bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of Administrative Data for the Surveillance of Mood and Anxiety Disorders
Authors: Kisely Stephen , Lin Elizabeth , Gilbert Charles , Smith Mark , Campbell Leslie-Anne , Vasiliadis Helen-Maria 
Published: December 2009

Objective: There is increasing interest in the use of administrative data for surveillance and research in Australia. The purpose of the present study was to evaluate the usefulness of such data for the surveillance of mood and anxiety disorder using databases from the following Canadian provinces: British Columbia, Ontario, Quebec and Nova Scotia. Method: A population-based record-linkage analysis was done using data from physician billings and hospital discharge abstracts, and community-based clinics using a case definition of ICD-9 diagnoses of 296.0–296.9, 311.0, and 300.0–300.9. Results: The prevalence of treated mood and/or anxiety disorder was similar in Nova Scotia, British Columbia, and Ontario at approximately 10%. The prevalence for Quebec was slightly lower at 8%. Findings from the provinces showed consistency across age and sex despite variations in data coding. Women tended to show a higher prevalence overall of mood and anxiety disorder than men. There was considerably more variation, however, when treated anxiety (300.0–300.9) and mood disorders (296.0–296.9, 311.0) were considered separately. Prevalence increased steadily to middle age, declining in the 50s and 60s, and then increased after 70 years of age. Conclusions: Administrative data can provide a useful, reliable and economical source of information for the surveillance of treated mood and/or anxiety disorder. Due to the lack of specificity, however, in the diagnoses and data capture, it may be difficult to conduct surveillance of mood and anxiety disorders as separate entities. These findings may have implications for the surveillance of mood and anxiety disorders in Australia with the development of a national network for the extraction, linkage and analysis of administrative data.
Effect of clenching on t2 and diffusion parameters of the masseter muscle
Authors: Chikui Toru , Shiraishi Tomoko , Ichihara Takahiro , Kawazu Toshiyuki , Hatakenaka Masamitsu , Kami Yukiko , Yuasa Kenji , Yoshiura Kazunori 
Published: December 2009

Background: Persistent muscle contractions during clenching are considered to be one reason for temporomandibular disorders. However, no report has evaluated the effect of clenching on the masticatory muscles, as measured by magnetic resonance imaging (MRI). Purpose: To investigate whether clenching has an effect on either T2 or the coefficients for diffusion of the masseter muscles (MM), and to evaluate the effect of the distribution of bite force on such indices. Material and Methods: Twenty-three subjects were examined. Bite force was measured by a pressure-sensitive sheet, and the force of the right and the left sides was calculated. MRI was used to evaluate T2, the apparent diffusion coefficient (ADC), and the primary (λ1), secondary (λ2), and tertiary eigenvalues (λ3). These indices on the stronger side of the bite force were compared to those on the weaker side. Thereafter, the indices were compared between at rest and during clenching. Results: There was no significant difference in any of the indices (T2, ADC, λ1, λ2, and λ3) between the side of stronger bite force and the side with weaker. T2 increased by clenching, and the difference was significant in the side with stronger bite force ( P = 0.006). ADC, λ1, λ2, and λ3 increased significantly by clenching ( P <0.01, P <0.01, P <0.01, and P <0.01, respectively) on both sides. The percentage of change of λ2 by clenching was 26.2±15.7% on the stronger side and 26.9±18.6% on the weaker side, which was significantly greater than either that of λ1 or λ3. Conclusion: The coefficients for diffusion of the MM were sensitive to change by clenching, and λ2 was the most sensitive. Moreover, the relative distribution of the bite forces had no effect on any of the indices.
Magnetic resonance imaging signal reduction may precede volume loss in the pituitary gland of transfusion-dependent beta-thalassemic patients
Authors: Hekmatnia Ali , Radmard Amir Reza , Rahmani Ali Asghar , Adibi Atoosa , Khademi Hooman 
Published: December 2009

Background: Pituitary iron overload in patients with transfusion-dependent beta-thalassemia may lead to delayed puberty. Magnetic resonance imaging (MRI) has the potential to estimate tissue iron concentration by detecting its paramagnetic effect and hypophyseal damage by measuring its dimensions indirectly. Purpose: To investigate the association of pituitary MRI findings and pubertal status in thalassemic patients as well as to demonstrate any priority in appearance of them. Material and Methods: Twenty-seven beta-thalassemic patients, aged 15–25 years, were divided into 13 with (group A) and 14 without hypogonadism (group B), matched by age, gender, duration of transfusion, and chelation therapy. Thirty-eight age- and sex-adjusted healthy control individuals were also included (group C). All participants underwent pituitary MRI using a 1.5T unit. Pituitary-to-fat signal intensity ratios (SIR) were calculated from coronal T2-weighted images. Estimated pituitary volumes were measured using pituitary height, width, and length on T1-weighted images. Results: The mean values of pituitary-to-fat SIRs were significantly lower in group A as compared with group B ( P <0.001), and likewise group B had statistically lower values than group C ( P=0.03). The pituitary height and volume were significantly decreased in group A compared to group B (P = 0.006 and P = 0.002, respectively), while these differences did not demonstrate statistically significance between groups B and C. Conclusion: Pituitary MRI findings such as signal intensity reduction and decrease in volume can be useful markers in estimating pituitary dysfunction in beta-thalassemic patients. Compared to healthy controls, lower values of pituitary-to-fat SIRs in thalassemic patients experiencing normal puberty, without marked decrease in volume, indicate that signal reduction may precede volume loss and could be expected first on MRI.
Randomized controlled non‐inferiority trial of a telehealth treatment for chronic stuttering: the Camperdown Program
Authors: Carey Brenda , O'Brian Sue , Onslow Mark , Block Susan , Jones Mark , Packman Ann 
Published: December 2009

Background: Although there are treatments that can alleviate stuttering in adults for clinically significant periods, in Australia there are barriers to the accessibility and availability of best‐practice treatment.Aims: This parallel group, non‐inferiority randomized controlled trial with multiple blinded outcome assessments investigated whether telehealth delivery of the Camperdown Program provides a non‐inferior alternative to face‐to‐face treatment for adults who stutter.Methods & Procedures: Forty participants who presented to a university speech clinic were randomized: 20 to the telehealth arm and 20 to the face‐to‐face arm. Exclusion criteria were age younger than 18 years, frequency of stuttering less than 2% of syllables stuttered and previous speech‐restructuring treatment within the past 12 months. The Camperdown Program for adults who stutter was the intervention. Primary outcome measures were frequency of stuttering measured in per cent syllables stuttered (%SS) before treatment and at 9 months post‐randomization and efficiency, measured by counting the number of speech pathologist contact hours used by each participant. Intention to treat analysis was conducted using last observation carried forward. Secondary outcome measures were speech naturalness, self‐reported stuttering severity, and treatment satisfaction.Outcomes & Results: There was no statistically or clinically significant difference in %SS between the two groups at 9 months post‐randomization. Analysis of covariance adjusting for baseline %SS showed telehealth had 0.8% absolute lower per cent syllables stuttered than face‐to‐face. There were also no differences in %SS between groups immediately post‐treatment, or at 6 months and 12 months post‐treatment (p = 0.9). In the second primary outcome measure, the telehealth group used statistically less contact time (221 min) on average than the face‐to‐face group (95% confidence interval = − 387 to − 56 min, p = 0.01).Conclusions & Implications: The results provide evidence to support the use of the Camperdown Program delivered by telehealth as an alternate to the face‐to‐face treatment delivery of this programme for adults who stutter. Such a model will increase accessibility to this evidence‐based treatment for adults currently isolated from treatment services.Trial registration: Current Controlled Trials ISRCTN 48954432.
Exploring Health Information Technology Innovativeness and its Antecedents in Canadian Hospitals
Authors: Jaana M. , Sicotte C. , Paré G. 
Published: December 2009

Summary
Objectives: The primary aim of this study was to assess the antecedents of health information technology (HIT) innovativeness in public hospitals. To do so, we built upon our own previous work to relate the level of HIT innovativeness to organizational capacity characteristics.
Methods: We conducted a survey of chief information officers (CIOs) in public hospitals in the two largest Canadian provinces to identify the level of HIT innovativeness in these settings and test nine research hypotheses derived from the proposed research model.
Results: A total of 106 completed questionnaires were received, which represents a response rate of 52%. Our findings indicate strong support for the research model. Seven out of nine hypotheses were supported indicating a significant relationship between HIT innovativeness and structural, financial, leadership, and knowledge sharing capacity characteristics. Results also reveal a moderate level of HIT innovativeness in the surveyed hospitals, with more emphasis on administrative systems and their integration than on clinical systems and emerging technologies.
Conclusions: This study demonstrates that organizational characteristics are related to HIT innovativeness; this relationship holds irrespective of the public or private nature of hospitals.
OmniSCOPE: Composing Universal Therapies
Authors: Carriço L. , de Sá M. 
Published: December 2009

Summary
Objectives: This paper presents Omni SCOPE, an environment for the development of mobile pervasive therapy artifacts. OmniSCOPE builds on SCOPE, a tool for the support of mobile psychotherapy. It aims at providing therapists with means to adjust and compose new therapeutic artifacts to suit their patients’ needs and new therapeutic approaches.
Methods: Given the positive results that emerged through the development and utilization of SCOPE, a previous single therapy version of Omni SCOPE, extensions were developed in order to enhance the artifacts, the data collection by patients and its consequent analysis by therapists. These extend the usage possibilities to new situations and therapies also targeting a wider range of users and were developed following a user-centered design approach.
Results: As results, we detail the extensions and how they support new activities and therapies illustrated by two case studies in which they are being currently evaluated. Initial results from the involved therapists’ assessment and future trends and directions are also discussed.
Conclusions: The features and accessible artifacts that can be composed with Omni-SCOPE have provided therapists with the possibility to enhance their therapy procedures and to reach a wider audience of patients even while out of the office. Additionally, the data gathering options that can be included within the therapeutic artifacts provide much more detail which can clearly facilitate diagnosis and posterior therapy adjustments.
Studying the Place of Technology to Lower Financial Barriers for Dietary Change
Authors: Maitland J. , Siek K. A. 
Published: December 2009

Summary
Background: Current dietary self-monitoring systems assume users have access to healthy foods and resources to effectively implement and monitor dietary behavioral change. Objectives: The purpose of this qualitative study is to understand the specific financial-related barriers that caregivers of low socioeconomic status encounter when attempting to make dietary behavior change.
Methods: In this qualitative study, we conducted a focus group and 14 in-person interviews with the primary caregivers of low socioeconomic families. Participants were recruited from a community considered to be ‘at risk’ through high levels of exposure to multiple modifiable risk factors for cardiovascular disease. All participants were English-speaking caregivers, who had children under eight years old. The families lived in an urban, public housing community. The focus group and interviews were transcribed and coded during data analysis sessions, then analyzed for emergent themes.
Results: We abstracted three main themes from the data. The caregivers of 17 families: 1) feared trying healthier food alternatives because of possibly wasting the food; 2) planned meals only when they had enough time, space, and financial security; and 3) defined produce as luxury items and often could only afford staple food items, such as meat and grains.
Conclusion: We challenge the community to design technological interventions to lower the financial barriers presented with existing information and communication technology available to low socioeconomic populations. In addition, we encourage interventions to foster a community’s social capital to decrease feelings of isolation and increase opportunities for cooperation.
Decision Support for Teletraining of COPD Patients
Authors: Wolf K.-H. , Gietzelt M. , Al Scharaa O. , Tegtbur U. , Haux R. , Marschollek M. , Song B. 
Published: December 2009

Summary
Background: Supervised physical training has been shown to promote rehabilitation of patients affected by chronic obstructive pulmonary disease (COPD). Currently, due to limited resources, not all COPD patients can be trained by an expert supervisor.
Objectives: The objective of our research is to construct a decision support system (DSS) which observes and controls physical ergometer training sessions of COPD patients.
Methods: A systematic literature review and expert interviews were carried out to build up the knowledge base for the DSS.
Results: Nine production rules were established and standardized by Drools and Arden Syntax. The developed software autonomously controls training sessions on a bicycle ergometer on the basis of vital signs data. Thus it offers a new way for the rehabilitation of COPD patients.
Conclusion: Evaluation with nine healthy subjects in a laboratory environment has confirmed its correct function, but the effects of its use for COPD patients’ rehabilitation and their quality of life have to be investigated in a further study.
IL-1R1/MyD88 Signaling Is Critical for Elastase-Induced Lung Inflammation and Emphysema
Authors: Couillin Isabelle , Vasseur Virginie , Charron Sabine , Gasse Pamela , Tavernier Marie , Guillet Julien , Lagente Vincent , Fick Lizette , Jacobs Muazzam , Coelho Fernando Rodrigues , Moser René , Ryffel Bernhard 
Published: December 2009

AbstractLung emphysema and fibrosis are severe complications of chronic obstructive pulmonary disease, and uncontrolled protease activation may be involved in the pathogenesis. Using experimental elastase-induced acute inflammation, we demonstrate here that inflammation and development of emphysema is IL-1R1 and Toll/IL-1R signal transduction adaptor MyD88 dependent; however, TLR recognition is dispensable in this model. Elastase induces IL-1β, TNF-α, keratinocyte-derived chemokine, and IL-6 secretion and neutrophil recruitment in the lung, which is drastically reduced in the absence of IL-1R1 or MyD88. Further, tissue destruction with emphysema and fibrosis is attenuated in the lungs of IL-1R1- and MyD88-deficient mice. Specific blockade of IL-1 by IL-1R antagonist diminishes acute inflammation and emphysema. Finally, IL-1β production and inflammation are reduced in mice deficient for the NALP3 inflammasome component apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and we identified uric acid, which is produced upon elastase-induced lung injury, as an activator of the NALP3/ASC inflammasome. In conclusion, elastase-mediated lung pathology depends on inflammasome activation with IL-1β production. IL-1β therefore represents a critical mediator and a possible therapeutic target of lung inflammation leading to emphysema.
Antigen Specificity Determines the Pro- or Antitumoral Nature of CD8+ T Cells
Authors: Cuff Simone , Dolton Garry , Matthews R. James , Gallimore Awen 
Published: December 2009

Abstract
Although CD8+ T cells are usually considered antitumoral, several recent studies report that the cells can also promote tumor progression. Using the melanoma cell line B16 as a murine model of pulmonary metastasis, we examined whether the pro- versus antitumoral effects of CD8+ T cells relate to their Ag specificity. Results of the study indicate that although CD8+ T cells specific for tumor Ags promote tumor rejection, CD8+ T cells specific for unrelated Ags promote tumor progression. We found the effect to be partly attributable to CD8+ T cells dampening effective antitumor NK cell responses. Notably, activation of CD8+ T cell responses by an unrelated stimulus, in this case infection with influenza virus, increased the number of pulmonary tumor nodules. These data provide a rationale for previously unexplained data identifying contrasting roles for CD8+ T cells in tumor progression.
Helicobacter pyloriInduces MAPK Phosphorylation and AP-1 Activation via a NOD1-Dependent Mechanism
Authors: Allison Cody C. , Kufer Thomas A. , Kremmer Elisabeth , Kaparakis Maria , Ferrero Richard L. 
Published: December 2009

AbstractHelicobacter pylori rapidly activates MAPKs and transcription factors, NF-κB and AP-1, in gastric epithelial cells following host attachment. Activation of these signal transducers is largely dependent on the cag pathogenicity island (cagPAI)-encoded Type IV Secretion System. H. pylori was shown to translocate peptidoglycan through the Type IV Secretion System, which is recognized by the pathogen recognition molecule, NOD1, thus resulting in NF-κB activation. The mechanisms of H. pylori-induced MAPK and AP-1 activation, however, are less well defined and therefore, we assessed the contribution of NOD1 to their activation. For this, we used gastric epithelial cell lines, stably expressing siRNA to either NOD1 or a control gene. In siNOD1-expressing cells stimulated with cagPAI+ H. pylori, we observed significant reductions in p38 and ERK phosphorylation (p &lt; 0.05), whereas the levels of Jnk phosphorylation remained unchanged. Consistent with a previous report, however, we were able to demonstrate NOD1-dependent Jnk phosphorylation by the invasive pathogen Shigella flexneri, highlighting pathogen-specific host responses to infection. We also show that NOD1 was essential for H. pylori induction of not only NF-κB, but also AP-1 activation, implying that NOD1 induces robust proinflammatory responses, in an attempt to rapidly control infection. Pharmacological inhibition of p38 and ERK activity significantly reduced IL-8 production in response to H. pylori, further emphasizing the importance of MAPKs in innate immune responses to the pathogen. Thus, for the first time we have shown the important role for NOD1 in MAPK and AP-1 activation in response to cagPAI+ H. pylori.
Novel Role for Aldose Reductase in Mediating Acute Inflammatory Responses in the Lung
Authors: Ravindranath Thyyar M. , Mong Phyllus Y. , Ananthakrishnan Radha , Li Qing , Quadri Nosirudeen , Schmidt Ann Marie , Ramasamy Ravichandran , Wang Qin 
Published: December 2009

Abstract
Exaggerated inflammatory responses and the resultant increases in alveolar-capillary permeability underlie the pathogenesis of acute lung injury during sepsis. This study examined the functions of aldose reductase (AR) in mediating acute lung inflammation. Transgenic mice expressing human AR (ARTg) were used to study the functions of AR since mice have low intrinsic AR activity. In a mild cecal ligation and puncture model, ARTg mice demonstrated an enhanced AR activity and a greater inflammatory response as evaluated by circulating cytokine levels, neutrophil accumulation in the lungs, and activation of Rho kinase in lung endothelial cells (ECs). Compared with WT lung cells, ARTg lung cells produced more IL-6 and showed augmented JNK activation in response to LPS stimulation ex vivo. In human neutrophils, AR activity was required for fMLP-included CD11b activation and up-regulation, respiratory burst, and shape changes. In human pulmonary microvascular ECs, AR activity was required for TNF-α-induced activation of the Rho kinase/MKK4/JNK pathway and IL-6 production, but not p38 activation or ICAM-1 expression. Importantly, AR activity in both human neutrophils and ECs was required for neutrophil adhesion to TNF-α-stimulated ECs. These data demonstrate a novel role for AR in regulating the signaling pathways leading to neutrophil-EC adhesion during acute lung inflammation.
DcR3 Protects Islet β Cells from Apoptosis through ModulatingAdcyap1andBank1Expression
Authors: Han Bing , Wu Jiangping 
Published: December 2009

AbstractThe islet primary nonfunction (PNF) is a serious problem in islet transplantation. In this study, we investigated whether DcR3-secreting transgenic (Tg) islets could reduce PNF. We generated Tg mice expressing human DcR3. The transgenically expressed DcR3 protected islets from IFN-γ plus IL-1β- or TNF-α plus IL-1β-induced dysfunction and apoptosis in vitro. The Tg islets presented significantly reduced PNF after transplantation. Mechanistically, in addition to the known FasL apoptotic pathway, components of two other apoptosis pathways, that is, HVEM/LTβR for the LIGHT pathway and DR3 for the TL1A pathway, were found to be expressed in islets. Recombinant LIGHT- and TL1A-induced islet apoptosis in the absence of the FasL/Fas pathway, as well as DcR3, could block such induction. These results for the first time demonstrated that LIGHT and TL1A were capable of inducing islet apoptosis in addition to FasL, while DcR3 protected the islets by blocking all three apoptosis pathways. By DNA microarray analysis, we discovered that Adcyap was up-regulated &gt;700-fold and Bank1 was down-regulated 50-fold in the cytokine-assaulted Tg islets, compared with WT islets. Forced overexpression of Adcyap1 by plasmid transfection or knockdown of Bank1 expression by small interfering RNA in insulinoma NIT-1 cells protected them from cytokine-triggered apoptosis, indicating that indeed DcR3 protects β cells via the action of these two downstream molecules. This study has revealed novel mechanisms by which DcR3 protects islet survival, and it has identified new therapeutic targets of diabetes.