bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pyeongwee-San extract (KMP6): a new anti-allergic effect
Authors: Han Na-Ra , Kim Hyung-Min , Jeong Hyun-Ja 
Published: November 2011

Abstract

Objectives
The prevalence of allergic diseases is increasing due to rapid industrialization and changes in lifestyle. Pyeongwee-San (KMP6) is a traditional Korean medicine that has been used as a basic prescription for digestive disorders. This study investigated the efficacy of KMP6 and its component hesperidin on experimental allergic models.

Methods
The anti-allergic effect of KMP6 was studied against a compound 48/80-induced systemic anaphylactic reaction and the ear swelling response. In addition, a human mast cell line (HMC-1) was used to analyze the activity of histidine decarboxylase. Passive cutaneous anaphylaxis (PCA) from immunoglobulin E (IgE) was used.

Key findings
KMP6 and hesperidin inhibited the compound 48/80-induced systemic anaphylactic reaction and the ear swelling response as well as histamine release, intracellular calcium levels and tryptase release from rat peritoneal mast cells. KMP6 inhibited histidine decarboxylase activity in stimulated HMC-1 cells and macrophages. In addition, KMP6 inhibited the PCA reaction induced by IgE as well as the levels of IgE, interleukin (IL)-4, IL-5, IL-6 and IL-13 in serum from mice.

Conclusions
These results suggest that KMP6 may exert an anti-allergic effect through not only the inhibition of mast cell degranulation but also the inhibition of histamine synthesis.
Arteriolar Function in Visceral Adipose Tissue Is Impaired in Human Obesity
Authors: Farb Melissa G. , Ganley-Leal Lisa , Mott Melanie , Liang YanMei , Ercan Bahadir , Widlansky Michael E. , Bigornia Sherman J. , Fiscale Antonino J. , Apovian Caroline M. , Carmine Brian , Hess Donald T. , Vita Joseph A. , Gokce Noyan 
Published: November 2011

Objective—
The purpose of this study was to characterize the relationship between adipose tissue phenotype and depot-specific microvascular function in fat.

Methods and Results—

In 30 obese subjects (age 42±11 years, body mass index 46±11 kg/m
2
) undergoing bariatric surgery, we intraoperatively collected visceral and subcutaneous adipose tissue and characterized depot-specific adipose phenotypes. We assessed vasomotor function of the adipose microvasculature using videomicroscopy of small arterioles (75–250 μm) isolated from different fat compartments. Endothelium-dependent, acetylcholine-mediated vasodilation was severely impaired in visceral arterioles, compared to the subcutaneous depot (
P
<0.001 by ANOVA). Nonendothelium dependent responses to papaverine and nitroprusside were similar. Endothelial nitric oxide synthase inhibition with N
ω
-nitro-
l
-arginine methyl ester reduced subcutaneous vasodilation but had no effect on severely blunted visceral arteriolar responses. Visceral fat exhibited greater expression of proinflammatory, oxidative stress-related, hypoxia-induced, and proangiogenic genes; increased activated macrophage populations; and had a higher capacity for cytokine production ex vivo.

Conclusion—
Our findings provide clinical evidence that the visceral microenvironment may be intrinsically toxic to arterial health providing a potential mechanism by which visceral adiposity burden is linked to atherosclerotic vascular disease. Our findings also support the evolving concept that both adipose tissue quality and quantity may play significant roles in shaping cardiovascular phenotypes in human obesity.
Regulation of Peroxisome Proliferator–Activated Receptor-γ by Angiotensin II Via Transforming Growth Factor-β1–Activated p38 Mitogen-Activated Protein Kinase in Aortic Smooth Muscle Cells
Authors: Subramanian Venkateswaran , Golledge Jonathan , Heywood Elizabeth B. , Bruemmer Dennis , Daugherty Alan 
Published: November 2011

Objective—
Peroxisome proliferator–activated receptor-γ (PPARγ) ligands attenuate angiotensin II (Ang II)–induced atherosclerosis through interactions with vascular smooth muscle cell (VSMC)–specific PPARγ in hypercholesterolemic mice. Therefore, the purpose of this study was to determine the mechanism of Ang II–mediated intracellular regulation of PPARγ in VSMCs.

Methods and Results—

Incubation of cultured mouse aortic VSMCs with Ang II for 24 hours reduced abundance of PPARγ protein, mRNA, and transcriptional activity (
P
<0.001). This effect was attenuated by an angiotensin type 1 receptor antagonist, losartan. Ang II–induced PPARγ reduction was dependent on stimulation of transforming growth factor (TGF)-β1 as demonstrated using either a neutralizing antibody or small interfering RNA (siRNA). Ang II–induced TGF-β1 secretion was dependent on epidermal growth factor receptor kinase activation through reactive oxygen species production. Inhibition of p38 mitogen-activated protein kinase by SB203580 or siRNA inhibited both Ang II– and TGF-β1–induced PPARγ reduction. Blockade of TGF-β1 decreased p38 phosphorylation induced by Ang II. siRNA–mediated inhibition of histone deacetylase 3 attenuated p38-mediated reductions in PPARγ abundance.

Conclusion—
These findings suggest that Ang II decreases PPARγ abundance in cultured VSMCs via an angiotensin type 1 receptor–dependent secretion of TGF-β1 via phosphorylation of p38 mitogen-activated protein kinase and histone deacetylase 3.
The Acute Effects of Changes to AV Delay on BP and Stroke Volume
Authors: Manisty Charlotte H. , Al-Hussaini Ali , Unsworth Beth , Baruah Resham , Pabari Punam A. , Mayet Jamil , Hughes Alun D. , Whinnett Zachary I. , Francis Darrel P. 
Published: November 2011

Background—
The AV delay optimization of biventricular pacemakers (cardiac resynchronization therapy) may maximize hemodynamic benefit but consumes specialist time to conduct echocardiographically. Noninvasive BP monitoring is a potentially automatable alternative, but it is unknown whether it gives the same information and similar precision (signal/noise ratio). Moreover, the immediate BP increment on optimization has been reported to decay away: it is unclear whether this is the result of an (undesirable) decrease in stroke volume or a (desirable) compensatory relief of peripheral vasoconstriction.

Methods and Results—

To discriminate between these alternative mechanisms, we measured simultaneous beat-to-beat stroke volume (flow) using Doppler echocardiography, and BP using finger photoplethysmography, during and after AV delay changes from 40 to 120 ms in 19 subjects with cardiac pacemakers. BP and stroke volume both increased immediately (
P
<0.001, within 1 heartbeat). BP showed a clear decline a few seconds later (average rate, −0.65 mm Hg/beat;
r
=0.95 [95% CI, 0.86–0.98]); in contrast, stroke volume did not decline (
P
=0.87). The immediate BP increment correlated strongly with the stroke volume increment (
r
=0.74,
P
<0.001). The signal/noise ratio was 3-fold better for BP than stroke volume (6.8±3.5 versus 2.3±1.4;
P
<0.001).

Conclusions—
Improving AV delay immediately increases BP, but the effect begins to decay within a few seconds. Reassuringly, this is because of compensatory vasodilatation rather than reduction in cardiac function. Pacemaker optimization will never be reliable unless there is an adequate signal/noise ratio. Using BP rather than Doppler minimizes noise. The early phase (before vascular compensation) has the richest signal lode.
Implantable Cardioverter Defibrillator Therapy in Adults With Congenital Heart Disease
Authors: Koyak Zeliha , de Groot Joris R. , Van Gelder Isabelle C. , Bouma Berto J. , van Dessel Pascal F.H.M. , Budts Werner , van Erven Lieselot , van Dijk Arie P.J. , Wilde Arthur A.M. , Pieper Petronella G. , Sieswerda Gertjan T. , Mulder Barbara J.M. 
Published: November 2011

Background—
The value of implantable cardioverter defibrillators (ICDs) in adults with congenital heart disease (CHD) is unknown. We investigated the long-term outcome after ICD implantation and developed a simple risk stratification score for ICD therapy.

Methods and Results—

A total of 136 adults with CHD and ICD (mean age±SD, 41±13 years; 67% male) were identified from 10 tertiary referral centers in the Netherlands and Belgium. The indication for ICD implantation was primary prevention in 50% of patients. Diagnoses included tetralogy of Fallot (51%), septal defects (20%), (congenitally corrected) transposition of the great arteries (13%), and other (16%). Thirty-nine patients (29%) received appropriate ICD shocks during a median follow-up of 4.6 years. Secondary prevention indication (hazard ratio [HR], 3.6; 95% CI, 1.3–9.5;
P=
0.009), coronary artery disease (HR, 2.7; 95% CI, 1.0–7.2;
P=
0.042), and symptomatic nonsustained ventricular tachycardia (NSVT; HR, 9.1; 95% CI, 2.8–29.2;
P=
0.001) were associated with appropriate ICD shocks. A risk score was developed to evaluate the likelihood of appropriate ICD shocks. The 8-year survival curve to first appropriate shocks was 94%, 57%, and 26% for low-, intermediate-, and high-risk patients, respectively. In primary prevention, symptomatic NSVTs (HR, 8.0; 95% CI, 2.3–27.1;
P=
0.001) and subpulmonary ventricular dysfunction (HR, 3.0; 95% CI, 1.2–12.6;
P
=0.02) were associated with appropriate shocks in univariable analysis. Inappropriate shocks occurred in 41 patients (30%). In addition, 40 patients (29%) experienced 45 implantation-related complications.

Conclusions—
Adults with CHD and ICDs receive high rates of appropriate and effective shocks. Patients with secondary prevention indication, coronary artery disease, and symptomatic NSVT are at highest risk of receiving appropriate ICD shocks. ICD implantation is accompanied by considerable morbidity, including inappropriate shocks and procedure- related complications.
Niacin Inhibits Vascular Inflammation via the Induction of Heme Oxygenase-1
Authors: Wu Ben J. , Chen Kang , Barter Philip J. , Rye Kerry-Anne 
Published: November 2011

Background—
Heme oxygenase-1 (HO-1) is a cytoprotective protein whose expression is consistently associated with therapeutic benefits in a number of pathological conditions such as atherosclerotic vascular disease and inflammation. Niacin is a pleiotropic drug that slows the progression of coronary artery disease and increases serum levels of the HO-1 enzymatic product bilirubin. This study asks if the cardioprotective properties of niacin involve the induction of HO-1.

Methods and Results—
New Zealand White rabbits received chow or chow supplemented with 0.6% (wt/wt) niacin for 2 weeks. Acute vascular inflammation was induced in the animals by placing a nonocclusive silastic collar around the left common carotid artery. At 24 hours after collar implantation, serum bilirubin and vascular, liver, and spleen HO-1 messenger RNA levels were significantly increased. Vascular inflammation was decreased in the niacin-supplemented animals compared with control. Treatment of the animals with tin protoporphyrin-IX, a global HO inhibitor, or HO-1 small interfering RNA to knock down carotid artery HO-1 attenuated the ability of niacin to inhibit vascular inflammation. Treatment of cultured human coronary artery endothelial cells with niacin increased HO-1 expression by activating the nuclear factor-E2–related factor 2/p38 mitogen-activated protein kinase signaling pathway and inhibiting tumor necrosis factor α–induced endothelial inflammation. The antiinflammatory effects of niacin in human coronary artery endothelial cells were mimicked by bilirubin and abolished by incubation with tin protoporphyrin-IX and knock down of nuclear factor-E2–related factor 2.

Conclusions—
Niacin activates HO-1 in vivo and in vitro. Induction of HO-1 may be partly responsible for the vascular protective properties of niacin.
Assessment of Carotid Plaque Stability Based on the Dynamic Enhancement Pattern in Plaque Components With Multidetector CT Angiography
Authors: Horie Nobutaka , Morikawa Minoru , Ishizaka Shunsuke , Takeshita Tomonori , So Gohei , Hayashi Kentaro , Suyama Kazuhiko , Nagata Izumi 
Published: November 2011

Background and Purpose—
Recent studies have investigated plaque morphology to determine patients who are at high risk of carotid atherosclerosis. In this study, we investigated whether a difference in dynamic enhancement pattern in plaque components could be useful to assess plaque stability with multidetector CT angiography.

Methods—
Fifty-nine lesions with moderate to severe carotid atherosclerosis in 51 patients (33 symptomatic, 18 asymptomatic) were consecutively included. Early- and delayed-phase images were obtained in 3 equivalent axial slices with multidetector CT angiography. Hounsfield units (HU) in the early phase were subtracted from those in the delayed phase in plaques (ΔHU) and compared with clinical features, MRI-based plaque characteristics, and histological findings with 20 surgical specimens acquired from carotid endarterectomy.

Results—

The ΔHU was significantly higher in asymptomatic than that in symptomatic presentation (
P
=0.02). With MRI, a higher ΔHU was negatively correlated with signal intensity on T1-weighted imaging (
r
=−0.56,
P
<0.0001). Histology confirmed that ΔHU was positively correlated with fibrous tissue (
r
=0.67,
P
=0.001) and negatively correlated with a lipid-rich necrotic core with hemorrhage (
r
=−0.70,
P
<0.001). Moreover, less neovascularization and inflammation was found in plaques with a higher ΔHU.

Conclusions—
Delayed-phase images provide information regarding the dynamic change in contrast media from the early arterial phase. An increase in HU from the early phase on multidetector CT angiography indicates plaque stability with more fibrous tissue and a less lipid-rich necrotic core, intraplaque hemorrhage, and neovascularization.
Sulcal Effacement on Fluid Attenuation Inversion Recovery Magnetic Resonance Imaging in Hyperacute Stroke
Authors: Kim Suk Jae , Ha Yeon Soo , Ryoo Sookyung , Noh Hyun Jin , Ha Sam-Yeol , Bang Oh Young , Kim Gyeong-Moon , Chung Chin-Sang , Lee Kwang Ho 
Published: November 2011

Background and Purpose—
The clinical significance of sulcal effacement has been widely investigated in CT studies, but the results are controversial. In this study, we evaluated the presence of perisylvian sulcal effacement (PSE) on fluid attenuation inversion recovery MRI and hypothesized that PSE may be related to collateral flow status together with hyperintense vessels on fluid attenuation inversion recovery in hyperacute stroke. In addition, we investigated whether an association between PSE and clinical outcome could be found in these patients.

Methods—
Consecutive patients with acute middle cerebral artery infarcts within 6 hours of symptom onset were included. All patients had internal carotid artery or middle cerebral artery occlusion and underwent MRI including FLAIR. The presence of PSE and hyperintense vessels on fluid attenuation inversion recovery and the collateral status and occurrence of early recanalization (ER) on conventional angiography were evaluated.

Results—
Of 139 patients, 79 (56.8%) had PSE. Multivariate testing revealed PSE was independently associated with collateral status. The association between hyperintense vessels and collaterals was different depending on PSE. Compared to PSE-positive and ER-negative patients, PSE-negative and ER-negative patients (odds ratio, 4.11; 95% confidence interval, 1.12–15.17) and PSE-negative and ER-positive patients (odds ratio, 34.62; 95% confidence interval, 5.75–208.60), but not PSE-positive and ER-positive patients, were more likely to experience favorable clinical outcomes (modified Rankin Scale score ≤2 at 3 months).

Conclusions—
PSE is independently associated with collateral status in patients with acute middle cerebral artery stroke. Moreover, PSE in conjunction with recanalization status can predict clinical outcomes in these patients.
The Cerebellum Generates Motor-to-Auditory Predictions: ERP Lesion Evidence
Authors: Knolle Franziska , Schröger Erich , Baess Pamela , Kotz Sonja A. 
Published: November 2011

Abstract
Forward predictions are crucial in motor action (e.g., catching a ball, or being tickled) but may also apply to sensory or cognitive processes (e.g., listening to distorted speech or to a foreign accent). According to the “internal forward model,” the cerebellum generates predictions about somatosensory consequences of movements. These predictions simulate motor processes and prepare respective cortical areas for anticipated sensory input. Currently, there is very little evidence that a cerebellar forward model also applies to other sensory domains. In the current study, we address this question by examining the role of the cerebellum when auditory stimuli are anticipated as a consequence of a motor act. We applied an N100 suppression paradigm and compared the ERP in response to self-initiated with the ERP response to externally produced sounds. We hypothesized that sensory consequences of self-initiated sounds are precisely predicted and should lead to an N100 suppression compared with externally produced sounds. Moreover, if the cerebellum is involved in the generation of a motor-to-auditory forward model, patients with focal cerebellar lesions should not display an N100 suppression effect. Compared with healthy controls, patients showed a largely attenuated N100 suppression effect. The current results suggest that the cerebellum forms not only motor-to-somatosensory predictions but also motor-to-auditory predictions. This extends the cerebellar forward model to other sensory domains such as audition.
Temporal- and Spatial-Scale Dependence of Three CMIP3 Climate Models in Simulating the Surface Temperature Trend in the Twentieth Century
Authors: Sakaguchi Koichi , Zeng Xubin , Brunke Michael A. 
Published: November 2011

Abstract
Motivated by increasing interests in regional- and decadal-scale climate predictions, this study systematically analyzed the spatial- and temporal-scale dependence of the prediction skill of global climate models in surface air temperature (SAT) change in the twentieth century. The linear trends of annual mean SAT over moving time windows (running linear trends) from two observational datasets and simulations by three global climate models [Community Climate System Model, version 3.0 (CCSM3.0), Climate Model, version 2.0 (CM2.0), and Model E-H] that participated in CMIP3 are compared over several temporal (10-, 20-, 30-, 40-, and 50-yr trends) and spatial (5° × 5°, 10° × 10°, 15° × 15°, 20° × 20°, 30° × 30°, 30° latitudinal bands, hemispheric, and global) scales. The distribution of root-mean-square error is improved with increasing spatial and temporal scales, approaching the observational uncertainty range at the largest scales. Linear correlation shows a similar tendency, but the limited observational length does not provide statistical significance over the longer temporal scales. The comparison of RMSE to climatology and a Monte Carlo test using preindustrial control simulations suggest that the multimodel ensemble mean is able to reproduce robust climate signals at 30° zonal mean or larger spatial scales, while correlation requires hemispherical or global mean for the twentieth-century simulations. Persistent lower performance is observed over the northern high latitudes and the North Atlantic southeast of Greenland. Although several caveats exist for the metrics used in this study, the analyses across scales and/or over running time windows can be taken as one of the approaches for climate system model evaluations.
The Southern Ocean and Its Climate in CCSM4
Authors: Weijer Wilbert , Sloyan Bernadette M. , Maltrud Mathew E. , Jeffery Nicole , Hecht Matthew W. , Hartin Corinne A. , van Sebille Erik , Wainer Ilana , Landrum Laura 
Published: November 2011

AbstractThe new Community Climate System Model, version 4 (CCSM4), provides a powerful tool to understand and predict the earth’s climate system. Several aspects of the Southern Ocean in the CCSM4 are explored, including the surface climatology and interannual variability, simulation of key climate water masses (Antarctic Bottom Water, Subantarctic Mode Water, and Antarctic Intermediate Water), the transport and structure of the Antarctic Circumpolar Current, and interbasin exchange via the Agulhas and Tasman leakages and at the Brazil–Malvinas Confluence. It is found that the CCSM4 has varying degrees of accuracy in the simulation of the climate of the Southern Ocean when compared with observations. This study has identified aspects of the model that warrant further analysis that will result in a more comprehensive understanding of ocean–atmosphere–ice dynamics and interactions that control the earth’s climate and its variability.
Global Warming Effects on U.S. Hurricane Damage
Authors: Emanuel Kerry 
Published: November 2011

Abstract
While many studies of the effects of global warming on hurricanes predict an increase in various metrics of Atlantic basin-wide activity, it is less clear that this signal will emerge from background noise in measures of hurricane damage, which depend largely on rare, high-intensity landfalling events and are thus highly volatile compared to basin-wide storm metrics. Using a recently developed hurricane synthesizer driven by large-scale meteorological variables derived from global climate models, 1000 artificial 100-yr time series of Atlantic hurricanes that make landfall along the U.S. Gulf and East Coasts are generated for four climate models and for current climate conditions as well as for the warmer climate of 100 yr hence under the Intergovernmental Panel on Climate Change (IPCC) emissions scenario A1b. These synthetic hurricanes damage a portfolio of insured property according to an aggregate wind-damage function; damage from flooding is not considered here. Assuming that the hurricane climate changes linearly with time, a 1000-member ensemble of time series of property damage was created. Three of the four climate models used produce increasing damage with time, with the global warming signal emerging on time scales of 40, 113, and 170 yr, respectively. It is pointed out, however, that probabilities of damage increase significantly well before such emergence time scales and it is shown that probability density distributions of aggregate damage become appreciably separated from those of the control climate on time scales as short as 25 yr. For the fourth climate model, damages decrease with time, but the signal is weak.