bluuebunny/crossref_metadata_2025_split huggingface dataset:
When peers count: The effects on integrated type II diabetes care of communication within general practitioner-only subgroups in interprofessional primary care teams
Authors: Compagni Amelia , Armeni Patrizio , Tasselli Stefano 
Published: March 2017

Background:
Primary care teams (hereafter referred to as primary care units [PCUs]) composed of general practitioners (GPs), nurses, and specialist doctors have recently been established in the Italian context, with the main aim of improving integrated care for chronic diseases.

Purposes:
The aim of the study was to assess whether the increased professional diversity of PCUs has resulted in an improvement in the integrated care of type II diabetes and to identify a potential mechanism mediating this effect.

Methodology/Approach:
We analyzed 213 PCUs, comparing their performance in integrated type II diabetes care at two time points. Using social categorization theory and a fixed effects regression analysis, we tested a mediation model in which the frequency of communication among GPs in the PCUs, that is, within-subgroup communication, mediates the relationship between PCU professional diversity and team performance in diabetes care.

Findings:
We show that when the professional diversity of the PCUs increases, integrated care of type II diabetes improves and better meets the standards of optimal care. Within-GP subgroup communication works as a mediating mechanism that translates the PCU professional diversity into better team performance. The mediation effect, however, is curvilinear. Beyond certain levels, within-subgroup communication can hamper PCUs’ capacity to work collaboratively in integrated type II diabetes care.

Practice Implications:
The article suggests that, when creating interprofessional primary care teams, managers might be able to steer teams toward a better performance by encouraging communication among peers of the same profession.
Self-Management Program for Heart Healthy Behavior Among Middle- and Old-Aged Korean Women at Risk for Metabolic Syndrome
Authors: Shin Nah-Mee , Choi JiWon , Cho InHae , Park Byung-Jun 
Published: March 2017

Background:
The prevalence of metabolic syndrome (MetS) has been increasing among Koreans, and middle-aged and older women are at risk of metabolic syndrome. Effective strategies to promote lifestyle modification need to be developed.

Objective:
We examined the effects of a self-management program on improving the cardiovascular health status and promoting healthy behaviors among overweight or obese Korean women at risk of metabolic syndrome.

Methods:
A pretest and posttest intervention design was used. Sixty women participated in a group teaching session. They also received a pedometer and a diary for self-monitoring. On the basis of blood test results, women's metabolic syndrome status was identified. Thirty women with metabolic syndrome received additional tailored counseling and weekly follow-up calls for 4 weeks, whereas 30 women without metabolic syndrome did not receive any tailored counseling or follow-up calls. Twenty-three women in the MetS group and 22 women in the non-MetS group completed the posttest.

Results:
Overall, women significantly improved their cardiovascular health status including systolic blood pressure, diastolic blood pressure, body mass index, low-density lipoprotein, triglycerides, number of metabolic syndrome risk factors, and 10-year risk estimates from pretest to posttest. Seventy-eight percent of the MetS group (n = 18) no longer had metabolic syndrome, whereas 5% of the non-MetS group (n = 1) became to have metabolic syndrome. Women significantly increased frequency and duration of walking per week and significantly decreased the time spent sitting.

Conclusions:
Promoting self-management for healthy behaviors might be effective for obese or overweight women to prevent metabolic syndrome and cardiovascular diseases, if it is tailored to their health needs.
Cochlear Transcriptome Following Acoustic Trauma and Dexamethasone Administration Identified by a Combination of RNA-seq and DNA Microarray
Authors: Maeda Yukihide , Omichi Ryotaro , Sugaya Akiko , Kariya Shin , Nishizaki Kazunori 
Published: March 2017

Aim:
To elucidate molecular mechanisms of noise-induced hearing loss (NIHL) and glucocorticoid therapy in the cochlea.

Background:
Glucocorticoids are used to treat many forms of acute sensorineural hearing loss, but their molecular action in the cochlea remains poorly understood.

Methods:
Dexamethasone was administered intraperitoneally immediately following acoustic overstimulation at 120 dB SPL for 2 hours to mice. The whole cochlear transcriptome was analyzed 12 and 24 hours following noise trauma and dexamethasone administration by both next-generation sequencing (RNA-seq) and DNA microarray. Differentially expressed genes (DEGs) with more than 2-fold changes after noise trauma and dexamethasone administration were identified. The functions of these DEGs were analyzed by David Bioinformatics Resources and a literature search.

Results:
Twelve hours after acoustic overstimulation, immune-related gene pathways such as “chemokine signaling activity,” “cytokine-cytokine receptor interaction,” and “cell adhesion molecules (CAMs) in the immune system” were significantly changed compared with the baseline level without noise. These DEGs were involved in immune and defense responses in the cochlea. Dexamethasone was administered to this NIHL model, and it modulated gene pathways of “cytokine-cytokine receptor interaction” and “cell adhesion molecules (CAMs) in the immune system” at 12 hours, compared with saline-injected control. Dexamethasone-dependent DEGs were also involved in immune and defense responses. A literature search showed that 10 other genes associated with hearing functions were regulated by dexamethasone both at 12 and 24 hours post-administration.

Conclusion:
Dexamethasone modulates the immune reaction in the traumatized cochlea following acoustic overstimulation. Dexamethasone may also regulate cochlear functions other than immunity.
Predicting Auditory Outcomes From Radiological Imaging in Cochlear Implant Patients With Cochlear Nerve Deficiency
Authors: Wei Xingmei , Li Yongxin , Chen Biao , Gong Yue , Fu Qian-Jie , Liu Ting , Cui Danmo , Su Qiaotong , Shi Ying 
Published: March 2017

Objective:
To compare imaging and outcome data in cochlear implant (CI) patients with and without cochlear nerve deficiency (CND).

Study Design:
Retrospective study comparing presurgical imaging (via high-resolution computed tomography and three-dimensional magnetic resonance imaging) to postsurgical auditory outcomes in CI patients with and without CND.

Patients:
Forty-three CI patients with CND diagnosed according to preoperative imaging were included in the CND group. A control group (non-CND; n = 43) was matched to the CND group in terms of age at implantation, CI device type, preoperative hearing threshold, and sex.

Results:
Across all subjects, internal auditory canal (IAC) diameter, cochlear nerve canal (CNC) diameter, and the number of nerve bundles were significantly correlated with all auditory outcome measures (p < 0.0125 in all cases). Across CND subjects, CNC diameter was significantly correlated with SIR, MUSS, and MAIS-IT/ MAIS scores (p < 0.0125 in all cases). Auditory outcomes were significantly poorer for CND patients with one rather than two nerve bundles. Across non-CND subjects, CNC diameter was significantly correlated only with SIR scores (p < 0.0125). IAC diameter, CNC diameter, and the number of nerve bundles were significantly smaller, and auditory outcomes were significantly poorer for the CND group than for the non-CND group (p < 0.05 in all cases). Results were similar when data only from patients ≤ 5 years old (n = 31) were analyzed.

Conclusions:
CNC diameter and the number of nerve bundles can significantly predict auditory outcomes for CI patients with CND. The results suggest that presurgical imaging may be useful in predicting CI outcomes for congenitally deaf patients.
Molecular mechanisms that mediate invasion and egress of malaria parasites from red blood cells
Authors: Alaganan Aditi , Singh Pallavi , Chitnis Chetan E. 
Published: March 2017

Purpose of review
Malaria parasites invade and multiply in diverse host cells during their complex life cycle. Some blood stage parasites transform into male and female gametocytes that are transmitted by female anopheline mosquitoes. The gametocytes are activated in the mosquito midgut to form male and female gametes, which egress from RBCs to mate and form a zygote. Here, we will review our current understanding of the molecular mechanisms that mediate invasion and egress by malaria parasites at different life cycle stages.

Recent findings
A number of key effector molecules such as parasite protein ligands for receptor-engagement during invasion as well as proteases and perforin-like proteins that mediate egress have been identified. Interestingly, these parasite-encoded effectors are located in internal, vesicular organelles and are secreted in a highly regulated manner during invasion and egress. Here, we will review our current understanding of the functional roles of these effectors as well as the signaling pathways that regulate their timely secretion with accurate spatiotemporal coordinates.

Summary
Understanding the molecular basis of key processes such as host cell invasion and egress by malaria parasites could provide novel targets for development of inhibitors to block parasite growth and transmission.
A role for intracellular and extracellular DEK in regulating hematopoiesis
Authors: Capitano Maegan L. , Broxmeyer Hal E. 
Published: March 2017

Purpose of review
Hematopoietic stem/progenitor cell fate decision during hematopoiesis is regulated by intracellular and extracellular signals such as transcription factors, growth factors, and cell-to-cell interactions. In this review, we explore the function of DEK, a nuclear phosphoprotein, on gene regulation. We also examine how DEK is secreted and internalized by cells, and discuss how both endogenous and extracellular DEK regulates hematopoiesis. Finally, we explore what currently is known about the regulation of DEK during inflammation.

Recent findings
DEK negatively regulates the proliferation of early myeloid progenitor cells but has a positive effect on the differentiation of mature myeloid cells. Inflammation regulates intracellular DEK concentrations with inflammatory stimuli enhancing DEK expression. Inflammation-induced nuclear factor-kappa B activation is regulated by DEK, resulting in changes in the production of other inflammatory molecules such as IL-8. Inflammatory stimuli in turn regulates DEK secretion by cells of hematopoietic origin. However, how inflammation-induced expression and secretion of DEK regulates hematopoiesis remains unknown.

Summary
Understanding how DEK regulates hematopoiesis under both homeostatic and inflammatory conditions may lead to a better understanding of the biology of HSCs and HPCs. Furthering our knowledge of the regulation of hematopoiesis will ultimately lead to new therapeutics that may increase the efficacy of hematopoietic stem cell transplantation.
International Sexual Partnerships May Be Shaped by Sexual Histories and Socioeconomic Status
Authors: Truong Hong-Ha M. , Mehrotra Megha , Montoya Orlando , Lama Javier R. , Guanira Juan V. , Casapía Martín , Veloso Valdiléa G. , Buchbinder Susan P. , Mayer Kenneth H. , Chariyalertsak Suwat , Schechter Mauro , Bekker Linda-Gail , Kallás Esper G. , Grant Robert M. 
Published: March 2017

Abstract
Exchange sex and higher education were associated with an increased likelihood of international sexual partnerships (ISPs). Exchange sex and older age were associated with an increased likelihood of condomless sex in ISPs. Educational and socioeconomic factors may create unbalanced power dynamics that influence exchange sex and condomless sex in ISPs.
Nocebo effects in clinical studies: hints for pain therapy
Authors: Klinger Regine , Blasini Maxie , Schmitz Julia , Colloca Luana 
Published: March 2017

Abstract

Introduction:
Nocebo-induced algesic responses occurring within clinical contexts present a challenge for health care practitioners working in the field of pain medicine.

Objectives:
Following the recent research on algesic nocebo effects, the scope of this review is to develop ethically acceptable strategies to help avoid, or at least reduce, nocebo responses within clinical settings.

Methods:
We reviewed relevant clinical studies that depict how patient-practitioner interactions may contribute to the reduction of nocebo responses.

Results:
A strong algesic nocebo effect may adversely impact a patient's condition by causing decreases in both the efficacy and effectiveness of interventions, as well as by promoting treatment nonadherence and discontinuation. These effects may be triggered through multiple channels and can lead to significant alterations in a patient's perception of pain, consequently producing a weakening of the specific positive effects of pharmacological, psychological, or physical pain-management interventions.

Conclusion:
To minimize nocebo effects in clinical settings, we identified and discussed five contextual aspects relevant to the treatment of patients with chronic pain: (1) negative patient–clinician communication and interaction during treatment; (2) emotional burden of patients during treatment with analgesic medication; (3) negative information provided via informational leaflets; (4) cued and contextual conditioning nocebo effects; and (5) patient's lack of positive information. Through an understanding of these elements, many preventive and ethically acceptable clinical actions can be taken to improve multidisciplinary pain treatment outcomes.
The Patients’ Perspective: Hematological Cancer Patients’ Experiences of Adverse Events as Part of Care
Authors: Bryant Jamie , Carey Mariko , Sanson-Fisher Rob , Turon Heidi , Wei Andrew , Kuss Bryone 
Published: March 2017

Objective
To describe in a sample of patients with a confirmed diagnosis of a hematological cancer: (a) the proportion who self-report experiencing an unexpected adverse event as part of their care; (b) how the adverse event was handled by the health-care organization; and (c) the sociodemographic, disease, and treatment characteristics associated with experiencing an adverse event.

Design
Cross sectional survey.

Setting
Three Australian hematological oncology treatment centers.

Participants
Individuals with a confirmed diagnosis of a hematological cancer.

Main Outcome Measures
Participants were asked if they had ever experienced an adverse event in their cancer care. Those who did were asked about their perceptions concerning what the adverse event was related to, how much harm the event caused, who identified the adverse event, and how the health-care organization responded to the adverse event.

Results
Forty-two participants (26.4%) perceived that they had experienced an unexpected adverse event as part of their care. Most were told about the event as soon as it happened (62%) and were given an explanation about why the event occurred (75%). Fewer were given information about how to take the matter further if they wished (43%). Participants who were unemployed, retired, disabled, or performed home duties and those whose employment status was “other” had higher odds of reporting an adverse event than those in full- or part-time employment.

Conclusions
There is a need for routinely querying patients during their treatment regarding the occurrence of unexpected adverse events. In addition, there is a need for improvement in the responses of health-care providers and the health-care system to these events in regard to full disclosure, apology, and options available to the patient for resolution.
Use of corticosteroids for pain control in cancer patients with bone metastases: a comprehensive literature review
Authors: Lim Fiona M.Y. , Bobrowski Adam , Agarwal Arnav , Silva Mauricio F. 
Published: March 2017

Purpose of review
Despite a limited understanding of the exact mechanism, corticosteroids are commonly employed for pain control in patients with bone metastases. The aim of this review was to evaluate the efficacy of corticosteroid-mediated pain control in patients with bone metastases associated with solid cancers.

Recent findings
A literature search was conducted using OVID MEDLINE and Embase databases (from 1946 up to July 19, 2016). Studies involving patients with bone metastases receiving corticosteroids as the primary means of pain control were included. Screening and data extraction were conducted by paired reviewers, with consensus established by discussion, or a third adjudicator. A total of 12 studies were included. Rates of pain relief achieved with corticosteroid use varied from 30 to 70%, but generally reflected moderate pain control. Corticosteroid use significantly reduced the incidence of pain flare alongside radiotherapy, reportedly by almost half of baseline pain severity. Adverse events were not documented consistently across studies, though grade two to three hyperglycemia was noted in approximately 2% of patients by some studies.

Summary
Recent evidence suggests that short-term corticosteroid use may provide moderate pain and pain flare control with radiotherapy for patients with bone metastases. The risk of developing adverse effects should be carefully considered prior to therapy initiation on a case-by-case basis.
Guiding the design of bacterial signaling interactions using a coevolutionary landscape
Authors: Cheng R. R. , Haglund E. , Tiee N. , Morcos F. , Levine H. , Adams J. A. , Jennings P. A. , Onuchic J. N. 
Published: March 2017

AbstractThe selection of amino acid identities that encode new interactions between two-component signaling (TCS) proteins remains a significant challenge. Recent work constructed a co-evolutionary landscape that can be used to select mutations to maintain signal transfer interactions betweenpartnerTCS proteins without introducing signal transfer between non-partners (crosstalk). A bigger challenge is to introduce mutations between non-natural partner TCS proteins using the landscape to enhance, suppress, or have a neutral effect on their basal signal transfer rates. This study focuses on the selection of mutations to a response regulator (RR) fromBacilus subtilisand its effect on phosphotransfer with a histidine kinase (HK) fromEscherichia Coli. Twelve single-point mutations of the RR protein are selected from the landscape and experimentally expressed to directly test the theoretical predictions on the effect of signal transfer. Differential Scanning Calorimetry is used to monitor any protein stability effects caused by the mutations, which could be detrimental to proper protein function. Of these proteins, seven mutants successfully perturb phosphoryl transfer activity in the computationally predicted manner between the TCS proteins. Furthermore, brute-force exhaustive mutagenesis approaches indicate that only 1% of mutations result in enhanced activity. In comparison, of the six mutations predicted to enhance phosphotransfer, two mutations exhibit a significant enhancement while two mutations are comparable to the wild-type. Thus co-evolutionary landscape theory offers significant improvement over traditional large-scale mutational studies in the efficiency of selecting mutations for protein engineering and design.
Identification of Candidate Drugs for Heart Failure using Tensor Decomposition-Based Unsupervised Feature Extraction Applied to Integrated Analysis of Gene Expression between Heart Failure and DrugMatrix Datasets
Authors: Taguchi Y-h. 
Published: March 2017

AbstractIdentifying drug target genes in gene expression profiles is not straightforward. Because a drug targets not mRNAs but proteins, mRNA expression of drug target genes is not always altered. In addition, the interaction between a drug and protein can be context dependent; this means that simple drug incubation experiments on cell lines do not always reflect the real situation during active disease. In this paper, I apply tensor decomposition-based unsupervised feature extraction to the integrated analysis of gene expression between heart failure and the DrugMatrix dataset where comprehensive data on gene expression during various drug treatments of rats were reported. I found that this strategy, in a fully unsupervised manner, enables us to identify a combined set of genes and compounds, for which various associations with heart failure were reported.
The Golgi matrix protein giantin is required for normal cilia function in zebrafish
Authors: Bergen Dylan J.M. , Stevenson Nicola L. , Skinner Roderick E.H. , Stephens David J. , Hammond Chrissy L. 
Published: March 2017

AbstractThe Golgi is essential for glycosylation of newly synthesised proteins including almost all cell-surface and extracellular matrix proteoglycans. Giantin, encoded by thegolgb1gene, is a member of the golgin family of proteins that reside within the Golgi stack but its function remains elusive. Loss-of-function of giantin in rats causes osteochondrodysplasia; knockout mice show milder defects, notably a cleft palate. In vitro, giantin has been implicated in Golgi organization, biosynthetic trafficking, and ciliogenesis. Here we show that loss-of-function of giantin in zebrafish, using either morpholino or knockout techniques, causes defects in cilia function. Giantin morphants have fewer cilia in the neural tube and those remaining are longer. Mutants have the same number of cilia in the neural tube but these cilia are also elongated. Scanning electron microscopy shows that loss of giantin results in an accumulation of material at the ciliary tip, consistent with a loss-of-function of retrograde intraflagellar transport. Mutants show milder defects than morphants consistent with adaptation to loss of giantin.Summary statementLoss of giantin following either morpholino injection or genome editing in zebrafish results in defects in ciliogenesis.