bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association between urinary adiponectin level and renal involvement in systemic lupus erythematous
Authors: Loghman Maryam , Haghighi Anousheh , Broumand Behrooz , Ataipour Yousef , Tohidi Maryam , Marzbani Caroline , Fakharran Mehdi 
Published: January 2014

AbstractAimTo assess association between urinary levels of adiponectin and severity of renal involvement in SLE patients. Also, this study aims to determine the value of urinary adiponectin levels to discriminate renal involvement in these patients.MethodsIn a multi‐center cross‐sectional survey, 50 consecutive patients diagnosed as having systemic lupus erythematosus (SLE) according to American College of Rheumatology criteria were classified into two groups with or without renal involvement (microscopic hematuria, reduced glomerular filtration rate < 25% of normal value, and proteinuria > 500 mg/24 h) which was confirmed by renal biopsy. Urinary adiponectin was measured by enzyme‐linked immunosorbent assay. SLE disease activity levels were assessed by SLE Disease Activity Index (SLEDAI) score.ResultsComparing urinary levels of adiponectin between the two groups indicated considerable discrepancy in this index between the groups with and without renal involvement (146.33 ± 258.83 ng/mL vs. 22.96 ± 44.33 ng/mL, P = 0.023). Also, urinary adiponectin/creatinine ratio was significantly higher in the former group (221.72 ± 414.58 vs. 19.99 ± 41.19, P = 0.019). Our study showed a higher mean SLEDAI score in those with renal involvement than others (23.60 ± 2.53 vs. 9.12 ± 3.03, P < 0.001). Multivariable linear regression analysis with the presence of potential confounders showed that the level of urinary adiponectin was significantly higher in those with renal involvement than other patients (β = 0.470, P = 0.023). The optimal cut‐off point for urinary adiponectin levels to discriminate renal involvement from normal renal state was 7.5 ng/mL, yielding a sensitivity of 80% and specificity of 52%.ConclusionUrinary levels of adiponectin are significantly elevated in SLE patients with renal involvement. The measurement of this biomarker can be helpful to discriminate impaired from normal renal function in SLE patients.
Symbiont‐driven sulfur crystal formation in a thiotrophic symbiosis from deep‐sea hydrocarbon seeps
Authors: Eichinger Irmgard , Schmitz‐Esser Stephan , Schmid Markus , Fisher Charles R. , Bright Monika 
Published: January 2014

SummaryThe siboglinid tubewormSclerolinum contortumsymbiosis inhabits sulfidic sediments at deep‐sea hydrocarbon seeps in theGulf ofMexico. A single symbiont phylotype in the symbiont‐housing organ is inferred from phylogenetic analyses of the 16Sribosomal ribonucleic acid (16S rRNA) gene and fluorescent in situ hybridization. The phylotype we studied here, and a previous study from an arctic hydrocarbon seep population, reveal identical 16S rRNAsymbiont gene sequences. While sulfide is apparently the energy source for the symbionts (and ultimately the gutless host), both partners also have to cope with its toxicity. This study demonstrates abundant large sulfur crystals restricted to the trophosome area. Based onRaman microspectroscopy and energy dispersiveX‐ray analysis, these crystals have the sameS8 sulfur configuration as the recently described small sulfur vesicles formed in the symbionts. The crystals reside adjacent to the symbionts in the trophosome. This suggests that their formation is either extra‐ or intracellular in symbionts. We propose that formation of these crystals provides both energy‐storage compounds for the symbionts and serves the symbiosis by removing excess toxic sulfide from host tissues. This symbiont‐mediated sulfide detoxification may have been crucial for the establishment of thiotrophic symbiosis and continues to remain an important function of the symbionts.
Vascular endothelial growth factor C is an indicator of lymph node metastasis in thoracic esophageal squamous cell carcinomas and its role in long‐term survival after surgery
Authors: Pan Xufeng , Mao Teng , Fang Wentao , Chen Wenhu 
Published: January 2014

AbstractBackgroundTo define the role of vascular endothelial growth factor C (VEGF‐C) on lymph node (LN) metastasis of human esophageal squamous cell carcinoma (ESCC), and to investigate its impact on overall survival.MethodsReal‐time polymerase chain reaction was introduced to quantify the expression of VEGF‐CmRNA. One hundred and eight samples (59 tumor tissue and 59 paired normal tissue) were analyzed.ResultsVEGF‐CmRNA expression was significantly higher in tumor tissues than in normal mucosa (P = 0.02). VEGF‐CmRNA expression was significantly higher in LN (+) patients than in LN (‐) patients (P = 0.04). VEGF‐CmRNA expression was related to a positive LN number (P = 0.06) and a positive LN station number (P = 0.04). VEGF‐CmRNA expression was significantly higher in stage III and IV patients than in stage I and II patients (P = 0.03). A logistic regression model showed that VEGF‐CmRNA and T status were independent risk factors for LN metastasis(P < 0.05). In univariate analysis, survival tended to be poorer in the VEGF‐CmRNA high expression group (22.0 months vs. 44.0 months, P = 0.08). A Cox regression model revealed that a positive LN station number was the only independent risk factor for overall survival (P < 0.01).ConclusionVEGF‐C was a useful indicator for LN metastasis in human ESCC, and it might have some influence on long‐term survival by affecting LN metastasis.
Towards patient self‐triage in the ophthalmic emergency department: sensitivity and specificity of a self‐triage instrument
Authors: Eijk Eva S.V. , Busschbach Jan J.V. , Monteban Helma , Timman Reinier , Wefers Bettink‐Remeijer Marijke 
Published: January 2014

AbstractPurposeTrained ophthalmic triage staff may not constantly be available in the emergency department of a specialized ophthalmic hospital, particularly at night. To support the current triage process, the aim of this study was to develop an ophthalmic instrument of patient self‐triage (ISET).MethodsA preliminary ISET, in the form of a pen‐and‐paper questionnaire, was refined and validated in a two‐step procedure. In a first explorative step, we compared the results of the ISET with the results of the regular triage process during the day, that is, triage by a trained triage assistant in a specialized ophthalmic hospital. As several patients needed guidance completing the questionnaire, the ISET was subsequently refined. The second step was to test the validity of the refined ISET by again comparing the outcome of this triage with that of the triage assistant in the emergency department.ResultsThe first explorative step involved 279 patients and the final validation step 298. During the validation step, sensitivity of the ISET was 94.3% and specificity 76.4%.ConclusionThe results show that the ISET is a sensitive and specific instrument for ophthalmic triage compared with a trained ophthalmic triage assistant.
Comparison and analysis of the animal models used to study the effect of morphine on tumour growth and metastasis
Authors: Afsharimani B , Doornebal C W , Cabot P J , Hollmann M W , Parat M‐O 
Published: January 2014

The effect of opioids on tumour growth and metastasis has been debated for many years, with recent emphasis on the possibility that they might influence the rate of disease‐free survival after tumour resection when used in the perioperative pain management of cancer surgery patients. The literature presents conflicting and inconclusive in vitro and in vivo data about the potential effect of opioids, especially morphine, on tumour growth and metastasis. To inform clinical practice, appropriate animal models are needed to test whether opioids alter the course of tumour growth and metastasis. Here, we review the literature on animal‐based studies testing the effect of morphine on cancer so far, and analyse differences between the models used that may explain the discrepancies in published results. Such analysis should elucidate the role of opioids in cancer and help define ideal pre‐clinical models to provide definitive answers.Linked ArticlesThis article is part of a themed section on Opioids: New Pathways to Functional Selectivity. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-2
Hypoxia activates 15‐PGDH and its metabolite 15‐KETE to promote pulmonary artery endothelial cells proliferation via ERK1/2 signalling
Authors: Ma Cui , Liu Yun , Wang Yanyan , Zhang Chen , Yao Hongmin , Ma Jun , Zhang Lei , Zhang Dandan , Shen Tingting , Zhu Daling 
Published: January 2014

Background and PurposeDysfunction and injury of endothelial cells in the pulmonary artery play critical roles in the hypertension induced by chronic hypoxia. One consequence of hypoxia is increased activity of 15‐hydroxyprostaglandin dehydrogenase (PGDH). Here, we have explored, in detail, the effects of hypoxia on the proliferation of pulmonary artery endothelial cells.Experimental ApproachWe used bromodeoxyuridine incorporation, cell‐cycle analysis, immunohistochemistry and Western blot analysis to study the effects of hypoxia, induced 15‐PGDH) activity and its product, 15‐keto‐6Z, 8Z, 11Z, 13E‐eicosatetraenoic acid (15‐KETE), on endothelial cell proliferation. Scratch‐wound and tube formation assays were also used to study migration of endothelial cells.Key Results15‐KETE increased DNA synthesis and enhanced the transition from the G0/G1 phase to the S phase in hypoxia. Inhibition of 15‐PGDH or siRNA for 15‐PGDH reversed these effects. 15‐KETE also activated the ERK1/2 signalling pathway. 15‐KETE‐induced cell migration and tube formation were reversed by blocking ERK1/2, but not the p38 MAPK pathway.Conclusions and ImplicationsHypoxia‐induced endothelial proliferation and migration, an important underlying mechanism contributing to hypoxic pulmonary vascular remodelling, appears to be mediated by 15‐PGDH and 15‐KETE, via the ERK1/2 signalling pathway.
Optimizing nanomedicine pharmacokinetics using physiologically based pharmacokinetics modelling
Authors: Moss Darren Michael , Siccardi Marco 
Published: January 2014

The delivery of therapeutic agents is characterized by numerous challenges including poor absorption, low penetration in target tissues and non‐specific dissemination in organs, leading to toxicity or poor drug exposure. Several nanomedicine strategies have emerged as an advanced approach to enhance drug delivery and improve the treatment of several diseases. Numerous processes mediate the pharmacokinetics of nanoformulations, with the absorption, distribution, metabolism and elimination (ADME) being poorly understood and often differing substantially from traditional formulations. Understanding how nanoformulation composition and physicochemical properties influence drug distribution in the human body is of central importance when developing future treatment strategies. A helpful pharmacological tool to simulate the distribution of nanoformulations is represented by physiologically based pharmacokinetics (PBPK) modelling, which integrates system data describing a population of interest with drug/nanoparticle in vitro data through a mathematical description of ADME. The application of PBPK models for nanomedicine is in its infancy and characterized by several challenges. The integration of property–distribution relationships in PBPK models may benefit nanomedicine research, giving opportunities for innovative development of nanotechnologies. PBPK modelling has the potential to improve our understanding of the mechanisms underpinning nanoformulation disposition and allow for more rapid and accurate determination of their kinetics. This review provides an overview of the current knowledge of nanomedicine distribution and the use of PBPK modelling in the characterization of nanoformulations with optimal pharmacokinetics.Linked ArticlesThis article is part of a themed section on Nanomedicine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue‐17
Functional selectivity and time‐dependence of μ‐opioid receptor desensitization at nerve terminals in the mouse ventral tegmental area
Authors: Lowe J D , Bailey C P 
Published: January 2014

Background and PurposeThe majority of studies examining desensitization of the μ‐opioid receptor (MOR) have examined those located at cell bodies. However, MORs are extensively expressed at nerve terminals throughout the mammalian nervous system. This study is designed to investigate agonist‐induced MOR desensitization at nerve terminals in the mouse ventral tegmental area (VTA).Experimental ApproachMOR function was measured in mature mouse brain slices containing the VTA using whole‐cell patch‐clamp electrophysiology. Presynaptic MOR function was isolated from postsynaptic function and the functional selectivity, time‐dependence and mechanisms of agonist‐induced MOR desensitization were examined.Key ResultsMORs located at GABAergic nerve terminals in the VTA were completely resistant to rapid desensitization induced by the high‐efficacy agonists DAMGO and Met‐enkephalin. MORs located postsynaptically on GABAergic cell bodies readily underwent rapid desensitization in response to DAMGO. However, after prolonged (>7 h) treatment with Met‐enkephalin, profound homologous MOR desensitization was observed. Morphine could induce rapid MOR desensitization at nerve terminals when PKC was activated.Conclusions and ImplicationsAgonist‐induced MOR desensitization in GABAergic neurons in the VTA is compartment‐selective as well as agonist‐selective. When MORs are located at cell bodies, higher‐efficacy agonists induce greater levels of rapid desensitization than lower‐efficacy agonists. However, the converse is true at nerve terminals where agonists that induce MOR desensitization via PKC are capable of rapid agonist‐induced desensitization while higher‐efficacy agonists are not. MOR desensitization induced by higher‐efficacy agonists at nerve terminals only takes place after prolonged receptor activation.Linked ArticlesThis article is part of a themed section on Opioids: New Pathways to Functional Selectivity. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-2
Regulatory role of the cannabinoid CB2 receptor in stress‐induced neuroinflammation in mice
Authors: Zoppi S , Madrigal J L , Caso J R , García‐Gutiérrez M S , Manzanares J , Leza J C , García‐Bueno B 
Published: January 2014

Background and PurposeStress exposure produces excitotoxicity and neuroinflammation, contributing to the cellular damage observed in stress‐related neuropathologies. The endocannabinoids provide a homeostatic system, present in stress‐responsive neural circuits. Here, we have assessed the possible regulatory role of cannabinoid CB2 receptors in stress‐induced excitotoxicity and neuroinflammation.Experimental ApproachWe used wild type (WT), transgenic overexpressing CB2 receptors (CB2xP) and CB2 receptor knockout (CB2‐KO) mice exposed to immobilization and acoustic stress (2 h·day−1 for 4 days). The CB2 receptor agonist JWH‐133 was administered daily (2 mg·kg−1, i.p.) to WT and CB2‐KO animals. Glutamate uptake was measured in synaptosomes from frontal cortex; Western blots and RT‐PCR were used to measure proinflammatory cytokines, enzymes and mediators in homogenates of frontal cortex.Key ResultsIncreased plasma corticosterone induced by stress was not modified by manipulating CB2 receptors. JWH‐133 treatment or overexpression of CB2 receptors increased control levels of glutamate uptake, which were reduced by stress back to control levels. JWH‐133 prevented the stress‐induced increase in proinflammatory cytokines (TNF‐α and CCL2), in NF‐κB, and in NOS‐2 and COX‐2 and in the consequent cellular oxidative and nitrosative damage (lipid peroxidation). CB2xP mice exhibited anti‐inflammatory or neuroprotective actions similar to those in JWH‐133 pretreated animals. Conversely, lack of CB2 receptors (CB2‐KO mice) exacerbated stress‐induced neuroinflammatory responses and confirmed that effects of JWH‐133 were mediated through CB2 receptors.Conclusions and ImplicationsPharmacological manipulation of CB2 receptors is a potential therapeutic strategy for the treatment of stress‐related pathologies with a neuroinflammatory component, such as depression.
Modifiable factors governing indoor fungal diversity and risk of asthma
Authors: Sharpe R. , Thornton C. R. , Osborne N. J. 
Published: January 2014

SummaryExposure to dampness and fungi in the home is a known risk factor for individuals with allergic asthma. Inadequate heating and ventilation may lead to dampness and concomitant increased exposure to spores of allergenic fungi such as Aspergillus and Penicillium. These fungi have been cultured from sputum of asthmatic and non‐asthmatic individuals, and implicated in the initiation or exacerbation of asthma. Indoor environmental factors influence the presence and concentrations of fungal propagules and, in turn, risk of asthma outcomes. This review aims to identify modifiable risk factors in the built environment that have been shown to influence fungal composition indoors, and to examine this association with the risk of asthma development and/or exacerbation. A complex interaction between residential characteristics, the built environment and the behaviour of people regulate the diversity and concentrations of indoor fungi. Modifiable factors include build age, architectural design, level of maintenance, variations in construction materials, presence of pets, heating and ventilation patterns. Risk of fungal contamination and asthma outcomes are also influenced by low occupant awareness concerning potential health effects and socio‐economic factors. Addressing these factors provides an opportunity to improve future housing interventions, though it is not clear how the built environment and occupant behaviours interact to modify the diversity of indoor fungi and resultant risk of asthma. A combination of housing improvements combined with awareness programmes and the alleviation of fuel poverty can be used to lower the allergen burden associated with damp homes. Further research is needed to identify factors that regulate the concentration and diversity of indoor fungi and how this may act as a modifier for asthma outcomes.
Homology and misdirection
Authors: Farris James S. 
Published: January 2014

AbstractHennig (1966) recognized symplesiomorphies as homologies, and that view is logically correct under the concept of homology (homogeny) prevalent among evolutionists since 1870. Nelson and Platnick (1981) instead wanted homology to exclude symplesiomorphies for reasons that they never made clear but which certainly included opposition to Hennig. They and some of their followers, most recently Platnick (2013) and Brower and de Pinna (2013), have continued to advocate that anti‐Hennigian position, often under the slogan “homology equals synapomorphy,” while ironically passing themselves off as cladists and often using ambiguous or falsified citations to pretend that legitimate phylogeneticists think likewise. Such authors have seldom shown much concern for accuracy or logic, with the result that a great deal of print has been wasted. Those problems can be avoided simply by maintaining a Hennigian view and so discarding the purported equivalence of homology and synapomorphy.
A Social Relational Network Perspective for MPA Science
Authors: Alexander Steven M. , Armitage Derek 
Published: January 2014

AbstractThis mini‐review outlines the emergence and benefit of applying a structurally explicit, social relational network perspective to inform the establishment and governance of marine protected area (MPAs) and MPA networks. This is an important conservation research and policy frontier. We draw on concepts from relational sociology and social network analysis to highlight the theoretical foundations of a social relational network perspective. Selected examples are used to: (1) illustrate the analytical utility and application of this network perspective to systematically examine attributes recognized as important for MPA establishment and governance; and (2) provide new insights on crucial practices and processes (e.g., knowledge exchange), core social attributes (e.g., social capital), and the roles and positions of diverse MPA actors.
Ecosystem Services as a Contested Concept: a Synthesis of Critique and Counter‐Arguments
Authors: Schröter Matthias , van der Zanden Emma H. , van Oudenhoven Alexander P.E. , Remme Roy P. , Serna‐Chavez Hector M. , de Groot Rudolf S. , Opdam Paul 
Published: January 2014

AbstractWe describe and reflect on seven recurring critiques of the concept of ecosystem services and respective counter‐arguments. First, the concept is criticized for being anthropocentric, whereas others argue that it goes beyond instrumental values. Second, some argue that the concept promotes an exploitative human–nature relationship, whereas others state that it reconnects society to ecosystems, emphasizing humanity's dependence on nature. Third, concerns exist that the concept may conflict with biodiversity conservation objectives, whereas others emphasize complementarity. Fourth, the concept is questioned because of its supposed focus on economic valuation, whereas others argue that ecosystem services science includes many values. Fifth, the concept is criticized for promoting commodification of nature, whereas others point out that most ecosystem services are not connected to market‐based instruments. Sixth, vagueness of definitions and classifications are stated to be a weakness, whereas others argue that vagueness enhances transdisciplinary collaboration. Seventh, some criticize the normative nature of the concept, implying that all outcomes of ecosystem processes are desirable. The normative nature is indeed typical for the concept, but should not be problematic when acknowledged. By disentangling and contrasting different arguments we hope to contribute to a more structured debate between opponents and proponents of the ecosystem services concept.
Hypopigmented macules secondary to imatinib for the treatment of chronic myeloid leukemia: a histopathologic and immunohistochemical study
Authors: Llamas‐Velasco Mar , Fraga Javier , Kutzner Heinz , Steegmann Juan Luis , García‐Diez Amaro , Requena Luis 
Published: January 2014

BackgroundA few series addressing the cutaneous side effects related to imatinib in the skin have been published, but only one described scarce histopathologic information in seven patients.ObjectiveTo characterize these lesions and compare the number of melanocytes between hypopigmented lesions and normal appearing skin.MethodsWe retrieved clinical data of the patients and performed 24 skin biopsies (13 from hypopigmented skin and 11 from normal‐appearing skin) within a cohort of 41 patients with chronic myeloid leukemia treated with imatinib. We classified the biopsies into three patterns.ResultsAbout 45% of patients presented with periocular hypopigmentation. Perifollicular fibrosis was observed in hypopigmented skin biopsies (76.9%) and in normal‐appearing skin (45.5%). Epidermal melanin, as determined with Masson‐Fontana staining, and melanocyte number, as evaluated with MiTF, Melan A and c‐kit immunostains, were lower in hypopigmented skin.ConclusionsHistopathologic study of hypopigmented macules demonstrates the presence of melanin with a statistically significant decrease in the number of melanocytes. Therefore, these findings differ from vitiligo, as melanocytes are present. Three histopathological patterns may be found, namely (a) perifollicular fibrosis, (b) lichen planopilaris‐like and (c) apparently normal skin. One of the most striking histopathologic finding consisted of the presence of perifollicular fibrosis in both hypopigmented lesions and apparently normal skin.