bluuebunny/crossref_metadata_2025_split huggingface dataset:
How do conflicts impact change in family businesses? The family system and familiness as a catalytic converter of change
Authors: Claßen Christina Anna Elisabeth , Schulte Reinhard 
Published: October 2017

PurposeThe purpose of this paper is to develop an understanding of how conflicts, caused by the specifics of family businesses – the familiness – impact change in family businesses.Design/methodology/approachThe analysis is based on 21 semi-structured in-depth interviews of German family business members. The authors followed the grounded theory approach.FindingsThis study gives evidence for family business-specific conflicts and family business-specific change and outlines how conflict impacts change. Findings show that a family system works like a recursive catalytic converter in family businesses.Research limitations/implicationsThis paper offers researchers a broader understanding and a comprehensive view of change in the family business. Although still limited by its exploratory approach, its insights can be valuable for researchers, practitioners and policy makers. The findings offer an operational base for future quantitative studies.Originality/valueUsing the new system theories approach the authors develop an understanding of how conflicts impact change in family businesses. The study explains how conflicts are managed in family business practice.
Evolution of human diet and effect of globalization on regional diet with emphasis to the Mediterranean diet
Authors: Haile Belay , Neme Kumera , Belachew Tefera 
Published: October 2017

Purpose
The Mediterranean Diet (MD) is an expression of different Mediterranean food cultures and lifestyles. It is characterized by high consumption of olive oil, vegetables, legumes, whole grain products, fruits and nuts. This paper aims to emphasize on the evolution of human diet from earliest human ancestors to current civilization, the effect of MD on human health and the role of globalization to shift traditional diet, particularly MD to processed foods.

Design/methodology/approach
Different published papers were collected from the internet by using the following phrases: evolution of human diet, human ancestors, the effect of globalization on a regional diet, Mediterranean diet, healthy food, food pyramid, evolution of human diet and effect of globalization on diet. Finally, the papers were read and summarized as a review paper.

Findings
MD has been accepted worldwide owing to its health impact such as prevention and control of type 2 diabetes, anti-inflammatory effects and decrease in the risk of cardiovascular diseases and incidence of Parkinson’s disease and Alzheimer’s disease. However, in conjunction with this discordance between our ancient, genetically determined biology and the nutritional, cultural and activity patterns of contemporary Western populations, many of the so-called diseases of civilization have emerged. Particularly, the food staples and food-processing procedures introduced during the Neolithic and Industrial periods have fundamentally altered nutritional characteristics of ancestral hominin diets. MD is currently under the risk of extinction for a result of the effects of globalization.

Originality/value
The review paper focuses on the evolution of human diet as an effect of globalization on the regional diet with emphasis on the MD. It specifically focuses on the link between diet and earliest human ancestors, about MD and its health benefit, diet pyramid and effect of globalization on regional diet.
Mutualistic interaction between dichloromethane‐ and chloromethane‐degrading bacteria in an anaerobic mixed culture
Authors: Chen Gao , Kleindienst Sara , Griffiths Daniel R. , Mack E. Erin , Seger Edward S. , Löffler Frank E. 
Published: October 2017

SummaryThe microbial mixed culture RM grows with dichloromethane (DCM) as the sole energy source generating acetate, methane, chloride and biomass as products. Chloromethane (CM) was not an intermediate during DCM utilization consistent with the observation that CM could not replace DCM as a growth substrate. Interestingly, cultures that received DCM and CM together degraded both compounds concomitantly. Transient hydrogen (H2) formation reaching a maximum concentration of 205 ± 13 ppmv was observed in cultures growing with DCM, and the addition of exogenous H2 at concentrations exceeding 3000 ppmv impeded DCM degradation. In contrast, CM degradation in culture RM had a strict requirement for H2. Following five consecutive transfers on CM and H2, Acetobacterium 16S rRNA gene sequences dominated the culture and the DCM‐degrader Candidatus Dichloromethanomonas elyunquensis was eliminated, consistent with the observation that the culture lost the ability to degrade DCM. These findings demonstrate that culture RM harbours different populations responsible for anaerobic DCM and CM metabolism, and further imply that the DCM and CM degradation pathways are mechanistically distinct. H2 generated during DCM degradation is consumed by the hydrogenotrophic CM degrader, or may fuel other hydrogenotrophic processes, including organohalide respiration, methanogenesis and H2/CO2 reductive acetogenesis.
Metagenomic assessment of the interplay between the environment and the genetic diversification of Acinetobacter
Authors: Garcia‐Garcera Marc , Touchon Marie , Brisse Sylvain , Rocha Eduardo P.C. 
Published: October 2017

SummaryMost bacteria have poorly characterized environmental reservoirs and unknown closely related species. This hampers the study of bacterial evolutionary ecology because both the environment and the genetic background of ancestral lineages are unknown. We combined metagenomics, comparative genomics and phylogenomics to overcome this limitation, to identify novel taxa and to propose environments where they can be isolated. We applied this method to characterize the ecological distribution of known and novel lineages of Acinetobacter spp. We observed two major environmental transitions at deep phylogenetic levels, splitting the genus into three ecologically differentiated clades. One of these has rapidly shifted towards host‐association by acquiring genes involved in bacteria‐eukaryote interactions. We show that environmental perturbations affect species distribution in predictable ways: bovines have very diverse communities of Acinetobacter, unless they were administered antibiotics, in which case they show highly uniform communities of Acinetobacter spp. that resemble those of humans. Our results uncover the diversity of bacterial lineages, overpassing the limitations of classical cultivation methods and highlight the role of the environment in shaping their evolution.
Transfer and analysis of Salmonella pdu genes in a range of Gram‐negative bacteria demonstrate exogenous microcompartment expression across a variety of species
Authors: Graf Laura , Wu Kent , Wilson James W. 
Published: October 2017

SummaryBacterial microcompartments (MCPs) are protein organelles that typically house toxic or volatile reaction intermediates involved in metabolic pathways. Engineering bacteria to express exogenous MCPs will allow these cells to gain useful functions involving molecule compartmentalization. We cloned a 38 kb region from the Salmonella enterica serovar Typhimurium genome containing the pdu 1,2 propanediol (1,2 PD) utilization and cob/cbi genes using the FRT‐Capture strategy to clone and transfer large genomic segments. We transferred this clone to a range of Gram‐negative bacteria and found the clone to be functional for 1,2 PD metabolism in a variety of species including S. Typhimurium Δpdu, Escherichia coli, Salmonella bongori, Klebsiella pneumoniae, Cronobacter sakazakii, Serratia marcescens, and different Pseudomonas species. We successfully isolated MCPs expressed from the clone from several, but not all, of these strains, and we observed this utilizing a range of different media and in the absence of protease inhibitor. We also present a mini‐prep protocol that allows rapid, small‐scale screening of strains for MCP production. To date, this is the first analysis of cloned, exogenous microcompartment expression across several different Gram‐negative backgrounds and provides a foundation for MCP use in a variety of bacterial species using a full, intact clone.
Simulation‐based Education to Ensure Provider Competency Within the Health Care System
Authors: Griswold Sharon , Fralliccardi Alise , Boulet John , Moadel Tiffany , Franzen Douglas , Auerbach Marc , Hart Danielle , Goswami Varsha , Hui Joshua , Gordon James A. 
Published: September 2017

AbstractThe acquisition and maintenance of individual competency is a critical component of effective emergency care systems. This article summarizes consensus working group deliberations and recommendations focusing on the topic “Simulation‐based education to ensure provider competency within the healthcare system.” The authors presented this work for discussion and feedback at the 2017 Academic Emergency Medicine Consensus Conference on “Catalyzing System Change Through Healthcare Simulation: Systems, Competency, and Outcomes,” held on May 16, 2017, in Orlando, Florida. Although simulation‐based training is a quality and safety imperative in other high‐reliability professions such as aviation, nuclear power, and the military, health care professions still lag behind in applying simulation more broadly. This is likely a result of a number of factors, including cost, assessment challenges, and resistance to change. This consensus subgroup focused on identifying current gaps in knowledge and process related to the use of simulation for developing, enhancing, and maintaining individual provider competency. The resulting product is a research agenda informed by expert consensus and literature review.
Body size variation and sexual size dimorphism across climatic gradients in the widespread treefrog Scinax fuscovarius (Anura, Hylidae)
Authors: Goldberg Javier , Cardozo Darío , Brusquetti Francisco , Bueno Villafañe Diego , Caballero Gini Andrea , Bianchi Carlos 
Published: September 2017

AbstractVariation in body size represents one of the crucial raw materials for evolution. However, at present, it is still being debated what is the main factor affecting body size or if the final body size is the consequence of several factors acting synergistically. To evaluate this, widespread species seem to be suitable models because the different populations occur along a geographical gradient and under contrasted climatic and environmental conditions. Here we describe the spatial pattern of variation in body size and sexual size dimorphism in the snouted treefrog Scinax fuscovarius (Anura, Hylidae) along a 10° range in latitude, 25° longitude, and 2000 m in altitude from Argentina, Brazil and Paraguay using an information‐theoretic approach to evaluate the support of the data for eight a priori hypotheses proposed in the literature to account for geographical body size, and three hypotheses for sexual size dimorphism variation. Body size of S. fuscovarius varied most dramatically with longitude and less so with latitude; frogs were largest in the northwestern populations. Body size was positively related with precipitation seasonality, and negatively with annual precipitation. Furthermore, the degree of sexual size dimorphism was greatest in the western populations with less annual precipitation, as the increase in body size was stronger for females. Our results on body size variation are consistent with two ecogeographical hypotheses, the starvation resistance and the water availability hypotheses, while our results on sexual size dimorphism in S. fuscovarius supports the differential‐plasticity hypothesis but the inverse to Rensch's rule and the parental investment hypothesis. Due to the weak association between environmental variables and body size and sexual size dimorphism variation, we stress that there are other factors, mainly those related to the life history, driving the geographical variation of S. fuscovarius.
The monoacylglycerol lipase inhibitor KML29 with gabapentin synergistically produces analgesia in mice
Authors: Crowe Molly S , Wilson Catheryn D , Leishman Emma , Prather Paul L , Bradshaw Heather B , Banks Matthew L , Kinsey Steven G 
Published: September 2017

Background and PurposeGabapentin is commonly prescribed for nerve pain but may also cause dizziness, sedation and gait disturbances. Similarly, inhibition of the endogenous cannabinoid enzyme monoacylglycerol lipase (MAGL) has antinociceptive and anti‐inflammatory properties but also induces sedation in mice at high doses. To limit these side effects, the present study investigated the analgesic effects of coadministering a MAGL inhibitor with gabapentin.Experimental ApproachMice subjected to the chronic constriction injury model of neuropathic pain were administered the MAGL inhibitor KML29 (1–40 mg·kg−1, i.p.), gabapentin (1–50 mg·kg−1, i.p.) or both compounds. Mice were tested for mechanical and cold allodynia. The function and expression of cannabinoid CB1 receptors in whole brain homogenates and lipid profile of spinal cords were assessed after repeated drug administration.Key ResultsThe combination of low‐dose KML29:gabapentin additively attenuated mechanical allodynia and synergistically reduced cold allodynia. The CB1 antagonist, rimonabant, partially reversed the anti‐allodynic effects of KML29:gabapentin in mechanical allodynia but not cold allodynia. The anti‐allodynic effects of KML29:gabapentin did not undergo tolerance in mechanical allodynia after repeated administration but produced mild tolerance in cold allodynia. High dose KML29 alone reduced CB1 receptor expression and function, but KML29:gabapentin reduced the density of CB1 receptors but did not alter their function. KML29:gabapentin influenced additional signalling pathways (including fatty acids) other than the pathways activated by a higher dose of either drug alone.Conclusion and ImplicationsThese data support the strategy of combining MAGL inhibition with a commonly prescribed analgesic as a therapeutic approach for attenuating neuropathic pain.
Dopamine D2 receptor signalling controls inflammation in acute pancreatitis via a PP2A‐dependent Akt/NF‐κB signalling pathway
Authors: Han Xiao , Li Bin , Ye Xin , Mulatibieke Tunike , Wu Jianghong , Dai Juanjuan , Wu Deqing , Ni Jianbo , Zhang Ruling , Xue Jing , Wan Rong , Wang Xingpeng , Hu Guoyong 
Published: September 2017

Background and PurposeDopamine has multiple anti‐inflammatory effects, but its role and molecular mechanism in acute pancreatitis (AP) are unclear. We investigated the role of dopamine signalling in the inflammatory response in AP.Experimental ApproachChanges in pancreatic dopaminergic system and effects of dopamine, antagonists and agonists of D1 and D2 dopamine receptors were analysed in wild‐type and pancreas‐specific Drd2−/− mice with AP (induced by caerulein and LPS or L‐arginine) and pancreatic acinar cells with or without cholecystokinin (CCK) stimulation. The severity of pancreatitis was assessed by measuring serum amylase and lipase and histological assessments. The NF‐κB signalling pathway was evaluated, and macrophage and neutrophil migration assessed by Transwell assay.Key ResultsPancreatic dopamine synthetase and metabolic enzyme levels were increased, whereas D1 and D2 receptors were decreased in AP. Dopamine reduced inflammation in CCK‐stimulated pancreatic acinar cells by inhibiting the NF‐κB pathway. Moreover, the protective effects of dopamine were blocked by a D2 antagonist, but not a D1 antagonist. A D2 agonist reduced pancreatic damage and levels of p‐IκBα, p‐NF‐κBp65, TNFα, IL‐1β and IL‐6 in AP. Pancreas‐specific Drd2−/− aggravated AP. Also, the D2 agonist activated PP2A and inhibited the phosphorylation of Akt, IKK, IκBα and NF‐κB and production of inflammatory cytokines and chemokines. Furthermore, it inhibited the migration of macrophages and neutrophils by reducing the expression of CCL2 and CXCL2. A PP2A inhibitor attenuated these protective effects of the D2 agonist.Conclusions and ImplicationsD2 receptors control pancreatic inflammation in AP by inhibiting NF‐κB activation via a PP2A‐dependent Akt signalling pathway.
Epigenetic regulation of melatonin receptors in neuropsychiatric disorders
Authors: Bahna Sarra G , Niles Lennard P 
Published: October 2017

Melatonin, the primary indoleamine hormone of the mammalian pineal gland, is known to have a plethora of neuroregulatory, neuroprotective and other properties. Melatonergic signalling is mediated by its two GPCRs, MT1 and MT2, which are widely expressed in the mammalian CNS. Melatonin levels and receptor expression often show a decrease during normal ageing, and this reduction may be accelerated in some disease states. Depleted melatonergic signalling has been associated with neuropsychiatric dysfunction and impairments in cognition, memory, neurogenesis and neurorestorative processes. The anticonvulsant and mood stabilizer, valproic acid (VPA), up‐regulates melatonin MT1 and/or MT2 receptor expression in cultured cells and in the rat brain. VPA is known to affect gene expression through several mechanisms, including the modulation of intracellular kinase pathways and transcription factors, as well as the inhibition of histone deacetylase (HDAC) activity. Interestingly, other HDAC inhibitors, such as trichostatin A, which are structurally distinct from VPA, can also up‐regulate melatonin receptor expression, unlike a VPA analogue, valpromide, which lacks HDAC inhibitory activity. Moreover, VPA increases histone H3 acetylation along the length of the MT1 gene promoter in rat C6 cells. These findings indicate that an epigenetic mechanism, linked to histone hyperacetylation/chromatin remodelling and associated changes in gene transcription, is involved in the up‐regulation of melatonin receptors by VPA. Epigenetic induction of MT1 and/or MT2 receptor expression, in areas where these receptors are lost because of ageing, injury or disease, may be a promising therapeutic avenue for the management of CNS dysfunction and other disorders.Linked ArticlesThis article is part of a themed section on Recent Developments in Research of Melatonin and its Potential Therapeutic Applications. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.16/issuetoc
Antidepressant‐like effects of BU10119, a novel buprenorphine analogue with mixed κ/μ receptor antagonist properties, in mice
Authors: Almatroudi Abdulrahman , Ostovar Mehrnoosh , Bailey Christopher P , Husbands Stephen M , Bailey Sarah J 
Published: October 2017

Background and PurposeThe κ receptor antagonists have potential for treating neuropsychiatric disorders. We have investigated the in vivo pharmacology of a novel buprenorphine analogue, BU10119, for the first time.Experimental ApproachTo determine the opioid pharmacology of BU10119 (0.3–3 mg·kg−1, i.p.) in vivo, the warm‐water tail‐withdrawal assay was applied in adult male CD1 mice. A range of behavioural paradigms was used to investigate the locomotor effects, rewarding properties and antidepressant or anxiolytic potential of BU10119. Additional groups of mice were exposed to a single (1 × 2 h) or repeated restraint stress (3× daily 2 h) to determine the ability of BU10119 to block stress‐induced analgesia.Key ResultsBU10119 alone was without any antinociceptive activity. BU10119 (1 mg·kg−1) was able to block U50,488, buprenorphine and morphine‐induced antinociception. The κ antagonist effects of BU10119 in the tail‐withdrawal assay reversed between 24 and 48 h. BU10119 was without significant locomotor or rewarding effects. BU10119 (1 mg·kg−1) significantly reduced the latency to feed in the novelty‐induced hypophagia task and reduced immobility time in the forced swim test, compared to saline‐treated animals. There were no significant effects of BU10119 in either the elevated plus maze or the light–dark box. Both acute and repeated restraint stress‐induced analgesia were blocked by pretreatment with BU10119 (1 mg·kg−1). Parallel stress‐induced increases in plasma corticosterone were not affected.Conclusions and ImplicationsBU10119 is a mixed κ/μ receptor antagonist with relatively short‐duration κ antagonist activity. Based on these preclinical data, BU10119 has therapeutic potential for the treatment of depression and other stress‐induced conditions.Linked ArticlesThis article is part of a themed section on Emerging Areas of Opioid Pharmacology. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.14/issuetoc
In-vitro effect of pembrolizumab on different T regulatory cell subsets
Authors: Toor S M , Syed Khaja A S , Alkurd I , Elkord E 
Published: September 2017

Summary
Programmed death-1 (PD-1) and interactions with PD-ligand 1 (PD-L1) play critical roles in the tumour evasion of immune responses through different mechanisms, including inhibition of effector T cell proliferation, reducing cytotoxic activity, induction of apoptosis in tumour-infiltrating T cells and regulatory T cell (Treg) expansion. Effective blockade of immune checkpoints can therefore potentially eliminate these detrimental effects. The aim of this study was to investigate the effect of anti-PD-1 antibody, pembrolizumab, on various Treg subpopulations. Peripheral blood mononuclear cells (PBMC) from healthy donors (HD) and primary breast cancer patients (PBC) were treated in vitro with pembrolizumab, which effectively reduced PD-1 expression in both cohorts. We found that PD-1 was expressed mainly on CD4+CD25+ T cells and pembrolizumab had a greater effect on PD-1 expression in CD4+CD25− T cells, compared to CD4+CD25+ cells. In addition, pembrolizumab did not affect the expression levels of Treg-related markers, including cytotoxic T lymphocyte antigen-4 (CTLA-4), CD15s, latency-associated peptide (LAP) and Ki-67. Moreover, we report that CD15s is expressed mainly on forkhead box P3 (FoxP3)−Helios+ Treg in HD, but it is expressed on FoxP3+Helios− Treg subset in addition to FoxP3−Helios+ Treg in PBC. Pembrolizumab did not affect the levels of FoxP3+/−Helios+/− Treg subsets in both cohorts. Taken together, our study suggests that pembrolizumab does not affect Treg or change their phenotype or function but rather blocks signalling via the PD-1/PD-L1 axis in activated T cells.