bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acute Hypertriglyceridemia Induces Platelet Hyperactivity That is Not Attenuated by Insulin in Polycystic Ovary Syndrome
Authors: Aye Myint Myint , Kilpatrick Eric S. , Aburima Ahmed , Wraith Katie S. , Magwenzi Simbarashe , Spurgeon B. , Rigby Alan S. , Sandeman Derek , Naseem Khalid M. , Atkin Stephen L. 
Published: March 2014

Background

Atherothrombosis is associated with platelet hyperactivity. Hypertriglyceridemia and insulin resistance (
IR
) are features of polycystic ovary syndrome (
PCOS
). The effect of induced hypertriglyceridemia on
IR
and platelet function was examined in young women with
PCOS
.

Methods and Results

Following overnight fasting, 13
PCOS
and 12 healthy women were infused with saline or 20% intralipid for 5 hours on separate days. Insulin sensitivity was measured using a hyperinsulinemic euglycaemic clamp in the final 2 hours of each infusion. Platelet responses to adenosine diphosphate (
ADP
) and prostacyclin (
PGI
2
) were measured by flow cytometric analysis of platelet fibrinogen binding and P‐selectin expression using whole blood taken during each infusion (at 2 hours) and at the end of each clamp. Lipid infusion increased triglycerides and reduced insulin sensitivity in both controls (median, interquartile range ) (5.25 [3.3, 6.48] versus 2.60 [0.88, 3.88] mg kg
−1
min
−1
,
P
<0.001) and
PCOS
(3.15 [2.94, 3.85] versus 1.06 [0.72, 1.43] mg kg
−1
min
−1
,
P
<0.001). Platelet activation by
ADP
was enhanced and ability to suppress platelet activation by
PGI
2
diminished during lipid infusion in both groups when compared to saline. Importantly, insulin infusion decreased lipid‐induced platelet hyperactivity by decreasing their response to 1 μmol/L
ADP
(78.7% [67.9, 82.3] versus 62.8% [51.8, 73.3],
P
=0.02) and increasing sensitivity to 0.01 μmol/L
PGI
2
(67.6% [39.5, 83.8] versus 40.9% [23.8, 60.9],
P
=0.01) in controls, but not in
PCOS
.

Conclusion

Acute hypertriglyceridemia induced IR, and increased platelet activation in both groups that was not reversed by insulin in
PCOS
subjects compared to controls. This suggests that platelet hyperactivity induced by acute hypertriglyceridemia and
IR
could contribute athero‐thrombotic risk.

Clinical Trial Registration
URL: www.isrctn.org. Unique Identifier: ISRCTN42448814.
Elites in Hard Times: The Hungarian Case in Comparative Conceptual Framework
Authors: Lengyel György 
Published: March 2014

AbstractHungary was seriously hit by the financial crisis of 2008. This article investigates how the Hungarian governing elites exploit the space of maneuvering in crisis management. One way to mitigate anti-government mass sentiments is the rhetoric of national self-defense. Besides these ideological tools, fundamental changes in the institutional setting and elite composition are on the agenda in Hungary. How these government responses can be analyzed by tools of the new elite paradigm and by concepts of comparative political institutionalism like majoritarian vs. consensual democracy, or simulated democracy and competitive authoritarianism are the major questions touched upon in the paper. We test the applicability of these concepts on the Hungarian political scene and investigate the efficiency of elites’ efforts concerning uncertainty reduction.
Clinical Outcomes Do Not Support Arthroscopic Posterior Capsular Release in Addition to Anterior Release for Shoulder Stiffness
Authors: Kim Yang-Soo , Lee Hyo-Jin , Park In-Joo 
Published: March 2014

Background: Arthroscopic capsular release is an effective treatment for shoulder stiffness, yet its extent is controversial. Purpose: To compare the clinical outcomes of arthroscopic capsular release in patients with and without posterior extended capsular release for shoulder stiffness. Study Design: Randomized controlled trial; Level of evidence, 1. Methods: Between January 2008 and March 2011, 75 patients who underwent arthroscopic capsular release for shoulder stiffness were enrolled and randomized into 2 groups. In group I (n = 37), capsular release was performed, including release of the rotator interval and anterior and inferior capsule. In group II (n = 38), capsular release was extended to the posterior capsule. The American Shoulder and Elbow Surgeons score, Simple Shoulder Test, visual analog scale for pain, and range of motion (ROM) were used for the evaluation before surgery and at 3, 6, and 12 months after surgery and at the last follow-up. Results: Preoperative demographic data of age, sex, symptom duration, and clinical outcomes showed no significant differences ( P > .05). The average follow-up was 18.4 months. Both groups showed significantly increased ROM at the last follow-up compared with preoperative ROM ( P < .05). At the last follow-up, no statistical differences were found ( P > .05) between groups I and II in American Shoulder and Elbow Surgeons score (91.3 vs 79.5), Simple Shoulder Test (83.3 vs 83.3), and visual analog scale (1.5 vs 2.2). There were also no statistical differences between the 2 groups at the last follow-up ( P > .05) in ROM: forward flexion, 145.2° vs 143.3°; external rotation with 90° of abduction, 88.1° vs 86.2°; external rotation at side, 88.9° vs 82.9°; and internal rotation, 9.1° vs 8.3°. Conclusion: Posterior extended capsular release might not be necessary in arthroscopic surgery for shoulder stiffness.
Infliximab attenuates inflammatory osteolysis in a model of periodontitis in Wistar rats
Authors: Gonçalves Davi C , Evangelista Rakel C , da Silva Rafael R , Santos Maria JS , Silva Francisco S , Aragão Karoline S , Brito Gerly AC , Lucena Herene BM , Leitão Renata C , Oriá Reinaldo B 
Published: March 2014

Periodontitis is a chronic inflammatory disease related to tooth loss in adults. Infliximab is a chimeric monoclonal antibody against TNF-α and is prescribed for the treatment of systemic inflammatory diseases. This study aimed to investigate the role of infliximab on experimental periodontal disease (EPD). EPD was induced by passing a 3.0 nylon thread around the upper left second molar in Wistar rats. Animals were either treated with intravenous infliximab (1, 5, 7, and 10 mg/kg) or saline solution 30 min before the periodontitis induction and were followed until they were sacrificed on the 11th day. A subset of rats was euthanized on the third day for analysis of gingival myeloperoxidase (MPO) and the blood MPO granulocyte index. In addition, we analyzed the bone loss index (BLI), the periodontal histopathological score, and the periodontal collagen network using confocal microscopy. We also analyzed metalloproteinase-1/-8, RANK, RANK-L, and osteoprotegerin in maxillary tissue by immunohistochemistry Gingival MPO, IL-1β, TNF-α were measured by ELISA. EPD caused leukocytosis, significant increases in BLI and gingival pro-inflammatory cytokines and cell infiltrates, with worse histopathological scores and periodontal collagen derangement. Infliximab (5 mg/kg) reduced granulocyte blood counts, gingival IL-1β, TNF-α, and MPO levels, diminished MMP-1/-8, RANK, and RANK-L bone immunolabeling with better periodontal histopathological scores and collagen network in comparison with the challenged saline group. We concluded that infliximab had significant anti-inflammatory and bone-protective effects in Wistar rats challenged by periodontitis.
A talin mutant that impairs talin-integrin binding in platelets decelerates αIIbβ3 activation without pathological bleeding
Authors: Stefanini Lucia , Ye Feng , Snider Adam K. , Sarabakhsh Kasra , Piatt Raymond , Paul David S. , Bergmeier Wolfgang , Petrich Brian G. 
Published: March 2014

Key PointsMice expressing a talin(L325R) mutant that binds to, but does not activate integrin αIIbβ3, have impaired hemostasis. Talin(W359A) reduces integrin binding, decelerates integrin activation and protects mice from thrombosis without pathological bleeding.
Monitoring early lung disease in cystic fibrosis: where are we now?
Authors: Duncan Julie A. , Aurora Paul 
Published: March 2014

Educational aimsTo understand which techniques are available to monitor early lung disease in cystic fibrosis, recognise difficulties inherent to each measure, and describe the use of tests in clinical practice or interventional trials.SummaryIt is a particular challenge to detect and monitor lung disease in children younger than 6 years old. Various methods exist that can reveal abnormality in young children, but each technique presents difficulties on performing the test or interpreting results. Most children with cystic fibrosis are now diagnosed shortly after birth, but it is still unclear how to evaluate new therapies, or at what age to initiate them. This review summarises current options for monitoring early disease, limitations of individual techniques and how evidence to date influences their use in research and clinical practice.Key pointsLung disease remains the major cause of morbidity and mortality in cystic fibrosisDespite clear improvements in outcomes such as nutrition, the benefit of early diagnosis by newborn screening on pulmonary health in cystic fibrosis has yet to be proven.Early lung disease is challenging to detect and monitor in young children with cystic fibrosis, but there is an urgent requirement to define useful outcome measures in this population, particularly as new treatments emerge.Many techniques are available, but difficulties with measurement or interpretation must be recognised when appraising past studies, considering their use in practice or as endpoints in clinical trials.There is no superior monitoring test at present, but emerging evidence from longitudinal studies in children with cystic fibrosis will help define which are most useful.
Support Healthy Lungs for Life: holding a spirometry event
Authors: Powell Pippa , Masefield Sarah , Anderson Lauren , Fletcher Monica 
Published: March 2014

SummaryThe aim of this article is to introduce you to the new European Respiratory Society (ERS)/European Lung Foundation (ELF) initiative “Healthy Lungs for Life”, and to provide you with ideas and guidance on ways that you can join in and take part in this exciting campaign. The article will focus on spirometry and how running a testing event in your community can help put lung health at the forefront of public thinking.
Association of Trypanosoma cruzi infection with risk factors and electrocardiographic abnormalities in northeast Mexico
Authors: Molina-Garza Zinnia Judith , Rosales-Encina José Luis , Mercado-Hernández Roberto , Molina-Garza Daniel P , Gomez-Flores Ricardo , Galaviz-Silva Lucio 
Published: March 2014

Abstract

Background
American trypanosomiasis is a major disease and public health issue, caused by the protozoan parasite Trypanosoma cruzi. The prevalence of T. cruzi has not been fully documented, and there are few reports of this issue in Nuevo Leon. The aim of this study was to update the seroprevalence rate of T. cruzi infection, including an epidemiological analysis of the risk factors associated with this infection and an electrocardiographic (ECG) evaluation of those infected.

Methods
Sera from 2,688 individuals from 10 municipalities in the state of Nuevo Leon, Mexico, were evaluated using an enzyme-linked immunosorbent assay and an indirect hemagglutination assay. An ECG case–control study was performed in subjects seropositive for T. cruzi and the results were matched by sex and age to seronegative residents of the same localities. A univariate analysis with χ2 and Fisher’s exact tests was used to determine the association between seropositivity and age (years), sex, and ECG changes. A multivariate analysis was then performed to calculate the odd ratios between T. cruzi seropositivity and the risk factors.

Results
The seropositive rate was 1.93% (52/2,688). In the ECG study, 22.85% (8/35) of the infected individuals exhibited ECG abnormalities. Triatoma gerstaeckeri was the only vector reported. The main risk factors were ceiling construction material (P ≤ 0.0024), domestic animals (P ≤ 0.0001), and living in rural municipalities (P ≤ 0.0025).

Conclusions
These findings demonstrate a 10-fold higher prevalence of Chagas disease than previously reported (0.2%), which implies a serious public health threat in northeastern Mexico. The epidemiological profile established in this study differs from that found in the rest of Mexico, where human populations live in close proximity to domiciliary triatomines.
Androgen receptor CAG repeats, non-random X chromosome inactivation, and loss of heterozygosity at Xq25 in relation to breast cancer risk
Authors: Chen Hui-Tzu , Wu Yao-Chung , Chen Shou-Tung , Tsai Hsien-Chang , Chien Yi-Chih 
Published: March 2014

Abstract

Background
The aim of this study was to examine the association of non-random X chromosome inactivation (XCI) and loss of heterozygosity (LOH) at Xq25 with breast cancer development.

Methods
Seventy-nine breast cancer patients, 39 female lung cancer patients, 30 other cancer patients and 77 healthy females were analysed for LOH using a panel of 11 microsatellite markers spanning Xq25. The androgen receptor (AR) gene was chosen as an XCI marker.

Results
LOH of at least one microsatellite locus at Xq25 was identified in 46/65 breast cancers examined, while only 10/25 cancers of other origins demonstrated LOH in this region (p = 0.014). The critical deletion region in breast cancer was around marker DXS1047 (47.23%). Moreover, we found that tissues from eight breast cancers showed LOH at all of the informative loci tested at Xq25, while the other 38 showed partial (interstitial or telomeric) alterations at Xq25. Interestingly, the pattern of XCI of these eight breast cancers tended to be non-random. We estimated the frequencies of AR alleles and found that women with two long AR alleles (≥21 CAG repeats) had an increased risk of developing breast cancer, while those with two short AR alleles (<21 CAG repeats) were likely to be normal (p = 0.00069).

Conclusions
The extraordinary high frequencies of LOH at Xq25 found in this study strongly imply that there might be one or more tumour suppressor genes (TSGs) related to the development of breast cancer at Xq25 in the Taiwanese female population.
Akt inhibitor MK-2206 promotes anti-tumor activity and cell death by modulation of AIF and Ezrin in colorectal cancer
Authors: Agarwal Ekta , Chaudhuri Anathbandhu , Leiphrakpam Premila D , Haferbier Katie L , Brattain Michael G , Chowdhury Sanjib 
Published: March 2014

Abstract

Background
There is extensive evidence for the role of aberrant cell survival signaling mechanisms in cancer progression and metastasis. Akt is a major component of cell survival-signaling mechanisms in several types of cancer. It has been shown that activated Akt stabilizes XIAP by S87 phosphorylation leading to survivin/XIAP complex formation, caspase inhibition and cytoprotection of cancer cells. We have reported that TGFβ/PKA/PP2A-mediated tumor suppressor signaling regulates Akt phosphorylation in association with the dissociation of survivin/XIAP complexes leading to inhibition of stress-dependent induction of cell survival.

Methods
IGF1R-dependent colon cancer cells (GEO and CBS) were used for the study. Effects on cell proliferation and cell death were determined in the presence of MK-2206. Xenograft studies were performed to determine the effect of MK-2206 on tumor volume. The effect on various cell death markers such as XIAP, survivin, AIF, Ezrin, pEzrin was determined by western blot analysis. Graph pad 5.0 was used for statistical analysis. P < 0.05 was considered significant.

Results
We characterized the mechanisms by which a novel Akt kinase inhibitor MK-2206 induced cell death in IGF1R-dependent colorectal cancer (CRC) cells with upregulated PI3K/Akt signaling in response to IGF1R activation. MK-2206 treatment generated a significant reduction in tumor growth in vivo and promoted cell death through two mechanisms. This is the first report demonstrating that Akt inactivation by MK-2206 leads to induction of and mitochondria-to-nuclear localization of the Apoptosis Inducing Factor (AIF), which is involved in caspase-independent cell death. We also observed that exposure to MK-2206 dephosphorylated Ezrin at the T567 site leading to the disruption of Akt-pEzrin-XIAP cell survival signaling. Ezrin phosphorylation at this site has been associated with malignant progression in solid tumors.

Conclusion
The identification of these 2 novel mechanisms leading to induction of cell death indicates MK-2206 might be a potential clinical candidate for therapeutic targeting of the subset of IGF1R-dependent cancers in CRC.
Development and validation of a health belief model based instrument for measuring factors influencing exercise behaviors to prevent osteoporosis in pre-menopausal women (HOPE)
Authors: Soleymanian Atoosa , Niknami Shamsaddin , Hajizadeh Ebrahim , Shojaeizadeh Davoud , Montazeri Ali 
Published: March 2014

AbstractBackgroundThe health belief model (HBM) is the most commonly used conceptual framework for evaluating osteoporosis health belief and behaviors. The purpose of this study was to develop and evaluate the psychometric properties of a health belief model based questionnaire for exercise behavior for preventing osteoporosis among women aged 30 years and over.MethodsThis was a cross sectional study of a convenience sample of women aged 30 years and over in Tehran, Iran using a theory-based instrument (HOPE). The instrument contained 39 items covering issues relate to osteoporosis prevention behavior. In this methodological study, exploratory and confirmatory factor analyses were used for psychometric evaluation. The Cronbach’s alpha coefficient and Intraclass Correlation Coefficient (ICC) was used to evaluate the reliability of the scale.ResultsIn all 240 women participated in the study. The mean age of participant was 39.2±7.8 years. The initial analysis extracted nine factors for the questionnaire that jointly accounted for 66.5% of variance observed. Confirmatory factor analysis showed that the data obtained was fit with Health Belief Model (HBM) and self-regulation construct (X2=1132.80, df=629, P<0.0001, CFI=0.94, GFI=0.91, RMSEA=0.05 and SRMR=0.06). The Cronbach’s alpha coefficient for the subscales ranged from 0.72 to 0.90 and Intraclass Correlation Coefficient (ICC) ranged from 0.71 to 0.98; well above acceptable thresholds.ConclusionsThe HOPE was found to be appropriate instrument for measuring health belief and self-regulation for prevention of osteoporosis.
Clinical and prognostic factors associated with diagnostic wait times by breast cancer detection method
Authors: Plotogea Amalia , Chiarelli Anna M , Mirea Lucia , Prummel Maegan V , Chong Nelson , Shumak Rene S , O’Malley Frances P , Holloway Claire MB ,   The Breast Screening Study Group
Published: March 2014

Abstract

Introduction
Although prognostic differences between screen-detected, interval and symptomatic breast cancers are known, factors associated with wait times to diagnosis among these three groups have not been studied.

Methods
Of the 16,373 invasive breast cancers diagnosed between January 1, 1995 and December 31, 2003 in a cohort of Ontario women aged 50 to 69, a random sample (N = 2,615) were selected for chart abstraction. Eligible women were classified according to detection method; screen-detected (n = 1181), interval (n = 319) or symptomatic (n = 406). Diagnostic wait time was calculated from the initial imaging or biopsy to breast cancer diagnosis. Logistic regression analysis examined associations between diagnostic wait times dichotomized as greater or less than the median and demographic, clinical and prognostic factors separately for each detection cohort.

Results
Women who underwent an open biopsy had significantly longer than median wait times to diagnosis, compared to women who underwent a fine needle aspiration or core biopsy; (screen-detected OR = 2.76, 95% CI = 2.14-3.56; interval OR = 2.56, 95% CI = 1.50-4.35; symptomatic OR = 5.56, 95% CI = 3.33-9.30). Additionally, screen-detected breast cancers diagnosed with stage II and symptomatic cancers diagnosed at stage III or IV had significantly shorter diagnostic wait times compared to those diagnosed at stage 1 (OR = 0.66 95% CI = 0.50-0.87 and OR = 0.46, 95% CI = 0.25-0.85 respectively).

Conclusions
Our study is consistent with expedited diagnostic work-up for breast cancers with more advanced prognostic features. Furthermore, women who had an open surgical biopsy had a greater than the median diagnostic wait time, irrespective of detection method.
Labor market policies and European crises
Authors: Bertola Giuseppe 
Published: March 2014

Abstract
This paper studies theoretically and empirically why and how labor policies may reduce productivity and employment in order to stabilize labor incomes and redistribute resources. It proposes a specific stylized model where the tradeoffs facing labor policies are influenced by structural factors, inspects the empirical relevance of this mechanism in European data, and outlines the proposed theoretical perspective’s implications for reform design in crisis-hit economies.

JEL codes

D78; J38
Leukocyte-associated Ig-like receptor-1 is a novel inhibitory receptor for surfactant protein D
Authors: Olde Nordkamp Marloes J M , van Eijk Martin , Urbanus Rolf T , Bont Louis , Haagsman Henk P , Meyaard Linde 
Published: March 2014

ABSTRACTThe collagenous C-type lectin, SP-D, is a multitrimeric glycoprotein present at mucosal surfaces and is involved in host defense against infections in mammals. SP-D has immunomodulatory properties, but the underlying mechanisms are incompletely understood. SP-D contains collagen domains. LAIR-1 is an inhibitory immune receptor at the cell surface of various immune-competent cells that binds collagen. We hypothesized that the immunomodulatory functions of SP-D can be mediated via interactions between its collagen domain and LAIR-1. Binding assays show that SP-D interacts via its collagenous domain with LAIR-1 and the related LAIR-2. This does not affect the mannan-binding capacities of SP-D, which induces cross-linking of LAIR-1 in a cellular reporter assay. Functional assays show that SP-D inhibits the production of FcαR-mediated reactive oxygen via LAIR-1. Our studies indicate that SP-D is a functional ligand of the immune inhibitory receptor LAIR-1. Thus, we have identified a novel pathway for the immunomodulatory functions of SP-D mediated via binding of its collagenous domains to LAIR-1. This may provide a mechanism for the unexplained immunomodulatory function of the collagenous domains of SP-D.