bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characteristics of chiropractors who manage people aged 65 and older: A nationally representative sample of 1903 chiropractors
Authors: Moore Craig , de Luca Katie , Wong Arnold Y. L. , Fernandez Matthew , Swain Michael , Hartvigsen Jan , Adams Jon , Peng Wenbo 
Published: April 2019

ObjectiveTo examine the prevalence and profile of chiropractors who frequently manage people aged 65 years and older.MethodsA national cross‐sectional survey collected practitioner characteristics, practice settings and clinical management characteristics. Multiple logistic regression was conducted on 1903 chiropractors to determine the factors associated with the frequent treatment of people 65 years and older.ResultsIn total, 73.5% of participants report “often” treating those aged 65 years and older. These chiropractors were associated with treating degenerative spine conditions (OR [odds ratio] 2.25; 95% [confidence interval] CI 1.72‐2.94), working in a non‐urban area (OR 1.85; 95% CI 1.35‐2.54), treating low back pain (referred/radicular) (OR 1.74; 95% CI 1.26‐2.40) and lower limb musculoskeletal disorders (OR 1.50; 95% CI 1.15‐1.96).ConclusionsThe majority of chiropractors report often providing treatment to older people. Our findings call for more research to better understand older patient complaints that are common to chiropractic practice and the care provided by chiropractors for this patient group.
Decreased effector regulatory T cells and increased activated CD4+ T cells in premature ovarian insufficiency
Authors: Kobayashi Mutsumi , Nakashima Akitoshi , Yoshino Osamu , Yoshie Masanori , Ushijima Akemi , Ito Masami , Ono Yosuke , Shima Tomoko , Kawamura Kazuhiro , Ishizuka Bunpei , Saito Shigeru 
Published: April 2019

AbstractProblemPremature ovarian insufficiency (POI) is a clinical syndrome defined by the loss of ovarian activity before 40 years old. An autoimmune mechanism is suggested to be involved in the development of POI. Therefore, we examined the relationship between peripheral blood regulatory T (Treg) cells and autoantibodies in POI.Method of studyThirty POI patients and 23 control women were enrolled in the study. Using flow cytometry, we measured the abundance of CD4+ T, CD4+CD69+ T, CD8+ T, CD8+CD69+ T, naive Treg, effector Treg, and FOXP3+ effector T cells in peripheral blood. Antinuclear and anti‐thyroglobulin antibody (Tg‐Ab) titers were measured in POI patients.ResultsThe number of CD4+ T or CD4+CD69+ T cells was significantly higher in POI patients (P = 0.045, and P = 0.030), and there were significantly fewer effector Treg cells in POI patients (P = 0.016) than in the controls. There were significant negative correlations between effector Treg cells and Tg‐Abs (r = −0.584, P = 0.0282), and between effector Treg cells and CD4+CD69+ T cells (r = −0.415, P = 0.0226) in POI patients.ConclusionThis is the first report of decreased numbers of effector Treg cells and increased CD4+CD69+ activated T cells in peripheral blood in POI, suggesting that POI is an autoimmune disease.
Naïve regulatory T cells in infancy: Associations with perinatal factors and development of food allergy
Authors: Collier Fiona , Ponsonby Anne‐Louise , O'Hely Martin , Tang Mimi L.K. , Saffery Richard , Molloy John , Gray Lawrence E. , Ranganathan Sarath , Burgner David , Allen Katrina J. , Brix Susanne , Vuillermin Peter J. ,   the BIS Investigator Group
Published: April 2019

AbstractBackgroundIn previous studies, deficits in regulatory T‐cell (Treg) number and function at birth have been linked with subsequent allergic disease. However, longitudinal studies that account for relevant perinatal factors are required. The aim of this study was to investigate the relationship between perinatal factors, naïve Treg (nTreg) over the first postnatal year and development of food allergy.MethodsIn a birth cohort (n = 1074), the proportion of nTreg in the CD4+ T‐cell compartment was measured by flow cytometry at birth (n = 463), 6 (n = 600) and 12 (n = 675) months. IgE‐mediated food allergy was determined by food challenge at 1 year. Associations between perinatal factors (gestation, labour, sex, birth size), nTreg at each time point and food allergy at 1 year were examined by linear regression.ResultsA higher proportion of nTreg at birth, larger birth size and male sex was each associated with higher nTreg in infancy. Exposure to labour, as compared to delivery by prelabour Caesarean section, was associated with a transient decrease nTreg. Infants that developed food allergy had decreased nTreg at birth, and the labour‐associated decrease in nTreg at birth was more evident among infants with subsequent food allergy. Mode of birth was not associated with risk of food allergy, and there was no evidence that nTreg at either 6 or 12 months were related to food allergy.ConclusionThe proportion of nTreg at birth is a major determinant of the proportion present throughout infancy, highlighting the importance of prenatal immune development. Exposure to the inflammatory stimulus of labour appears to reveal differences in immune function among infants at risk of food allergy.
Peer problems, bullying involvement, and affective decision‐making in adolescence
Authors: Flouri Eirini , Papachristou Efstathios 
Published: April 2019

We investigated, using a cross‐lagged design, the longitudinal association of bullying involvement and peer problems with affective decision‐making in adolescence (ages 11 and 14 years) in 13,888 participants of the Millennium Cohort Study. Affective decision‐making (risk‐taking, quality of decision‐making, risk adjustment, deliberation time, and delay aversion) was measured with the Cambridge Gambling Task, bullying involvement (bully, bully–victim, victim, or ‘neutral’ status) with self‐report measures, and peer problems with the parent‐reported Strengths and Difficulties Questionnaire. In general, peer problems were associated with decision‐making in the unadjusted model but not after controlling for confounding. However, bullying involvement was related to decision‐making even after adjustment. Compared to ‘neutral’ males, bullies and bully–victims improved over time in risk adjustment, and bully–victims in deliberation time, too. In both sexes, bullies showed more risk‐taking compared to their ‘neutral’ counterparts. It seems that bullies are more sensitive to reward (or less sensitive to punishment) than those not involved in bullying. The finding that male bullies show improvement in decision‐making warrants further research.
Statement of contribution

What is already known on this subject?

In adults, decision‐making deficits and social exclusion or rejection are linked

In youth, only two studies have explored this link with gambling tasks measuring real‐world difficulties in decision‐making.

Both studies were cross‐sectional and small‐scale.

What does this study add?

We explore this link in adolescence, using a large, general population longitudinal sample and the Cambridge Gambling Task.

Bullies were more sensitive to reward (or less sensitive to punishment) than those not involved in bullying.

Male bullies improved over time in risk adjustment, a finding that warrants further research.
Global effects of non‐native tree species on multiple ecosystem services
Authors: Castro‐Díez Pilar , Vaz Ana Sofia , Silva Joaquim S. , van Loo Marcela , Alonso Álvaro , Aponte Cristina , Bayón Álvaro , Bellingham Peter J. , Chiuffo Mariana C. , DiManno Nicole , Julian Kahua , Kandert Susanne , La Porta Nicola , Marchante Hélia , Maule Hamish G. , Mayfield Margaret M. , Metcalfe Daniel , Monteverdi M. Cristina , Núñez Martín A. , Ostertag Rebecca , Parker Ingrid M. , Peltzer Duane A. , Potgieter Luke J. , Raymundo Maia , Rayome Donald , Reisman‐Berman Orna , Richardson David M. , Roos Ruben E. , Saldaña Asunción , Shackleton Ross T. , Torres Agostina , Trudgen Melinda , Urban Josef , Vicente Joana R. , Vilà Montserrat , Ylioja Tiina , Zenni Rafael D. , Godoy Oscar 
Published: April 2019

ABSTRACTNon‐native tree (NNT) species have been transported worldwide to create or enhance services that are fundamental for human well‐being, such as timber provision, erosion control or ornamental value; yet NNTs can also produce undesired effects, such as fire proneness or pollen allergenicity. Despite the variety of effects that NNTs have on multiple ecosystem services, a global quantitative assessment of their costs and benefits is still lacking. Such information is critical for decision‐making, management and sustainable exploitation of NNTs. We present here a global assessment of NNT effects on the three main categories of ecosystem services, including regulating (RES), provisioning (PES) and cultural services (CES), and on an ecosystem disservice (EDS), i.e. pollen allergenicity. By searching the scientific literature, country forestry reports, and social media, we compiled a global data set of 1683 case studies from over 125 NNT species, covering 44 countries, all continents but Antarctica, and seven biomes. Using different meta‐analysis techniques, we found that, while NNTs increase most RES (e.g. climate regulation, soil erosion control, fertility and formation), they decrease PES (e.g. NNTs contribute less than native trees to global timber provision). Also, they have different effects on CES (e.g. increase aesthetic values but decrease scientific interest), and no effect on the EDS considered. NNT effects on each ecosystem (dis)service showed a strong context dependency, varying across NNT types, biomes and socio‐economic conditions. For instance, some RES are increased more by NNTs able to fix atmospheric nitrogen, and when the ecosystem is located in low‐latitude biomes; some CES are increased more by NNTs in less‐wealthy countries or in countries with higher gross domestic products. The effects of NNTs on several ecosystem (dis)services exhibited some synergies (e.g. among soil fertility, soil formation and climate regulation or between aesthetic values and pollen allergenicity), but also trade‐offs (e.g. between fire regulation and soil erosion control). Our analyses provide a quantitative understanding of the complex synergies, trade‐offs and context dependencies involved for the effects of NNTs that is essential for attaining a sustained provision of ecosystem services.
Epigenetic silencing of SOCS5 potentiates JAK‐STAT signaling and progression of T‐cell acute lymphoblastic leukemia
Authors: Sharma Nitesh D. , Nickl Christian K. , Kang Huining , Ornatowski Wojciech , Brown Roger , Ness Scott A. , Loh Mignon L. , Mullighan Charles G. , Winter Stuart S. , Hunger Stephen P. , Cannon Judy L. , Matlawska‐Wasowska Ksenia 
Published: April 2019

AbstractActivating mutations in cytokine receptors and transcriptional regulators govern aberrant signal transduction in T‐cell lineage acute lymphoblastic leukemia (T‐ALL). However, the roles played by suppressors of cytokine signaling remain incompletely understood. We examined the regulatory roles of suppressor of cytokine signaling 5 (SOCS5) in T‐ALL cellular signaling networks and leukemia progression. We found that SOCS5 was differentially expressed in primary T‐ALL and its expression levels were lowered in HOXA‐deregulated leukemia harboring KMT2A gene rearrangements. Here, we report that SOCS5 expression is epigenetically regulated by DNA methyltransferase‐3A‐mediated DNA methylation and methyl CpG binding protein‐2‐mediated histone deacetylation. We show that SOCS5 negatively regulates T‐ALL cell growth and cell cycle progression but has no effect on apoptotic cell death. Mechanistically, SOCS5 silencing induces activation of JAK‐STAT signaling, and negatively regulates interleukin‐7 and interleukin‐4 receptors. Using a human T‐ALL murine xenograft model, we show that genetic inactivation of SOCS5 accelerates leukemia engraftment and progression, and leukemia burden. We postulate that SOCS5 is epigenetically deregulated in T‐ALL and serves as an important regulator of T‐ALL cell proliferation and leukemic progression. Our results link aberrant downregulation of SOCS5 expression to the enhanced activation of the JAK‐STAT and cytokine receptor‐signaling cascade in T‐ALL.
Higher human lymphocyte antigen class I expression in early‐stage cancer cells leads to high sensitivity for cytotoxic T lymphocytes
Authors: Akazawa Yu , Nobuoka Daisuke , Takahashi Mari , Yoshikawa Toshiaki , Shimomura Manami , Mizuno Shoichi , Fujiwara Toshiyoshi , Nakamoto Yasunari , Nakatsura Tetsuya 
Published: April 2019

AbstractHuman lymphocyte antigen (HLA) class I molecules play a central role in cytotoxic T lymphocytes (CTL)‐based antitumor immunity. However, the expression rate of HLA class I in cancer cells remains a topic of discussion. We compared HLA class I expression levels between cancer cells and surrounding non–tumorous hepatocytes in 20 early‐stage hepatocellular carcinoma (HCC) patients by immunohistochemistry using EMR 8‐5. The expression levels of HLA class I were classified as negative, incomplete positive or complete positive. Similarly, for various types of solid cancers, HLA class I expression was examined. For the HLA class I expression in cancer cells, among 20 HCC patients, 13 were complete positive, 3 were incomplete positive, and 4 were negative. In addition, 15 (75.0%) had higher expression levels of HLA class I in cancer cells compared with that in surrounding non–tumorous hepatocytes. An interferon‐γ (IFN‐γ) enzyme‐linked immunospot (ELISPOT) assay indicated that cancer cells with positive expression of HLA class I had strong sensitivity to antigen‐specific CTL. We suggested that HLA class I expression in cancer cells could be involved in the clinical prognosis of HCC patients. Similarly, 66.7%, 100.0%, 66.7% and 62.5% of patients with early‐stage pancreatic, gallbladder, esophageal and breast cancers, respectively, had higher expression levels of HLA class I in cancer cells than in surrounding normal tissue cells. We suggest that in several early‐stage solid cancers, including HCC, HLA class I expression levels in cancer cells are higher than that in surrounding normal tissue cells, which could result in the anti–tumor effect of CTL‐based cancer immunotherapy.
Independent relationships between bone mineral density, regional body fat and insulin sensitivity in white males
Authors: Loh Wann Jia , Stevenson John C. , Godsland Ian F. 
Published: April 2019

AbstractBackgroundAdiposity and insulin sensitivity may affect bone mineral density (BMD), but the confounding effect of weight hinders discrimination of independent associations. We explored whether regional fat masses and insulin sensitivity are independently related to BMD.Materials and methodsRelationships between total and regional body fat, insulin sensitivity and measures of BMD in 8 different regions were evaluated in a cross section of 590 generally healthy, white males, 274 of whom received measurement of insulin sensitivity (Si) using the intravenous glucose tolerance test. Measurements included total, android and gynoid fat and lean body mass and regional BMDs by dual‐energy X‐ray absorptiometry. Linear regression analyses were combined in a mediation analysis to explore associations with each regional BMD.ResultsWeight correlated positively with total fat mass (R2 = 0.67, P < 0.001) and negatively with Si (R2 = 0.14, P < 0.001). Body composition measures were consistently positively related to BMD in all regions except lumbar and thoracic spine. Accounting for body weight rendered negative majority of associations between total and regional fat masses and BMDs. An independent association between android fat and spine BMD was particularly apparent. Si was positively associated with total and limb BMD (P < 0.01) specifically among exercisers. Accounting for Si diminished the associations of total fat (negative) and lean body mass (positive) with total and limb BMD.ConclusionAndroid fat is independently negatively associated with spine BMD. Among those taking exercise, increased insulin sensitivity is associated with higher limb BMD and may underlie positive associations between lean body mass and BMD.
Clinical implications of the oncometabolite succinate in SDHx‐mutation carriers
Authors: Eijkelenkamp Karin , Osinga Thamara E. , Links Thera P. , van der Horst‐Schrivers Anouk N.A. 
Published: April 2019

AbstractSuccinate dehydrogenase (SDH) mutations lead to the accumulation of succinate, which acts as an oncometabolite. Germline SDHx mutations predispose to paraganglioma (PGL) and pheochromocytoma (PCC), as well as to renal cell carcinoma and gastro‐intestinal stromal tumors. The SDHx genes were the first tumor suppressor genes discovered which encode for a mitochondrial enzyme, thereby supporting Otto Warburg's hypothesis in 1926 that a direct link existed between mitochondrial dysfunction and cancer. Accumulation of succinate is the hallmark of tumorigenesis in PGL and PCC. Succinate accumulation inhibits several α‐ketoglutarate dioxygenases, thereby inducing the pseudohypoxia pathway and causing epigenetic changes. Moreover, SDH loss as a consequence of SDHx mutations can lead to reprogramming of cell metabolism. Metabolomics can be used as a diagnostic tool, as succinate and other metabolites can be measured in tumor tissue, plasma and urine with different techniques. Furthermore, these pathophysiological characteristics provide insight into therapeutic targets for metastatic disease. This review provides an overview of the pathophysiology and clinical implications of oncometabolite succinate in SDHx mutations.
Mesh Parametrization Driven by Unit Normal Flow
Authors: Zhao Hui , Su Kehua , Li Chenchen , Zhang Boyu , Yang Lei , Lei Na , Wang Xiaoling , Gortler Steven J. , Gu Xianfeng 
Published: April 2019

AbstractBased on mesh deformation, we present a unified mesh parametrization algorithm for both planar and spherical domains. Our approach can produce intermediate frames from the original meshes to the targets. We derive and define a novel geometric flow: ‘unit normal flow (UNF)’ and prove that if UNF converges, it will deform a surface to a constant mean curvature (CMC) surface, such as planes and spheres. Our method works by deforming meshes of disk topology to planes, and spherical meshes to spheres. Our algorithm is robust, efficient, simple to implement. To demonstrate the robustness and effectiveness of our method, we apply it to hundreds of models of varying complexities. Our experiments show that our algorithm can be a competing alternative approach to other state‐of‐the‐art mesh parametrization methods. The unit normal flow also suggests a potential direction for creating CMC surfaces.
Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer
Authors: Lippert Trenton , Borlongan Cesario V. 
Published: April 2019

SummaryAimsHyperbaric oxygen therapy (HBOT) has been widely used as postinjury treatment; however, we investigate its ability to mitigate potential damage as a preconditioning option. Here, we tested the hypothesis that HBOT preconditioning mitigates cell death in primary rat neuronal cells (PRNCs) through the transfer of mitochondria from astrocytes.MethodsPrimary rat neuronal cells were subjected to a 90‐minute HBOT treatment at 2.5 absolute atmospheres prior to either tumor necrosis factor‐alpha (TNF‐alpha) or lipopolysaccharide (LPS) injury to simulate the inflammation‐plagued secondary cell death associated with stroke and traumatic brain injury (TBI). After incubation with TNF‐alpha or LPS, the cell viability of each group was examined.ResultsThere was a significant increase of cell viability accompanied by mitochondrial transfer in the injury groups that received HBOT preconditioning compared to the injury alone groups (44 ± 5.2 vs 68 ± 4.48, n = 20,P < 0.05). The transfer of mitochondria directly after HBOT treatment was visualized by capturing images in 5‐minute intervals, which revealed that the robust transfer of mitochondria begins soon after HBOT and persisted throughout the treatment.ConclusionThis study shows that HBOT preconditioning stands as a robust prophylactic treatment for sequestration of inflammation inherent in stroke and TBI, possibly facilitating the transfer of resilient mitochondria from astrocytes to inflammation‐susceptible neuronal cells in mitigating cell death.
Urolithin A‐activated autophagy but not mitophagy protects against ischemic neuronal injury by inhibiting ER stress in vitro and in vivo
Authors: Ahsan Anil , Zheng Yan‐Rong , Wu Xiao‐Li , Tang Wei‐Dong , Liu Meng‐Ru , Ma Shi‐Jia , Jiang Lei , Hu Wei‐Wei , Zhang Xiang‐Nan , Chen Zhong 
Published: April 2019

AbstractAimMitochondrial autophagy (mitophagy) clears damaged mitochondria and attenuates ischemic neuronal injury. Urolithin A (Uro‐A) activates mitophagy in mammal cells and Caenorhabditis elegans. We explored neuroprotection of Uro‐A against ischemic neuronal injury.MethodsMice were subjected to middle cerebral artery occlusion. The brain infarct and neurological deficit scores were measured. The N2a cells and primary cultured mice cortical neurons were subjected to oxygen‐glucose deprivation and reperfusion (OGD/R). Uro‐A was incubated during OGD/R, and cell injury was determined by MTT and LDH. Autophagosomes were visualized by transfecting mCherry‐microtubule‐associated protein 1 light chain 3 (LC3). The protein levels of LC3‐II, p62, Translocase Of Inner Mitochondrial Membrane 23 (TIMM23), and cytochrome c oxidase subunit 4 isoform 1 (COX4I1) were detected by Western blot. The ER stress markers, activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), were determined by reverse transcription‐polymerase chain reaction (RT‐PCR).ResultsUrolithin A alleviated OGD/R‐induced injury in N2a cells and neurons and reduced ischemic brain injury in mice. Uro‐A reinforced ischemia‐induced autophagy. Furthermore, Uro‐A‐conferred protection was abolished by 3‐methyladenine, suggesting the requirement of autophagy for neuroprotection. However, mitophagy was not further activated by Uro‐A. Instead, Uro‐A attenuated OGD/R‐induced ER stress, which was abolished by 3‐methyladenosine. Additionally, neuroprotection was reversed by ER stress inducer.ConclusionUrolithin A protected against ischemic neuronal injury by reinforcing autophagy rather than mitophagy. Autophagy activation by Uro‐A attenuated ischemic neuronal death by suppressing ER stress.
The fatal flaws of compassionate conservation
Authors: Oommen Meera Anna , Cooney Rosie , Ramesh Madhuri , Archer Michael , Brockington Daniel , Buscher Bram , Fletcher Robert , Natusch Daniel J.D. , Vanak Abi T. , Webb Grahame , Shanker Kartik 
Published: April 2019

Article impact statement: Wallach et al.’s framing of compassionate conservation is flawed and impractical and could be dangerous for people, wildlife, and ecosystems.