bluuebunny/crossref_metadata_2025_split huggingface dataset:
Forest fragmentation may endanger a plant‐insect interaction: the case of the highly specialist native aphid Neuquenaphis staryi in Chile
Authors: Figueroa Christian C. , Niemeyer Hermann M. , Cabrera‐Brandt Marco , Briones Lucía M. , Lavandero Blas , Zúñiga‐Reinoso Alvaro , Ramírez Claudio C. 
Published: December 2017

Abstract

The diversity and distribution of the genetic variation in forest phytophagous insect populations can be highly sensitive to forest fragmentation. This should be particularly evident for monophagous insects living on endangered host plants.

The aphid Neuquenaphis staryi uses the tree Nothofagus alessandrii, commonly named Ruil, exclusively as a host. Nothofagus alessandrii is an endemic and endangered species whose distribution is highly fragmented in the unique Maulino temperate forests of the coastal range of Central Chile.

Here, we provide proof of the specialist status of N. staryi and provide evidence on the genetic diversity and structure of their populations sampled on distinct remnant fragments of the Ruil forest. A sample representing 480 individuals collected from five fragments of Ruil forests revealed 147 distinct multilocus genotypes at six microsatellite loci. Clonal diversity and other genetic parameters were consistent with aphids reproducing by cyclic parthenogenesis and showed few signs of diversity loss.

The genetic differentiation among populations was significant as evidenced by the presence of at least three genetic clusters, which are mostly explained by low migration due to geographic barriers that restrict aphid dispersion.

Our results suggest that forest fragmentation imposes genetic discontinuities on a highly specialised phytophagous insect, which may have important implications for the conservation status of this ancient aphid‐plant interaction.
Critical involvement of atypical chemokine receptor CXCR7 in allergic airway inflammation
Authors: Chang Hung‐Chih , Huang Po‐Han , Syu Fu‐Sheng , Hsieh Chia‐Hung , Chang Sunny Li‐Yun , Lu Jean , Chen Hui‐Chen 
Published: December 2017

SummaryTrafficking and recruitment of immune cells to the site of inflammation with spatial and temporal synchronization is crucial for the development of allergic airway inflammation. Particularly, chemokines are known to be key players in these processes. Previous studies revealed that the CXCL12/CXCR4 axis plays an important role in regulating allergic airway inflammation. However, the role of CXCR7, a recently discovered second receptor for CXCL12, in regulating airway inflammation has not been explored. Initially, CXCR7 was considered as a decoy receptor; however, numerous subsequent studies revealed that engagement of CXCR7 triggered its own signalling or modulated CXCR4‐mediated signalling. In the present study, we detected the expression of CXCR7 in airway epithelial cells. Use of a lentiviral delivery system to knock down the expression of CXCR7 in the lung of sensitized mice abrogated the cardinal features of asthma, indicating that CXCR7 plays a role in regulating allergic airway inflammation. The activation of mitogen‐activated protein kinase and Akt signalling in response to CXCL12 in the mouse epithelial cell line MLE‐12 was reduced when CXCR7 expression was knocked down. However, either knockdown or overexpression of CXCR7 in MLE‐12 did not affect CXCL12‐mediated calcium influx, indicating that CXCR7 does not modulate CXCR4‐mediated signalling, and that it functions as a signalling receptor rather than a decoy receptor. Finally, we found that the expression of chemokine CCL2 is regulated by CXCR7/CXCL12‐mediated signalling through β‐arrestin in airway epithelial cells. Hence, regulating the expression of CCL2 in airway epithelial cells may be one mechanism by which CXCR7 participates in regulating allergic airway inflammation.
The NLRC4 Inflammasome
Authors: Duncan Joseph A. , Canna Scott W. 
Published: December 2017

Summary15 years ago, the fundamental biology of an inflammatory signaling complex eventually dubbed “the inflammasome” began to unravel in chronologic parallel with the discovery that many inflammatory diseases were associated with its hyperactivity. Though the genetic origins of Familial Mediterranean Fever (FMF, caused my mutations in MEFV) were discovered first, it would take nearly two decades before the mechanistic connections to a PYRIN inflammasome were made. In the interim, the intensive study of the NLRP3 inflammasome, and the diseases associated with its hyperactivation, have largely dictated the paradigm of inflammasome composition and function. Despite impressive gains, focusing on NLRP3 left gaps in our understanding of inflammasome biology. Foremost among these gaps were how inflammasomes become activated and the connections between inflammasome structure and function. Fortunately, work in another inflammasome inducer, NLRC4, grew to fill those gaps. The current understanding of the NLRC4 inflammasome is perhaps the most comprehensive illustration of the inflammasome paradigm: trigger (e.g. cytosolic flagellin), sensor (NAIP), nucleator (NLRC4), adaptor (ASC), and effector (CASP1). Detailed work has also identified observations that challenge this paradigm. Simultaneously, the features unique to each inflammasome offer a lesson in contrast, providing perspectives on inflammasome activation, regulation, and function. In this review, we endeavor to highlight recent breakthroughs related to NLRC4 inflammasome structure and activation, important in vivo work in infection and systemic inflammation, and the characterization of a spectrum of human NLRC4‐associated autoinflammatory diseases.
Tuning inflammation and immunity by the negative regulators IL‐1R2 and IL‐1R8
Authors: Molgora Martina , Supino Domenico , Mantovani Alberto , Garlanda Cecilia 
Published: December 2017

SummaryInterleukin‐1 receptor family members (ILRs) and Toll‐Like Receptors (TLRs) are key players in immunity and inflammation and are tightly regulated at different levels. Most cell types, including cells of the innate and adaptive immune system express ILRs and TLRs. In addition, IL‐1 family members are emerging as key players in the differentiation and function of innate and adaptive lymphoid cells. IL‐1R2 and IL‐1R8 (also known as TIR8 or SIGIRR) are members of the ILR family acting as negative regulators of the IL‐1 system. IL‐1R2 binds IL‐1 and the accessory protein IL‐1RAcP without activating signaling and can be released as a soluble form (sIL‐1R2), thus modulating IL‐1 availability for the signaling receptor. IL‐1R8 dampens ILR‐ and TLR‐mediated cell activation and it is a component of the receptor recognizing human IL‐37. Here, we summarize our current understanding of the structure and function of IL‐1R2 and IL‐1R8, focusing on their role in different pathological conditions, ranging from infectious and sterile inflammation, to autoimmunity and cancer‐related inflammation. We also address the emerging evidence regarding the role of IL‐1R8 as a crucial checkpoint molecule in NK cells in anti‐cancer and antiviral activity and the potential therapeutic implications of IL‐1R8 blockade in specific pathological contexts.
Regulation and function of interleukin‐36 cytokines
Authors: Bassoy Esen Yonca , Towne Jennifer E , Gabay Cem 
Published: December 2017

SummaryThe interleukin (IL)‐36 cytokines include 3 agonists, IL‐36α, IL‐36β, and IL‐36γ that bind to a common receptor composed of IL‐36R and IL‐1RAcP to stimulate inflammatory responses. IL‐36Ra is a natural antagonist that binds to IL‐36R, but does not recruit the co‐receptor IL‐1RAcP and does not stimulate any intracellular responses. The IL‐36 cytokines are expressed predominantly by epithelial cells and act on a number of cells including immune cells, epithelial cells, and fibroblasts. Processing of the N‐terminus is required for full agonist or antagonist activity for all IL‐36 members. The role of IL‐36 has been extensively demonstrated in the skin where it can act on keratinocytes and immune cells to induce a robust inflammatory response that has been implicated in psoriatic disorders. Emerging data also suggest a role for this cytokine family in pulmonary and intestinal physiology and pathology.
Biology of IL‐38 and its role in disease
Authors: van de Veerdonk Frank L. , de Graaf Dennis M. , Joosten Leo AB , Dinarello Charles A. 
Published: December 2017

SummaryIL‐38 belongs to the IL‐36 cytokines, which in turn are part of the IL‐1 family. The first biological function of IL‐38 described was blocking the activation of the IL‐36R signaling similar to IL‐36Ra. Since IL‐36 cytokines require processing in order to become fully active, it is likely that IL‐38 also must be processed to become maximally active. However, the protease(s) responsible for this is currently not known. In addition of IL‐38 binding IL‐36R, it has been proposed it can also interact with the co‐receptor TIGIRR2. IL‐38 is expressed in several tissues including tonsils, placenta, heart and brain, and IL‐38 has been implicated in a wide variety of diseases including cardiovascular and autoimmune disease. Here, we discuss the discovery and biological function of IL‐38, and its role in the pathogenesis of a wide variety of diseases.
Identifying risk factors associated with infection in patients with chronic leg ulcers
Authors: Bui Ut T , Edwards Helen , Finlayson Kathleen 
Published: December 2017

Leg ulcers are hard to heal. Infection causes delayed healing, negatively impacting patients’ quality of life, the healthcare system, and society. Early recognition of patients at high risk of infection is essential to prevent complications and reduce negative impacts. However, at present, factors associated with infection in this population are not yet clearly understood.The study aimed to identify factors that were significantly associated with infection in chronic leg ulcers. A sample of 561 patients with chronic leg ulcers, who were previously recruited at outpatient clinics and community settings within Australia between 2008 and 2015, were selected for the current analysis. The prevalence of infection in the sample at study recruitment was 7.8%.A multivariate logistic regression model was used to identify factors associated with infection. The study identified 7 factors that were significantly independently associated with infection, including depression, chronic pulmonary disease, anti‐coagulant use, calf ankle circumference ratio < 1.3, ulcer area ≥ 10 cm2, slough in the wound bed tissue, and ulcers with heavy exudate.These findings could assist clinicians in the early recognition of patients at risk of infection and individualise treatment for these patients, thereby promoting wound healing.
Handing Off the Older Patient: Improved Documentation of Geriatric Assessment in Transitions of Care
Authors: Blomberg Ben A. , Mulligan Rebekah C. , Staub Stephen J. , Hanson Laura C. , Drickamer Margaret A. , Dale Maureen C. 
Published: December 2017

ObjectivesTo improve assessment and documentation of function, cognition, and advance care planning (ACP) in admission and discharge notes on an Acute Care of the Elderly (ACE) unit.DesignContinuous quality improvement intervention with episodic data review.SettingACE unit of an 866‐bed academic tertiary hospital.ParticipantsHousestaff physicians rotating on the ACE unit (N = 31).InterventionIntroduction of templated notes, housestaff education, leadership outreach, and posted reminders.MeasurementsDocumentation of function, cognition, and ACP were assessed through chart review of a weekly sample of the ACE unit census and scored using predefined criteria.ResultsMedical records (N = 172) were reviewed. At baseline, 0% of admission and discharge notes met minimum documentation criteria for all 3 domains (function, cognition, ACP). Documentation of function and cognition was completely absent at baseline. After the intervention, there was marked improvement in all measures, with 64% of admission notes and 94% of discharge notes meeting minimum documentation criteria or better in all 3 domains.ConclusionA quality improvement intervention using geriatric‐specific note templates, housestaff training, and reminders increased documentation of function, cognition and ACP for postacute care.
Mechanisms of neuroprotection against ischemic insult by stress‐inducible phosphoprotein‐1/prion protein complex
Authors: Beraldo Flavio H. , Ostapchenko Valeriy G. , Xu Jason Z. , Di Guglielmo Gianni M. , Fan Jue , Nicholls Peter J. , Caron Marc G. , Prado Vania F. , Prado Marco A. M. 
Published: December 2017

AbstractStress‐inducible phosphoprotein 1 (STI1) acts as a neuroprotective factor in the ischemic brain and its levels are increased following ischemia. Previous work has suggested that some of these STI1 actions in a stroke model depend on the recruitment of bone marrow‐derived stem cells to improve outcomes after ischemic insult. However, STI1 can directly increase neuroprotective signaling in neurons by engaging with the cellular prion protein (PrPC) and activating α7 nicotinic acetylcholine receptors (α7nAChR). Given that α7nAChR activation has also been involved in neuroprotection in stroke, it is possible that STI1 can have direct actions on neurons to prevent deleterious consequences of ischemic insults. Here, we tested this hypothesis by exposing primary neuronal cultures to 1‐h oxygen‐glucose deprivation (OGD) and reperfusion and assessing signaling pathways activated by STI1/PrPC. Our results demonstrated that STI1 treatment significantly decreased apoptosis and cell death in mouse neurons submitted to OGD in a manner that was dependent on PrPC and α7nAChR, but also on the activin A receptor 1 (ALK2), which has emerged as a signaling partner of STI1. Interestingly, pharmacological inhibition of the ALK2 receptor prevented neuroprotection by STI1, while activation of ALK2 receptors by bone morphogenetic protein 4 (BMP4) either before or after OGD was effective in decreasing neuronal death induced by ischemia. We conclude that PrPC/STI1 engagement and its subsequent downstream signaling cascades involving α7nAChR as well as the ALK2 receptor may be activated in neurons by increased levels of STI1. This signaling pathway protects neurons from ischemic insults.
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Complications of botulinum toxin injection for masseter hypertrophy: Incidence rate from 2036 treatments and summary of causes and preventions
Authors: Peng Hsien‐Li Peter , Peng Jui‐Hui 
Published: December 2017

SummaryBackgroundMasseter hypertrophy is a common, prominent feature in many Asian patients, and correction procedures are often requested for esthetic reasons. Toxin masseter injections have a high efficacy and safety profile, but the risks of a variety of side effects or complications remain.ObjectivesThe categorization of various complications was based on etiology, with a presentation of the author's own incidence rates for consideration and comparison.MethodsSix hundred and eighty patients received a total of 2036 sessions of toxin injection for masseter hypertrophy from 2011 to 2016, and complications or complaints were recorded through follow‐up on a by‐treatment basis. Complications were grouped together based on etiology and discussed.ResultsOf 2036 sessions, temporary mastication force decrease was reported after 611 (30%), bruising after 51 (2.5%), headaches after 12 (0.58%), smile limitation after 3 (0.15%), paradoxical bulging after 10 (0.49%), sunken cheeks (subzygomatic volume loss) after 9 (0.44%), and sagging after 4 (0.20%).ConclusionsMasseter injections remain very safe. To further decrease the incidence rate, injections should only be inside the recommended safety zone, a quadrilateral within the muscle that avoids most important local structures. Keeping injections inside the safe zone, and ideally in 3‐4 different locations at least 1 cm from any border, is crucial for the prevention of complications.
Bank Capital and Lending Relationships
Authors: SCHWERT MICHAEL 
Published: December 2017

ABSTRACTThis paper investigates the mechanisms behind the matching of banks and firms in the loan market and the implications of this matching for lending relationships, bank capital, and credit provision. I find that bank‐dependent firms borrow from well‐capitalized banks, while firms with access to the bond market borrow from banks with less capital. This matching of bank‐dependent firms with stable banks smooths cyclicality in aggregate credit provision and mitigates the effects of bank shocks on the real economy.
Effect of organic acids or probiotics alone or in combination on growth performance, nutrient digestibility, enzyme activities, intestinal morphology and gut microflora in broiler chickens
Authors: Rodjan P. , Soisuwan K. , Thongprajukaew K. , Theapparat Y. , Khongthong S. , Jeenkeawpieam J. , Salaeharae T. 
Published: December 2017

SummaryA feeding trial was conducted to determine the effect of organic acids or probiotics alone or in combination on growth performance, nutrient digestibility, enzyme activity, intestinal morphology and gut microflora in broiler chickens (Ross308). A completely randomized design was used, with 1,440 broiler chicks across four treatments and five replications of 72 chicks each. The chicks in the control treatment were fed on a control diet (CD), whereas for the other treatment groups, the CD was supplemented with 0.2 g/kg organic acids (CDOA), probiotics (CDP) or a combination of organic acids and probiotics (CDOAP). All the chicks were fed ad libitum during the feeding trial throughout 35 days. A total of 20 chicks were randomly allotted to individual metabolic cages to measure the nutrient digestibility (35–42 days) and the digestive enzyme activities (42 days). The intestinal morphology and gut microflora of 80 chicks were examined at the end of experiment. There were no significant (p > .05) differences in the feed intake, body weight gain or feed conversion ratio of the chicks across the four dietary treatments. The crude fibre digestibility was significantly increased in chicks fed on CDOA or CDOAP relative to CD (p < .05). Nutrient utilization, in terms of digestive enzyme activities and excreta thermal property, was unchanged by any supplementation. The chicks fed on the CDOAP had significantly higher duodenal villi height and crypt depth than the chicks fed on CDOA (p < .05). This dietary treatment dramatically improved gut microflora by decreasing the population of Escherichia coli and increasing the Lactobacillus spp.:E. coli ratio. Based on our investigations, supplementation of organic acids and probiotics in chick diets can increase the ability to digest crude fibre and villus height and decrease intestinal E. coli without impairing growth performance.
Spiritual Struggles and Health: Assessing the Influence of Socioeconomic Status
Authors: Krause Neal , Pargament Kenneth I. , Ironson Gail 
Published: December 2017

AbstractGrowing evidence suggests that spiritual struggles may play a major role in explaining the relationship between religion and health. Even so, there are significant gaps in the literature. More specifically, researchers do not know enough about how spiritual struggles arise in the first place. This study has two major goals. The first is to see whether socioeconomic status is associated with spiritual struggles. The second is to see whether spiritual struggles are associated with physical health. A conceptual model is tested that contains the following core hypotheses: (1) individuals with lower levels of educational attainment are more likely to encounter chronic economic difficulties; (2) people who experience ongoing financial strain are more likely to live in rundown neighborhoods; (3) people who live in dilapidated neighborhoods will be more angry than their well‐to‐do counterparts; (4) people who are more angry will, in turn, be more likely to experience spiritual struggles; and (5) greater spiritual struggles will be associated with more symptoms of physical illness. Data from a recent nationwide survey (N = 2,146) provide empirical support for each hypothesis.
Rapid legacy‐dependent succession of lichen assemblages after forest fires: Insights from two boreal regions
Authors: Lõhmus Piret , Lõhmus Asko , Hämäläinen Aino 
Published: December 2017

AbstractQuestions(i) What is the impact of legacy structures on lichen assemblage development up to two decades post‐fire? (ii) How does that impact vary among ecological groups? (iii) Are charcoal‐inhabiting lichen assemblages regionally distinct?LocationHemiboreal pine forests, Estonia, and middle‐boreal pine forests, eastern Finland.MethodsWe performed standard lichen surveys (4 hr effort per 2 ha plot; on all substrates 0–2 m from the forest floor) and measured forest structure in 18 burned sites (nine in Finland and nine in Estonia). The sites included both old (15–21 years) and recent (9 years) fires, and half of the latter had been harvested for timber. We analysed lichen assemblages (full assemblages and different ecological groups) in relation to site factors (GLM for species richness; multivariate techniques for assemblage composition).ResultsLichen assemblages on burned sites (altogether 187 species recorded) were regionally distinct and, additionally, significantly affected by the large variation in legacy and regeneration abundance among sites. Species richness was negatively related to abundance of fallen trees 9 years after fire but the relationship was positive 15–21 years post‐fire; this pattern indicated a change from the initial damage effect to a substrate‐providing effect of the fire. Microlichens and vegetatively dispersing lichens appeared more sensitive to disturbance (including harvesting), whereas macrolichens were more responsive to substrate provision. The main structural influences on lichens inhabiting charred substrates (67 species recorded in total) were similar to the factors affecting the composition of full lichen assemblages.ConclusionsWithin 10 years post‐fire, initial disturbance‐related damage to forest lichen assemblages was replaced by the dominance of substrate‐providing factors (legacies, regeneration). These damage and recovery phases differ among lichen groups, but are consistent between hemi‐ and middle‐boreal regions. The availability of post‐fire legacies, including charred surfaces, is of critical importance for the management of burned areas in modern landscapes.
Gene–Environment Interplay and Individual Differences in Behavior
Authors: Anreiter Ina , Sokolowski H. Moriah , Sokolowski Marla B. 
Published: December 2017

ABSTRACTIndividuals of the same species display remarkable variation in behavior, even in identical contexts. Increasing complexity in behavioral phenotypes brings with it an increase in individual variation in the manifestation of those phenotypes, and human behavior undoubtedly stands at the pinnacle of complexity. In this article, we discuss current knowledge of gene–environment interplay and how the complex interactions of genes, experiences, epigenetics, and developmental timing give rise to individual differences in behavior.