bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of daily noise exposure monitoring on annual rates of hearing loss in industrial workers
Authors: Rabinowitz Peter M , Galusha Deron , Kirsche Sharon R , Cullen Mark R , Slade Martin D , Dixon-Ernst Christine 
Published: December 2010

ObjectivesOccupational noise-induced hearing loss (NIHL) is prevalent, yet evidence on the effectiveness of preventive interventions is lacking. The effectiveness of a new technology allowing workers to monitor daily at-ear noise exposure was analysed.MethodsWorkers in the hearing conservation program of an aluminium smelter were recruited because of accelerated rates of hearing loss. The intervention consisted of daily monitoring of at-ear noise exposure and regular feedback on exposures from supervisors. The annual rate of change in high frequency hearing average at 2, 3 and 4 KHz before intervention (2000–2004) and 4 years after intervention (2006–2009) was determined. Annual rates of loss were compared between 78 intervention subjects and 234 controls in other company smelters matched for age, gender and high frequency hearing threshold level in 2005.ResultsIndividuals monitoring daily noise exposure experienced on average no further worsening of high frequency hearing (average rate of hearing change at 2, 3 and 4 KHz=–0.5 dB/year). Matched controls also showed decelerating hearing loss, the difference in rates between the two groups being significant (p<0.0001). Analysis of a subset of intervention subjects matched to controls for initial rate of hearing loss showed a similar trend but the difference was not statistically significant (p=0.06).ConclusionMonitoring daily occupational noise exposure inside hearing protection with ongoing administrative feedback apparently reduces the risk of occupational NIHL in industrial workers. Longer follow-up of these workers will help determine the significance of the intervention effect. Intervention studies for the prevention of NIHL need to include appropriate control groups.
The contribution of major risk factors and job strain to occupational class differences in coronary heart disease incidence: the MONICA Brianza and PAMELA population-based cohorts
Authors: Ferrario Marco M , Veronesi Giovanni , Chambless Lloyd E , Sega Roberto , Fornari Carla , Bonzini Matteo , Cesana Giancarlo 
Published: December 2010

ObjectivesWe investigated the contribution of major coronary heart disease (CHD) risk factors and job strain to occupational class differences in CHD incidence in a pooled-cohort prospective study in northern Italy.Methods2964 men aged 25–74 from four northern Italian population-based cohorts were investigated at baseline and followed for first fatal or non-fatal CHD event (171 events). Standardised procedures were used for baseline risk factor measurements, follow-up and validation of CHD events. Four occupational classes were derived from the Erikson–Goldthorpe–Portocarero social class scheme: higher and lower professionals and administrators, non-manual workers, skilled and unskilled manual workers, and the self-employed. HRs were estimated with Cox models.ResultsAmong CHD-free subjects, with non-manual workers as the reference group, age-adjusted excess risks were found for professionals and administrators (+84%, p=0.02), the self-employed (+72%, p=0.04) and manual workers (+63%, p=0.04). The relationship was consistent across different CHD diagnostic categories. Adjusting for major risk factors only slightly reduced the reported excess risks. In a sub-sample of currently employed subjects, adjusting for major risk factors, sport physical activity and job strain reduced the excess risk for manual workers (relative change = −71.4%) but did not substantially modify the excess risks of professionals and administrators and the self-employed.ConclusionsIn our study, we found higher CHD incidence rates for manual workers, professionals and administrators, and the self-employed, compared to non-manual workers. When the entire spectrum of job categories is considered, the job strain model helped explain the CHD excess risk for manual workers but not for other occupational classes.
Real-time performance analysis of multiprocessor systems with shared memory
Authors: Schliecker Simon , Ernst Rolf 
Published: January 2011

Predicting timing behavior is key to reliable real-time system design and verification, but becomes increasingly difficult for current multiprocessor systems on chip. The integration of formerly separate functionality into a single multicore system introduces new intercore timing dependencies resulting from the common use of the now shared resources. This feedback of system timing on local timing makes traditional performance analysis approaches inappropriate.
This article presents a general methodology to model the shared resource traffic and consider its effect on the local task execution. The aggregate busy time captures the timing of multiple accesses to a shared memory far better than the traditional models that focus on the timing of individual events. An iterative approach is proposed to tackle the analysis dependencies that exist in systems with event-driven task activation and dynamic resource arbitration.
Anti-DLL4 Inhibits Growth and Reduces Tumor-Initiating Cell Frequency in Colorectal Tumors with Oncogenic KRAS Mutations
Authors: Fischer Marcus , Yen Wan-Ching , Kapoun Ann M. , Wang Min , O'Young Gilbert , Lewicki John , Gurney Austin , Hoey Timothy 
Published: December 2010

Abstract
KRAS mutations are frequent in colorectal cancer (CRC) and are associated with clinical resistance to treatment with the epidermal growth factor receptor (EGFR)–targeted monoclonal antibodies. Delta-like 4 ligand (DLL4) is an important component of the Notch signaling pathway and mediates stem cell self-renewal and vascular development. DLL4 inhibition in colon tumor cells reduces tumor growth and stem cell frequency. Considering the need for new drugs to treat colon cancers with oncogenic KRAS mutations, we examined in this study the efficacy of anti-DLL4 antibodies in KRAS mutant tumors in a panel of early passage colon tumor xenograft models derived from patients. Consistent with clinical findings, mutant KRAS colorectal xenograft tumors were insensitive to the EGFR therapeutic antibody cetuximab, whereas KRAS wild-type tumors responded to cetuximab. In contrast, anti-DLL4 was efficacious against both wild-type and mutant KRAS colon tumors as a single agent and in combination with irinotecan. Further analysis of mutant KRAS tumors indicated that the anti-DLL4/irinotecan combination produced a significant decrease in colon cancer stem cell frequency while promoting apoptosis in tumor cells. Our findings provide a rationale for targeting DLL4-Notch signaling for improved treatment of CRC patients with activating KRAS mutations. Cancer Res; 71(5); 1520–5. ©2010 AACR.
CXCR4 Promotes Oral Squamous Cell Carcinoma Migration and Invasion through Inducing Expression of MMP-9 and MMP-13 via the ERK Signaling Pathway
Authors: Yu Tao , Wu Yingying , Helman Joseph I. , Wen Yuming , Wang Changmei , Li Longjiang 
Published: January 2011

Abstract
The increased migration and invasion of oral squamous cell carcinoma cells are key events in the development of metastasis to the lymph nodes and distant organs. Although the chemokine receptor CXCR4 and its ligand, stromal cell–derived factor-1α, have been found to play an important role in tumor invasion, its precise role and potential underlying mechanisms remain largely unknown. In this study, we showed that knockdown of CXCR4 significantly decreased Tca8113 cells migration and invasion, accompanied with the reduction of MMP-9 and MMP-13 expression. Inhibition of ligand binding to CXCR4 by a specific antagonist TN14003, also led to reduced cancer cell migration and invasion. Because the degradation of the extracellular matrix and the basement membrane by proteases, such as matrix metalloproteinases (MMP) is critical for migration and invasion of cancer cells, we investigated the expression of several MMPs and found that the expression of functional MMP-9 and MMP-13 was selectively decreased in CXCR4 knockdown cells. More importantly, decreased cell migration and invasion of CXCR4 knockdown cells were completely rescued by exogenous expression of MMP-9 or MMP-13, indicating that the two MMPs are downstream targets of CXCR4-mediated signaling. Furthermore, we found the level of phosphorylated extracellular signal-regulated kinase (ERK) was significantly decreased in CXCR4-silenced cells, suggesting that ERK may be a potential mediator of CXCR4-regulated MMP-9 and MMP-13 expression in Tca8113 cells. Taken together, our results strongly suggest the underlying mechanism of CXCR4 promoting Tca8113 migration and invasion by regulating MMP-9 and MMP-13 expression perhaps via activation of the ERK signaling pathway. Mol Cancer Res; 9(2); 161–72. ©2011 AACR.
Systemic and Targeted Delivery of Semaphorin 3A Inhibits Tumor Angiogenesis and Progression in Mouse Tumor Models
Authors: Casazza Andrea , Fu Xi , Johansson Irja , Capparuccia Lorena , Andersson Fredrik , Giustacchini Alice , Squadrito Mario Leonardo , Venneri Mary Anna , Mazzone Massimiliano , Larsson Erik , Carmeliet Peter , De Palma Michele , Naldini Luigi , Tamagnone Luca , Rolny Charlotte 
Published: January 2011

Objective—
The role of semaphorins in tumor progression is still poorly understood. In this study, we aimed at elucidating the regulatory role of semaphorin 3A (SEMA3A) in primary tumor growth and metastatic dissemination.

Methods and Results—
We used 3 different experimental approaches in mouse tumor models: (1) overexpression of SEMA3A in tumor cells, (2) systemic expression of SEMA3A following liver gene transfer in mice, and (3) tumor-targeted release of SEMA3A using gene modified Tie2-expressing monocytes as delivery vehicles. In each of these experimental settings, SEMA3A efficiently inhibited tumor growth by inhibiting vessel function and increasing tumor hypoxia and necrosis, without promoting metastasis. We further show that the expression of the receptor neuropilin-1 in tumor cells is required for SEMA3A-dependent inhibition of tumor cell migration in vitro and metastatic spreading in vivo.

Conclusion—
In sum, both systemic and tumor-targeted delivery of SEMA3A inhibits tumor angiogenesis and tumor growth in multiple mouse models; moreover, SEMA3A inhibits the metastatic spreading from primary tumors. These data support the rationale for further investigation of SEMA3A as an anticancer molecule.
Primary Prevention of Sudden Cardiac Death in Silent Cardiac Sarcoidosis
Authors: Mehta Davendra , Mori Neil , Goldbarg Seth H. , Lubitz Steven , Wisnivesky Juan P. , Teirstein Alvin 
Published: December 2010

Background—
Cardiac involvement in sarcoidosis is often silent and may lead to sudden death. This study was designed to assess the value of programmed electric stimulation of the ventricle (PES) for risk stratification in patients with sarcoidosis and evidence of preclinical cardiac involvement on imaging studies.

Methods and Results—

Patients with biopsy-proven systemic sarcoidosis but without cardiac symptoms who had evidence of cardiac sarcoidosis on positron emission tomography (PET) or cardiac MRI (CMR) were included. All patients underwent baseline evaluation, echocardiographic assessment of left ventricular function, and programmed electric stimulation of the ventricle. Patients were followed for survival and arrhythmic events. Seventy-six patients underwent PES of the ventricle. Eight (11%) were inducible for sustained ventricular arrhythmias and received an implantable defibrillator. None of the noninducible patients received a defibrillator. Left ventricular ejection fraction was lower in patients with inducible ventricular arrhythmia (36.4±4.2% versus 55.8±1.5%,
P
<0.05). Over a median follow-up of 5 years, 6 of 8 patients in the group with inducible ventricular arrhythmias had ventricular arrhythmia or died, compared with 1 death in the negative group (
P
<0.0001).

Conclusions—
In patients with biopsy-proven sarcoidosis and evidence of cardiac involvement on PET or CMR alone, positive PES may help to identify patients at risk for ventricular arrhythmia. More importantly, patients in this cohort with a negative PES appear to have a benign course within the first several years following diagnosis. PES may help to guide the use of implantable cardioverter defibrillators in this population.
Regional Thicknesses and Thickening of Compacted and Trabeculated Myocardial Layers of the Normal Left Ventricle Studied by Cardiovascular Magnetic Resonance
Authors: Dawson Dana K. , Maceira Alicia M. , Raj Vimal J. , Graham Catriona , Pennell Dudley J. , Kilner Philip J. 
Published: December 2010

Background—
We used cardiovascular magnetic resonance (CMR) to study normal left ventricular (LV) trabeculation as a basis for differentiation from pathological noncompaction.

Methods and Results—

The apparent end-diastolic (ED) and end-systolic (ES) thicknesses and thickening of trabeculated and compacted myocardial layers were measured in 120 volunteers using a consistent selection of basal, mid, and apical CMR short-axis slices. All had a visible trabeculated layer in 1 or more segments. The compacted but not the trabeculated layer was thicker in men than in women (
P
<0.01 at ED and ES). When plotted against age, the trabeculated and compacted layer thicknesses demonstrated opposite changes: an increase of the compact layer after the fourth decade at both ED and ES (
P
<0.05) but a decrease of the trabeculated layer. There was age-related preservation of total wall thickness at ED but an increase at ES (
P
<0.05). The compacted layer thickened, whereas the trabeculated layer thinned with systole, but neither change differed between sexes. With age, the most trabeculated LV segments showed significantly greater systolic thinning of trabeculated layers and, conversely, greater thickening of the compact segments (
P
<0.05). Total wall thickening is neither sex nor age dependent. There were no sex differences in the trabeculated/compacted ratio at ES or ED, but the ES trabeculated/compacted ratio was smaller in older (50 to 79 years) versus younger (20 to 49 years) groups (
P
<0.05).

Conclusions—
We demonstrated age- and sex-related morphometric differences in the apparent trabeculated and compacted layer thicknesses and systolic thinning of the visible trabeculated layer that contrasts with compacted myocardial wall thickening.
Evaluation of Polymer-Based Comparator Drug-Eluting Stents Using a Rabbit Model of Iliac Artery Atherosclerosis
Authors: Nakazawa Gaku , Nakano Masataka , Otsuka Fumiyuki , Wilcox Josiah N. , Melder Robert , Pruitt Sean , Kolodgie Frank D. , Virmani Renu 
Published: January 2011

Background—
Although atherosclerotic models, especially in the rabbit, have existed for a long time, a comparative study of various drug-eluting stent (DES) implantations in atherosclerotic arteries have not been systematically studied.

Methods and Results—

New Zealand White rabbits (n=44) with induced atheroma received bilateral iliac artery stents: bare metal stent (BMS) (Driver) or a stent eluting zotarolimus (ZES) (Endeavor), sirolimus (SES) (Cypher), or everolimus (EES) (Xience V). After 28 days, tissues were harvested for histomorphometric analyses,
en face
analysis of endothelial coverage, and expression of endothelial nitric oxide synthase (eNOS). Area measurements of external elastic lamina and stent area were similar. Neointimal area was significantly less in all DES versus BMS, which was least in SES and EES; similar trends were noted for cell proliferation. Uncovered struts were greater for SES and EES and least in BMS, whereas ZES were in between and associated with the least fibrin. Macrophages of the neointima were significantly less for all DES relative to BMS. Plaque calcification underneath stents, however, was significantly greater in SES and ZES than in BMS. Although endothelial coverage in between struts was comparable between BMS and DES, there was significantly greater expression of eNOS in BMS and ZES relative to EES and SES.

Conclusions—
The rabbit atherosclerotic model of stenting showed delayed healing and significantly greater reduction of neointima following implantation of SES and EES; however, delayed healing was less in ZES with greater neointima (but less than BMS), endothelial regrowth, and eNOS expression.
Autoantibodies Against the Fibrinolytic Receptor, Annexin A2, in Cerebral Venous Thrombosis
Authors: Cesarman-Maus Gabriela , Cantú-Brito Carlos , Barinagarrementeria Fernando , Villa Rosario , Reyes Elba , Sanchez-Guerrero Jorge , Hajjar Katherine A. , Latorre Ethel Garcia 
Published: December 2010

Background and Purpose—
Cerebral venous thrombosis (CVT) may be a manifestation of underlying autoimmune disease. Antibodies against annexin A2 (anti-A2Ab) coincide with antiphospholipid syndrome, in which antiphospholipid antibodies (aPLA) are associated with thrombosis in any vascular bed. Annexin A2, a profibrinolytic receptor and binding site for β2-glycoprotein-I, the main target for aPLA, is highly expressed on cerebral endothelium. Here we evaluate the prevalence of anti-A2Ab in CVT.

Methods—
Forty individuals with objectively documented CVT (33 women and 7 men) and 145 healthy controls were prospectively studied for hereditary and acquired prothrombotic risk factors, classical aPLA, and anti-A2Ab.

Results—

One or more prothrombotic risk factors were found in 85% of CVT subjects, (pregnancy/puerperium in 57.5%, classical aPLA in 22.5%, and hereditary procoagulant risk factors in 17.5%). Anti-A2Ab (titer >3 SD) were significantly more prevalent in patients with CVT (12.5%) than in healthy individuals (2.1%,
P
<0.01, OR, 5.9).

Conclusions—
Anti-A2Ab are significantly associated with CVT and may define a subset of individuals with immune-mediated cerebral thrombosis.
White Matter Damage and the Effect of Matrix Metalloproteinases in Type 2 Diabetic Mice After Stroke
Authors: Chen Jieli , Cui Xu , Zacharek Alex , Cui Yisheng , Roberts Cynthia , Chopp Michael 
Published: December 2010

Background and Purpose—
Diabetes mellitus leads to a higher risk of ischemic stroke and worse outcome compared to the general population. However, there have been few studies on white matter (WM) damage after stroke in diabetes mellitus. We therefore investigated WM damage after stroke in mice with diabetes mellitus.

Methods—

BKS.Cg-
m
+/+
Lepr

db

/J
(db/db) type 2 diabetes mellitus mice and db
+
non-diabetes mellitus mice were subjected to middle cerebral artery occlusion. Functional outcome, immunostaining, zymography, Western blot, and polymerase chain reaction were used.

Results—

After stroke, mice with diabetes mellitus exhibited significantly increased lesion volume and brain hemorrhagic and neurological deficits compared to mice without diabetes mellitus. Bielshowsky silver, luxol fast blue, amyloid precursor protein, and NG2 expression were significantly decreased, indicating WM damage, and matrix metalloproteinase (MMP)-9 activity was significantly increased in the ischemic brain of mice with diabetes mellitus. Subanalysis of similar lesions in mice with and without diabetes mellitus demonstrated mice with diabetes mellitus had significantly increased WM damage than in mice without diabetes mellitus (
P
<0.05). To investigate the mechanism underlying diabetes mellitus-induced WM damage, oxygen–glucose deprivation-stressed premature oligodendrocyte and primary cortical neuron cultures were used. High glucose increased MMP-2, MMP-9, cleaved caspase-3 levels, and apoptosis, as well as decreased cell survival and dendrite outgrowth in cultured primary cortical neuron. High glucose increased MMP-9, cleaved caspase-3 level, and apoptosis, and decreased cell proliferation and cell survival in cultured oligodendrocytes. Inhibition of MMP by GM6001 treatment significantly decreased high glucose-induced cell death and apoptosis in cultured primary cortical neuron and oligodendrocytes but did not alter dendrite outgrowth in primary cortical neuron.

Conclusions—
Mice with diabetes mellitus have increased brain hemorrhage and show more severely injured WM than mice without diabetes mellitus after stroke. MMP-9 upregulated in mice with diabetes mellitus may exacerbate WM damage after stroke in mice with diabetes mellitus.
Soluble Glycoprotein VI Is Raised in the Plasma of Patients With Acute Ischemic Stroke
Authors: Al-Tamimi Mohammad , Gardiner Elizabeth E. , Thom Jim Y. , Shen Yang , Cooper Matthew N. , Hankey Graeme J. , Berndt Michael C. , Baker Ross I. , Andrews Robert K. 
Published: December 2010

Background and Purpose—
Ischemic stroke induced by thrombosis may be triggered by atherosclerotic plaque rupture and collagen-induced platelet activation. Collagen induces glycoprotein VI shedding.

Methods—
We measured plasma-soluble glycoprotein VI (sGPVI) by enzyme-linked immunosorbent assay in 159 patients with acute (<7-day) ischemic stroke and age/sex-matched community-based control subjects.

Results—

sGPVI was elevated in stroke compared with controls (
P
=0.0168). ORs were higher in Quartile 4 for stroke cases (
P
=0.0121), and sGPVI was significantly elevated in stroke associated with large artery disease across Quartiles 2 to 4 and small artery disease in Quartile 4. sGPVI decreased 3 to 6 months after antiplatelet treatment, consistent with elevated sGPVI due to platelet activation during the thrombotic event. sGPVI correlated with P-selectin (
P
=0.0007) and was higher in individuals with the GPVI
a
haplotype (
P
=0.024).

Conclusion—
Glycoprotein VI shedding is implicated in the pathology of acute ischemic stroke.
Variation in in vitro hatch of potato cyst nematodes in response to different potato cultivars inoculated with isolates of arbuscular mycorrhizal fungi
Authors: Haydock Patrick , Jones Peter , Deliopoulos Thomas 
Published: January 2011

AbstractSix potato (Solanum tuberosum) cultivars (Home Guard, Bintje, British Queen, Maris Piper, Pentland Dell and Saturna) were inoculated with Vaminoc (a commercial mixture of three selected arbuscular mycorrhizal fungal (AMF) isolates) and with two of the individual AMF isolates present in Vaminoc, Glomus intraradices (BioRize BB-E) and Glomus mosseae (isolate BEG 12). Root length colonisation by AMF at 6 weeks after shoot emergence ranged from 49 to 54%, with Vaminoc exhibiting the highest percentage. In comparison with control plants, AMF-inoculated plants accelerated the in vitro hatch (21% mean increase) of the potato cyst nematode (PCN) species Globodera pallida (but not of G. rostochiensis) in potato root leachate collected 3 weeks after shoot emergence. The effects of mycorrhization on PCN hatch were broadly similar across the six potato cultivars. This consistency supports the potential use of AMF inoculation of potato plants as part of an integrated pest management strategy for G. pallida.