Ay Hakan , Singhal Aneesh B. , Greer David M. , Harris Gordon J. , Halpern Elkan , Koroshetz Walter J. , Smith Wade S.
Published: July 2009

Background and Purpose—

Multimodal imaging is gaining an important role in acute stroke. The benefit of obtaining additional clinically relevant information must be weighed against the detriment of increased cost, delaying time to treatment, and adverse events such as contrast-induced nephropathy. Use of National Institutes of Health Stroke Scale (NIHSS) score to predict a proximal arterial occlusion (PO) is suggested by several case series as a viable method of selecting cases appropriate for multimodal imaging.

Methods—

Six hundred ninety-nine patients enrolled in a prospective cohort study involving CT angiographic imaging in acute stroke were dichotomized according to the presence of a PO, including a subgroup of 177 subjects with middle cerebral artery M1 occlusion.

Results—

The median NIHSS score of patients found to have a PO was higher than the overall median (9 versus 5,
P
<0.0001). The median NIHSS score of patients with middle cerebral artery M1 occlusion was 14. NIHSS score ≥10 had 81% positive predictive value for PO but only 48% sensitivity with the majority of subjects with PO presenting with lower NIHSS scores. All patients with NIHSS score ≥2 would need to undergo angiographic imaging to detect 90% of PO.

Conclusions—

High NIHSS score correlates with the presence of a proximal arterial occlusion in patients presenting with acute cerebral ischemia. No NIHSS score threshold can be applied to select a subgroup of patients for angiographic imaging without failing to capture the majority of cases with clinically important occlusive lesions. The finding of minimal clinical deficits should not deter urgent angiographic imaging in otherwise appropriate patients suspected of acute stroke.
Structure and Modification of the South Pacific Eastern Subtropical Mode Water
Authors: Sato Kanako , Suga Toshio
Published: July 2009

Using all available temperature and salinity profiles obtained by Argo floats from July 2004 to June 2007, this study investigated the structure and modification of the South Pacific Eastern Subtropical Mode Water (SPESTMW). Based on the observed characteristics of the vertical minima of potential vorticity over the subtropical South Pacific, SPESTMW is defined as water with potential vorticity magnitude less than 2.5 × 10−10 m−1 s−1 and thickness exceeding 40 m. It is found between 35°–5°S and 160°–70°W and has a temperature of 13°–26°C, salinity greater than 34.0, and density of 24.5–25.8 kg m−3 at its core.

This study confirmed that vertical changes in temperature and salinity tend to compensate for each other in terms of density changes, resulting in favorable salt fingering conditions, as previously reported. By analyzing many profiles of Argo data in spring immediately after the SPESTMW formation period, its temperature and salinity are vertically uniform in the formation region, but large vertical gradients of temperature and salinity are found downstream from that region, even in the SPESTMW core. Consequently, the low potential vorticity signature of SPESTMW spread much wider than its signature as a thermostad. The Argo data also captured the seasonal changes of the vertical gradients of temperature and salinity at the SPESTMW core; these gradients increased as the seasons progressed, even in the formation region. Therefore, SPESTMW is truly vertically uniform water (i.e., thermostad, halostad, and pycnostad simultaneously) only immediately after the formation period. Afterward, it is only pycnostad. This seasonal evolution is related to temperature and salinity diffusion due to salt fingering in a manner similar to the rapid modification of interannual anomalies as shown by previous research. The temperature and salinity near the SPESTMW core and lower region decreased soon after its formation.
The Temporal and Spatial Distribution of Carbon Dioxide Emissions from Fossil-Fuel Use in North America
Authors: Gregg J. S. , Losey L. M. , Andres R. J. , Blasing T. J. , Marland G.
Published: July 2009

Refinements in the spatial and temporal resolution of North American fossil-fuel carbon dioxide (CO2) emissions provide additional information about anthropogenic aspects of the carbon cycle. In North America, the seasonal and spatial patterns are a distinctive component to characterizing anthropogenic carbon emissions. The pattern of fossil-fuel-based CO2 emissions on a monthly scale has greater temporal and spatial variability than the flux aggregated to the national annual level. For some areas, monthly emissions can vary by as much as 85% for some fuels when compared with monthly estimates based on a uniform temporal and spatial distribution. The United States accounts for the majority of North American fossil carbon emissions, and the amplitude of the seasonal flux in emissions in the United States is greater than the total mean monthly emissions in both Canada and Mexico. Nevertheless, Canada and Mexico have distinctive seasonal patterns as well. For the continent, emissions were aggregated on a 5° × 10° latitude–longitude grid. The monthly pattern of emissions varies on both a north–south and east–west gradient and evolves through the time period analyzed (1990–2007). For many areas in North America, the magnitude of the month-to-month variation is larger than the total annual emissions from land use change, making the characterization of emissions patterns essential to understanding humanity’s influence on the carbon cycle.
Method Development for Estimating Sensible Heat Flux over the Tibetan Plateau from CMA Data
Authors: Yang Kun , Qin Jun , Guo Xiaofeng , Zhou Degang , Ma Yaoming
Published: July 2009

To clarify the thermal forcing of the Tibetan Plateau, long-term coarse-temporal-resolution data from the China Meteorological Administration have been widely used to estimate surface sensible heat flux by bulk methods in many previous studies; however, these estimates have seldom been evaluated against observations. This study at first evaluates three widely used bulk schemes against Tibet instrumental flux data. The evaluation shows that large uncertainties exist in the heat flux estimated by these schemes; in particular, upward heat fluxes in winter may be significantly underestimated, because diurnal variations of atmospheric stability were not taken into account. To improve the estimate, a new method is developed to disaggregate coarse-resolution meteorological data to hourly according to statistical relationships derived from high-resolution experimental data, and then sensible heat flux is estimated from the hourly data by a well-validated flux scheme. Evaluations against heat flux observations in summer and against net radiation observations in winter indicate that the new method performs much better than previous schemes, and therefore it provides a robust basis for quantifying the Tibetan surface energy budget.
Observations of Seven African Easterly Waves in the East Atlantic during 2006
Authors: Zawislak Jonathan , Zipser Edward J.
Published: July 2009

The African Monsoon Multidisciplinary Analyses (AMMA) experiment and its downstream NASA extension, NAMMA, provide an unprecedented detailed look at the vertical structure of consecutive African easterly waves. During August and September 2006, seven easterly waves passed through the NAMMA domain: two waves developed into Tropical Cyclones Debby and Helene, two waves did not develop, and three waves were questionable in their role in the development of Ernesto, Florence, and Gordon. NCEP Global Data Assimilation System (GDAS) analyses are used to describe the track of both the vorticity maxima and midlevel wave trough associated with each of the seven easterly waves. Dropsonde data from NAMMA research flights are used to describe the observed wind structure and as a tool to evaluate the accuracy of the GDAS to resolve the structure of the wave. Finally, satellite data are used to identify the relationship between convection and the organization of the wind structure. Results support a necessary distinction between the large-scale easterly wave trough and smaller-scale vorticity centers within the wave. An important wave-to-wave variability is observed: for NAMMA waves, those waves that have a characteristically high-amplitude wave trough and well-defined low-level circulations (well organized) may contain less rainfall, do not necessarily develop, and are well resolved in the analysis, whereas low-amplitude (weakly organized) NAMMA waves may have stronger vorticity centers and large persistent raining areas and may be more likely to develop, but are not well resolved in the analysis.
Projected Changes in Mean and Extreme Precipitation in Africa under Global Warming. Part I: Southern Africa
Authors: Shongwe M. E. , van Oldenborgh G. J. , van den Hurk B. J. J. M. , de Boer B. , Coelho C. A. S. , van Aalst M. K.
Published: July 2009

This study investigates likely changes in mean and extreme precipitation over southern Africa in response to changes in radiative forcing using an ensemble of global climate models prepared for the Intergovernmental Panel on Climate Change (IPCC) Fourth Assessment Report (AR4). Extreme seasonal precipitation is defined in terms of 10-yr return levels obtained by inverting a generalized Pareto distribution fitted to excesses above a predefined high threshold. Both present (control) and future climate precipitation extremes are estimated. The future-to-control climate ratio of 10-yr return levels is then used as an indicator for the likely changes in extreme seasonal precipitation.

A Bayesian approach to multimodel ensembling is adopted. The relative weights assigned to each of the model simulations is determined from bias, convergence, and correlation. Using this method, the probable limits of the changes in mean and extreme precipitation are estimated from their posterior distribution.

Over the western parts of southern Africa, an increase in the severity of dry extremes parallels a statistically significant decrease in mean precipitation during austral summer months. A notable delay in the onset of the rainy season is found in almost the entire region. An early cessation is found in many parts. This implies a statistically significant shortening of the rainy season.

A substantial reduction in moisture influx from the southwestern Indian Ocean during austral spring is projected. This and the preaustral spring moisture deficits are possible mechanisms delaying the rainfall onset in southern Africa. A possible offshore (northeasterly) shift of the tropical–temperate cloud band is consistent with more severe droughts in the southwest of southern Africa and enhanced precipitation farther north in Zambia, Malawi, and northern Mozambique.

This study shows that changes in the mean vary on relatively small spatial scales in southern Africa and differ between seasons. Changes in extremes often, but not always, parallel changes in the mean precipitation.
An Evaluation of ENSO Asymmetry in the Community Climate System Models: A View from the Subsurface
Authors: Zhang Tao , Sun De-Zheng , Neale Richard , Rasch Philip J.
Published: July 2009

The asymmetry between El Niño and La Niña is a key aspect of ENSO that needs to be simulated well by models in order to fully capture the role of ENSO in the climate system. Here the asymmetry between the two phases of ENSO in five successive versions of the Community Climate System Model (CCSM1, CCSM2, CCSM3 at T42 resolution, CCSM3 at T85 resolution, and the latest CCSM3 + NR, with the Neale and Richter convection scheme) is evaluated. Different from the previous studies, not only is the surface signature of ENSO asymmetry examined, but so too is its subsurface signature. By comparing the differences among these models as well as the differences between the models and the observations, an understanding of the causes of the ENSO asymmetry is sought.

An underestimate of the ENSO asymmetry is noted in all of the models, but the latest version with the Neale and Richter scheme (CCSM3 + NR) is getting closer to the observations than the earlier versions. The net surface heat flux is found to damp the asymmetry in the SST field in both the models and observations, but the damping effect in the models is weaker than that in the observations, thus excluding a role of the surface heat flux in contributing to the weaker asymmetry in the SST anomalies associated with ENSO. Examining the subsurface signatures of ENSO—the thermocline depth and the associated subsurface temperature for the western and eastern Pacific—reveals the same bias; that is, the asymmetry in the models is weaker than that in the observations.

The analysis of the corresponding Atmospheric Model Intercomparison Project (AMIP) runs in conjunction with the coupled runs suggests that the weaker asymmetry in the subsurface signatures in the models is related to the lack of asymmetry in the zonal wind stress over the central Pacific, which in turn is due to a lack of sufficient asymmetry in deep convection (i.e., the nonlinear dependence of the deep convection on SST). In particular, the lack of a westward shift in the deep convection in the models in response to a cold phase SST anomaly is found as a common factor that is responsible for the weak asymmetry in the models. It is also suggested that a more eastward extension of the deep convection in response to a warm phase SST anomaly may also help to increase the asymmetry of ENSO. The better performance of CCSM3 + NR is apparently linked to an enhanced convection over the eastern Pacific during the warm phase of ENSO. Apparently, either a westward shift of deep convection in response to a cold phase SST anomaly or an increase of convection over the eastern Pacific in response to a warm phase SST anomaly leads to an increase in the asymmetry of zonal wind stress and therefore an increase in the asymmetry of subsurface signal, favoring an increase in ENSO asymmetry.
The Amplification of the ENSO Forcing over Equatorial Amazon
Authors: Misra Vasubandhu
Published: July 2009

The remote influence of the El Niño–Southern Oscillation (ENSO) strongly manifests over the equatorial Amazon (EA)—including parts of southern Venezuela, Guyana, French Guiana, and Suriname—when there is a large-scale anomalous upper-level divergence over continental tropical South America. Modeling studies conducted in this paper suggest that it is because of the modulation of the local diurnal cycle of the moisture flux convergence, which results in the local amplification of the ENSO signal over the EA. Further, it is shown that the local land surface feedback plays a relatively passive but important role of maintaining these interannual precipitation anomalies over the EA region.
The Airborne Demonstrator for the Direct-Detection Doppler Wind Lidar ALADIN on ADM-Aeolus. Part I: Instrument Design and Comparison to Satellite Instrument
Authors: Reitebuch Oliver , Lemmerz Christian , Nagel Engelbert , Paffrath Ulrike , Durand Yannig , Endemann Martin , Fabre Frederic , Chaloupy Marc
Published: July 2009

The global observation of profiles of the atmospheric wind speed is the highest-priority unmet need for global numerical weather prediction. Satellite Doppler lidar is the most promising candidate to meet the requirements on global wind profile observations with high vertical resolution, precision, and accuracy. The European Space Agency (ESA) decided to implement a Doppler wind lidar mission called the Atmospheric Dynamics Mission Aeolus (ADM-Aeolus) to demonstrate the potential of the Doppler lidar technology and the expected impact on numerical weather forecasting. An airborne prototype of the instrument on ADM-Aeolus was developed to validate the instrument concept and retrieval algorithms with realistic atmospheric observations before the satellite launch. It is the first airborne direct-detection Doppler lidar for atmospheric observations, and it is operating at an ultraviolet wavelength of 355 nm. The optical design is described in detail, including the single-frequency pulsed laser and the two spectrometers to resolve the Doppler frequency shift from molecular Rayleigh and aerosol Mie backscatter. The airborne prototype is representative of the spaceborne instrument, and their specific differences are discussed.
Wavelet Analysis on the Variability, Teleconnectivity, and Predictability of the Seasonal Rainfall of Taiwan
Authors: Kuo Chun-Chao , Gan Thian Yew , Yu Pao-Shan
Published: July 2009

Using wavelet analysis, the variability and oscillations of November–January (NDJ) and January–March (JFM) rainfall (1974–2006) of Taiwan and seasonal sea surface temperature (SST) of the Pacific Ocean were analyzed. From the scale-average wavelet power (SAWP) computed for the seasonal rainfall, it seems that the data exhibit interannual oscillations at a 2–4-yr period. On the basis of correlation fields between decadal component removed wavelet PC (DCR-WPC1) of seasonal rainfall and decadal component removed scale-averaged wavelet power (DCR-SAWP) of SST of Pacific Ocean at one-season lead time, SST of some domains of the western Pacific Ocean (July–September SST around 0°–30°N, 120°–160°E; October–December SST around 0°–60°N, 125°E–160°W) were selected as predictors to predict seasonal NDJ and JFM rainfall of Taiwan at one-season lead time, respectively, using an Artificial Neural Network calibrated by the Genetic Algorithm (ANN-GA). The ANN-GA was first calibrated using the 1975–99 data and independently validated using 2000–06 data. In terms of summary statistics such as the correlation coefficient, root-mean-square error (RMSE), and Hanssen–Kuipers (HK) scores, the prediction of seasonal rainfall of northern and western Taiwan using ANN-GA are generally good for both calibration and validation stages, but not so for southeastern Taiwan because the seasonal rainfall of the former are much more significantly correlated to the SST of selected sectors of the Pacific Ocean than the latter.
Mesoscale Surface Pressure and Temperature Features Associated with Bow Echoes
Authors: Adams-Selin Rebecca D. , Johnson Richard H.
Published: July 2009

This study examines observed mesoscale surface pressure, temperature, and wind features of bow echoes. Bow-echo events in the area of the Oklahoma Mesonet are selected for study to take advantage of high-resolution surface data. Thirty-six cases are identified using 2-km-resolution radar reflectivity data over a 4-yr period (2002–05); their surface features are interrogated using the mesonet data. Distinct surface features usually associated with squall lines, the mesohigh and cold pool, are found to also accompany bow echoes. A common surface pattern preceding bowing is identified. Prior to new bowing development, the mesohigh surges ahead of the convective line while the cold pool remains centered behind it. Surface winds shift to a ground-relative outflow pattern upon arrival of the mesohigh surge. Approximately 30 min later, a new bowing segment forms with its apex slightly to the left (with respect to the direction of system motion) of the mesohigh surge. The cold pool follows the convective line as it bows. This process is termed the “pressure surge–new bowing” cycle, and a conceptual model is presented. In one representative case, the surface signature of a gravity wave, identified through spatial and temporal filtering, is tracked. It is presumed to be generated by deep heating within the convective line. The wave moved at nearly 35 m s−1 and has heretofore been undetected in mesoanalysis studies. Two other distinct features, a sharp pressure rise and temperature drop, were also observed at all mesonet stations affected by the system. Possible explanations for these features in terms of a gravity current, gravity wave, or atmospheric bore are explored.