bluuebunny/crossref_metadata_2025_split huggingface dataset:
Optimal prosthesis sizing in transcatheter aortic valve implantation by exclusive use of three‐dimensional transoesophageal echocardiography
Authors: Kretzschmar Daniel , Lauten Alexander , Goebel Bjoern , Doenst Torsten , Poerner Tudor C. , Ferrari Markus , Figulla Hans R. , Hamadanchi Ali 
Published: October 2014

SummaryPurposeThe assessment of aortic annular size is critical, and inappropriate sizing is thought to be a main reason of paravalvular aortic regurgitation. Multidetector computed tomograph is associated with the risk of contrast nephropathy. For optimal evaluation of the complex structure of the aortic annulus, three‐dimensional (3D)‐methods should be used. We therefore sought to determine the value of 3D‐transoesophageal echocardiography (3D‐TEE) for appropriate sizing.MethodsHundred and one patients (mean age 81·4 years) with symptomatic aortic valve stenosis (AS) and high surgical risk profile (mean log. EuroScore 28·8%) being scheduled for transcatheter aortic valve implantation (TAVI) were included. 2D‐ and 3D‐TEE were performed before the procedure to evaluate the aortic annulus diameter.ResultsMaximum, minimum and mean (max diameter + min diameter/2) annulus diameters were 24·7, 23·1 and 23. 9 mm in 3D‐TEE and compared to 22·6 mm in 2D‐TEE (P<0·001; 0·07; <0·001). The interobserver variability for 3D‐TEE was low with a mean difference of 0·18 mm compared to 2D‐TEE with 0·59 mm. The application of 3D‐TEE caused a change of prosthesis size selection in 40% of patients compared to 2D‐TEE. In this study, we implanted three different types of catheter‐mounted valves (Edwards‐SAPIEN™ XT valve, CoreValve™ and JenaValve™). Final angiography confirmed valve competence (mild insufficiency) in 91%, and there was no aortic regurgitation greater than moderate in the follow‐up echocardiographic evaluation.ConclusionAssessment of aortic annulus dimensions for TAVI size selection can safely be performed with 3D‐TEE only. Based on our results with significantly higher annulus diameter compared to 2D‐TEE, we recommend 3D‐TEE to reduce prosthesis undersizing.
Volatiles from non‐host aromatic plants repel tea green leafhopper Empoasca vitis
Authors: Zhang Zhengqun , Luo Zongxiu , Gao Yu , Bian Lei , Sun Xiaoling , Chen Zongmao 
Published: October 2014

AbstractThe tea green leafhopper, Empoasca vitis Göthe (Hemiptera: Cicadellidae), is a serious pest of tea crops in China. The effectiveness of five aromatic non‐host plants, Corymbia citriodora (Hook.) (Myrtaceae), Ocimum basilicum L. (Lamiaceae), Lavandula pinnata L. (Lamiaceae), Ruta graveolens L. (Rutaceae), and Rosmarinus officinalis L. (Lamiaceae), was investigated to determine their ability to suppress E. vitis on tea plants. Volatile organic compounds derived from L. pinnata, R. officinalis, and C. citriodora were found to repel leafhoppers and to mask the host's odors. Intercropping L. pinnata and C. citriodora with tea plants significantly reduced the E. vitis population levels in the tea plantation associated with higher population densities of generalist predators. The volatile compounds from the five non‐host plants were collected by headspace absorption under field conditions, and the 10 major components were identified. Qualitative and quantitative differences were found among the five odor profiles. Moreover, the emission dynamics of non‐host volatiles were monitored. Non‐host volatile emissions showed two peak periods, one in the spring and one in the autumn period. These peaks were almost consistent with the population dynamics of E. vitis. Our findings suggested that this newer approach to ecologically based, sustainable pest management implemented via intercropping with non‐host aromatic plants such as L. pinnata and C. citriodora offers a promising alternative to chemical control of the leafhopper population.
Survival for patients with chronic leukemias in the US and Britain: Age‐related disparities and changes in the early 21st century
Authors: Pulte Dianne , Redaniel Maria Theresa , Bird Jenny , Jeffreys Mona 
Published: October 2014

AbstractBackgroundChronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML) are highly treatable conditions occurring primarily in older patients. Lower survival among older people has been reported in both conditions, but newer treatments may change both the overall survival rate and the relative risk associated with aging. Here, we examine survival for patients with CLL and CML in the United States (US) and England.MethodsPatients with CLL and CML were identified from the Surveillance, Epidemiology, and End Results (US) and National Cancer Registry (England). Five‐year relative survival was calculated by major age group. Excess hazard ratios (EHR) by age were calculated for each condition, and multivariable analysis was performed to adjust for the following potential confounders: gender, race or ethnic group (US only), period of diagnosis, and a measure of socioeconomic deprivation (England only).ResultsFive‐year relative survival increased for both CLL and CML in both England and the US between 1996–2000 and 2006–2010. However, relative age‐related disparities persisted. For CLL, the EHR for death was 9.44 (7.84–11.36) in the US and 6.14 (5.65–6.68) in England for ages 85+ compared to ages 55–64. For CML, the EHR was 3.52 (3.17–3.90) in the US and 4.54 (4.13–4.98) in England for ages 75+ compared to ages 45–64.ConclusionsSurvival improved for patients with chronic leukemias in the early 21st century. However, age‐related disparities persist, despite clinical trial evidence that treatment in older adults with chronic leukemia can be safe and effective. Further research to determine the reasons for the lower survival in older patients and greater awareness of this problem may improve survival for older patients with chronic leukemia.
Clinical outcome after failure of hypomethylating therapy for myelodysplastic syndrome
Authors: Lee Je‐Hwan , Choi Yunsuk , Kim Sung‐Doo , Kim Dae‐Young , Lee Jung‐Hee , Lee Kyoo‐Hyung , Lee Sang‐Min , Lee Won‐Sik , Joo Young‐Don 
Published: October 2014

AbstractAround half of patients with myelodysplastic syndrome (MDS) fail to respond to hypomethylating therapy (HMT) and most responders progress within 2 yr. Retrospective studies report poor outcomes after HMT failure. Here, we analyzed the outcomes of patients suffering HMT failure. Of 149 patients with MDS treated with either azacitidine or decitabine, 91 who experienced HMT failure were included in the study. Median overall survival (OS) was 12.1 months: 16.2 months for lower‐risk MDS and 9.3 months for higher‐risk MDS. Disease status and progression to acute myeloid leukemia (AML) at the time of HMT failure were independent prognostic factors for OS. Fifty‐four patients received one or more treatment modalities, and 23 received allogeneic hematopoietic cell transplantation (HCT). The objective response to non‐transplant treatments was poor (11–17%), whereas 17 transplanted patients showed a complete response. OS probability at 2 yr post‐HCT was 60.9%: 78.6% for patients receiving HCT during MDS and 33.3% for those receiving HCT after developing AML. In conclusion, the clinical outcome of patients after HMT failure was poor. Long‐term disease‐free survival was observed in approximately 50% of patients who received allogeneic HCT. Therefore, allogeneic HCT should be performed early in appropriate patients, and particularly before progression to AML.
Human‐caused habitat fragmentation can drive rapid divergence of male genitalia
Authors: Heinen‐Kay Justa L. , Noel Holly G. , Layman Craig A. , Langerhans R. Brian 
Published: October 2014

AbstractThe aim of this study rests on three premises: (i) humans are altering ecosystems worldwide, (ii) environmental variation often influences the strength and nature of sexual selection, and (iii) sexual selection is largely responsible for rapid and divergent evolution of male genitalia. While each of these assertions has strong empirical support, no study has yet investigated their logical conclusion that human impacts on the environment might commonly drive rapid diversification of male genital morphology. We tested whether anthropogenic habitat fragmentation has resulted in rapid changes in the size, allometry, shape, and meristics of male genitalia in three native species of livebearing fishes (genus:Gambusia) inhabiting tidal creeks across six Bahamian islands. We found that genital shape and allometry consistently and repeatedly diverged in fragmented systems across all species and islands. Using a model selection framework, we identified three ecological consequences of fragmentation that apparently underlie observed morphological patterns: decreased predatory fish density, increased conspecific density, and reduced salinity. Our results demonstrate that human modifications to the environment can drive rapid and predictable divergence in male genitalia. Given the ubiquity of anthropogenic impacts on the environment, future research should evaluate the generality of our findings and potential consequences for reproductive isolation.
Evolutionary conservation—evaluating the adaptive potential of species
Authors: Eizaguirre Christophe , Baltazar‐Soares Miguel 
Published: October 2014

AbstractDespite intense efforts, biodiversity around the globe continues to decrease. To cease this phenomenon, we urgently need a better knowledge not only of the true extent of biodiversity, but also of the evolutionary potential of species to respond to environmental change. These aims are the heart of the developing field of Evolutionary conservation. Here, after describing problems associated with implementing evolutionary perspectives into management, we outline how evolutionary principles can contribute to efficient conservation programmes. We then introduce articles from this special issue on Evolutionary conservation, outlining how each study or review provides tools and concepts to contribute to efficient management of species or populations. Ultimately, we highlight what we believe can be future research avenues for evolutionary conservation.
Relationships between each category of 25‐item frailty risk assessment (Kihon Checklist) and newly certified older adults under Long‐Term Care Insurance: A 24‐month follow‐up study in a rural community in Japan
Authors: Fukutomi Eriko , Okumiya Kiyohito , Wada Taizo , Sakamoto Ryota , Ishimoto Yasuko , Kimura Yumi , Chen Wen‐Ling , Imai Hissei , Kasahara Yoriko , Fujisawa Michiko , Otsuka Kuniaki , Matsubayashi Kozo 
Published: October 2014

AimThe 25‐item Kihon Checklist (KCL) is the official self‐administered questionnaire tool to screen frail older adults, consisting of seven categories: physical strength, nutritional status, oral function, houseboundness, cognitive function, depression risk and a score of more than 9 out of 1–20 items. The aim of the present study was to evaluate the relationships between each category of the KCL and newly certified cases under the Long‐Term Care Insurance (LTCI) in Japan during 24 months.MethodThe study population consisted of 883 community‐dwelling adults aged 65 years or older uncertified by LTCI completing a questionnaire, which included the KCL and scales of basic/advanced activities of daily living (ADL), quality of life (QOL), and depressive symptoms. The participants were categorized into the risk or non‐risk group depending on the official criteria of each KCL category. The outcome was the incidence of newly certified cases by LTCI during 24 months. The difference between the risk and non‐risk group was analyzed by Cox regression hazard models.ResultsScores in basic/advanced ADL and QOL were higher, and the score in the geriatric depression scale was lower in the non‐risk than the risk group in KCL criteria. In men, the incidence of newly certified cases was higher in the risk group of the physical strength category after adjusting for age and the other categories of the KCL.ConclusionThe physical strength category in men was the only significant predictor of the incidence of newly certified cases by LTCI. Further studies are required to improve the assessment item of cognitive function in KCL under LTCI. Geriatr Gerontol Int 2015; 15: 864–871.
Regulatory T cells in B‐cell‐deficient and wild‐type mice differ functionally and in expression of cell surface markers
Authors: Ellis Jason S. , Braley‐Mullen Helen 
Published: October 2014

SummaryNOD.H‐2h4 mice develop spontaneous autoimmune thyroiditis (SAT) with chronic inflammation of thyroids by T and B cells. B‐cell deficient (B–/–) mice are resistant to SAT but develop SAT if regulatory T (Treg) cells are transiently depleted. We established a transfer model using splenocytes from CD28–/– B–/– mice (effector cells and antigen‐presenting cells) cultured with or without sorted Treg cells from Foxp3‐GFP wild‐type (WT) or B–/– mice. After transfer to mice lacking T cells, mice given Treg cells from B–/– mice had significantly lower SAT severity scores than mice given Treg cells from WT mice, indicating that Treg cells in B–/– mice are more effective suppressors of SAT than Treg cells in WT mice. Treg cells from B–/– mice differ from WT Treg cells in expression of CD27, tumour necrosis factor receptor (TNFR) II p75, and glucocorticoid‐induced TNFR‐related protein (GITR). After transient depletion using anti‐CD25 or diphtheria toxin, the repopulating Treg cells in B–/– mice lack suppressor function, and expression of CD27, GITR and p75 is like that of WT Treg cells. If B–/– Treg cells develop with B cells in bone marrow chimeras, their phenotype is like that of WT Treg cells. Addition of B cells to cultures of B–/– Treg and T effector cells abrogates their suppressive function and their phenotype is like that of WT Treg cells. These results establish for the first time that Treg cells in WT and B–/– mice differ both functionally and in expression of particular cell surface markers. Both properties are altered after transient depletion and repopulation of B–/– Treg cells, and by the presence of B cells during Treg cell development or during interaction with effector T cells.
Transcriptomic analysis of mononuclear phagocyte differentiation and activation
Authors: Hume David A. , Freeman Tom C. 
Published: October 2014

SummaryMonocytes and macrophages differentiate from progenitor cells under the influence of colony‐stimulating factors. Genome‐scale data have enabled the identification of the sets of genes that are associated with specific functions and the mechanisms by which thousands of genes are regulated in response to pathogen challenge. In large datasets, it is possible to identify large sets of genes that are coregulated with the transcription factors that regulate them. They include macrophage‐specific genes, interferon‐responsive genes, early inflammatory genes, and those associated with endocytosis. Such analyses can also extract macrophage‐associated signatures from large cancer tissue datasets. However, cluster analysis provides no support for a signature that distinguishes macrophages from antigen‐presenting dendritic cells, nor the classification of macrophage activation states as classical versus alternative, or M1 versus M2. Although there has been a focus on a small subset of lineage‐enriched transcription factors, such as PU.1, more than half of the transcription factors in the genome can be expressed in macrophage lineage cells under some state of activation, and they interact in a complex network. The network architecture is conserved across species, but many of the target genes evolve rapidly and differ between mouse and human. The data and publication deluge related to macrophage biology require the development of new analytical tools and ways of presenting information in an accessible form.
Control of macrophage 3D migration: a therapeutic challenge to limit tissue infiltration
Authors: Maridonneau‐Parini Isabelle 
Published: October 2014

SummaryMacrophages are professional migrating cells found in all body tissues from the early embryonic stages till the end of the adult life. Tissue macrophages do not only play beneficial roles. In several diseases, macrophages recruited from blood monocytes have a deleterious action such as favoring cancer progression and destroying tissues in chronic inflammation. To migrate in 3D environments, all leukocytes use the amoeboid movement while macrophages use the amoeboid and the mesenchymal migration modes. Mesenchymal migration takes place in dense matrices and involves podosomes and proteolysis of the extracellular matrix to create paths. Podosome disruption has been correlated with reduced mesenchymal migration of macrophages and unaffected amoeboid migration. Therefore, podosomes are proposed as a therapeutic target. Inhibiting podosome regulators that are only expressed in macrophages and few cell types would avoid collateral effects often encountered when ubiquitous proteins are used as drug targets. With the current status of our knowledge on human macrophage podosomes and 3D migration, the tyrosine kinase Hck appears to be a good candidate.
Beyond macrophages: the diversity of mononuclear cells in tuberculosis
Authors: Srivastava Smita , Ernst Joel D. , Desvignes Ludovic 
Published: October 2014

SummaryMycobacterium tuberculosis, the bacterium that causes tuberculosis (TB), is an intracellular pathogen of mononuclear phagocytes. Although M. tuberculosis has traditionally been thought to survive and replicate in macrophages, recent work in our laboratory and others has revealed that M. tuberculosis infects multiple subsets of mononuclear phagocytes in vivo and in vitro. In experimental animals, M. tuberculosis infects no fewer than five distinct cell subsets in the lungs, including resident alveolar macrophages and 4 types of cells that recruited to the lungs in response to inflammatory signals: neutrophils, monocytes, interstitial macrophages, and dendritic cells. A characteristic of the adaptive immune response in TB is that it is delayed for several weeks following infection, and we have determined that this delay is due to prolonged residence of the bacteria in lung phagocytes prior to acquisition of the bacteria by dendritic cells. Among the mechanisms used by M. tuberculosis to delay acquisition by dendritic cells is to inhibit apoptosis of alveolar macrophages and neutrophils, which sequester the bacteria and prevent their acquisition by dendritic cells in the early stages of infection. We hypothesize that each infected cell subset makes a distinct contribution to the overall biology of M. tuberculosis and allows the bacteria to evade elimination by T‐cell responses and to avoid rapid killing by antimycobacterial drugs.
Macrophage phenotypes in atherosclerosis
Authors: Colin Sophie , Chinetti‐Gbaguidi Giulia , Staels Bart 
Published: October 2014

SummaryInitiation and progression of atherosclerosis depend on local inflammation and accumulation of lipids in the vascular wall. Although many cells are involved in the development and progression of atherosclerosis, macrophages are fundamental contributors. For nearly a decade, the phenotypic heterogeneity and plasticity of macrophages has been studied. In atherosclerotic lesions, macrophages are submitted to a large variety of micro‐environmental signals, such as oxidized lipids and cytokines, which influence the phenotypic polarization and activation of macrophages resulting in a dynamic plasticity. The macrophage phenotype spectrum is characterized, at the extremes, by the classical M1 macrophages induced by T‐helper 1 (Th‐1) cytokines and by the alternative M2 macrophages induced by Th‐2 cytokines. M2 macrophages can be further classified into M2a, M2b, M2c, and M2d subtypes. More recently, additional plaque‐specific macrophage phenotypes have been identified, termed as Mox, Mhem, and M4. Understanding the mechanisms and functional consequences of the phenotypic heterogeneity of macrophages will contribute to determine their potential role in lesion development and plaque stability. Furthermore, research on macrophage plasticity could lead to novel therapeutic approaches to counteract cardiovascular diseases such as atherosclerosis. The present review summarizes our current knowledge on macrophage subsets in atherosclerotic plaques and mechanism behind the modulation of the macrophage phenotype.
Regulation and consequences of monocytosis
Authors: Dutta Partha , Nahrendorf Matthias 
Published: October 2014

SummaryMonocytes are part of the vertebrate innate immune system. Blood monocytes are produced by bone marrow and splenic progenitors that derive from hematopoietic stem cells (HSCs). In cardiovascular disease, such as atherosclerosis and myocardial infarction, HSCs proliferate at higher levels that in turn increase production of hematopoietic cells, including monocytes. Once produced in hematopoietic niches, monocytes intravasate blood vessels, circulate, and migrate to sites of inflammation. Monocyte recruitment to atherosclerotic plaque and the ischemic heart depends on various chemokines, such as CCL2, CX3CL1, and CCL5. Once in tissue, monocytes can differentiate into macrophages and dendritic cells. Macrophages are end effector cells that regulate the steady state and tissue healing, but they can also promote disease. At sites of inflammation, monocytes and macrophages produce inflammatory cytokines, which can exacerbate disease progression. Macrophages can also phagocytose tissue debris and produce pro‐healing cytokines. Additionally, macrophages are antigen‐presenting cells and can prime T cells. The tissue environment, including cytokines and types of inflammation, instructs macrophage specialization. Understanding monocytosis and its consequences in disease will reveal new therapeutic opportunities without compromising steady state functions.
Salinity as a Limiting Factor for Biological Condition in Mining‐Influenced Central Appalachian Headwater Streams
Authors: Timpano Anthony J. , Schoenholtz Stephen H. , Soucek David J. , Zipper Carl E. 
Published: October 2014

AbstractRecent studies have found that Appalachian coal mining causes increased surface water salinity, and that benthic macroinvertebrate communities in salinized mining‐influenced streams differ from communities in streams draining unmined areas. Understanding the role of salinity in shaping these communities is challenging because such streams are often influenced by a variety of stressors in addition to salinity. We characterized associations of salinity with biotic condition while isolating salinity from other stressors through rigorous site selection. We used a multimetric index of biotic condition to characterize benthic macroinvertebrate communities in headwater streams in the Central Appalachian Ecoregion of Virginia across a gradient of sulfate‐dominated salinity. We found strong negative seasonal correlations between biotic condition and three salinity measures (specific conductance, total dissolved solids, and SO42− concentration). We found no evidence to suggest stressors other than salinity as significant influences on biotic condition in these streams. Our results confirm negative associations of salinity with benthic macroinvertebrate community condition, as observed in other studies. Thus, our findings demonstrate that elevated salinity is an important limiting factor for biological condition in Central Appalachian headwater streams.