bluuebunny/crossref_metadata_2025 huggingface dataset:
Physical Inactivity Rapidly Induces Insulin Resistance and Microvascular Dysfunction in Healthy Volunteers
Authors: Hamburg Naomi M. , McMackin Craig J. , Huang Alex L. , Shenouda Sherene M. , Widlansky Michael E. , Schulz Eberhard , Gokce Noyan , Ruderman Neil B. , Keaney John F. , Vita Joseph A.
Published: October 2007

Objectives—

Sedentary lifestyle increases the risk of cardiovascular disease and diabetes. Vascular dysfunction contributes to atherogenesis and has been linked to insulin resistance.

Methods and Results—

We measured insulin sensitivity by glucose tolerance test and vascular function by ultrasound and venous occlusion plethysmography in 20 healthy subjects (14 men, 6 women) at baseline and during 5 days of bed rest. Bed rest led to a 67% increase in the insulin response to glucose loading (
P
<0.001) suggesting increased insulin resistance and produced increases in total cholesterol and triglycerides. Bed rest led to decreased reactive hyperemia in the forearm (1317±404 to 1112±260 mL/min,
P
=0.01) and the calf (28.5±7.0 to 22.2±8.7 mL/min/dL,
P
=0.003) indicating impaired microvascular function. Bed rest decreased brachial artery diameter and increased systolic blood pressure suggesting increased basal arterial tone. There were no changes in circulating inflammatory markers arguing against systemic inflammation as a mechanism for vascular dysfunction in this setting.

Conclusions—

Physical inactivity was associated with the development of insulin resistance, dyslipidemia, increased blood pressure, and impaired microvascular function in healthy volunteers. Our findings may provide insight into the pathogenesis of vascular disease in sedentary individuals and emphasize that even short-term physical inactivity may have adverse metabolic and vascular consequences.
Aortic
Msx2-Wnt
Calcification Cascade Is Regulated by TNF-α–Dependent Signals in Diabetic
Ldlr
−/−
Mice
Authors: Al-Aly Ziyad , Shao Jian-Su , Lai Chung-Fang , Huang Emily , Cai Jun , Behrmann Abraham , Cheng Su-Li , Towler Dwight A.
Published: October 2007

Objective—

Aortic calcification is prevalent in type II diabetes (T2DM), enhancing morbidity and tracking metabolic syndrome parameters.
Ldlr
−/−
mice fed high-fat “Westernized” diets (HFD) accumulate aortic calcium primarily in the tunica media, mediated via osteogenic morphogens and transcriptional programs that induce aortic alkaline phosphatase (ALP). Because elevated TNF-α is characteristic of obesity with T2DM, we examined contributions of this inflammatory cytokine.

Methods and Results—

HFD promoted obesity, hyperglycemia, and hyperlipidemia, and upregulated serum TNF-α in
Ldlr
−/−
mice. Serum haptoglobin (inflammatory marker) was increased along with aortic expression of
BMP2
,
Msx2
,
Wnt3a
, and
Wnt7a
. Dosing with the TNF-α neutralizing antibody infliximab did not reduce obesity, hypercholesterolemia, or hyperglycemia; however, haptoglobin, aortic
BMP2
,
Msx2
,
Wnt3a
, and
Wnt7a
and aortic calcium accumulation were downregulated by infliximab. Mice with vascular TNF-α augmented by a transgene (
SM22-TNFαTg
) driven from the
SM22
promoter upregulated aortic
Msx2
,
Wnt3a
, and
Wnt7a.
Furthermore,
SM22-TNFαTg;TOPGAL
mice exhibited greater aortic β-galactosidase reporter staining versus
TOPGAL
sibs, indicating enhanced mural Wnt signaling. In aortic myofibroblast cultures, TNF-α upregulated
Msx2
,
Wnt3a
,
Wnt7a
, and
ALP. ALP
induction was inhibited by Dkk1, an antagonist of paracrine Wnt actions.

Conclusions—

TNF-α promote aortic
Msx2-Wnt
programs that contribute to aortic calcium accumulation in T2DM.
Novel Mechanism and Role of Angiotensin II–Induced Vascular Endothelial Injury in Hypertensive Diastolic Heart Failure
Authors: Yamamoto Eiichiro , Kataoka Keiichiro , Shintaku Haruo , Yamashita Takuro , Tokutomi Yoshiko , Dong Yi-Fei , Matsuba Shinji , Ichijo Hidenori , Ogawa Hisao , Kim-Mitsuyama Shokei
Published: October 2007

Objective—

The mechanism and role of angiotensin II–induced vascular endothelial injury is unclear. We examined the molecular mechanism of angiotensin (AII)-induced vascular endothelial injury and its significance for hypertensive diastolic heart failure.

Methods and Results—

We compared the effect of valsartan and amlodipine on Dahl salt-sensitive hypertensive rats (DS rats). Valsartan improved vascular endothelial dysfunction of DS rats more than amlodipine, by inhibiting endothelial apoptosis and eNOS uncoupling more. Moreover, valsartan inhibited vascular apoptosis signal-regulating kinase 1 (ASK1) more than amlodipine. Thus, AT1 receptor contributed to vascular endothelial apoptosis, eNOS uncoupling, and ASK1 activation of DS rats. Using ASK1
−/−
mice, we examined the causative role of ASK1 in endothelial apoptosis and eNOS uncoupling. AII infusion in wild-type mice markedly caused vascular endothelial apoptosis and eNOS uncoupling accompanied by vascular endothelial dysfunction, whereas these effects of AII were absent in ASK1
−/−
mice. Therefore, ASK1 participated in AII-induced vascular endothelial apoptosis and eNOS uncoupling. Using tetrahydrobiopterin, we found that eNOS uncoupling was involved in vascular endothelial dysfunction in DS rats with established diastolic heart failure.

Conclusion—

AII-induced vascular endothelial apoptosis and eNOS uncoupling were mediated by ASK1 and contributed to vascular injury in diastolic heart failure of salt-sensitive hypertension.
Activated Protein C Decreases Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand by an EPCR- Independent Mechanism Involving Egr-1/Erk-1/2 Activation
Authors: O’Brien Lee A. , Richardson Mark A. , Mehrbod Sean F. , Berg David T. , Gerlitz Bruce , Gupta Akanksha , Grinnell Brian W.
Published: October 2007

Background—

APC is an antithrombotic and antiinflammatory serine protease that plays an important role in vascular function. We report that APC can suppress the proapoptotic mediator TRAIL in human umbilical vein endothelial cells, and we have investigated the signaling mechanism.

Methods and Results—

APC inhibited endothelial TRAIL expression and secretion and its induction by cell activation. To explore the mechanism, we examined factors associated with TRAIL regulation and demonstrated that APC increased the level of EGR-1, a transcriptional factor known to suppress the TRAIL promoter. APC also induced a significant increase in phosphorylation of ERK-1/2, required to activate EGR-1 expression. Activation of ERK-1/2 was dependent on the protease activated receptor-1 (PAR-1), but independent of the endothelial protein C receptor (EPCR). Using siRNA, we found that the effect of APC on the EGR-1/ERK signaling required for TRAIL inhibition was dependent on the S1P1 receptor and S1P1 kinase.

Conclusions—

Our data suggest that APC may provide cytoprotective activity by activating the ERK pathway, which upregulates EGR-1 thereby suppressing the expression of TRAIL. Moreover, we provide evidence that APC can induce a cell signaling response through a PAR-1/S1P1-dependent but EPCR-independent mechanism.
Serum Matrix Metalloproteinase-8 Concentrations Are Associated With Cardiovascular Outcome in Men
Authors: Tuomainen Anita M. , Nyyssönen Kristiina , Laukkanen Jari A. , Tervahartiala Taina , Tuomainen Tomi-Pekka , Salonen Jukka T. , Sorsa Timo , Pussinen Pirkko J.
Published: October 2007

Objective—

In culture studies matrix metalloproteinase (MMP)-8 thins the protecting fibrous cap of the atherosclerotic plaque thereby increasing its vulnerability. Results on the association of serum MMP-8 concentrations and cardiovascular diseases (CVD) are, however, scarce and contradictory.

Methods and Results—

We analyzed the association between CVD or subclinical atherosclerosis and serum MMP-8 and tissue inhibitor of metalloproteinase-1 (TIMP-1) concentrations of 1018 men with the follow-up time of 10 years. MMP-8 concentrations or MMP-8/TIMP-1 ratios were higher in men with prevalent CVD or subclinical atherosclerosis at baseline than those without. In men free of CVD at baseline, MMP-8 concentrations associated with acute myocardial infarction, death from coronary heart disease (CHD), CVD, or from any cause with relative risks (RR) (95% CI) of 1.138 (1.009 to 1.284), 1.188 (1.034 to 1.365), 1.171 (1.026 to 1.338), and 1.136 (1.018 to 1.269), respectively, and MMP-8/TIMP-1 ratio with CHD death with an RR of 1.206 (1.028 to 1.414) per standard deviation (SD) increase. In men with no prevalent CVD but with subclinical atherosclerosis at baseline, elevated serum MMP-8 concentration predicted CVD death with an RR of 3.03 (1.09 to 8.44). TIMP-1 concentrations alone had no predictive value.

Conclusions—

The results indicate that serum MMP-8 concentrations are elevated in prevalent or subclinical atherosclerosis and associate with the worst cardiovascular outcome.
Hepatic PGC-1β Overexpression Induces Combined Hyperlipidemia and Modulates the Response to PPARα Activation
Authors: Lelliott Christopher J. , Ljungberg Anna , Ahnmark Andrea , William-Olsson Lena , Ekroos Kim , Elmgren Anders , Arnerup Gunnel , Shoulders Carol C. , Oscarsson Jan , Lindén Daniel
Published: October 2007

Objective—

Previous studies have indicated that the hyperlipidemia and gene expression changes induced by a short-term high-fat diet (HFD) are mediated through the peroxisome proliferator-activated receptor γ coactivator (PGC)-1β, and that in vitro both PGC-1β and PGC −1α increase PPARα-mediated transcriptional activities. Here, we examined the in vivo effects of these two coactivators in potentiating the lipid lowering properties of the PPARα agonist Wy14,643 (Wy).

Methods and Results—

C57BL/6 mice were fed chow or HFD and transduced with adenoviruses encoding PGC-1α or PGC-1β. On chow, hepatic PGC-1β overexpression caused severe combined hyperlipidemia including elevated plasma apolipoprotein B levels. Hepatic triglyceride secretion, DGAT1, and FAT/CD36 expression were increased whereas PPARα and hepatic lipase mRNA levels were reduced. PGC-1β overexpression blunted Wy-mediated changes in expression levels of PPARα and downstream genes. Furthermore, PGC-1β did not potentiate Wy-stimulated fatty acid oxidation in primary hepatocytes. PGC-1β and PGC-1α overexpression did not alter SREBP-1c, SREBP-1c target gene expression, nor hepatic triglyceride content. On HFD, PGC-1β overexpression decreased hepatic SREBP-1c, yet increased FAS and ACCα mRNA and plasma triglyceride levels.

Conclusions—

Hepatic PGC-1β overexpression caused combined hyperlipidemia independent of SREBP-1c activation. Hepatic PGC-1β overexpression reduced the potentially beneficial effects of PPARα activation on gene expression. Thus, inhibition of hepatic PGC-1β may provide a therapy for treating combined hyperlipidemia.
Propagated Endothelial Ca
2+
Waves and Arteriolar Dilation In Vivo
Authors: Tallini Yvonne N. , Brekke Johan Fredrik , Shui Bo , Doran Robert , Hwang Seong-min , Nakai Junichi , Salama Guy , Segal Steven S. , Kotlikoff Michael I.
Published: October 2007

To study endothelial cell (EC)– specific Ca
2+
signaling in vivo we engineered transgenic mice in which the Ca
2+
sensor GCaMP2 is placed under control of endogenous connexin40 (Cx40) transcription regulatory elements within a bacterial artificial chromosome (BAC), resulting in high sensor expression in arterial ECs, atrial myocytes, and cardiac Purkinje fibers. High signal/noise Ca
2+
signals were obtained in Cx40
BAC
-GCaMP2 mice within the ventricular Purkinje cell network in vitro and in ECs of cremaster muscle arterioles in vivo. Microiontophoresis of acetylcholine (ACh) onto arterioles triggered a transient increase in EC Ca
2+
fluorescence that propagated along the arteriole with an initial velocity of ≈116 μm/s (n=28) and decayed over distances up to 974 μm. The local rise in EC Ca
2+
was followed (delay, 830±60 ms; n=8) by vasodilation that conducted rapidly (mm/s), bidirectionally, and into branches for distances exceeding 1 mm. At intermediate distances (300 to 600 μm), rapidly-conducted vasodilation occurred without changing EC Ca
2+
, and additional dilation occurred after arrival of a Ca
2+
wave. In contrast, focal delivery of sodium nitroprusside evoked similar local dilations without Ca
2+
signaling or conduction. We conclude that in vivo responses to ACh in arterioles consists of 2 phases: (1) a rapidly-conducted vasodilation initiated by a local rise in EC Ca
2+
but independent of EC Ca
2+
signaling at remote sites; and (2) a slower complementary dilation associated with a Ca
2+
wave that propagates along the endothelium.
Dilated and Hypertrophic Cardiomyopathy Mutations in Troponin and α-Tropomyosin Have Opposing Effects on the Calcium Affinity of Cardiac Thin Filaments
Authors: Robinson Paul , Griffiths Peter J. , Watkins Hugh , Redwood Charles S.
Published: October 2007

Dilated cardiomyopathy and hypertrophic cardiomyopathy (HCM) can be caused by mutations in thin filament regulatory proteins of the contractile apparatus. In vitro functional assays show that, in general, the presence of dilated cardiomyopathy mutations decreases the Ca
2+
sensitivity of contractility, whereas HCM mutations increase it. To assess whether this functional phenomenon was a direct result of altered Ca
2+
affinity or was caused by altered troponin–tropomyosin switching, we assessed Ca
2+
binding of the regulatory site of cardiac troponin C in wild-type or mutant troponin complex and thin filaments using a fluorescent probe (2-[4′-{iodoacetamido}aniline]-naphthalene-6-sulfonate) attached to Cys35 of cardiac troponin C. The Ca
2+
-binding affinity (pCa
50
=6.57±0.03) of reconstituted troponin complex was unaffected by all of the HCM and dilated cardiomyopathy troponin mutants tested, with the exception of the troponin I Arg145Gly HCM mutation, which caused an increase (ΔpCa
50
=+0.31±0.05). However, when incorporated into regulated thin filaments, all but 1 of the 10 troponin and α-tropomyosin mutants altered Ca
2+
-binding affinity. Both HCM mutations increased Ca
2+
affinity (ΔpCa
50
=+0.41±0.02 and +0.51±0.01), whereas the dilated cardiomyopathy mutations decreased affinity (ΔpCa
50
=−0.12±0.04 to −0.54±0.04), which correlates with our previous functional in vitro assays. The exception was the troponin T Asp270Asn mutant, which caused a significant decrease in cooperativity. Because troponin is the major Ca
2+
buffer in the cardiomyocyte sarcoplasm, we suggest that Ca
2+
affinity changes caused by cardiomyopathy mutant proteins may directly affect the Ca
2+
transient and hence Ca
2+
-sensitive disease state remodeling pathways in vivo. This represents a novel mechanism for this class of mutation.
Inhibition of
N
-Ethylmaleimide–Sensitive Factor Protects Against Myocardial Ischemia/Reperfusion Injury
Authors: Calvert John W. , Gundewar Susheel , Yamakuchi Munekazu , Park Pierce C. , Baldwin William M. , Lefer David J. , Lowenstein Charles J.
Published: October 2007

Exocytosis of endothelial granules promotes thrombosis and inflammation and may contribute to the pathophysiology of early reperfusion injury following myocardial ischemia. TAT-NSF700 is a novel peptide that reduces endothelial exocytosis by inhibiting the ATPase activity and disassembly activity of
N
-ethylmaleimide–sensitive factor (NSF), a critical component of the exocytic machinery. We hypothesized that TAT-NSF700 would limit myocardial injury in an in vivo murine model of myocardial ischemia/reperfusion injury. Mice were subjected to 30 minutes of ischemia followed by 24 hours of reperfusion. TAT-NSF700 or the scrambled control peptide TAT-NSF700scr was administered intravenously 20 minutes before the onset of ischemia. Myocardial ischemia/reperfusion caused endothelial exocytosis, myocardial infarction, and left ventricular dysfunction. However, TAT-NSF700 decreased von Willebrand factor levels after myocardial ischemia/reperfusion, attenuated myocardial infarct size by 47%, and preserved left ventricular structure and function. These data suggest that drugs targeting endothelial exocytosis may be useful in the treatment of myocardial injury following ischemia/reperfusion.
Spatiotemporal Relationship Between Intracellular Ca
2+
Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts
Authors: Warren Mark , Huizar José F. , Shvedko Alexander G. , Zaitsev Alexey V.
Published: October 2007

Normal “master–slave” relationship between the action potential (AP) and intracellular Ca
2+
transient (Ca
i
T) is sometimes altered during ventricular fibrillation (VF). The nature of AP/Ca
i
T dissociation during VF and its role in inducing wavebreaks (WBs) remain unclear. We simultaneously mapped AP (RH237) and Ca
i
T (Rhod-2) during VF in blood-perfused pig hearts. We computed AP and Ca
i
T dominant frequency (DF) and Ca
i
T delay in each AP cycle. We identified WBs as singularity points in AP phase movies and sites of conduction block (CB) as sites where an AP wavefront failed to propagate. We analyzed spatiotemporal relationship between abnormal AP/Ca
i
T sequences and CB sites. We used a calcium chelator (BAPTA-AM) to abolish Ca
i
T and test its involvement in WB formation. During VF, the DF difference between AP and Ca
i
T was <10% of the respective values in 95% of pixels, and 80% of all Ca
i
T upstrokes occurred during the initial 25% of the excitation cycle. Aberrant sequences of AP and Ca
i
T occurred almost exclusively near CB sites but could be traced to normal wavefront sequences away from CB sites. Thus, apparent AP/Ca
i
T dissociation was largely attributable to spatial uncertainty of the absolute position of block of each wave. BAPTA-AM reduced Ca
i
T amplitude to 30.5±12.9% of control and the DF of AP from 12.2±1.6 to 10.4±1.3Hz (
P
<0.01), but did not significantly alter WB incidence (0.76±0.19 versus 0.72±0.19SP/mm
2
). These results do not support presence of spontaneous, non–voltage-gated Ca
i
Ts during VF and suggest that AP/Ca
i
T dissociation is a consequence rather than a cause of wave fragmentation.
C-Terminal Truncation of Connexin43 Changes Number, Size, and Localization of Cardiac Gap Junction Plaques
Authors: Maass Karen , Shibayama Junko , Chase Sharon E. , Willecke Klaus , Delmar Mario
Published: October 2007

Haplodeficient mice expressing carboxyl-terminally truncated Cx43 (K258stop/KO), instead of the wild-type Cx43 isoform, reach adulthood and reveal no abnormalities in heart morphology. Here, we have analyzed the expression of K258stop protein and the morphology of gap junctions in adult hearts of these mice. Coimmunofluorescence analysis revealed reduced juxtaposition of K258stop with other junctional proteins at the intercalated disc. Immunoprecipitation studies documented changes in the interaction with previously described Cx43 binding proteins. Quantitative transmission electron and confocal microscopy confirmed the localization of K258stop gap junctions to the periphery of the intercalated disc and further revealed an increase in the size of K258stop gap junction plaques and a reduction in their number. Dual whole cell patch clamp analysis confirmed that K258stop gap junctions were functional, with single channel properties similar to those described in exogenous systems. We conclude that the carboxyl-terminal domain of Cx43 (Cx43CT) is involved in regulating the localization, number and size of Cx43 plaques in vivo. Conversely, protein interactions or posttranslational modifications taking place within the Cx43CT are not required for the assembly of functional gap junctions in the intercalated disc.
Connexin45 Cannot Replace the Function of Connexin40 in Conducting Endothelium-Dependent Dilations Along Arterioles
Authors: Wölfle Stephanie E. , Schmidt Volker J. , Hoepfl Bernd , Gebert Andreas , Alcoléa Sébastien , Gros Daniel , de Wit Cor
Published: October 2007

Intercellular communication through gap junctions coordinates vascular tone by the conduction of vasomotor responses along the vessel wall. Gap junctions in arterioles are composed of different connexins (Cxs) (Cx40, Cx37, Cx45, Cx43), but it is unknown whether Cxs are interchangeable. We used mice with a targeted replacement of Cx40 by Cx45 (Cx40KI45) to explore whether Cx45 can functionally replace Cx40 in arterioles. Arterioles were locally stimulated using acetylcholine, bradykinin, adenosine, and K
+
in the cremaster of Cx40KI45, Cx40-deficient (Cx40ko), and wild-type mice, and diameter changes were assessed by intravital microscopy. Additionally, arterial pressure was measured by telemetry and Cx expression verified by immunofluorescence. Acetylcholine initiated a local dilation of a similar amplitude in all genotypes (≈50%), which was rapidly conducted to upstream sites (1200 μm distance) without attenuation in wild type. In marked contrast, the remote dilation was significantly reduced in Cx40ko (25±3%) and Cx40KI45 (24±2%). Likewise, dilations initiated by bradykinin application were conducted without attenuation up to 1200 μm in wild type but not in Cx40ko and Cx40KI45. Adenosine-induced dilations and K
+
-induced constrictions were conducted similarly with decaying amplitude in all genotypes. Arterial pressure was strongly elevated in Cx40ko (161±1 versus 116±2 mm Hg) but only moderately in Cx40KI45 (133±8 mm Hg). This demonstrates that Cx40 function is critical for the conduction of acetylcholine and bradykinin dilations and cannot be substituted by Cx45. Therefore, unique properties of Cx40 are required for endothelial signal conduction, whereas nonspecific restoration of communication maintains additional functions related to blood pressure control.
The 1997–98 Summer Rainfall Season in Southern Africa. Part I: Observations
Authors: Lyon Bradfield , Mason Simon J.
Published: October 2007

Following the onset of the strong El Niño of 1997–98 historical rainfall teleconnection patterns and dynamical model predictions both suggested an enhanced likelihood of drought for southern Africa, but widespread dry conditions failed to materialize. Results from a diagnostic study of NCEP–NCAR reanalysis data are reported here demonstrating how the large- and regional-scale atmospheric circulations during the 1997–98 El Niño differed from previous events. Emphasis is placed on the January–March 1998 season and comparisons with the strong 1982–83 El Niño, although composites of eight events occurring between 1950 and 2000 are also considered. In a companion paper, simulation runs from three atmospheric general circulation models (AGCMs), and forecasts from three fully coupled models are employed to investigate the extent to which the anomalous atmospheric circulation patterns during the 1997–98 El Niño may have been anticipated.

Observational results indicate that the 1997–98 El Niño displayed significant differences from both the 1982–83 episode and the composite event. An unusually strong Angola low, exceptionally high sea surface temperatures (SSTs) in the western Indian and eastern tropical South Atlantic Oceans, and an enhanced northerly moisture flux from the continental interior and the western tropical Indian Ocean all appear to have contributed to more seasonal rainfall in 1997–98 over much of the southern Africa subcontinent than in past El Niño events.
Changes of the Boreal Winter Hadley Circulation in the NCEP–NCAR and ECMWF Reanalyses: A Comparative Study
Authors: Song Hua , Zhang Minghua
Published: October 2007

Both the ECMWF and the NCEP–NCAR reanalyses show a strengthening of the atmospheric Hadley circulation in boreal winter over the last 50 years, but the intensification is much stronger in the ECMWF than in the NCEP–NCAR reanalysis. This study focuses on the difference of these trends in the two reanalyses. It is shown that trends in the Hadley circulation in the two reanalyses differ mainly over the tropical western Pacific. This difference is found to be consistent with respective trends of the atmospheric transport of moist static energy, longwave cloud radiative forcing, and upper-level clouds in the two reanalyses. Two independent datasets of upper-level cloud cover and sea level pressure from ship-based measurements are then used to evaluate the reanalyses over the tropical western Pacific. They are found to be more consistent with the trends in the NCEP–NCAR reanalysis than those in the ECMWF reanalysis. The results suggest a weakening of the vertical motion associated with the Hadley circulation in the tropical western Pacific.
Rapid Holocene Deglaciation of the Labrador Sector of the Laurentide Ice Sheet
Authors: Carlson Anders E. , Clark Peter U. , Raisbeck Grant M. , Brook Edward J.
Published: October 2007

Retreat of the Laurentide Ice Sheet (LIS) following the Last Glacial Maximum 21 000 yr BP affected regional to global climate and accounted for the largest proportion of sea level rise. Although the late Pleistocene LIS retreat chronology is relatively well constrained, its Holocene chronology remains poorly dated, limiting our understanding of its role in Holocene climate change and sea level rise. Here new 10Be cosmogenic exposure ages on glacially deposited boulders are used to date the final disappearance of the Labrador sector of the LIS (LS-LIS). These data suggest that following the deglaciation of the southeastern Hudson Bay coastline at 8.0 ± 0.2 cal ka BP, the southwestern margin of the LS-LIS rapidly retreated ∼600 km in 140 yr and most likely in ∼600 yr at a rate of ∼900 m yr−1, with final deglaciation by 6.8 ± 0.2 10Be ka. The disappearance of the LS-LIS ∼6.8 10Be ka and attendant reduction in freshwater runoff may have induced the formation of Labrador Deep Seawater, while the loss of the high albedo surface may have initiated the Holocene Thermal Maximum in eastern Canada and southern Greenland. Moreover, the rapid melting just prior to ∼6.8 10Be ka indicates that the remnant LIS may be the primary source of a postulated rapid rise in global sea level of ∼5 m that occurred sometime between 7.6 and 6.5 cal ka BP.
Zonal Jet Structure and the Leading Mode of Variability
Authors: Eichelberger Scott J. , Hartmann Dennis L.
Published: October 2007

An observational analysis of the Northern Hemisphere circulation during winter reveals that the leading mode of variability depends on longitude. In particular, the first EOF of the zonal-mean circulation differs over the Atlantic and Pacific sectors. These results provide motivation for a series of model runs where a simple GCM is used to investigate the effects of the zonal jet structure on the leading mode of variability in the Northern Hemisphere. Model results indicate that the leading mode of variability depends on the distance between the eddy-driven and subtropical jets. When the jets are well separated, the leading mode of variability describes latitudinal shifting of the eddy-driven jet. However, when the two jets are nearly collocated, pulsing of the combined jet dominates the variability. This change coincides with a weakening of the positive feedback between the eddies and zonal flow anomalies. These results provide a possible explanation for the reduced amplitude of the Northern Annular Mode in the Pacific sector relative to that in the Atlantic sector during Northern Hemisphere winter.
The ENSO–Asian Monsoon Interaction in a Coupled Ocean–Atmosphere GCM
Authors: Li Ying , Lu Riyu , Dong Buwen
Published: October 2007

In this study, the authors evaluate the (El Niño–Southern Oscillation) ENSO–Asian monsoon interaction in a version of the Hadley Centre coupled ocean–atmosphere general circulation model (CGCM) known as HadCM3. The main focus is on two evolving anomalous anticyclones: one located over the south Indian Ocean (SIO) and the other over the western North Pacific (WNP). These two anomalous anticyclones are closely related to the developing and decaying phases of the ENSO and play a crucial role in linking the Asian monsoon to ENSO. It is found that the HadCM3 can well simulate the main features of the evolution of both anomalous anticyclones and the related SST dipoles, in association with the different phases of the ENSO cycle.

By using the simulated results, the authors examine the relationship between the WNP/SIO anomalous anticyclones and the ENSO cycle, in particular the biennial component of the relationship. It is found that a strong El Niño event tends to be followed by a more rapid decay and is much more likely to become a La Niña event in the subsequent winter. The twin anomalous anticyclones in the western Pacific in the summer of a decaying El Niño are crucial for the transition from an El Niño into a La Niña. The El Niño (La Niña) events, especially the strong ones, strengthen significantly the correspondence between the SIO anticyclonic (cyclonic) anomaly in the preceding autumn and WNP anticyclonic (cyclonic) anomaly in the subsequent spring, and favor the persistence of the WNP anomaly from spring to summer. The present results suggest that both El Niño (La Niña) and the SIO/WNP anticyclonic (cyclonic) anomalies are closely tied with the tropospheric biennial oscillation (TBO). In addition, variability in the East Asian summer monsoon, which is dominated by the internal atmospheric variability, seems to be responsible for the appearance of the WNP anticyclonic anomaly through an upper-tropospheric meridional teleconnection pattern over the western and central Pacific.
Deep Convective System Evolution over Africa and the Tropical Atlantic
Authors: Futyan Joanna M. , Del Genio Anthony D.
Published: October 2007

In the tropical African and neighboring Atlantic region there is a strong contrast in the properties of deep convection between land and ocean. Here, satellite radar observations are used to produce a composite picture of the life cycle of convection in these two regions. Estimates of the broadband thermal flux from the geostationary Meteosat-8 satellite are used to identify and track organized convective systems over their life cycle. The evolution of the system size and vertical extent are used to define five life cycle stages (warm and cold developing, mature, cold and warm dissipating), providing the basis for the composite analysis of the system evolution. The tracked systems are matched to overpasses of the Tropical Rainfall Measuring Mission satellite, and a composite picture of the evolution of various radar and lightning characteristics is built up.

The results suggest a fundamental difference in the convective life cycle between land and ocean. African storms evolve from convectively active systems with frequent lightning in their developing stages to more stratiform conditions as they dissipate. Over the Atlantic, the convective fraction remains essentially constant into the dissipating stages, and lightning occurrence peaks late in the life cycle. This behavior is consistent with differences in convective sustainability in land and ocean regions as proposed in previous studies.

The area expansion rate during the developing stages of convection is used to provide an estimate of the intensity of convection. Reasonable correlations are found between this index and the convective system lifetime, size, and depth.
Impact of the Atlantic Warm Pool on the Summer Climate of the Western Hemisphere
Authors: Wang Chunzai , Lee Sang-ki , Enfield David B.
Published: October 2007

The Atlantic warm pool (AWP) is a large body of warm water that comprises the Gulf of Mexico, the Caribbean Sea, and the western tropical North Atlantic. Located to its northeastern side is the North Atlantic subtropical high (NASH), which produces the tropical easterly trade winds. The easterly trade winds carry moisture from the tropical North Atlantic into the Caribbean Sea, where the flow intensifies, forming the Caribbean low-level jet (CLLJ). The CLLJ then splits into two branches: one turning northward and connecting with the Great Plains low-level jet (GPLLJ), and the other continuing westward across Central America into the eastern North Pacific. The easterly CLLJ and its westward moisture transport are maximized in the summer and winter, whereas they are minimized in the fall and spring. This semiannual feature results from the semiannual variation of sea level pressure in the Caribbean region owing to the westward extension and eastward retreat of the NASH.

The NCAR Community Atmospheric Model and observational data are used to investigate the impact of the climatological annual mean AWP on the summer climate of the Western Hemisphere. Two groups of the model ensemble runs with and without the AWP are performed and compared. The model results show that the effect of the AWP is to weaken the summertime NASH, especially at its southwestern edge. The AWP also strengthens the summertime continental low over the North American monsoon region. In response to these pressure changes, the CLLJ and its moisture transport are weakened, but its semiannual feature does not disappear. The weakening of the easterly CLLJ increases (decreases) moisture convergence to its upstream (downstream) and thus enhances (suppresses) rainfall in the Caribbean Sea (in the far eastern Pacific west of Central America). Model runs show that the AWP’s effect is to always weaken the southerly GPLLJ. However, the AWP strengthens the GPLLJ’s northward moisture transport in the summer because the AWP-induced increase of specific humidity overcomes the weakening of southerly wind, and vice versa in the fall. Finally, the AWP reduces the tropospheric vertical wind shear in the main development region that favors hurricane formation and development during August–October.
The Plane-Parallel Albedo Bias of Liquid Clouds from MODIS Observations
Authors: Oreopoulos Lazaros , Cahalan Robert F. , Platnick Steven
Published: October 2007

The authors present the global plane-parallel shortwave albedo bias of liquid clouds for two months, July 2003 and January 2004. The cloud optical properties necessary to perform the bias calculations come from the operational Moderate Resolution Imaging Spectroradiometer (MODIS) Terra and MODIS Aqua level-3 datasets. These data, along with ancillary surface albedo and atmospheric information consistent with the MODIS retrievals, are inserted into a broadband shortwave radiative transfer model to calculate the fluxes at the atmospheric column boundaries. The plane-parallel homogeneous (PPH) calculations are based on the mean cloud properties, while independent column approximation (ICA) calculations are based either on 1D histograms of optical thickness or joint 2D histograms of optical thickness and effective radius. The (positive) PPH albedo bias is simply the difference between PPH and ICA albedo calculations. Two types of biases are therefore examined: 1) the bias due to the horizontal inhomogeneity of optical thickness alone (the effective radius is set to the grid mean value) and 2) the bias due to simultaneous variations of optical thickness and effective radius as derived from their joint histograms. The authors find that the global bias of albedo (liquid cloud portion of the grid boxes only) is ∼+0.03, which corresponds to roughly 8% of the global liquid cloud albedo and is only modestly sensitive to the inclusion of horizontal effective radius variability and time of day, but depends strongly on season and latitude. This albedo bias translates to ∼3–3.5 W m−2 of bias (stronger negative values) in the diurnally averaged global shortwave cloud radiative forcing, assuming homogeneous conditions for the fraction of the grid box not covered by liquid clouds; zonal values can be as high as 8 W m−2. Finally, the (positive) broadband atmospheric absorptance bias is about an order of magnitude smaller than the albedo bias. The substantial magnitude of the PPH bias underlines the importance of predicting subgrid variability in GCMs and accounting for its effects on cloud–radiation interactions.
Regional Climate Model Simulation of U.S.–Mexico Summer Precipitation Using the Optimal Ensemble of Two Cumulus Parameterizations
Authors: Liang Xin-Zhong , Xu Min , Kunkel Kenneth E. , Grell Georg A. , Kain John S.
Published: October 2007

The fifth-generation Pennsylvania State University–NCAR Mesoscale Model (MM5)-based regional climate model (CMM5) simulations of U.S.–Mexico summer precipitation are quite sensitive to the choice of Grell or Kain–Fritsch convective parameterization. An ensemble based on these two parameterizations provides superior performance because distinct regions exist where each scheme complementarily captures certain observed signals. For the interannual anomaly, the ensemble provides the most significant improvement over the Rockies, Great Plains, and North American monsoon region. For the climate mean, the ensemble has the greatest impact on skill over the southeast United States and North American monsoon region, where CMM5 biases associated with the individual schemes are of opposite sign. Results are very sensitive to the specific methods used to generate the ensemble. While equal weighting of individual solutions provides a more skillful result overall, considerable further improvement is achieved when the weighting of individual solutions is optimized as a function of location.
Gang Membership as a Risk Factor for Adolescent Violent Victimization
Authors: Taylor Terrance J. , Peterson Dana , Esbensen Finn-Aage , Freng Adrienne
Published: October 2007

Youth gangs and violence have received substantial scholarly and public attention during the past two decades. While most of the extant research on youth gang members has focused on their offending behaviors, few quantitative studies have been conducted to examine the link between gang membership and violent victimization. The current study uses data from a multi-site study of youth to explore potential factors related to this increased risk. These findings suggest that gang members are more likely to experience violent victimization, as well as greater frequency of victimization, than do non-gang members. Furthermore, gang membership remains a significant correlate of the annual prevalence of victimization net other individual, family, peer, school, and situational factors. The relationship, however, is complex and dependent upon the type of victimization examined.
Prosecutorial Discretion and the Imposition of Mandatory Minimum Sentences
Authors: Ulmer Jeffery T. , Kurlychek Megan C. , Kramer John H.
Published: October 2007

In Pennsylvania, the imposition of mandatory minimum sentences presents an important opportunity to examine relatively “pure” prosecutorial discretion over sentencing outcomes. The authors present a multilevel analysis of the prosecutorial decision to apply a mandatory minimum among mandatory-eligible offenders sentenced for drug crimes or as repeat, “three-strikes” offenders. They find that prosecutors' decisions to apply the mandatory minimum are significantly affected by the type and characteristics of offenses and guideline sentence recommendations, prior record, mode of conviction, and gender. They also find that Hispanic males are more likely to receive mandatory minimums and that Black–White differences in mandatory application increase with county percentage Black. The authors frame and interpret their analysis and findings in light of the uncertainty reduction theory of prosecutorial discretion, the view of courts as communities, and an integrative focal concerns perspective on criminal justice decision-making.
Pathways to Childlessness and Late-Life Outcomes
Authors: Dykstra Pearl A. , Wagner Michael
Published: October 2007

Via a simultaneous analysis of different life course pathways (marital, occupational, and childbearing histories) and different outcomes, this article addresses the question When does childlessness matter in late life and how? Survey data from Amsterdam ( N = 661) and Berlin, Germany ( N = 516) are used. Lifelong childlessness results in smaller networks among men and women in Amsterdam and Berlin, and in the Dutch sample it leads to higher income levels. Dutch men who have never had children and Dutch women who have outlived their children have relatively low life satisfaction levels. In Germany, marital history is a more powerful predictor of life satisfaction in old age than parental history. The findings attest to the importance of distinguishing lifelong childlessness from outliving one's children and of considering the consequences of childlessness for a variety of life domains.
Clinical Comparison of Fixation Methods for Patellar Bone Quadriceps Tendon Autografts in Anterior Cruciate Ligament Reconstruction
Authors: Gorschewsky Ottmar , Stapf Robert , Geiser Laurent , Geitner Ulrich , Neumann Wolfram
Published: October 2007

Background

Recently, the use of the quadriceps tendon transplant with bone block (patellar bone quadriceps tendon autografts) for anterior cruciate ligament reconstruction has increasingly been reported.

Hypothesis

Clinical results after the implantation of a patellar bone quadriceps tendon autograft fixed with cross-pins or screws will show no significant difference between the 2 techniques with regard to stability, function, and subjective satisfaction. Study Design: Cohort study; Level of evidence, 2.

Methods

Between 1998 and 2004, 193 patients with anterior cruciate ligament ruptures were implanted with a patellar bone quadriceps tendon autograft. For 100 of these patients, fixation was carried out using absorbable cross-pins, and for the remaining 93, fixation was carried out using absorbable screws. The results were evaluated by means of International Knee Documentation Committee, Noyes, and Lysholm scores, as well as KT-1000 arthrometer measurement and subjective satisfaction.

Results

The mean follow-up postoperative control period was 29 months. In the International Knee Documentation Committee overall evaluation, the pin group showed a significantly better result (P = .03). The values of the Noyes score produced no significant differences. The mean value of the Lysholm score was 94 points in the screw group and 89 points in the pin group (P < .001). Overall, 90% of the patients subjectively judged their conditions as good or very good.

Conclusion

With both operating processes examined, 80% to 90% of the cases achieved good to very good results. The use of cross-pins can be recommended for fixing patellar bone quadriceps tendon autografts.
Isolated Anterior Cruciate Ligament Reconstruction in Patients with Chronic Anterior Cruciate Ligament Insufficiency Combined with Grade II Valgus Laxity
Authors: Hara Kenji , Niga Sadao , Ikeda Hiroo , Cho Sadahiro , Muneta Takeshi
Published: October 2007

Background

There is no consensus about whether isolated anterior cruciate ligament reconstruction using multistrand hamstring tendon with nonoperative treatment for chronic medial collateral ligament injury is sufficient.

Purpose

To assess clinical outcome for patients with chronic anterior cruciate ligament injury and accompanying grade II valgus laxity who received medial hamstring anterior cruciate ligament reconstruction alone. Results were compared with those of patients with isolated chronic anterior cruciate ligament injury without valgus laxity.

Study Design

Cohort study; Level of evidence, 2.

Methods

Two hundred eighty-nine patients with isolated anterior cruciate ligament injury were compared with 53 patients with accompanying valgus laxity (minimum follow-up, 24 months). The following parameters were compared between the 2 groups at the last follow-up: range of motion, KT-1000 arthrometer value, pivot-shift test result, Lysholm knee scale, knee extensor muscle strength, return to sporting activities, subjective recovery, and International Knee Documentation Committee grade. Differences in clinical outcome were evaluated between those with preoperative International Knee Documentation Committee grade B and grade C and between those with grade A and grade B or C at final evaluation.

Results

Postoperative KT-1000 arthrometer value averaged 1.2 mm for those with isolated anterior cruciate ligament injury and 1.6 mm for those with accompanying valgus laxity (not significant, P = .281). There was no significant difference between these 2 groups regarding the other items. In patients with preoperative valgus laxity, KT-1000 arthrometer values at final evaluation between patients with preoperative grade B and C were not significantly different. The value for subjects with grade A at final evaluation was 1.3 mm and for those with grade B or C at final evaluation was 2.7 mm ( P = .065).

Conclusion

There was no clinically significant difference regarding outcome of anterior cruciate ligament multistrand hamstring reconstruction alone for 90% of patients with grade II valgus laxity who regained medial stability with nonoperative management compared with those who underwent the same anterior cruciate ligament reconstruction for an isolated anterior cruciate ligament tear.
Biomechanical and Anatomical Assessment after Knee Hyperextension Injury
Authors: Fornalski Stefan , McGarry Michelle H. , Csintalan Rick P. , Fithian Donald C. , Lee Thay Q.
Published: October 2007

Background

Knee hyperextension can be a serious and disabling injury in both the athletic and general patient population. Understanding the pathoanatomy and pathomechanics is critical for accurate surgical soft tissue reconstructions.

Purpose

To quantify the effects of knee hyperextension injury on knee laxity in a human cadaveric model and to qualitatively assess the anatomical injury pattern through surgical dissection.

Study Design

Descriptive laboratory study.

Methods

Six fresh-frozen cadaveric knees were rigidly mounted on a custom knee testing system that simulates clinical laxity tests. The knee laxity measurements consisted of anterior-posterior laxity, internal-external rotational laxity, and varus-valgus laxity using a custom testing setup and a Microscribe 3DLX system. The laxity data were collected at both 30° and 90° of knee flexion for the intact specimens and then after 15° and 30° hyperextension injury. After biomechanical assessment a detailed dissection was performed to document the injured structures in the knee. Repeated-measures analysis of variance with a Tukey post hoc test ( P < .05) was used for statistical comparison.

Results

The results from this study suggest progressive damage to translational and rotational knee soft-tissue restraints with increasing knee hyperextension. Knee hyperextension to 30° caused the most significant increase in anterior-posterior and rotational laxity. Anatomical dissections showed a general injury pattern to the posterolateral corner, partial femoral anterior cruciate ligament avulsion in 4 of 6 specimens, and no gross posterior cruciate ligament injuries.

Conclusion

Injuries to the posterolateral corner of the knee can result from isolated knee hyperextension.

Clinical Relevance

The clinician should be aware of the potential for posterolateral corner injuries with isolated knee hyperextension. This will allow early surgical planning and primary surgical repair.