bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metformin modulates cardiac endothelial dysfunction, oxidative stress and inflammation in irradiated rats: A new perspective of an antidiabetic drug
Authors: Karam Heba M. , Radwan Rasha R. 
Published: July 2019

AbstractCardiovascular disease is one of the most pivotal disorders after radiotherapy. The aim of this study investigates the possible protective effect of metformin against gamma radiation‐induced heart damage in male rats. Group 1 (control) received saline, group 2 was whole body gamma‐irradiated 5 Gy, group 3 was orally administered metformin 50 mg/kg/day for 2 weeks, group 4 received metformin 50 mg/kg/day for 1 week, then exposed to whole‐body gamma radiation at a dose of 5 Gy and continued with metformin for further 1 week. The results revealed that the administration of metformin to irradiated rats significantly ameliorated the changes in cardiac biomarkers (LDH and CK‐MB) compared with irradiated group. Heart catalase and SOD activities showed normal level when compared with the irradiated group. Also, NF‐κB, IL‐6 and TNF‐ α levels were markedly decreased compared with the corresponding values of irradiated group. Consequently, metformin reduced E‐selectin as well ICAM and VCAM‐1. These results confirmed by histopathological examination. In conclusion, concomitant administration of metformin during radiotherapy acts as a potent heart protector from oxidative stress, inflammatory mediators and endothelial dysfunction induced damages. Results thus hold a great promise for a new implication of an antidiabetic drug (metformin) as adjunct to radiotherapy.
The characteristics of antibiotic resistance and phenotypes in 29 outer‐membrane protein mutant strains in Aeromonas hydrophila
Authors: Li Zeqi , Wang Yuqian , Li Xiaoyan , Lin Zhenping , Lin Yuexu , Srinivasan Ramanathan , Lin Xiangmin 
Published: July 2019

SummaryAlthough many typical outer‐membrane proteins (OMPs) have been well characterized, the biological functions of many OMPs remain largely elusive. In this study, we successfully constructed 29 OMP knockout strains in the pathogen Aeromonas hydrophila, which account for about 50% of all predicted OMPs in this bacterial species. We then further validated the antibiotics' susceptibility characteristics against 20 antimicrobial reagents in these mutants considering several phenotypes. Our results showed that a total of 22 OMP mutants affected the susceptibility to at least one antibiotic. The deletion of some OMPs, such as ΔlamB and ΔbamA, revealed very important roles in the resistance to certain antibiotics. However, not a single OMP mutant presented a constant behaviour to all of the tested antibiotics, suggesting the existence of a complex intercellular regulation mechanism and a protein–protein interaction network underlying the OMP homeostasis in the presence of antibiotics. Meanwhile, some OMP mutants also affected biofilm formation, ECPase and haemolytic activity, and carbon resources utilization. This report demonstrates the biological functions of OMPs on a large scale and most of results have not been reported in A. hydrophila.
Functional responses of three guilds of spiders: Comparing single‐ and multiprey approaches
Authors: Benhadi‐Marín Jacinto , Pereira José A. , Sousa José P. , Santos Sónia A. P. 
Published: July 2019

AbstractSpiders are successful natural enemies of pests occurring throughout the different strata of an agroecosystem. The study of their functional responses can provide information related to the potential effectiveness of different species and guilds on reducing a pest population. However, multiple prey availability may change the functional response of a predator. In this study, the functional responses of three species of spiders in single‐prey and multiple‐prey experiments were modelled. The spider species Haplodrassus rufipes, Araniella cucurbitina and Synema globosum were chosen as being representatives of ground runners, orb‐weavers and ambushers, respectively. Three prey species were selected: a target prey, the Mediterranean fruit fly Ceratitis capitata and two alternate prey species, the flour moth Ephestia kuehniella and the house cricket Acheta domesticus. When the selected target prey C. capitata was supplied in the single‐prey experiments, the most and the least efficient spider species were H. rufipes and S. globosum, respectively. However, opposite results were obtained when alternative preys were supplied. Also, A. cucurbitina significantly changed its functional response with the presence of alternative prey species. Considering the prey preference during the multiple‐prey experiments, A. domesticus, used as representative of a heavy, long‐sized and highly motile prey, was avoided whereas C. capitata, the target pest used as representative of light, small‐sized and moderately motile prey was preferred by the three species of spiders. Ephestia kuehniella, used as representative of light, medium‐sized and low motile prey was occasionally consumed. Each guild could include efficient predators against pests according to its hunting strategies and the ecological exploited niches. Orb‐weavers could be efficient predators against flying pests; ambushers such as S. globosum could contribute to the reduction of the populations of flower‐visiting pests, whereas active ground hunters may also play an important role preying on pests that develop a part or all of its life cycle in the ground. However, further research on feeding behaviour such as prey switching is needed for a better understanding of the effectiveness of spiders as natural enemies.
Childhood maltreatment and treatment outcome in psychotic disorders: a systematic review and meta‐analysis
Authors: Thomas S. , Höfler M. , Schäfer I. , Trautmann S. 
Published: July 2019

ObjectiveChildhood maltreatment (CM) plays an important role in the aetiology and course of psychotic disorders and is associated with characteristics that could be relevant for treatment. We aimed to conduct a systematic review and meta‐analysis on the association between CM and treatment outcome in psychotic disorders.MethodsTreatment outcome was defined as change in psychotic symptoms or in social or occupational functioning between first and last reported measurement in the course of a pharmacological and/or psychological treatment.ResultsTwelve treatment results from seven studies (636 patients, average treatment duration: 59.2 weeks) were included. CM was related to poorer treatment outcomes in psychotic disorders (OR = 1.51, 95% CI = [1.08, 2.10]). There is evidence that this association might increase with illness duration and increasing age and might be stronger in schizophrenia samples.ConclusionsChildhood maltreatment is highly understudied with regard to treatment outcome in psychotic disorders. The need for more studies is emphasized by the fact that this meta‐analysis reveals evidence for a poorer treatment response in patients with CM. If this association is confirmed, the identification of patients with CM and the consideration of associated clinical and biological conditions could contribute to improve treatment outcome in psychotic disorders.
Impact of specialist and primary care stop smoking support on socio‐economic inequalities in cessation in the United Kingdom: a systematic review and national equity analysis
Authors: Smith Caroline E. , Hill Sarah E. , Amos Amanda 
Published: July 2019

AbstractAimTo assess the impact of UK specialist and primary care‐based stop smoking support on socio‐economic inequalities in cessation.MethodsSystematic review and narrative synthesis, with a national equity analysis of stop smoking services (SSS). Ten bibliographic databases were searched for studies of any design, published since 2012, which evaluated specialist or primary care‐based stop smoking support by socio‐economic status (SES) or within a disadvantaged group. Studies could report on any cessation‐related outcome. National Statistics were combined to estimate population‐level SSS reach and impact among all smokers by SES. Overall, we included 27 published studies and three collated, national SSS reports for England, Scotland and Northern Ireland (equivalent data for Wales were unavailable).ResultsPrimary care providers and SSS in the United Kingdom were particularly effective at engaging and supporting disadvantaged smokers. Low SES groups were more likely to have their smoking status assessed, to receive general practitioner brief cessation advice/SSS referral and to attempt a quit with SSS support. Although disadvantaged SSS clients were less successful in quitting, increased service reach offset these lower quit rates, resulting in higher service impact among smokers from low SES groups. Interventions that offer tailored and targeted support have the potential to improve quit outcomes among disadvantaged smokers.ConclusionsEquity‐orientated stop smoking support can compensate for lower quit rates among disadvantaged smokers through the use of equity‐based performance targets, provision of targeted services and the development of tailored interventions.
Are animal models of addiction useful?
Authors: Field Matt , Kersbergen Inge 
Published: July 2019

AbstractBackgroundPre‐clinical research involving non‐human animals has made important contributions to our understanding of risk factors for addiction, neuroadaptations that follow chronic drug exposure and to the development of some efficacious pharmacotherapies for addiction. Despite these contributions, we argue that animal models of addiction have impeded progress in our understanding of addiction and its treatment in humans.ArgumentFirst, the majority of pharmacological treatments that were initially developed using animal models have failed to prove effective for the treatment of addiction in humans, resulting in a huge waste of resources. Secondly, we demonstrate that prevailing animal models that portray addiction as a disorder of compulsion and habit cannot be reconciled with observations that psychoactive drug use in humans is a goal‐directed operant behaviour that remains under the control of its consequences, even in people who are addicted. Thirdly, addiction may be a uniquely human phenomenon that is dependent on language, which necessarily limits the validity of animal models. Finally, we argue that addicted brains must be understood as one component of broader networks of symptoms and environmental and social factors that are impossible to model in laboratory animals.ConclusionsA case can be made that animal models of addiction have not served us well in understanding and treating addiction in humans. It is important to reconsider some widely held beliefs about the nature of addictive behaviour in humans that have arisen from the zeal to translate observations of laboratory animals.
SIRT1 gene polymorphisms are associated with nondiabetic type 1 cardiorenal syndrome
Authors: Hou Jiebin , Xie Xinyue , Tu Qingxian , Li Jie , Ding Jiarong , Shao Guojian , Jiang Qianfeng , Yuan Li , Lai Xueli 
Published: July 2019

AbstractType 1 cardiorenal syndrome (CRS1) is characterized by acute cardiac disease (e.g., acute heart failure [AHF]), leading to acute kidney injury. Sirtuin 1 (SIRT1), an NAD+‐dependent deacylase, has been found to be associated with CRS1. To confirm whether a correlation exists between SIRT1 variants and the risk of CRS1, the association between the prevalence of CRS1 and single‐nucleotide polymorphisms (SNPs) within the SIRT1 gene was investigated in AHF patients. A total of 316 Chinese AHF participants (158 patients with CRS1 and 158 age‐ and sex‐matched controls) were recruited for the present observational study to investigate the association between nine common SIRT1 SNPs (i.e., rs7895833 G > A, rs10509291 T > A, rs3740051 A > G, rs932658 A > C, rs33957861 C > T, rs7069102 C > G, rs2273773 T > C, rs3818292 A > G, and rs1467568 A > G) and the susceptibility to CRS1. Significant differences in genotype distribution between the control and CRS1 groups were found for rs7895833 and rs1467568. After applying a Bonferroni adjustment, the A allele of rs7895833 was still found to be protective (p = 0.001; odds ratio [OR] = 0.77) against CRS1 in this study population. The AA genotype of rs7895833 and the GA genotype of rs1467568 were associated with a significantly reduced risk of CRS1 (OR = 0.23 and 0.49, respectively). rs7895833 and rs1467568 were further analyzed as a haplotype, and the GA haplotype (rs7895833‐rs1467568) exhibited a significant association with CRS1 (p = 0.008), while the AA haplotype showed a significant protective effect (p = 0.022). Our study showed that SIRT1 rs7895833 and rs1467568 polymorphisms had a significant effect on the risk of developing CRS1 in a population in China.
Hospitalisation for medication misadventures among older adults with and without dementia: A 5‐year retrospective study
Authors: Mullan Judy , Burns Pippa , Mohanan Lita , Lago Luise , Jordan Margaret , Potter Jan 
Published: July 2019

AbstractObjectivesTo compare rates and trends in hospital admissions due to medication misadventure for older adults (≥65 years) with and without dementia.MethodsA retrospective analysis of hospital admissions that occurred between 2012 and 2016, for medication misadventures among older adults living in regional Australia.ResultsMedication misadventures contributed to 10 555 (4.6%) of the total 228 165 admissions for older adults over the study period. Among these admissions, older adults with dementia were three times more likely to be hospitalised with medication misadventures (14.0%), than their non‐dementia counterparts (4.2%). Medication misadventures relating to “anticoagulants” and “opioids/related analgesics” accounted for the majority of admissions (24.3% dementia vs 30.7% non‐dementia).ConclusionsThis study highlights that the proportion of older adults hospitalised for a medication misadventure is much higher among those with dementia, than those without dementia. Strategies should target older adults, and especially those with dementia, to reduce medication‐related harm and improve patient safety.
Basophil degranulation in response to IgE ligation is controlled by a distinctive circadian clock in asthma
Authors: Spadaro Giuseppe , Giurato Giorgio , Stellato Cristiana , Marone Gianni , Casolaro Vincenzo 
Published: July 2019

AbstractBackgroundSeveral factors may contribute to the circadian variability of clinical manifestations in asthma and allergy. Basophils play a pivotal role in allergic inflammation. However, evidence for a functional clock governing the effector function of these cells is sparse and contradictory. We have systematically sampled the 24‐hour response of basophils to IgE‐ and non‐IgE‐dependent ligands in asthma to understand their possible contribution to the diurnal variations of allergic symptoms.MethodsLeukocytes were collected every 4 hours for 24 hours from 10 patients with moderate, persistent asthma and 10 matched, nonallergic controls, and then incubated with concentrations of anti‐IgE, formyl‐methionyl‐leucylphenylalanine (fMLP), or the Ca2+ ionophore, A23187. Histamine release (HR) was tested for time‐of‐day‐ or disease‐related variability by conventional statistics and for 24‐hour rhythmicity by the cosinor method.ResultsHR induced by anti‐IgE was significantly increased at 08:00 vs. 20:00 in basophils from asthmatics but not controls. No significant differences were seen at any time in the response to A23187, while the response to fMLP was significantly higher at 08:00 vs. 20:00 in controls but not asthmatics. The basophil response to anti‐IgE, but not fMLP or A23187, varied significantly across the 24 hours in asthma, and its amplitude, percent rhythm, and acrophase were comparable to those of peak expiratory flow or serum cortisol.ConclusionUsing an integrated statistical approach, we show that basophil responsiveness undergoes significant circadian variability and that distinct patterns of rhythmicity can be recognized depending on the signal delivered, the activation parameters assessed, and the disease status.
Mindfulness‐based cognitive therapy is associated with distinct resting‐state neural patterns in patients with generalized anxiety disorder
Authors: Zhao Xing‐Rong , Chen Zhuang‐Fei , Kang Chuan‐Yuan , Liu Rui‐Xiang , Bai Jun‐Yun , Cao Yu‐Ping , Cheng Yu‐Qi , Xu Xiu‐Feng , Zhang Ya‐Lin 
Published: July 2019

AbstractIntroductionMindfulness‐based cognitive therapy (MBCT) may be effective for generalized anxiety disorder (GAD); however, the neural mechanism is poorly understood. In this study, we examined the potential neural mechanisms through which MBCT may reduce anxiety in patients with mild‐to‐moderate GAD.MethodsEight weekly group MBCT sessions (2 h each) were conducted with 32 GAD patients. Resting‐state functional magnetic resonance imaging (fMRI) was used, along with clinical and mindfulness profiles. A regional homogeneity (ReHo) approach was applied, and resting‐state functional connectivity in the default mode network (DMN) using the posterior cingulate cortex (PCC) seed was examined.ResultsMBCT reduced the anxiety and increased the mindfulness abilities of patients. After MBCT, patients had reduced ReHo in broad regions of the limbic system, along with increased DMN functional connectivity in the anterior cingulate cortex (ACC) and bilateral insula. Overlapping regions of reduced ReHo and increased DMN functional connectivity were observed in the mid‐cingulate cortex (MCC) and bilateral insula. The increased PCC‐ACC and PCC‐insula functional connectivity following MBCT were related to anxiety improvements, suggesting a potential therapeutic mechanism for mindfulness‐based therapies.DiscussionGroup MBCT treatment appears to have effectively reduced anxiety symptoms in patients with mild‐to‐moderate GAD. Activation and functional connectivity appeared significantly different across some limbic regions after MBCT treatment. The salience network showed reduced ReHo and increased connectivity to the PCC. The DMN functional connectivity of the MCC may indicate reduced anxiety and improved mindfulness in GAD patients.
Childcare policies and services in Hong Kong after the handover: Beyond a feminist critique
Authors: Xia Lily L. L. , Ma Joyce L. C. 
Published: July 2019

AbstractThis article reviews the development of childcare policies and services in Hong Kong after the handover, gauging it with two standards: promoting the equal development of children and gender equality in our society. Statistics derived from data taken from multiple sources show that the government has been sticking to a “positive non‐intervention approach” to welfare development and that the male breadwinner/female carer model prevalent in this region was shaped and strengthened by current childcare policies and services. The current provision of childcare services is insufficient to guarantee the equal use of childcare among children of different socioeconomic backgrounds, or to ease the tension between the needs of childcare and job requirements in a family, or to emancipate married women from the domestic sphere. A “generative welfare approach” that collects fiscal resources and redistributes them strategically with a systemic mind‐set has been suggested for social policy and service planning, including spending the money in the right place, launching smart and practical policies that can achieve both pragmatic effects and ideological improvement in the area of gender equality, providing financial support or subsidies to a company for the provision of parental leave, and increasing the provision of quality childcare services.
Single and combined BTK and PI3Kδ inhibition with acalabrutinib and ACP‐319 in pre‐clinical models of aggressive lymphomas
Authors: Spriano Filippo , Tarantelli Chiara , Gaudio Eugenio , Gerlach Magdalena M. , Priebe Valdemar , Cascione Luciano , Bernasconi Elena , Targa Altea , Mascia Michele , Dirnhofer Stefan , Stathis Anastasios , Zucca Emanuele , Bertoni Francesco 
Published: July 2019

SummaryThe B‐cell receptor and the phosphatidylinositol 3‐kinase (PI3K) signalling pathways, together with their downstream partners, represent important therapeutic targets for B‐cell lymphomas. Here, we evaluated the activity of acalabrutinib (ACP‐196) and ACP‐319 (AMG‐319), second generation inhibitors of Bruton tyrosine kinase (BTK) and PI3Kδ inhibitor, respectively, in lymphoma pre‐clinical models. The two compounds showed activity in activated B‐cell‐like diffuse large B‐cell lymphoma (ABC DLBCL), mantle cell lymphoma and marginal zone lymphoma. Two in vivo experiments with ABC DLBCL and MCL xenografts confirmed the effect of the single agents. Benefit was achieved by exposing the lymphoma cell lines to both acalabrutinib and ACP‐319. Two cell lines presented a discordant response to first and second generation BTK inhibitors, probably due to the inhibition by ibrutinib of kinases other than BTK. In conclusion, our data sustain the on‐going current trials with acalabrutinib and ACP‐319 as single agents and provide the basis for the investigation of their combination as well.
Upregulation of adenosine A2A receptor and downregulation of GLT1 is associated with neuronal cell death in Rasmussen's encephalitis
Authors: He Xinghui , Chen Fan , Zhang Yifan , Gao Qing , Guan Yuguang , Wang Jing , Zhou Jian , Zhai Feng , Boison Detlev , Luan Guoming , Li Tianfu 
Published: July 2019

AbstractRasmussen encephalitis (RE) is a severe pediatric inflammatory brain disease characterized by unilateral inflammation and atrophy of the cerebral cortex, drug‐resistant focal epilepsy and progressive neurological and cognitive deterioration. The etiology and pathogenesis of RE remain unclear. Our previous results demonstrated that the adenosine A1 receptor (A1R) and the major adenosine‐removing enzyme adenosine kinase play an important role in the etiology of RE. Because the downstream pathways of inhibitory A1R signaling are modulated by stimulatory A2AR signaling, which by itself controls neuro‐inflammation, glial activation and glial glutamate homeostasis through interaction with glutamate transporter GLT‐1, we hypothesized that maladaptive changes in adenosine A2A receptor (A2AR) expression are associated with RE. We used immunohistochemistry and Western blot analysis to examine the expression of A2ARs, glutamate transporter‐I (GLT‐1) and the apoptotic marker Bcl‐2 in surgically resected cortical specimens from RE patients (n = 18) in comparison with control cortical tissue. In lesions of the RE specimen we found upregulation of A2ARs, downregulation of GLT‐1 and increased apoptosis of both neurons and astroglia. Double staining revealed colocalization of A2ARs and Bcl‐2 in RE lesions. These results suggest that maladaptive changes in A2AR expression are associated with a decrease in GLT‐I expression as a possible precipitator for apoptotic cell loss in RE. Because A2AR antagonists are already under clinical evaluation for Parkinson's disease, the A2AR might likewise be a tractable target for the treatment of RE.