bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low‐power laser irradiation in salivary glands reduces glycemia in streptozotocin‐induced diabetic female rats
Authors: Fukuoka Cíntia Yuki , Torres Schröter Gabriella , Nicolau José , Simões Alyne 
Published: October 2016

Low‐power laser irradiation (LPLI) has been extensively employed to modulate inflammation in vitro and in vivo. Previous reports from our group indicated that LPLI might regulate glycemia in diabetic animals. Diabetes results in chronic hyperglycemia and therefore chronic inflammation by upregulation of inflammatory markers such as the high mobility group box 1 (HMGB1) protein. Thus this study aimed to analyze the LPLI effects upon blood glucose levels, plasma insulin and HMGB1 concentrations in a diabetes experimental rat model. Streptozotocin‐induced diabetic rats were irradiated in the salivary glands area with a diode laser applied at 660 nm, 70 mW, 20 J/cm2, 22.4 J, with a spot area of 0.028 cm2 and its effects were evaluated. LPLI significantly reduced diabetic rat hyperglycemia, without changing insulin or HMGB1 plasma levels, but possibly by ameliorating the insulin resistance in these animals. These findings suggest that LPLI might have a systemic effect, but more studies are necessary to better understand its mechanisms.
Fasting blood glucose measured by peroxidase‐glucose oxidase (PGO) method (A), showing a reduction of diabetic animals glycemia after LPLI. LPLI probably reduced the hyperglycemia in diabetes by improving the insulin resistance in these animals (B). C n = 10, CL n = 10, D n = 7 and DL n = 8. Data are expressed as mean ± SD; * P < 0.05 vs. respective control group; # P < 0.05 vs. D group.magnified imageFasting blood glucose measured by peroxidase‐glucose oxidase (PGO) method (A), showing a reduction of diabetic animals glycemia after LPLI. LPLI probably reduced the hyperglycemia in diabetes by improving the insulin resistance in these animals (B). C n = 10, CL n = 10, D n = 7 and DL n = 8. Data are expressed as mean ± SD; * P < 0.05 vs. respective control group; # P < 0.05 vs. D group.
The Effects of Aging and Sex Steroid Deficiency on the Murine Skeleton Are Independent and Mechanistically Distinct
Authors: Ucer Serra , Iyer Srividhya , Kim Ha-Neui , Han Li , Rutlen Christine , Allison Kelly , Thostenson Jeff D , de Cabo Rafael , Jilka Robert L , O'Brien Charles , Almeida Maria , Manolagas Stavros C 
Published: October 2016

ABSTRACT

Old age and sex steroid deficiency are the two most critical factors for the development of osteoporosis. It remains unknown, however, whether the molecular culprits of the two conditions are similar or distinct. We show herein that at 19.5 months of age—a time by which the age-dependent decline of cortical and cancellous bone mass and cortical porosity were fully manifested in C57BL/6J mice—these animals remained functionally estrogen sufficient. Transgenic mice with conditional expression of mitochondria-targeted catalase—a potent H2O2 inactivating enzyme—in cells of the myeloid lineage (mitoCAT;LysM-Cre mice) were protected from the loss of cortical, but not cancellous, bone caused by gonadectomy in either sex. Consistent with these findings, in vitro studies with ERα-deficient Prx1+ cells and gonadectomized young adult mice showed that in both sexes decreased ERα signaling in Prx1+ cells leads to an increase in SDF1, a.k.a. CXCL12, an osteoclastogenic cytokine whose effects were abrogated in macrophages from mitoCAT;LysM-Cre mice. In contrast to sex steroid deficiency, the adverse effects of aging on either cortical or cancellous bone were unaffected in mitoCAT;LysM-Cre mice. On the other hand, attenuation of H2O2 generation in cells of the mesenchymal lineage targeted by Prx1-Cre partially prevented the loss of cortical bone caused by old age. Our results suggest the effects of sex steroid deficiency and aging on the murine skeleton are independent and result from distinct mechanisms. In the former, the prevailing mechanism of the cortical bone loss in both sexes is increased osteoclastogenesis caused by estrogen deficiency; this is likely driven, at least in part, by mesenchymal/stromal cell–derived SDF1. Decreased osteoblastogenesis, owing in part to increased H2O2, combined with increased osteoclastogenesis caused by aging mechanisms independent of estrogen deficiency, are the prevailing mechanisms of the loss of cortical bone with old age. © 2016 American Society for Bone and Mineral Research.
Red blood cell exchange: 2015 American Society for Apheresis consensus conference on the management of patients with sickle cell disease
Authors: Sarode Ravi , Ballas Samir K. , Garcia Alicia , Kim Haewon C , King Karen , Sachais Bruce , Williams Lance A. 
Published: October 2016

AbstractThe American Society for Apheresis (ASFA) conducted a one‐day consensus conference on red blood cell exchange (RBCx) in sickle cell disease (SCD) during its annual meeting in San Antonio, TX, on May 5, 2015. The authors of this article, a subcommittee of ASFA's Clinical Applications Committee, developed several questions with regard to pathophysiology of SCD and use of RBCx in the management of various complications. These questions were provided to the seven invited speakers who are the experts in the field of SCD. Two experts in the field moderated the proceedings of the conference, which was attended by more than 150 participants. After each presentation, there was a summary of the main points by the moderators and an open discussion with questions from the audience. A video recording of the proceedings, as well as each presentation, was made available to the authors. Each author's summary was reviewed and approved by the respective speaker before submission of this manuscript. The subcommittee also developed several key questions to generate a consensus amongst the speakers on key issues for using RBCx for patients with SCD.
Lipid modulation of skeletal muscle mass and function
Authors: Lipina Christopher , Hundal Harinder S 
Published: October 2016

AbstractLoss of skeletal muscle mass is a characteristic feature of various pathologies including cancer, diabetes, and obesity, as well as being a general feature of ageing. However, the processes underlying its pathogenesis are not fully understood and may involve multiple factors. Importantly, there is growing evidence which supports a role for fatty acids and their derived lipid intermediates in the regulation of skeletal muscle mass and function. In this review, we discuss evidence pertaining to those pathways which are involved in the reduction, increase and/or preservation of skeletal muscle mass by such lipids under various pathological conditions, and highlight studies investigating how these processes may be influenced by dietary supplementation as well as genetic and/or pharmacological intervention.
Doxorubicin inhibits muscle inflammation after eccentric exercise
Authors: Huang Sheng‐Chih , Wu Jin‐Fu , Saovieng Suchada , Chien Wei‐Horng , Hsu Ming‐Fen , Li Xiao‐Fei , Lee Shin‐Da , Huang Chih‐Yang , Huang Chih‐Yang , Kuo Chia‐Hua 
Published: October 2016

AbstractBackgroundDoxorubicin, a widely used anti‐tumour drug, is known to cause muscle loss in cancer patients.MethodsFollowing an acute dose of doxorubicin injection (2.5 mg/kg per body weight), we examined macrophage distribution in rat soleus muscle challenged by eccentric exercise (downhill running). Long‐term doxorubicin treatment (one injection every 3 days) on muscle mass and survival were also determined.ResultsUnder non‐exercised condition, increased tumour necrosis factor (TNF)‐alpha mRNA and decreased IL‐10 mRNA were observed in soleus muscle of doxorubicin‐treated rats, compared with saline‐treated control rats. However, increases in inflammation score (leukocyte infiltration), nitrotyrosine level, and M1 macrophage (CD68+) invasion in exercised soleus muscle were absent in doxorubicin‐treated rats, whereas increased M2 macrophage (CD163+) localization in exercised muscle was less affected by doxorubicin. Despites coenzyme Q (Q10) supplementation significantly elevated TNF‐alpha mRNA, nitrotyrosine, and anti‐oxidant gamma‐glutamylcysteine synthetase (GCS) levels in non‐exercised soleus muscle, these pro‐inflammatory responses were also abolished in doxorubicin‐treated rats. Results from long‐term doxorubicin treatment show a significant muscle loss followed by an accelerated death, which cannot be reversed by Q10 supplementation.Conclusions(i) Doxorubicin impairs inflammation mechanism by depleting M1 macrophage in exercised skeletal muscle; (ii) Muscle loss and accelerated death during prolonged doxorubicin treatment cannot be reversed by Q10 supplementation.
Effects of Water Loss on New Mexico Spadefoot Toad (Spea multiplicata) Development, Spleen Cellularity, and Corticosterone Levels
Authors: Bagwill April L. , Lovern Matthew B. , Worthington Thomas A. , Smith Loren M. , McMurry Scott T. 
Published: October 2016

ABSTRACTAmphibian metamorphosis is complex and larval morphology and physiology are completely restructured during this time. Amphibians that live in unpredictable environments are often exposed to stressors that can directly and indirectly alter physiological systems during development, with subsequent consequences (carryover effects) later in life. In this study, we investigated the effects of water level reduction on development rate, spleen size and cellularity, and examined the role of corticosterone levels in premetamorphic, metamorphic, and postmetamorphic New Mexico spadefoot toads (Spea multiplicata). Based on previous studies, we hypothesized that declining water level would increase tadpole developmental rate, but with the trade‐off of increasing corticosterone to a level that would subsequently affect spleen size and cellularity, thus prolonging potential immunological suppression. Declining water levels increased developmental rate by 3 days; however, there were no significant body size effects. Corticosterone (CORT) was negatively correlated with total length, snout vent length, body weight, and spleen weight at metamorphosis, suggesting that size at metamorphosis and the immune system may be affected by excessive CORT levels. When compared to other studies, our results support the view that multiple factors may be acting as stressors in the field affecting amphibian responses, and simple pathways as tested in this study may not adequately represent field conditions.
Characteristics of C‐terminal, β‐amyloid peptide binding fragment of neuroprotective protease inhibitor, cystatin C
Authors: Spodzieja Marta , Kalejta Katarzyna , Kołodziejczyk Aleksandra S. , Maszota‐Zieleniak Martyna , Rodziewicz‐Motowidło Sylwia , Żmudzińska Wioletta , Czaplewska Paulina 
Published: October 2016

AbstractCystatin C originally identified as a cysteine proteases inhibitor has a broad spectrum of biological roles ranging from inhibition of extracellular cysteine protease activities, bone resorption, and modulation of inflammatory responses to stimulation of fibroblasts proliferation. There is an increasing number of evidence to suggest that human cystatin C (hCC) might play a protective role in the pathophysiology of sporadic Alzheimer's disease.In vivo and in vitro results well documented the association of hCC with Aβ and the hCC‐induced inhibition of Aβ fibril formation. In our earlier work, using a combination of selective proteolytic methods and MS spectroscopy, C‐terminal fragment hCC(101‐117) was identified as the Aβ‐binding region. The fragment of Aβ peptide responsible for the complex formation with hCC was found in the middle, highly hydrophobic part, Aβ(17‐24). Structures and affinities of both Aβ and hCC binding sites were characterized by the enzyme‐linked immunosorbent assay‐like assay, by surface plasmon resonance, and by nano‐ESI‐FTICR MS of the hCC–Aβ‐binding peptide complexes. In the in vitro inhibition studies, the binding cystatin sequence, hCC(101‐117), revealed the highest relative inhibitory effect toward Aβ‐fibril formation.Herein, we present further studies on molecular details of the hCC‐Aβ complex. With Ala substitution, affinity experiments, and enzyme‐linked immunosorbent assay‐like assays for the Aβ‐binding fragment, hCC(101‐117), and its variants, the importance of individual amino acid residues for the protein interaction was evaluated. The results were analyzed using hCC(101‐117) nuclear magnetic resonance structural data with molecular dynamics calculations and molecular modeling of the complexes. The results point to conformational requirements and special importance of some amino acid residues for the protein interaction. The obtained results might be helpful for the design of low molecular compounds modulating the biological role of both proteins. Copyright © 2016 John Wiley & Sons, Ltd.
Effect of Nitroglycerin on the Performance of MR Coronary Angiography
Authors: Heer Tobias , Reiter Stephanie , Trißler Markus , Höfling Berthold , von Knobelsdorff‐Brenkenhoff Florian , Pilz Günter 
Published: October 2016

PurposeTo systematically investigate the effect of sublingual glyceryl trinitrate (nitroglycerin=nitro=glyceryl trinitrate=GTN=C3H5N3O9 [NTG]) on the diagnostic performance of MR coronary artery imaging (MRCA) to detect relevant coronary artery disease (CAD).Materials and MethodsThirty‐five healthy volunteers and 25 patients with suspected or proven CAD (all in sinus rhythm) underwent MRCA before and after NTG using a contrast‐agent free, three‐dimensional, navigator‐based, steady state free precession acquisition (voxel size 1.0 × 0.7 × 0.7 mm3) at 1.5 Tesla. Target parameters were stenosis detection (>50%), visible vessel length (straightened planar reconstruction) and vessel diameter (curved planar reconstruction, measured proximal/medial/distal). In patients, invasive coronary angiography served as reference.ResultsNTG led to increase of the coronary diameter both in healthy volunteers (right coronary artery [RCA]: 3.2 to 3.7 mm, P < 0.001; left anterior descending coronary artery [LAD]: 2.9 to 3.4 mm, P = 0.009; left circumflex coronary artery [LCx]: 2.8 to 3.3 mm, P < 0.001) and patients (RCA 3.5 to 4.0 mm, P = 0.01; LAD 3.3 to 3.7 mm, P = 0.008; LCx: 2.9 to 3.3 mm, P = 0.03). Visible vessel length increased after NTG for the LAD (volunteers: 72 to 84 mm, P = 0.03; patients: 56 to 78 mm, P = 0.01) and for LCx (volunteers: 48 to 60 mm, P = 0.02). Sensitivity to detect > 50% stenosis improved after NTG from 88.0 to 96%, specificity from 46.5 to 69.8%, diagnostic accuracy from 61.8 to 79.4% and positive/negative predictive value from 48.9 to 64.9% and 87.0 to 96.8%, respectively.ConclusionSublingual administration of NTG significantly enhanced the visibility of the coronary arteries and improved the detection of coronary artery stenosis.Level of Evidence: 2J. MAGN. RESON. IMAGING 2017;45:1419–1428
Ultrashort echo time MRI biomarkers of asthma
Authors: Sheikh Khadija , Guo Fumin , Capaldi Dante P.I. , Ouriadov Alexei , Eddy Rachel L. , Svenningsen Sarah , Parraga Grace ,   for the Canadian Respiratory Research Network
Published: October 2016

PurposeTo develop and assess ultrashort echo‐time (UTE) magnetic resonance imaging (MRI) biomarkers of lung function in asthma patients.Materials and MethodsThirty participants including 13 healthy volunteers and 17 asthmatics provided written informed consent to UTE and pulmonary function tests in addition to hyperpolarized‐noble‐gas 3T MRI and computed tomography (CT) for asthmatics only. The difference in MRI signal‐intensity (SI) across four lung volumes (full‐expiration, functional‐residual‐capacity [FRC], FRC+1L, and full‐inspiration) was determined on a voxel‐by‐voxel basis to generate dynamic proton‐density (DPD) maps. MRI ventilation‐defect‐percent (VDP), UTE SI, and DPD values as well as CT radiodensity were determined for whole lung and individual lobes.ResultsMean SI at full‐expiration (P < 0.01), FRC (P < 0.05), and DPD (P < 0.01) were greater in healthy volunteers compared to asthmatics. In asthmatics, UTE SI at full‐expiration and DPD were correlated with FEV1/FVC (SI r = 0.73/P = 0.002; DPD r = 0.75/P = 0.003), RV/TLC (SI r = –0.57/P = 0.02), or RV (DPD r = –0.62/P = 0.02), CT radiodensity (SI r = 0.83/P = 0.006; DPD r = 0.71/P = 0.01), and lobar VDP (SI rs = –0.33/P = 0.02; DPD rs = –0.47/P = 0.01).ConclusionIn patients with asthma, UTE SI and dynamic proton‐density were related to pulmonary function measurements, whole lung and lobar VDP, as well as CT radiodensity. Thus, UTE MRI biomarkers may reflect ventilation heterogeneity and/or gas‐trapping in asthmatics using conventional equipment, making this approach potentially amenable for clinical use.Level of Evidence: 2J. Magn. Reson. Imaging 2017;45:1204–1215
Cost‐effectiveness analysis of multiparametric MRI with increased active surveillance for low‐risk prostate cancer in Australia
Authors: Gordon Louisa G. , James Robbie , Tuffaha Haitham W. , Lowe Anthony , Yaxley John 
Published: October 2016

PurposeTo evaluate the cost‐effectiveness of multiparametric magnetic resonance imaging (mpMRI) to diagnose prostate cancer and direct all low‐risk patients into active surveillance (AS).Materials and MethodsA Markov cohort model was developed to assess three scenarios: 1) no mpMRI and current AS; 2) mpMRI and current AS; and 3) mpMRI and increased AS. Men were tracked from diagnosis to end‐of‐life. Estimates to populate the model were derived from systematic reviews, meta‐analyses, epidemiological publications, and national cost reports. An Australian Government perspective was used. Outcomes included healthcare costs, survival, quality‐adjusted life years (QALYs), number of biopsies, and significant and insignificant cancers. Extensive sensitivity analyses were undertaken to address possible variation in the modeled inputs.ResultsMean lifetime costs per patient were AU$23,191 for Scenario 1, AU$23,387 for Scenario 2 and AU$21,064 for Scenario 3. Corresponding QALYs were 7.81, 7.77, 7.83 for Scenarios 1, 2, and 3, respectively. At the current uptake of AS in Australia, mpMRI alone does not appear cost‐effective (16.9% likelihood). However, mpMRI with AS for all men with low‐risk disease is strongly cost‐effective (86.9% likelihood) at a willingness‐to‐pay AU$50,000 per QALY gained. For the mpMRI options, for every 1000 men suspected of prostate cancer, using mpMRI would avoid 340 biopsies, detect an additional 20 significant cancers, and detect 10 fewer insignificant cancers.ConclusionDiagnosis of prostate cancer through mpMRI technology would be cost‐effective if it leads to increased uptake of AS for men with confirmed very‐low‐ or low‐risk prostate cancer.Level of Evidence: 2J. MAGN. RESON. IMAGING 2017;45:1304–1315
Whole‐tumor apparent diffusion coefficient measurements in nephroblastoma: Can it identify blastemal predominance?
Authors: Littooij Annemieke S. , Sebire Neil J. , Olsen Øystein E. 
Published: October 2016

PurposeTo explore the potential relation between whole‐tumor apparent diffusion coefficient (ADC) parameters in viable parts of tumor and histopathological findings in nephroblastoma.Materials and MethodsChildren (n = 52) with histopathologically proven nephroblastoma underwent diffusion‐weighted magnetic resonance imaging (MRI) (1.5T) before preoperative chemotherapy. Of these, 25 underwent an additional MRI after preoperative chemotherapy, shortly before resection. An experienced reader performed the whole‐tumor ADC measurements of all lesions, excluding nonenhancing areas. An experienced pathologist reviewed the postoperative specimens according to standard SIOP guidelines. Potential associations between ADC parameters and proportions of histological subtypes were assessed with Pearson's or Spearman's rank correlation coefficient depending on whether the parameters tested were normally distributed. In case the Mann–Whitney U‐test revealed significantly different ADC values in a subtype tumor, this ADC parameter was used to derive a receiver operating characteristic (ROC) curve.ResultsThe 25th percentile ADC at presentation was the best ADC metric correlated with proportion of blastema (Pearson's r = –0.303, P = 0.026). ADC after preoperative treatment showed moderate correlation with proportion stromal subtype at histopathology (r = 0.579, P = 0.002). By ROC analysis, the optimal threshold of median ADC for detecting stromal subtype was 1.362 × 10−3 mm2/s with sensitivity and specificity of 100% (95% confidence interval [CI] 0.65–1.00) and 78.9% (95% CI 0.57–0.92), respectively.ConclusionADC markers in nephroblastoma are related to stromal subtype histopathology; however, identification of blastemal predominant tumors using whole‐tumor ADC measurements is probably not feasible.Level of Evidence: 3J. MAGN. RESON. IMAGING 2017;45:1316–1324
Using a Jiles‐Atherton vector hysteresis model for isotropic magnetic materials with the finite element method, Newton‐Raphson method, and relaxation procedure
Authors: Guérin Christophe , Jacques Kévin , Sabariego Ruth V. , Dular Patrick , Geuzaine Christophe , Gyselinck Johan 
Published: October 2016

AbstractThis paper deals with the use of a Jiles‐Atherton vector hysteresis model included in 2D finite element modeling. The hysteresis model is only valid for isotropic materials. It is implemented with the vector potential formulation in 2D along with electric circuit equations to account for a possible external circuit. The Newton‐Raphson algorithm is used with a relaxation procedure, whereby at each iteration, the relaxation coefficient is sought so as to minimize the Euclidean norm of the residual of the finite element nonlinear system of equations. We have simulated several numerical examples with the proposed approach. First, simulations on a square domain were conducted so as to validate the model. We have further simulated a T‐shaped magnetic circuit (exhibiting rotating flux) and a 3‐phase 3‐limb transformer model. For these 2 cases, the eddy current losses in the laminations are taken into account by a low‐frequency model. We have finally performed simulations on the TEAM workshop problem 32, which consists of a 3‐limb transformer with 2 windings, for which current and local magnetic flux density measurements are available. We obtained a good agreement between computed and measured results.