bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intrinsic permeability of materials ranging from sand to rock-fill using natural air convection tests
Authors: Côté Jean , Fillion Marie-Hélène , Konrad Jean-Marie 
Published: May 2011

Air convection within coarse rock-fills enhances winter-time heat extraction from underlying soils. Modeling this phenomenon requires the knowledge of intrinsic permeability. This study focuses on the measurement of intrinsic permeability using natural air convection within a 1 m3 test cell. Upward heat flow conditions are applied to various specimens. Test results are analyzed using a theoretical solution of natural convection in a square enclosure. Four materials were studied, with effective particle sizes (d10) ranging from 90 to 150 mm and porosities ranging from 0.37 to 0.41. The results showed that intrinsic permeability increases with increasing d10. The experimental results were adequately predicted by the Kozeny–Carman and Chapuis equations. Only slight deviations were observed, which is considered acceptable given that these equations were developed for materials with much smaller values of d10. The experimental results of this study confirm the value of intrinsic permeability recently used in a study of natural convection within a rock-fill dam in northern Quebec, Canada.
FUNCTIONAL AND MORPHOLOGICAL EFFECTS OF INDIRECT GRADUAL ELONGATION OF PERIPHERAL NERVE: ELECTROPHYSIOLOGICAL AND MORPHOLOGICAL CHANGES AT DIFFERENT ELONGATION RATES
Authors: Kubota Shigeki , Nishiura Yasumasa , Hara Yuki , Saijilafu  , Abe Ichiro , Ochiai Naoyuki 
Published: May 2011

We investigated the neuropathy induced by leg lengthening histological evaluation using teased nerve fiber specimens and electrophysiological evaluation. Indirect elongation of the sciatic nerve associated with leg lengthening was performed at 1 and 3 mm/day over 30 mm in rats. Electrophysiological evaluation was performed immediately and 60 days after the end of elongation, teased nerve fiber specimens were prepared, and the mean axonal diameter was calculated. The electrophysiological results were more wrong, and the recovery was poorer, in the 3-mm than in the 1-mm group. In the 1-mm group, the nerve conduction velocity (NCV) and the duration of the compound nerve action potential (C-NAP) recovered to a level close to the intact side, but the decrease in the amplitude of the C-NAP persisted. In the teased fiber study, while paranodal demyelination was observed in both groups immediately after elongation, demyelination was decreased in the 1-mm group indicationg recovery compared to the 3-mm group. Paranodal demyelination caused by indirect nerve elongation is considered to have induced electrophysiological disorders.Electrophysiological and morphological damages appeared to be more severe according to elongation speed. The nerve disorder were remained even at 1 mm per day in 60 days.
ARTHROSCOPIC ASSISTED BONE GRAFTING FOR EARLY STAGES OF KIENBÖCK'S DISEASE
Authors: Pegoli L. , Ghezzi A. , Cavalli E. , Luchetti R. , Pajardi G. 
Published: May 2011

Kienböck's disease is known for its difficulty in being diagnosed and treated at early stages; option treatments are few and most of them quite aggressive. The author describes his experience with arthroscopic assisted lunate bone grafting. Three patients with diagnosis of stage I avascular necrosis of the lunate (average age: 45 years), were treated. Before surgical procedure, the patients underwent to a conservative treatment. After harvesting the bone graft from the volar surface of the radius, arthroscopic bone grafting was performed.At an average follow-up of 13.5 months (9–15), all the patients show a normal density of the lunate and no arthritic changes in radiographs. The MRI confirmed the lunate vascularity.The number of patients is definitely small, due also to the rarity of the disease and the difficulty in diagnosis, but, despite the very high learning curve, could be the proper first choice of treatment.
Integrated, Genome-Wide Screening for Hypomethylated Oncogenes in Salivary Gland Adenoid Cystic Carcinoma
Authors: Shao Chunbo , Sun Wenyue , Tan Marietta , Glazer Chad A. , Bhan Sheetal , Zhong Xiaoli , Fakhry Carole , Sharma Rajni , Westra William H. , Hoque Mohammad O. , Moskaluk Christopher A. , Sidransky David , Califano Joseph A. , Ha Patrick K. 
Published: May 2011

Abstract
Purpose: Salivary gland adenoid cystic carcinoma (ACC) is a rare malignancy that is poorly understood. To look for relevant oncogene candidates under the control of promoter methylation, an integrated, genome-wide screen was conducted.
Experimental Design: Global demethylation of normal salivary gland cell strains using 5-aza-2′-deoxycytidine (5-aza-dC) and trichostatin A (TSA), followed by expression array analysis was conducted. ACC-specific expression profiling was generated using expression microarray analysis of primary ACC and normal samples. Next, the two profiles were integrated to identify a subset of genes for further validation of promoter demethylation in ACC versus normal. Finally, promising candidates were further validated for mRNA, protein, and promoter methylation levels in larger ACC cohorts. Functional validation was then conducted in cancer cell lines.
Results: We found 159 genes that were significantly re-expressed after 5-aza-dC/TSA treatment and overexpressed in ACC. After initial validation, eight candidates showed hypomethylation in ACC: AQP1, CECR1, C1QR1, CTAG2, P53AIP1, TDRD12, BEX1, and DYNLT3. Aquaporin 1 (AQP1) showed the most significant hypomethylation and was further validated. AQP1 hypomethylation in ACC was confirmed with two independent cohorts. Of note, there was significant overexpression of AQP1 in both mRNA and protein in the paraffin-embedded ACC cohort. Furthermore, AQP1 was upregulated in 5-aza-dC/TSA–treated SACC83. Finally, AQP1 promoted cell proliferation and colony formation in SACC83.
Conclusions: Our integrated, genome-wide screening method proved to be an effective strategy for detecting novel oncogenes in ACC. AQP1 is a promising oncogene candidate for ACC and is transcriptionally regulated by promoter hypomethylation. Clin Cancer Res; 17(13); 4320–30. ©2011 AACR.
Expression Signatures of the Lipid-Based Akt Inhibitors Phosphatidylinositol Ether Lipid Analogues in NSCLC Cells
Authors: Zhang Chunyu , Elkahloun Abdel G. , Liao Hongling , Delaney Shannon , Saber Barbara , Morrow Betsy , Prendergast George C. , Hollander M. Christine , Gills Joell J. , Dennis Phillip A. 
Published: May 2011

Abstract
Activation of the serine/threonine kinase Akt contributes to the formation, maintenance, and therapeutic resistance of cancer, which is driving development of compounds that inhibit Akt. Phosphatidylinositol ether lipid analogues (PIA) are analogues of the products of phosphoinositide-3-kinase (PI3K) that inhibit Akt activation, translocation, and the proliferation of a broad spectrum of cancer cell types. To gain insight into the mechanism of PIAs, time-dependent transcriptional profiling of five active PIAs and the PI3K inhibitor LY294002 (LY) was conducted in non–small cell lung carcinoma cells using high-density oligonucleotide arrays. Gene ontology analysis revealed that genes involved in apoptosis, wounding response, and angiogenesis were upregulated by PIAs, whereas genes involved in DNA replication, repair, and mitosis were suppressed. Genes that exhibited early differential expression were partitioned into three groups; those induced by PIAs only (DUSP1, KLF6, CENTD2, BHLHB2, and PREX1), those commonly induced by PIAs and LY (TRIB1, KLF2, RHOB, and CDKN1A), and those commonly suppressed by PIAs and LY (IGFBP3, PCNA, PRIM1, MCM3, and HSPA1B). Increased expression of the tumor suppressors RHOB (RhoB), KLF6 (COPEB), and CDKN1A (p21Cip1/Waf1) was validated as an Akt-independent effect that contributed to PIA-induced cytotoxicity. Despite some overlap with LY, active PIAs have a distinct expression signature that contributes to their enhanced cytotoxicity. Mol Cancer Ther; 10(7); 1137–48. ©2011 AACR.
NFBD1/MDC1 Regulates Cav1 and Cav2 Independently of DNA Damage and p53
Authors: Wilson Kathleen A. , Colavito Sierra A. , Schulz Vincent , Wakefield Patricia Heffernan , Sessa William , Tuck David , Stern David F. 
Published: May 2011

Abstract
NFBD1/MDC1 is involved in DNA damage checkpoint signaling and DNA repair. NFBD1 binds to the chromatin component γH2AX at sites of DNA damage, causing amplification of ataxia telangiectasia-mutated gene (ATM) pathway signaling and recruitment of DNA repair factors. Residues 508–995 of NFBD1 possess transactivation activity, suggesting a possible role of NFBD1 in transcription. Furthermore, NFBD1 influences p53-mediated transcription in response to adriamycin. We sought to determine the role of NFBD1 in ionizing radiation (IR)–responsive transcription and if NFBD1 influences transcription independently of p53.
Using microarray analysis, we identified genes altered upon NFBD1 knockdown. Surprisingly, most NFBD1 regulated genes are regulated in both the absence and presence of IR, thus pointing toward a novel function for NFBD1 outside of the DNA damage response. Furthermore, NFBD1 knockdown regulated genes mostly independent of p53 knockdown. These genes are involved in pathways including focal adhesion signaling, carbohydrate metabolism, and insulin signaling.
We found that CAV1 and CAV2 mRNA and protein levels are reduced by both NFBD1 knockdown and knockout independently of IR and p53. NFBD1-depleted cells exhibit some similar phenotypes to Cav1-depleted cells. Furthermore, like Cav1-depletion, NFBD1 shRNA increases Erk phosphorylation. Thus, Cav1 could act as a mediator of the DNA-damage independent effects of NFBD1 in mitogenic signaling. Mol Cancer Res; 9(6); 766–81. ©2011 AACR.
A Detailed Cardiovascular Characterization of Obesity Without the Metabolic Syndrome
Authors: Lind Lars , Siegbahn Agneta , Ingelsson Erik , Sundström Johan , Ärnlöv Johan 
Published: May 2011

Objective—
Although obesity without metabolic disturbances has been regarded as harmless, we have recently shown that obese subjects without the metabolic syndrome (MetS) has an increased risk of cardiovascular (CV) disorders and mortality during long-term follow-up. To investigate the basis for that increased risk, we studied the impact of obesity without MetS on multiple markers of subclinical CV disease.

Methods and Results—

At age 70, 1016 subjects were investigated in the Prospective Investigation of the Vasculature in Uppsala Seniors study. According to body mass index (BMI)/MetS status, they were categorized as normal weight (BMI <25 kg/m
2
) without MetS (National Cholesterol Education Program criteria, n=319), normal weight with MetS (n=19), overweight (BMI 25 to 29.9 kg/m
2
) without MetS (n=333), overweight with MetS (n=94), obese (BMI ≥30 kg/m
2
) without MetS (n=102), and obese with MetS (n=118). Several different measurements of endothelial reactivity, arterial compliance (plethysmography and ultrasound), carotid artery atherosclerosis, and echocardiography were performed, and 7 markers of coagulation/fibrinolysis were measured. Subjects with obesity without MetS showed impaired vasoreactivity, a more echolucent carotid artery wall, increased left ventricular mass and function together with impaired coagulation/fibrinolysis compared with normal-weight subjects without the MetS (
P
<0.05 to 0.001). The majority of these disturbances were also seen in overweight subjects without the MetS.

Conclusion—
In contrast to some previous studies, our data do not support that obesity without MetS is a benign condition, because obesity without MetS was associated with impairments in multiple markers of subclinical CV disease. This was also the case for overweight subjects without the MetS.
Hepatic Steatosis, Obesity, and the Metabolic Syndrome Are Independently and Additively Associated With Increased Systemic Inflammation
Authors: Ndumele Chiadi E. , Nasir Khurram , Conceiçao Raquel D. , Carvalho Jose A.M. , Blumenthal Roger S. , Santos Raul D. 
Published: May 2011

Objective—
The goal of this study was to assess the independent and collective associations of hepatic steatosis, obesity, and the metabolic syndrome with elevated high-sensitivity C-reactive protein (hs-CRP) levels.

Methods and Results—
We evaluated 2388 individuals without clinical cardiovascular disease between December 2004 and December 2006. Hepatic steatosis was diagnosed by ultrasound, and the metabolic syndrome was defined using National Heart, Lung, and Blood Institute criteria. The cut point of ≥3 mg/L was used to define high hs-CRP. Multivariate logistic regression was used to assess the independent and collective associations of hepatic steatosis, obesity, and the metabolic syndrome with high hs-CRP. Steatosis was detected in 32% of participants, 23% met criteria for metabolic syndrome, and 17% were obese. After multivariate regression, hepatic steatosis (odds ratio [OR] 2.07; 95% CI 1.68 to 2.56), obesity (OR 3.00; 95% CI 2.39 to 3.80), and the metabolic syndrome (2.39; 95% CI 1.88 to 3.04) were all independently associated with high hs-CRP. Combinations of these factors were associated with an additive increase in the odds of high hs-CRP, with individuals with 1, 2, and 3 factors having ORs for high hs-CRP of 1.92 (1.49 to 2.48), 3.38 (2.50 to 4.57), and 4.53 (3.23 to 6.35), respectively.

Conclusion—
Hepatic steatosis, obesity, and the metabolic syndrome are independently and additively associated with increased odds of high hs-CRP levels.
Beta 2 Microglobulin and the Risk for Cardiovascular Events in Patients With Asymptomatic Carotid Atherosclerosis
Authors: Amighi Jasmin , Hoke Matthias , Mlekusch Wolfgang , Schlager Oliver , Exner Markus , Haumer Markus , Pernicka Elisabeth , Koppensteiner Renate , Minar Erich , Rumpold Helmut , Schillinger Martin , Wagner Oswald 
Published: May 2011

Background and Purpose—
Atherosclerosis is a chronic inflammatory disease. Ongoing inflammation is associated with elevated levels of beta 2 microglobulin (B2M). We investigated B2M levels in a large cohort of patients with carotid atherosclerosis for the occurrence of major adverse cardiovascular events.

Methods—
One thousand five of 1286 consecutive, neurologically asymptomatic patients with carotid atherosclerosis were followed for a median of 3 years (interquartile range, 2.5 to 3.5) for the occurrence of major adverse cardiovascular events, a composite of myocardial infarction, percutaneous coronary intervention, coronary bypass graft, stroke, and death.

Results—

We recorded 359 major cardiovascular events in 271 (27%) patients. B2M was significantly associated with the occurrence of major adverse cardiovascular events. With increasing quartiles of B2M, the adjusted hazard ratios were 1.19 (95% CI, 0.81 to 1.73), 1.51 (95% CI, 1.05 to 2.18), and 1.88 (95% CI, 1.26 to 2.79) compared with the lowest quartile, respectively (
P
<0.001). Adjusted hazard ratios for the occurrence of death, myocardial infarction, and stroke for increasing quartiles of B2M were 1.25 (95% CI, 0.92 to 1.70), 1.52 (95% CI, 1.12 to 2.06), and 1.62 (95% CI, 1.16 to 2.67) compared with the lowest quartile, respectively (
P
<0.001). Through statistical estimation of improvement in risk stratification, addition of B2M to baseline risk factors improved the risk stratification for major cardiovascular events, at least as much as high-sensitivity C-reactive protein or even better.

Conclusions—
B2M was independently and significantly associated with adverse cardiovascular outcome in patients with prevalent asymptomatic carotid atherosclerosis.
Phosphatidylinositol-3-Kinase Gamma Plays a Central Role in Blood–Brain Barrier Dysfunction in Acute Experimental Stroke
Authors: Jin Rong , Song Zifang , Yu Shiyong , Piazza Abigail , Nanda Anil , Penninger Josef M. , Granger D. Neil , Li Guohong 
Published: May 2011

Background and Purpose—
Phosphoinositide 3-kinase (PI3K)-γ is linked to inflammation and oxidative stress. This study was conducted to investigate the role of the PI3Kγ in the blood–brain barrier dysfunction and brain damage induced by focal cerebral ischemia/reperfusion.

Methods—
Wild-type and PI3Kγ knockout mice were subjected to middle cerebral artery occlusion (60 minutes) followed by reperfusion. Evans blue leakage, brain edema, infarct volumes, and neurological deficits were examined. Oxidative stress, neutrophil infiltration, and matrix metallopeptidase-9 were assessed. Activation of nuclear factor-κB and expression of proinflammatory and pro-oxidative genes were studied.

Results—
PI3Kγ deficiency significantly reduced blood–brain barrier permeability and brain edema formation, which were time-dependently correlated with preventing the degradation of the tight junction protein, claudin-5, and the basal lamina protein, collagen IV, and the phosphorylation of myosin light chain in brain microvessels. PI3Kγ deficiency suppressed ischemia/reperfusion-induced nuclear factor-κB p65 (Ser536) phosphorylation and the expression of the pro-oxidant enzyme NADPH oxidase (Nox1, Nox2, and Nox4) and proinflammatory adhesion molecules (E- and P-selectin, intercellular adhesion molecule-1) at different time points. These molecular changes were associated with significant inhibition of oxidative stress (superoxide production and malondialdehyde content), neutrophil infiltration, and matrix metallopeptidase-9 expression/activity in PI3Kγ knockout mice. Eventually, PI3Kγ deficiency significantly reduced infarct volumes and neurological scores at 24 hours after ischemia/reperfusion.

Conclusions—
Our results provide the first direct demonstration that PI3Kγ plays a significant role in ischemia/reperfusion-induced blood–brain barrier disruption and brain damage. Future studies need to explore PI3Kγ as a potential target for stroke therapy.
Using Administrative Databases to Calculate Framingham Scores Within a Large Health Care Organization
Authors: Ekundayo Olaniyi James , Vassar Stefanie D. , Williams Linda S. , Bravata Dawn M. , Cheng Eric M. 
Published: May 2011

Background and Purpose—
Framingham calculators are typically implemented in 1-on-1 settings to determine if a patient is at high risk for development of cardiovascular disease in the next 10 years. Because health care administrative datasets are including more clinical information, we explored how well administrative data-derived Framingham scores could identify persons who would have stroke develop in the next year.

Methods—
Using a nested case-control design, we compared all 313 persons who had a first-time stroke at 5 Veterans Administration Medical Centers with a random sample of 25 361 persons who did not have a first-time stroke in 2008. We compared Framingham scores and risk using administrative data available at the end of 2007.

Results—

Stroke patients had higher risk profile than controls: older age, higher systolic blood pressure and total cholesterol, more likely to have diabetes, cardiovascular disease, left ventricular hypertrophy, and more likely to use treatment for blood pressure (
P
<0.05). The mean Framingham generalized cardiovascular disease score (18.0 versus 14.5) as well as the mean Framingham stroke-specific score (13.2 versus 10.2) was higher for stroke cases than controls (both
P
<0.0001). The c-statistic for the generalized cardiovascular disease score was 0.68 (95% CI, 0.65–0.70) and for the stroke score was 0.64 (95% CI, 0.62–0.67).

Conclusions—
Persons who had a stroke develop in the next year had a worse Framingham risk profile, as determined by administrative data. Future studies should examine how to improve the stroke predictive tools and to identify the appropriate populations and uses for applying stroke risk predictive tools.
Understanding Reasons for Delay in Seeking Acute Stroke Care in an Underserved Urban Population
Authors: Hsia Amie W. , Castle Amanda , Wing Jeffrey J. , Edwards Dorothy F. , Brown Nina C. , Higgins Tara M. , Wallace Jasmine L. , Koslosky Sara S. , Gibbons M. Chris , Sánchez Brisa N. , Fokar Ali , Shara Nawar , Morgenstern Lewis B. , Kidwell Chelsea S. 
Published: May 2011

Background and Purpose—
Few patients arrive early enough at hospitals to be eligible for emergent stroke treatment. There may be barriers specific to underserved, urban populations that need to be identified before effective educational interventions to reduce delay times can be developed.

Methods—
A survey of respondents' likely action in a hypothetical stroke situation was given to 253 community volunteers in the catchment areas of a large urban community hospital. Concurrently, 100 structured interviews were conducted in the same hospital with patients with acute stroke or a proxy.

Results—
In this predominantly urban, black population, if faced with a hypothetical stroke, 89% of community volunteers surveyed said they would call 911 first, and few felt any of the suggested potential barriers applied to them. However, only 12% of patients with stroke interviewed actually called 911 first (OR, 63.9; 95% CI, 29.5 to 138.2). Instead, 75% called a relative/friend. Eighty-nine percent of patients with stroke reported significant delay in seeking medical attention, and almost half said the reason for the delay was thinking the symptoms were not serious and/or they would self-resolve. For those arriving by ambulance, only 25% did so because they thought it would be faster, whereas 35% cited having no other transportation options.

Conclusions—
In this predominantly black urban population, although 89% of community volunteers report the intent of calling 911 during a stroke, only 12% of actual patients with stroke did so. Further research is needed to determine and conquer the barriers between behavioral intent and actual behavior to call 911 for witnessed stroke.
Trigger Factors and Their Attributable Risk for Rupture of Intracranial Aneurysms
Authors: Vlak Monique H.M. , Rinkel Gabriel J.E. , Greebe Paut , van der Bom Johanna G. , Algra Ale 
Published: May 2011

Background and Purpose—
Little is known about activities that trigger rupture of an intracranial aneurysm. Knowledge on what triggers aneurysmal rupture increases insight into the pathophysiology and facilitates development of prevention strategies. We therefore aimed to identify and quantify trigger factors for aneurysmal rupture and to gain insight into the pathophysiology.

Methods—
During a 3-year period, 250 patients with aneurysmal subarachnoid hemorrhage completed a structured questionnaire regarding exposure to 30 potential trigger factors in the period soon before subarachnoid hemorrhage (hazard period) and for usual frequency and intensity of exposure. We assessed relative risks (RR) of rupture after exposure to triggers with the case-crossover design comparing exposure in the hazard period with the usual frequency of exposure. Additionally, we calculated population-attributable risks.

Results—
Eight triggers increased the risk for subarachnoid hemorrhage: coffee consumption (RR, 1.7; 95% CI, 1.2–2.4), cola consumption (RR, 3.4; 95% CI,1.5–7.9), anger (RR, 6.3; 95% CI, 4.6–25), startling (RR, 23.3; 95% CI, 4.2–128), straining for defecation (RR, 7.3; 95% CI, 2.9–19), sexual intercourse (RR, 11.2; 95% CI, 5.3–24), nose blowing (RR, 2.4; 95% CI, 1.3–4.5), and vigorous physical exercise (RR, 2.4; 95% CI, 1.2–4.2). The highest population-attributable risks were found for coffee consumption (10.6%) and vigorous physical exercise (7.9%).

Conclusions—
We identified and quantified 8 trigger factors for aneurysmal rupture. All triggers induce a sudden and short increase in blood pressure, which seems a possible common cause for aneurysmal rupture. Some triggers are modifiable, and further studies should assess whether reduction of exposure to these factors or measures preventing sudden increase in blood pressure decrease the risk of rupture in patients known to have an intracranial aneurysm.