bluuebunny/crossref_metadata_2025_split huggingface dataset:
Buddhist ‘Genesis’ as a Narrative of Conflict Transformation: A Re-reading of the Aggañña-sutta
Authors: Satha-Anand Suwanna 
Published: February 2014

AbstractSince January 2004, violent conflicts in the deep South of Thailand have caused 4,453 deaths, 7,239 injuries in 10,386 violent incidents. The numbers are increasing every day. Myriads of studies, strategies and proposals have been put forth to address and redress this deep-rooted problem. This paper is a modest attempt to find analysis and inspiration from the rich cultural resources of Buddhism to address the question of conflict and conflict transformation in Thai society.The Buddhist “Genesis” or The Agganna-sutta has been analyzed by Thai and Western Buddhist scholars as offering an allegorical tale which details a long, inter-dependent process of human beings’ moral degradation on the one hand, and socio-political evolution on the other. This is considered to be the Buddhist equivalent of the Genesis without God.This paper offers a re-reading of this important sutta as a narrative of conflict and conflict transformation. It argues that the personal conflict of the two young Brahmins aspiring to be fully ordained is transcended and transformed by the Buddha's allegorical tale of human socio-political evolution. This paper offers an analysis of the narration and demonstrates that in the narrating process, the Buddha was “substituting” the Hindu creation myth with the Discourse on What is Primary (Agganna-sutta). This narrative replacement subverts the deep-rooted cultural force of the Hindu creation myth which serves as a cosmological justification for a hierarchy of classes/castes in the social world. Once the creation Hindu myth is de-mythologized, the structure of meaning for the personal conflict of the two Brahmins evaporates. In this way, the Buddha's approach to conflict transformation addresses three dimensions simultaneously, namely, the personal, the socio-political and the cosmological.This re-reading is one paradigmatic example of how to revitalize Buddhism to function as an agent of social transformation by offering a Buddhist creative approach to conflict transformation.
Incidence and risk analysis of aortic aneurysm and aortic dissection among patients with systemic lupus erythematosus: a nationwide population-based study in Taiwan
Authors: Wang S-H , Chang Y-S , Liu C-J , Lai C-C , Chen T-J , Chen W-S 
Published: February 2014

Objective The objective of our study was to determine the incidence rates and risk factors of aortic aneurysm and aortic dissection among patients with systemic lupus erythematosus (SLE) using a nationwide population-based data set. Methods We conducted a retrospective cohort study using data from the Taiwan National Health Insurance database. Patients with SLE and age-, sex- and comorbidity-matched control patients without SLE were identified. The primary endpoint was the first occurrence of aortic aneurysm or aortic dissection. The incidence rate ratios (IRRs) were calculated based on a 95% confidence interval (CI). A Cox proportional-hazards model was used to evaluate the risk factors for aortic aneurysm and aortic dissection in the SLE cohort. Results Among the 15,209 patients with SLE (89.9% women and mean age of 38.3 years), 20 developed aortic aneurysm and 13 developed aortic dissection (overall incidence rate, 4.26 per 10,000 person-years). Compared with the control patients, the overall IRR for developing aortic aneurysm or aortic dissection was 3.34 (95% CI, 1.71–6.91; p < 0.001). The IRRs for aortic aneurysm or aortic dissection were 2.98 (95% CI, 1.41–6.70, p = 0.018) for women and 5.50 (95% CI, 1.10–53.15, p = 0.020) for men. Multivariate Cox regression analysis showed that age, male sex, an SLE diagnosis greater than three years prior and hypertension were associated with aortic aneurysm and aortic dissection. Conclusion Aortic aneurysm and aortic dissection occur at higher rates in SLE patients than in people without SLE and a longer disease duration is associated with a higher risk of these rare vascular complications.
Endovenous laser ablation for saphenous vein insufficiency: Short- and mid-term results of 230 procedures
Authors: Altin Firat H , Aydin Selim , Erkoc Kamuran , Gunes Tevfik , Eygi Bortecin , Kutas Baris H 
Published: February 2014

Objective The present study aimed to evaluate the efficacy of endovenous laser ablation with a 1470-nm laser and to analyze the short- to mid-term results of endovenous laser ablation procedures to treat great saphenous vein insufficiency. Method In this retrospective study, 200 patients (230 limbs) with symptomatic varicose veins secondary to great saphenous vein insufficiency treated with 1470-nm endovenous laser ablation were studied. Patients were evaluated clinically on the first day, first week, first month, and sixth month after the operation. Treated limbs were evaluated as separate treatment events. Results The short-term occlusion rate was 99% and mid-term occlusion rate was 100%. Induration or swelling was the most common minor complication (13%). No major complication such as deep venous thrombosis and pulmonary embolus occurred. Preoperatively documented mean venous clinical severity score significantly reduced from 4.9 ± 2.3 to 2.5 ± 1.1 ( p < 0.05). Conclusion Endovenous laser ablation procedure of great saphenous vein with a 1470-nm diode laser is a minimally invasive, safe, and efficient treatment option in all-suitable patients with high short- and mid-term success rate.
Insulin Pump Patient Characteristics and Glucose Control in the Hospitalized Setting
Authors: Kannan Subramanian , Satra Ankita , Calogeras Ellen , Lock Patricia , Lansang M. Cecilia 
Published: February 2014

Introduction: Patients’ knowledge of their insulin pumps and glucose control during hospitalization has not been studied. Aim: The aim was to study the determinants of glycemic control in patients using continuous subcutaneous insulin infusion (CSII) in the hospital. Methods: Three groups of patients were identified: those who did not need any inpatient education and continued on CSII (gorup A), those who received education then continued on CSII (group B), and those for whom CSII was not appropriate and were treated with multiple daily insulin injections (gorup C). We compared the measures of glycemic control between the 3 groups and analyzed which variables impacted glucose control. Results: There were 50 patients, with 51 hospital admissions, 57% males, mean age 48 ± 13 years, 86% had type 1 diabetes (T1DM). The mean DM duration was 26 ± 14 years, mean duration of CSII use was 8.7 ± 6 years, and mean HbA1c was 7.6 ± 1.4%. The mean duration of hospital stay was 5.6 ± 4.6 days. Mean blood glucose (BG) and frequency of hyperglycemia and hypoglycemic events among the 3 groups adjusted for their duration of hospital stay were not statistically different. None of the patients developed diabetic ketoacidosis while using their pump. Stepwise multivariate analysis revealed knowledge of hypoglycemia correction was the single most important predictor of mean BG (P < .001). Conclusion: Patients who received inpatient education performed similarly to patients who did not need inpatient education. Patients who receive inpatient education on CSII fare similar as patients who did not require inpatient education.
Endothelial Smad4 restrains the transition to hematopoietic progenitors via suppression of ERK activation
Authors: Lan Yu , He Wenyan , Li Zhuan , Wang Yu , Wang Jun , Gao Jiao , Wang Weili , Cheng Tao , Liu Bing , Yang Xiao 
Published: February 2014

Key PointsEndothelial Smad4 is a physiological suppressor that functions specifically during the transition to hematopoietic progenitors. Endothelial Smad4 lies upstream of the subaortic microenvironment to control the hematopoietic fate of aortic endothelium.
Distinct clustering of symptomatic burden among myeloproliferative neoplasm patients: retrospective assessment in 1470 patients
Authors: Geyer Holly L. , Scherber Robyn M. , Dueck Amylou C. , Kiladjian Jean-Jacques , Xiao Zhijian , Slot Stefanie , Zweegman Sonja , Sackmann Federico , Fuentes Ana Kerguelen , Hernández-Maraver Dolores , Döhner Konstanze , Harrison Claire N. , Radia Deepti , Muxi Pablo , Besses Carlos , Cervantes Francisco , Johansson Peter L. , Andreasson Bjorn , Rambaldi Alessandro , Barbui Tiziano , Vannucchi Alessandro M. , Passamonti Francesco , Samuelsson Jan , Birgegard Gunnar , Mesa Ruben A. 
Published: February 2014

Key Points
Distinct clusters exist within polycythemia vera, essential thrombocythemia, and myelofibrosis. Clusters are not direct surrogates for current prognostic scores.
Genotype-specific small-molecule therapy for cystic fibrosis
Authors: Thursfield Rebecca M. , Davies Jane C. 
Published: February 2014

Educational aimsTo allow the reader to refresh their knowledge of the underlying gene and protein defects in cystic fibrosisTo provide an understanding of new therapies developed and those in developmentTo attain a thorough understanding of the need for different therapies for different mutationsTo inform the reader of the potential benefits for their patients of this new class of drugsSummaryThe prognosis for patients with cystic fibrosis (CF) has improved greatly over the past 30 years but the median age of survival is still only to the patients late 30s. New treatments are required to decrease morbidity and improve mortality. The basic defect in CF lies in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, mutations of which lead to a dysfunctional CFTR protein. The way in which the protein is defective differs between the six so-called mutation classes. An understanding of these classes has led to the development of mutation-specific small-molecule treatments.Class I mutations are caused by the presence of a premature termination codon. Ataluren is a systemic agent that allows read-through of the mutated mRNA and translation of full-length protein. A phase III clinical trial has recently been completed. In class II mutations, the most common of which is Phe508del (previously termed ΔF508), the resulting CFTR protein is misfolded and is not trafficked through the cytoplasm to the cell membrane. CFTR-corrector drugs seek to facilitate such trafficking; recently increased understanding of the complex nature of the misfolding events may explain why this approach is, to date, rather difficult. Improvements in CFTR protein function have been achievedin vivoand clinical trial data are beginning to emerge. It may be necessary to use correctors with potentiators and combination trials of two correctors, VX-809 and VX-661, with or without the CFTR potentiator ivacaftor are underway. The latter was initially developed and tested in patients with the class III mutation Gly551Asp (previously termed G551D). In cells with this mutation, CFTR protein reaches the cell surface but fails to respond to cellular signals to open and conduct chloride. Ivacaftor increases the probability that the channel is open and has led to significant clinical benefit in patients with the Gly551Asp mutation; it is now being investigated in other class III and some class IV mutations.Ivacaftor is the first genotype-specific treatment to demonstrate clinical efficacy and to be approved for licence. Other compounds are currently in development and the field is optimistic that drugs for other genotypes will not be far behind.
Nabla discrete fractional Grüss type inequality
Authors: Güvenilir A Feza , Kaymakçalan Billur , Peterson Allan C , Taş Kenan 
Published: February 2014

Abstract
Properties of the discrete fractional calculus in the sense of a backward difference are introduced and developed. Here, we prove a more general version of the Grüss type inequality for the nabla fractional case. An example of our main result is given.

MSC: 39A12, 34A25, 26A33, 26D15, 26D20.
Autocrine ligands of the epithelial growth factor receptor mediate inflammatory responses to diesel exhaust particles
Authors: Parnia Sam , Hamilton Lynnsey M , Puddicombe Sarah M , Holgate Stephen T , Frew Anthony J , Davies Donna E 
Published: February 2014

Abstract

Background
Diesel exhaust is associated with cardiovascular and respiratory mortality and morbidity. Acute exposure leads to increased IL-8 expression and airway neutrophilia, however the mechanism of this response is unknown. Objectives: As cigarette smoke-induced IL-8 expression by epithelial cells involves transactivation of the epidermal growth factor receptor (EGFR), we studied the effects of diesel exhaust particles (DEP) on IL-8 release and the role of the EGFR.

Methods
Primary bronchial epithelial cells (PBEC) were exposed to DEPs or carbon black. IL-8 and EGFR ligand expression (transforming growth factor alpha (TGFα), heparin-binding EGF-like growth factor, and amphiregulin (AR)) were assessed by quantitative RT-PCR and ELISA.

Results
DEP, but not carbon black, caused a dose-dependent increase in mitogen-activated protein kinase (MAPK) activation and IL-8 expression, however above 50 μg/ml there was an increase in cytotoxicity. At 50 μg/ml, DEPs stimulated transcription and release of IL-8 and EGFR ligands. IL-8 release was blocked by EGFR neutralizing antibodies, an EGFR-selective tyrosine kinase inhibitor and by the metalloprotease inhibitor, GM6001, which blocks EGFR ligand shedding. Neutralizing antibodies to AR, TGFα and heparin-binding (HB)-EGF reduced DEP-induced IL-8 by >50%. Conclusion Expression of IL-8 in response to DEPs is dependent on EGFR activation and that autocrine production of EGFR ligands makes a substantial contribution to this response. Capsule Summary: This study identifies a mechanism whereby diesel particles stimulates IL-8 release from bronchial epithelial cells. This mechanism may help to explain the recruitment of neutrophils into the airways of people exposed to particulate air pollution.
DNA methylation profiling in the thalamus and hippocampus of postnatal malnourished mice, including effects related to long-term potentiation
Authors: Weng Xiaoling , Zhou Daizhan , Liu Fatao , Zhang Hong , Ye Junyi , Zhang Zhou , Zhang Di , Wang Yinan , Tao Liming , Cao Lan , Kan Mengyuan , Wang Ting , Feng Guoyin , Qin Xiaolan , Sun Jihui , He Lin , Liu Yun 
Published: February 2014

AbstractBackgroundDNA methylation has been viewed as the most highly characterized epigenetic mark for genome regulation and development. Postnatal brains appear to exhibit stimulus-induced methylation changes because of factors such as environment, lifestyle, and diet (nutrition). The purpose of this study was to examine how extensively the brain DNA methylome is regulated by nutrition in early life.ResultsBy quantifying the total amount of 5-methylcytosine (5mC) in the thalamus and the hippocampus of postnatal malnourished mice and normal mice, we found the two regions showed differences in global DNA methylation status. The methylation level in the thalamus was much higher than that in the hippocampus. Then, we used a next-generation sequencing (NGS)-based method (MSCC) to detect the whole genome methylation of the two regions in malnourished mice and normal mice. Notably, we found that in the thalamus, 500 discriminable variations existed and that approximately 60% were related to neuronal development or psychiatric diseases. Pathway analyses of the corresponding genes highlighted changes for 9 genes related to long-term potentiation (5.3-fold enrichment, P = 0.033).ConclusionsOur findings may help to indicate the genome-wide DNA methylation status of different brain regions and the effects of malnutrition on brain DNA methylation. The results also indicate that postnatal malnutrition may increase the risk of psychiatric disorders.
Italian family paediatricians’ approach and management of celiac disease: a cross-sectional study in Puglia Region, 2012
Authors: Fortunato Francesca , Martinelli Domenico , Cozza Vanessa , Ciavarella Pierpaolo , Valente Anna , Cazzato Teresa , Piazzolla Ruggiero , Prato Rosa , Pedalino Biagio 
Published: February 2014

AbstractBackgroundCeliac disease (CD) is a chronic autoimmune illness of the small intestine triggered by gluten consumption in genetically predisposed individuals. CD presentation is not limited to the gastrointestinal tract and it is still under-diagnosed. Complete resolution of clinical manifestations follows if a gluten-free diet is adopted. In western countries, CD prevalence is approximately 1%. Age of onset is often between 6 months and 7 years.We assessed the approach to diagnosis and management of celiac patients by the paediatricians in Puglia Region, Italy.MethodsWe conducted a cross-sectional survey among the 589 Apulian Family Paediatricians (FPs) during January 2011-January 2012 using a self-administered web-based standardized questionnaire including self-assessment of their knowledge, diagnostic path and type of management they would follow for CD, clinical information on their celiac patients. We assessed associations among the explored variables by defining double-entry contingency tables and calculating Odds Ratio (OR) with 95% Confidence Intervals (CIs).ResultsThe 218 (37%) FPs participating in the study reported 1,020 CD patients (representing approximately 1% of the child population covered by the enrolled FPs). Of them, 55% were female; 45% were aged 5–10 years. Weight loss and stunting were the main reported symptoms at diagnosis (41%). The majority (98%) of FPs requested anti-transglutaminase antibody (tTG-Ab) titres for CD diagnosis. Approximately 78% of FPs recommended gluten introduction in the diet of infants at the age of 6 months; 12% and 8% recommended introduction of gluten before and after 6 months of age respectively.The degree of knowledge for either CD diagnosis making process or CD related diseases was medium/high in 97% and 82% of the participating FPs respectively. FPs (83%) who had a medium or high degree of knowledge of CD patients’ diet were more likely to experience low or no difficulty in providing their patients with dietary advices (OR:5.5; 95%CI:1.7-17.5).ConclusionsApulian FPs report a good degree of knowledge of CD, its diagnosis and its management. We will diffuse results and recommendations to all paediatricians in the Region. Actions aiming to continued education on CD in medical under and postgraduate trainings are crucial to prevent under-diagnosis.
Evidence for synergistic effects of PRNP and ATP7Bmutations in severe neuropsychiatric deterioration
Authors: Forbes Nauzer , Goodwin Susan , Woodward Kevin , Morgan David G , Brady Lauren , Coulthart Michael B , Tarnopolsky Mark A 
Published: February 2014

AbstractBackgroundWilson’s disease (WD), a rare cause of neuropsychiatric deterioration, is associated with mutations in theATP7Bgene. Prion diseases are also rare causes of neuropsychiatric deterioration that can occur sporadically without an identifiable cause, or can be attributed to mutations in thePRNPgene.Case presentationHere we describe a biological “experiment of nature” in which a patient presented with severe neuropsychiatric decline and strong biochemical evidence of WD. Genetic analysis revealed that he was a compound heterozygote for twoATP7Bsequence variants (c.2165dupT, p.Arg723Glufs*32; and c.4039G > A, p.Gly1347Ser), the first having been reported once previously, and the second being novel. In addition, the patient was heterozygous for aPRNPvariant, c.160G > A, p.Gly54Ser, that has been reported in a neuropsychiatric patient only once previously in association with a similarly severe clinical course of neuropsychiatric disease and early age of onset, but no accompanying information onATP7Bgenotype. Of particular interest was the observation that the patient’s older sister, who carried the sameATP7Bgenotype and laboratory evidence for biochemical WD but was clinically asymptomatic, lacked thePRNPvariant allele.ConclusionsWe propose that synergism may occur between at least some allelic variants ofATP7BandPRNP, possibly exerted through effects on cellular copper metabolism.
Severe maternal morbidity and maternal near miss in the extremes of reproductive age: results from a national cross- sectional multicenter study
Authors: Oliveira Fernando César , Surita Fernanda Garanhani , Pinto e Silva João Luiz , Cecatti José Guilherme , Parpinelli Mary Angela , Haddad Samira M , Costa Maria Laura , Pacagnella Rodolfo Carvalho , Sousa Maria Helena , Souza João Paulo ,   The Brazilian Network for Surveillance of Severe Maternal Morbidity Study Group
Published: February 2014

Abstract

Background
The aim of this study was to assess severe maternal morbidity (SMM) and near miss (NM) cases among adolescent girls and women over 35 years of age in the Brazilian Network for Surveillance of Severe Maternal Morbidity, using a set of standard criteria, compared to pregnant women aged 20 to 34 years.

Methods
A cross-sectional multicenter study conducted in 27 referral obstetric units in Brazil. All pregnant women admitted to these centers during a one-year period of prospective surveillance were screened to identify cases of maternal death (MD), NM and other SMM. Indicators of maternal morbidity and mortality were evaluated for the three age groups. Sociodemographic, clinical and obstetric characteristics, gestational and perinatal outcomes, main causes of morbidity and delays in care were also compared. Two multiple analysis models were performed, to estimate the adjusted prevalence ratio for identified factors that were independently associated with the occurrence of severe maternal outcome (SMO = MNM + MD).

Results
Among SMM and MD cases identified, the proportion of adolescent girls and older women were 17% each. The risk of MNM or death was 25% higher among older women. Maternal near miss ratio and maternal mortality ratios increased with age, but these ratios were also higher among adolescents aged 10 to 14, although the absolute numbers were low. On multivariate analysis, younger age was not identified as an independent risk factor for SMO, while this was true for older age (PR 1.25; 1.07-1.45).

Conclusions
SMO was high among women below 14 years of age and increased with age in Brazilian pregnant women.