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[PMID]: 29524919
[Au] Autor:Nawrot TS; Saenen ND; Schenk J; Janssen BG; Motta V; Tarantini L; Cox B; Lefebvre W; Vanpoucke C; Maggioni C; Bollati V
[Ad] Address:Centre for Environmental Sciences, Hasselt University, Hasselt, Belgium; Department of Public Health & Primary Care, Leuven University, Leuven, Belgium. Electronic address: tim.nawrot@uhasselt.be.
[Ti] Title:Placental circadian pathway methylation and in utero exposure to fine particle air pollution.
[So] Source:Environ Int;114:231-241, 2018 Mar 07.
[Is] ISSN:1873-6750
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:In mammals, a central clock maintains the daily rhythm in accordance with the external environment. At the molecular level, the circadian rhythm is maintained by epigenetic regulation of the Circadian pathway. Here, we tested the role of particulate matter with an aerodynamic diameter ≤ 2.5 m (PM ) exposure during gestational life on human placental Circadian pathway methylation, as an important molecular target for healthy development. In 407 newborns, we quantified placental methylation of CpG sites within the promoter regions of the following genes: CLOCK, BMAL1, NPAS2, CRY1-2 and PER1-3 using bisulfite-PCR-pyrosequencing. Daily PM exposure levels were estimated for each mother's residence, using a spatiotemporal interpolation model. We applied mixed-effects models to study the methylation status of the Circadian pathway genes and in utero PM exposure, while adjusting for a priori chosen covariates. In a multi-gene model, placental Circadian pathway methylation was positively and significantly (p < 0.0001) associated with 3rd trimester PM exposure. Consequently, the single-gene models showed relative methylation differences [Log(fold change)] in placental NPAS2 (+0.16; p = 0.001), CRY1 (+0.59; p = 0.0023), PER2 (+0.36; p = 0.0005), and PER3 (+0.42; p = 0.0008) for an IQR increase (8.9 g/m ) in 3rd trimester PM exposure. PM air pollution, an environmental risk factor leading to a pro-inflammatory state of the mother and foetus, is associated with the methylation pattern of genes in the Circadian pathway. The observed alterations in the placental CLOCK epigenetic signature might form a relevant molecular mechanism through which fine particle air pollution exposure might affect placental processes and foetal development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 2293465 MEDLINE  
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[PMID]: 29524918
[Au] Autor:Guimond S; Padani S; Lutz O; Eack S; Thermenos H; Keshavan M
[Ad] Address:Department of Psychiatry, Beth Israel Deaconess Medical Center, Massachusetts Mental Health Center Division of Public Psychiatry, MA 02115, USA; Department of Psychiatry, Harvard Medical School, Boston, MA 02115, USA. Electronic address: sguimond@bidmc.harvard.edu.
[Ti] Title:Impaired regulation of emotional distractors during working memory load in schizophrenia.
[So] Source:J Psychiatr Res;101:14-20, 2018 Mar 02.
[Is] ISSN:1879-1379
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Schizophrenia (SZ) patients exhibit deficits in emotion regulation that affect their daily functioning. There is evidence that the prefrontal cortex plays an important role in emotion regulation. However, it remains unclear how this brain region is involved in emotion regulation deficits in SZ, and how such deficits impact performance on cognitively demanding tasks. We examined how happy and fearful emotional distractors impact performance on working memory (WM) tasks of varying difficulty (0-back, 2-back), and brain activity using fMRI. Participants were 20 patients with SZ and 20 healthy controls (HC) matched on age, sex, race, and IQ. A significant 3-way interaction showed that SZ patients had lower performance compared to HC when exposed to fearful and happy distractors, but only during the 2-back task. Second-level fMRI between-group analysis revealed that compared to SZ patients, HC showed significantly greater increase in brain activity with WM load in the left IFG (BA 45) when exposed to fearful distractors. Less brain activity in this region was also associated with reduction in SZ patients' performance during higher WM load and the presence of fearful distractors. SZ patients had difficulty in performing a WM task when regulating emotions, and they failed to show the emotion-specific modulation of the left IFG observed in HC. These results suggest that SZ patients have difficulty with emotion regulation demands during effortful cognitive tasks. This also provides us with potential insight on how emotion regulation could be rehabilitated in SZ using cognitive training.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524886
[Au] Autor:Shan Z; An N; Qin J; Yang J; Sun H; Yang W
[Ad] Address:Clinical Laboratory, Children's Hospital Affiliated to Zhengzhou University, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou City, Henan Province, China.
[Ti] Title:Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/-catenin signaling.
[So] Source:Biomed Pharmacother;101:769-776, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Substantial evidence has demonstrated the involvement of long non-coding RNAs (lncRNAs) in the development and progression of colorectal cancer (CRC) via their regulation on cancer cell proliferation, apoptosis, invasion and metastasis pathways. The current study aimed to understand the role of lncRNA Linc00675 in the progression and metastasis of CRC and to identify the potential lncRNA-miRNA interactions and signaling pathways underlying the mechanisms of action of Linc00675 in CRC. Our data firstly demonstrated the down-regulation of Linc00675 in both CRC cells and clinical CRC tissues. Expression of Linc00675 was also relatively low in metastatic tumors and advanced tumors. Further studies also showed that overexpression of Linc00675 inhibited the proliferation, invasion and migration of CRC cells. In addition, our data also revealed the negative regulation of miR-942 by Linc00675 and the relatively higher expression of miR-942 in clinical CRC tissues. More importantly, the inhibitory effect of Linc00675 on proliferation, invasion and migration of HCT116 cells was also significantly attenuated in the presence of miR-942 mimic, suggesting that down-regulation of miR-942 represented one of the mechanisms by which Linc00675 inhibited the proliferation and metastasis of CRC. Furthermore, we also demonstrated the inhibition of Wnt/-catenin signaling in the Linc00675/miR-942 regulated pathway in CRC cells. Taken together, our findings suggested Linc00675 as a potential molecular marker and target for the diagnosis and treatment of CRC and enhanced the current understanding on the mechanisms of action of Linc00675 in CRC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524884
[Au] Autor:Noitem R; Yuajit C; Soodvilai S; Muanprasat C; Chatsudthipong V
[Ad] Address:Department of Physiology, Faculty of Science, Mahidol University, Ratchathewi, Bangkok, Thailand.
[Ti] Title:Steviol slows renal cyst growth by reducing AQP2 expression and promoting AQP2 degradation.
[So] Source:Biomed Pharmacother;101:754-762, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Overexpression of aquaporin 2 (AQP2) was observed and suggested to be involved in fluid secretion leading to cyst enlargement in polycystic kidney disease (PKD). The cyst expansion deteriorates the renal function and, therefore, therapies targeting cyst enlargement are of clinical interest. Of note, inhibition of vasopressin function using vasopressin 2 receptor (V2R) antagonist which decreased cAMP production along with AQP2 production and function can slow cyst growth in ADPKD. This finding supports the role of AQP2 in cyst enlargement. Steviol, a major metabolite of the sweetening compound stevioside, was reported to retard MDCK cyst growth and enlargement by inhibiting CFTR activity. Interestingly, its efficacy was found to be higher than that of CFTR -172. Since steviol was also found to produce diuresis in rodent, it is likely that steviol might have an additional effect in retarding cyst progression, such as inhibition of AQP2 expression and function. Here, we investigated the effect of steviol on AQP2 function and on cyst growth using an in vitro cyst model (MDCK and Pkd1 cells). We found that steviol could markedly inhibit cyst growth by reducing AQP2 expression in both Pkd1 and MDCK cells. Real-time PCR also revealed that steviol decreased AQP2 mRNA expression level as well. Moreover, a proteasome inhibitor, MG-132, and the lysosomotropic agent, hydroxychloroquine (HCQ) were found to abolish the inhibitory effect of steviol in Pkd1 cells. Increased lysosomal enzyme marker (LAMP2) expression following steviol treatment clearly confirmed the involvement of lysosomes in steviol action. In conclusion, our finding showed for the first time that steviol slowed cyst growth, in part, by reducing AQP2 transcription, promoted proteasome, and lysosome-mediated AQP2 degradation. Due to its multiple actions, steviol is a promising compound for further development in the treatment of PKD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524875
[Au] Autor:Jang HN; Back SK; Sung JH; Kang YS; Jurng J; Seo YC
[Ad] Address:Dept. of Environmental Engineering, Yonsei University, Wonju, 220-710, Republic of Korea.
[Ti] Title:The simultaneous capture of mercury and fine particles by hybrid filter with powder activated carbon injection.
[So] Source:Environ Pollut;237:531-540, 2018 Mar 07.
[Is] ISSN:1873-6424
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The hybrid filter (HF) was newly designed and operated with powder activated carbon (PAC) injection to capture mercury and fine particulate matter in the coal power plant. With PAC injection in HF operation, the capture efficiency of elemental mercury was clearly enhanced. When the injection rate of PAC increased from 0 to 20 mg/m , the speciation fraction of elemental mercury significantly decreased from 85.19% to 3.76% at the inlet of the hybrid filter. The speciation fraction of oxidized mercury did not vary greatly, whereas the particulate mercury increased from 1.31% to 94.04%. It was clearly observed that the HF played a role in the capture of mercury and fine PM by leading the conversion of elemental mercury as particulate mercury and the growth of PM via electrode discharge in the HF operation with PAC injection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 2293465 MEDLINE  
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[PMID]: 29524869
[Au] Autor:Melo S
[Ad] Address:Queen's Management School, Queen's University Belfast, Riddel Hall, 185 Stranmillis Road, Belfast, BT9 5EE, Northern Ireland, UK. Electronic address: s.melo@qub.ac.uk.
[Ti] Title:The role of place on healthcare quality improvement: A qualitative case study of a teaching hospital.
[So] Source:Soc Sci Med;202:136-142, 2018 Mar 02.
[Is] ISSN:1873-5347
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:This article examines how the built environment impacts, and is impacted by, healthcare staff day to day practice, care outcomes and the design of new quality and patient safety (Q&PS) projects. It also explores how perceptions of the built environment affect inter-professional dynamics. In doing so, it contributes to the overlooked interplay between the physical, social, and symbolic dimensions associated with a hospital's place. The study draws on 46 in-depth semi-structured interviews conducted at a large teaching hospital in Portugal formed by two buildings. Interview transcripts were analysed inductively using thematic analysis. The major contribution of this study is to advance the understanding of the interactions among the different dimensions of place on Q&PS improvement. For example, findings indicate that some of the characteristics of the physical infrastructure of the hospital have a negative impact on the quality of care provided and/or significantly limit the initiatives that can be implemented to improve it, including refurbishment works. However, decisions on refurbishment works were also influenced by the characteristics of the patient population, hospital budget, etc. Likewise, clinicians' emotional reactions to the limitations of the buildings depended on their expectations of the buildings and the symbolic projections they attributed to them. Nevertheless, differences between clinicians' expectations regarding the physical infrastructure and its actual features influenced clinicians' views on Q&PS initiatives designed by non-clinicians.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 2293465 MEDLINE  
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[PMID]: 29524868
[Au] Autor:Hunter BM
[Ad] Address:King's College London, Department of International Development, Strand Campus, London WC2R 2LS, UK. Electronic address: benjamin.hunter@kcl.ac.uk.
[Ti] Title:Brokerage in commercialised healthcare systems: A conceptual framework and empirical evidence from Uttar Pradesh.
[So] Source:Soc Sci Med;202:128-135, 2018 Mar 02.
[Is] ISSN:1873-5347
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In many contexts there are a range of individuals and organisations offering healthcare services that differ widely in cost, quality and outcomes. This complexity is exacerbated by processes of healthcare commercialisation. Yet reliable information on healthcare provision is often limited, and progress to and through the healthcare system may depend on knowledge drawn from prior experiences, social networks and the providers themselves. It is in these contexts that healthcare brokerage emerges and third-party actors facilitate access to healthcare. This article presents a novel framework for studying brokerage of access to healthcare, and empirical evidence on healthcare brokerage in urban slums in Lucknow, Uttar Pradesh. The framework comprises six areas of interest that have been derived from sociological and political science literature on brokerage. A framework approach was used to group observational and interview data into six framework charts (one for each area of interest) to facilitate close thematic analysis. A cadre of women in Lucknow's urban slums performed healthcare brokerage by encouraging use of particular healthcare services, organising travel, and mediating communications and fee negotiations with providers. The women emphasised their personal role in facilitating access to care and encouraged dependency on their services by withholding information from users. They received commission payments from healthcare programmes, and sometimes from users and hospitals as well, but were blamed for issues beyond their control. Disruption to their ability to facilitate low-cost healthcare meant some women lost their positions as brokers, while others adapted by leveraging old and new relationships with hospital managers. Brokerage analysis reveals how people capitalise on the complexity of healthcare systems by positioning themselves as intermediaries. Commercialised healthcare systems offer a fertile environment for such behaviours, which can undermine attainment of healthcare entitlements and exacerbate inequities in healthcare access.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 2293465 MEDLINE  
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[PMID]: 29524867
[Au] Autor:Pike IL; Hilton C; sterle M; Olungah O
[Ad] Address:School of Anthropology, University of Arizona, PO Box 20031, Tucson, AZ 85721, United States. Electronic address: ilpike@email.arizona.edu.
[Ti] Title:Low-intensity violence and the social determinants of adolescent health among three East African pastoralist communities.
[So] Source:Soc Sci Med;202:117-127, 2018 Feb 23.
[Is] ISSN:1873-5347
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Recently, strong pleas have emerged to place the health of adolescents on the global health agenda. To reposition adolescence front and center, scholars argue that we must work toward a richly contextualized approach that considers the role that social environments play in shaping the final stages of growth and development. We aim to contribute to this deeper understanding of the social determinants of global adolescent health by offering a case study of three nomadic pastoralist communities from northern Kenya. In addition to noteworthy political and economic marginalization, East African pastoralist communities also contend with chronic, low intensity intercommunity conflict. Data collected over five extensive visits from 2008 to 2011, include the 10-19 year olds from 215 randomly sampled Pokot, Samburu, and Turkana households. Using a case/control design, we sampled two sites per ethnic community: one directly affected and one less affected by intercommunity violence. Our nutritional findings indicate that teens ages 15-19 years old had significantly higher anthropometric values compared to younger teens. Living in a wealthier household is associated with greater height, body mass indices, and summed skinfolds for boys but not for girls. Anthropometric measures were influenced by household and community variation in the mixed-effects, multi-level regression models. The Self-Report Questionnaire (SRQ-20) was used to assess psychosocial health, with higher scores associated with living in a community directly affected by violence and having lost a loved one due to violence. Our findings highlight the unique nature of adolescent health challenges but also the central role even subtle differences across communities and households play in shaping young people's experiences. With few studies to document the lived experience of pastoralist youth as they move toward adulthood, examining how such challenging socioeconomic environment shapes health seems long overdue.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 2293465 MEDLINE  
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[PMID]: 29524863
[Au] Autor:Kasselman LJ; Vernice NA; DeLeon J; Reiss AB
[Ad] Address:Winthrop Research Institute and Department of Medicine, NYU Winthrop Hospital, Mineola, NY, USA. Electronic address: lkasselman@nyuwinthrop.org.
[Ti] Title:The gut microbiome and elevated cardiovascular risk in obesity and autoimmunity.
[So] Source:Atherosclerosis;271:203-213, 2018 Mar 02.
[Is] ISSN:1879-1484
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Cardiovascular disease associated with obesity and autoimmunity is the leading cause of death in these populations and significant residual risk remains despite current treatment approaches. Obesity, type 1 diabetes mellitus (T1DM), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE) are linked to chronic inflammation, and subjects with these disorders have characteristic shifts in their gut microbiome composition. Recent data suggest that alterations in gut microbial and metabolic composition may be responsible, in part, for induction of chronic inflammation, thus promoting cardiovascular disease. Common microbiome changes observed in obesity, T1DM, RA, and SLE include a decrease in the ratio of bacteria, such as Gram-positive Firmicutes to Gram-negative Bacteroidetes, as well as an overabundance or depletion of certain species, including Prevotella copri. The consequent effects of these shifts include alterations in the metabolic composition of the gut, hyper-activation of toll-like receptor 4 (TLR-4), upregulation of inflammatory pathways, e.g. c-Jun N-terminal kinase and nuclear factor-kappa B (NFκB), increased intestinal permeability, increased C-reactive protein, and increased levels of trimethylamine N-oxide (TMAO). Differential microbiome compositions may also explain sex differences observed in autoimmunity, where a male gut microbiome promotes anti-inflammatory processes as compared to a female pro-inflammatory gut microbiome. Intervention at the level of the microbiota appears to attenuate symptoms in these inflammatory syndromes with probiotic treatment, such as Lactobacilli, playing a uniquely beneficial role in restoring intestinal health, decreasing inflammation, and reducing cardiovascular disease. This review will discuss obesity, T1DM, RA, and SLE in the context of how each unique microbiome profile contributes to elevated cardiovascular risk.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 2293465 MEDLINE  
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[PMID]: 29524862
[Au] Autor:Damen MSMA; Dos Santos JC; Hermsen R; Adam van der Vliet J; Netea MG; Riksen NP; Dinarello CA; Joosten LAB; Heinhuis B
[Ad] Address:Department of Internal Medicine and Radboud Center for Infectious Diseases (RCI), Nijmegen, The Netherlands.
[Ti] Title:Interleukin-32 upregulates the expression of ABCA1 and ABCG1 resulting in reduced intracellular lipid concentrations in primary human hepatocytes.
[So] Source:Atherosclerosis;271:193-202, 2018 Mar 02.
[Is] ISSN:1879-1484
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:BACKGROUND AND AIMS: The role of interleukin (IL-)32 in inflammatory conditions is well-established, however, the mechanism behind its role in atherosclerosis remains unexplained. Our group reported a promoter single nucleotide polymorphism in IL-32 associated with higher high-density lipoprotein (HDL) concentrations. We hypothesize that endogenous IL-32 in liver cells, a human monocytic cell line and carotid plaque tissue, can affect atherosclerosis by regulating (HDL) cholesterol homeostasis via expression of cholesterol transporters/mediators. METHODS: Human primary liver cells were stimulated with recombinant human (rh)TNFα and poly I:C to study the expression of IL-32 and mediators in cholesterol pathways. Additionally, IL-32 was overexpressed in HepG2 cells and overexpressed and silenced in THP-1 cells to study the direct effect of IL-32 on cholesterol transporters expression and function. RESULTS: Stimulation of human primary liver cells resulted in induction of IL-32α, IL-32 and IL-32γ mRNA expression (p < 0.01). A strong correlation between the expression of IL-32γ and ABCA1, ABCG1, LXRα and apoA1 was observed (p < 0.01), and intracellular lipid concentrations were reduced in the presence of endogenous IL-32 (p < 0.05). Finally, IL32γ and ABCA1 mRNA expression was upregulated in carotid plaque tissue and when IL-32 was silenced in THP-1 cells, mRNA expression of ABCA1 was strongly reduced. CONCLUSIONS: Regulation of IL-32 in human primary liver cells, HepG2 and THP-1 cells strongly influences the mRNA expression of ABCA1, ABCG1, LXRα and apoA1 and affects intracellular lipid concentrations in the presence of endogenous IL-32. These data, for the first time, show an important role for IL32 in cholesterol homeostasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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